Eterinary Bstetrics: - Dr. S.Balasubramanian

VGO-421
VETERINARY OBSTETRICS
(1+1)
- Dr. S.Balasubramanian
VGO 411: VETERINARY OBSTETRICS (1+1)
MODULE-1: DEVELOPMENT OF FETUS - FETAL MEMBRANES - PLACENTA
PREIMPLANTATION CHANGES
When the embryo undergoes the cleavage and blastocyst formation, the uterus undergoes changes
preparing the way for implantation.
The characteristic changes during this phase are:
• The muscular activity and tonicity of the uterus is decreased to help to retain the blastocysts in
the uterine lumen.
• Blood supply to the uterine epithelium gets increased. In some species, this is more along the
side of the uterus at which implantation takes place.
• At the time of implantation
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o Amino acid and protein content shows marked changes in the uterine fluid.
o In rabbit, the concentration of most amino acids is much higher in uterine fluid at
implantation than in blood serum.
o Glycine, alanine, taurine and glutamic acid are particularly abundant and their
concentration is progesterone dependent.
o In cow, the concentrations of free amino acids in uterine fluid is high and is reported to
undergo cyclic variation.
• Changes occur in the secretory activity of glandular and surface epithelium of the
endometrium.
• High molecular weight compounds (proteins, carbohydrates, mucopolysaccharides) are broken
down, and low molecular weight derivatives, along with glycogen and fats accumulate. This
material along with cellular debris and extra vasated leukocytes in the uterine lumen forms the
histotrophe (Uterine milk).
• Before the chorioallantoic placenta is established, during the early period of uterine life, this
uterine milk provides nourishment for the embryo.
• In rabbits, about 80 h post coitum and in sheep from nine days blastocyst stage, histotrophe
play an vital role.
• In farm animals, the placenta is of epitheliochorial or syndesmochorial type and the association
between fetal and maternal blood is not very close.
• Histotrophic nutrition is therefore important not only in the early stages of uterine life, but
throughout gestation.
• The hormonal basis of implantation varies widely
o Progesterone plays a major role in determining the preimplantation changes in the
uterus.
o The balance between estrogen and progesterone is probably more important than the
absolute levels of either alone.
o In rats, estrogen priming is required for sensitizing the endometrium for implantation.
IMPLANTATION
• In animals, the term implantation often refers to the attachment of the placental membranes
to the endometrium.
INTRODUCTION
• True implantation is a phenomenon observed in rodents and humans.

• The conceptus/blastocyst that penetrates the uterine mucosa by penetrating and phagocytizing
the uterine luminal epithelium and “ buries” as they migrate into the uterine stroma.
• The conceptus temporarily disappears beneath the surface. This invasive process is
accompanied by transformation and proliferation of uterine stromal cells (referred to as
decidualization) in the vicinity of the developing blastocyst.
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• In contrast, implantation in domestic animals is superficial and non-invasive and involves
phases of trophoblast-uterine epithelial cell apposition and adhesion and never disappears
from the luminal compartment.
• When pig trophoblast is placed in an ectopic site, e.g., the kidney capsule, it does exhibit
invasive properties. This invasive property appears to result from blastocyst production of
proteolytic enzymes such as plasminogen activator; but, invasive implantation is prevented by
uterine epithelial secretion of protease (plasmin/trypsin) inhibitors that coat the blastocyst
and protect the uterus from this protease.
• During implantation in domestic animals, an outgrowth of extra-embryonic mesoderm
originates from the embryoblast and migrates between the trophectoderm and endoderm. This
mesodermal layer will split and combine with the trophectoderm to form the chorion and
endoderm to form the yolk sac.
IMPLANTATION IN PIGS
• Pig blastocysts begin to attach to the uterine surface on day 13 with attachment completed
across the trophoblastic surface between days 18 to 24.
• Attachment is through interdigitation of uterine and trophoblastic microvilli covering the
interface between the two layers, except where the trophoblast overlies the openings of
uterine glands.
• The trophoblastic surface in these areas becomes modified to form specialized absorptive
structures (areolae) that allow nutrient uptake by the developing conceptus.
IMPLANTATION IN RUMINANTS
• Placental attachment involves both caruncular and intercaruncular areas of the uterine
endometrium.
• A transitory attachment first occurs as cow and ewe trophoblasts develop finger-like villi
(papillae) that project into the lumen of the uterine glands. These papillae provide a temporary
anchor and absorptive structure for the conceptus as more complete attachment progresses.
• Loss of trophoblastic surface microvilli permits close surface contact with uterine epithelial
microvilli.
• The uterine epithelium presses into the trophoblastic surface, interlocking with the cytoplasmic
projections on the trophoblast surface until the trophoblast microvilli redevelop forming a
more complex attachment.
Binucleate Giant Cells (BNGCs)
• Attachment is characterized by the appearance of binucleate giant cells (characterized as being

quite large and have two nuclei) arising from uninucleate cells of the trophoblast.
• In the sheep, BNGCs first appear at about day 14 and in the cow, between days 18 and 20.
• These cells originate from the trophoblast cells and are believed to be formed continuously
throughout gestation.
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Binucleate giant cells(BNGCs)
Source: P.L.Senger (2003).
• BNGCs constitute around 20 per cent of the fetal placenta.

• During development, these cells migrate from the chorionic epithelium and invade and fuse
with under lying uterine surface epithelial cells to form multinucleate cells or a syncytium.
• The BNGCs are believed to transfer complex molecules from the fetal to the maternal placenta.
• The syncytium may be involved in immunologic protection of the conceptus or transfer of
placental lactogen synthesized by binucleate cells.
IMPLANTATION IN MARE
• Implantation or attachment does not occur until days 24-40.

• Early attachment is through interdigitation between surface epithelium of the embryonic
vesicle and uterine lining.
• Specialized chorionic girdle cell form around the spherical vesicle, detach around day 35 and
invade the uterine endometrium to form the endometrial cups, that produce equine chorionic
gonadotrophin.
Endometrial cups
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• Endometrial cup formation may protect the trophoblast from maternal immune attack.
• Microvillous attachment becomes more complex as the microvilli branch and coalesce to give
rise to thousands of micro-cotyledonary structures that hold the placenta firmly in place.
Microcotyledon
MATERNAL RECOGNITION OF PREGNANCY (MRP)
DEFINITION
Establishment of pregnancy involves interactions between two interdependent systems defined as:
• Uterus, and
• Conceptus (embryo and extra embryonic membranes)
Two Interdependent System
• At the appropriate time, the conceptus must produce steroid hormones and /or proteins to
signal its presence to the maternal system.
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• This signal is necessary for corpus luteum (CL) maintenance, production of progesterone and
continued endometrial development and secretory activity.
• This phenomenon was described by Short (1969) as “Maternal Recognition of Pregnancy”
(MRP).
MECHANISM OF MRP
• If the conceptus fails to signal its presence at exactly the correct time, the function of CL is
terminated by the luteolytic action of prostaglandin F2 alpha (PGF2 alpha) from the uterus. This
ensures that the female will return to estrus and mate at frequent intervals until a successful
pregnancy is established.
• Uterine PGF2 alpha, is produced by endometrium of cows, ewes, mares and sows and causes
morphologic regression of CL and cessation of progesterone production.
• The effect of conceptus is luteostatic, since progesterone production is maintained at a level
comparable to that of dioestrus during pregnancy.
• Basal secretion of luteinizing hormone (LH) from the anterior pituitary is also essential for CL
maintenance and function during pregnancy.
Non pregnant PGF2 alpha is released in an endocrine

direction during estrus cycle (non
pregnant) to cause regression of CL.
Pregnant Secretion is however, in an exocrine

direction during pregnancy and PGF2
alpha is, therefore, unable to exert its
luteolytic effect on the CL.
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TIME OF MATERNAL RECOGNITION OF PREGNANCY (MRP) IN DOMESTIC ANIMALS
Species Day of MRP Day of definite Attachment

Cow 16-17 18-22
Ewe 12-13 16
Mare 14-16 36-38
Sow 12 18
EARLY EMBRYONIC DEVELOPMENT
• There are certain terms which are commonly used in embryonic development. These terms
have subtly different uses depending on the species and the context in which they are used.
• Fusion of the male and female pronuclei (Syngamy) results in the zygote becoming an embryo.
TERMINOLOGY
The terms embryo, conceptus and fetus are often used interchangeably to describe the developing
organism.
• Embryo is defined as an organism in the early stages of development. In general, an embryo has
not acquired an anatomical form that is readily recognizable in appearance as a member of the
specific species. During early stages of development, it is impossible to distinguish the pig
embryo from the cow embryo, except by skilled embryologists.
• Fetus is defined as a potential offspring that is still within the uterus, but is generally
recognizable as a member of a given species. Fetus is often thought of as a more advanced form
of an embryo.
• Conceptus is defined as the product of conception. It includes:
o The embryo during the early embryonic stage.
o The embryo and extraembryonic membranes during the pre implantation stage, and
o The fetus and placenta during the post-attachment phase.
PRE-ATTACHMENT DEVELOPMENT OF EMBRYO
• Following fertilization, embryo must undergo certain developments before it is capable of

attaching to the uterus.
• Fertilization results in the formation of male and female nuclei and cell is called an ootid, the
largest single cell in the body and is characterized by having an enormous cytoplasmic volume
relative to nuclear volume.
• Fusion of the male and female pronuclei occurs and the single-celled embryo is now called a
zygote.
• The zygote undergoes a series of mitotic divisions called cleavage divisions dividing the embryo
into cells each of which are called blastomeres. As a result of the cleavage divisions an embryo
gains cell number but still contains the same total mass of cytoplasm it had when it was a 1-cell
zygote.
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• Each blastomere undergoes subsequent divisions yielding 4, 8 and then 16 daughter cells.
• In the early stages of embryogenesis, each blastomere has the potential to develop into
separate healthy offspring, a property called totipotency. Totipotency is a term used to
describe the ability of a single cell (blastomere) to give rise to a complete, fully formed
individual.
• When the resultant embryo is a solid ball of cells where individual blastomeres can no longer be
counted accurately, the early embryo is called a morula.
• Within the morula, compaction of the outer cells occur causing cells to separate into two
distinct populations, the inner and outer cells.
• Cells in the inner portion of the morula develop gap junctions that allow for intercellular
communication and may enable the inner cells to remain in a defined cluster.
• The outer cells of the morula develop cell-to-cell adhesions known as tight junctions that are
believed to alter the permeability of the outer cells.
• Fluid begins to accumulate inside the embryo. This fluid accumulation is brought about by an
active sodium pump in the outer cells of the morula that pump sodium ions into the center
portion of the morula. This build-up of ions causes the ionic concentration of the fluid
surrounding the inner cells of the morula to increase. As the ionic strength inside the morula
increases, water diffuses through the zona pellucida into the embryo and begins to form a fluid
filled cavity called a blastocele. The embryo is now called a blastocyst.
• The embryo becomes partitioned into two distinct cellular populations, the inner cell mass
(ICM) and the trophoblast (TE).
o The inner cell mass will give rise to the body of the embryo.
o The trophoblastic cells will become the fetal component of the placenta.
• As the blastocyst continues to undergo mitosis, fluid continues to fill the blastocoele and the
pressure within the embryo increases.
• Growth and fluid accumulation is accompanied by the production of proteolytic enzymes by the
trophoblastic cells that weaken the zona pellucida so that it ruptures easily as growth of the
blastocyst continues.
• Finally, the blastocyst itself begins to contract and relax. Such behavior causes intermittent
pressure pulses. These pressure pulses coupled with continued growth and enzymatic
degradation cause the zona pellucida to rupture.
• Zona develops a small crack or fissure through which the cells of the blastocyst squeeze out,
escaping from their confines.
• The blastocyst now becomes a free-floating embryo within the lumen of the uterus and is
totally dependent on the uterine environment for survival.
DEVELOPMENT OF EXTRAEMBRYONIC MEMBRANES
• Following hatching, the conceptus undergoes massive growth.

o In the cow, the blastocyst is about 3 mm in diameter around day 13, which undergoes
maximum growth to 250 mm in length within the next four days and appears as a
filamentous thread. By day 18 of gestation, the blastocyst occupies space in both uterine
horns.
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o In the sow, the development of blastocyst is even more dramatic, where it grows from
2mm spheres on day 10 to about 200 mm in length in the next 24-48 h reaching lengths
of 800-1000 mm by day 16 (growth is at a rate of 4-8 mm/h).
• The dramatic growth of the conceptus is due largely to development of a set of membranes
called the extraembryonic membranes.
• The pig, sheep and cow are characterized as having filamentous or threadlike blastocysts prior
to attachment.
• In the mare, however, blastocysts do not change into a thread like structure but remain
spherical.
• The extraembryonic membranes are a set of four anatomically distinct membranes that
originate from the
o Trophoblast
o Endoderm
o Mesoderm, and
o Embryo.
• As the hatched blastocyst begins to grow, it develops an additional layer called primitive
endoderm just beneath, but in contact with the inner cell mass which continues to grow
downwards eventually lining the trophoblast.
• At the same time, it also forms an evagination at the ventral portion of the inner cell mass to
form the yolk sac, a transient extra embryonic membrane that regresses in size as the
conceptus develops.
• As the blastocyst continues to expand, the newly formed double membrane (the trophoblast
and mesoderm) becomes the chorion. Further development of the blastocyst causes the
chorion to push upward in the dorso lateral region of the conceptus and begins to surround it.
• The chorion begins to send “wing-like” projections above the embryo, the amnion begins to
form. Fusion of the chorion over the dorsal portion of the embryo results in formation of a
complete sac called amnion around the embryo.
• The amnion is filled with fluid and serves
o To hydraulically protect the embryo from mechanical perturbations.
o As an anti-adhesion material to prevent tissues in the rapidly developing embryo from
adhering to each other.
• The amnionic vesicle can be palpated in the cow between days 30 and 45 and feels like a small,
turgid balloon inside the uterus. The embryo, however, is quite fragile during this early period
and amnionic vesicle palpation should be performed with caution.
• During the same time that the amnion is developing, a small evagination from the posterior
region of the primitive gut begins to form. This sac-like evagination is referred to as the
allantoic sac that collects liquid waste from the embryo.
• As the embryo grows, the allantois continues to expand and eventually will make contact with
the chorion.
• When the allantois reaches a certain volume, it presses against the chorion and eventually fuses
with it. When fusion takes place the two membranes are called the allantochorion. The
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allantochorionic membrane is the fetal contribution to the placenta and will provide the surface
for attachments to the endometrium.
SCHEMATIC REPRESENTATION OF EXTRAEMBRYONIC MEMBRANES DEVELOPMENT
Source: Redrawn from Patten (1964). Foundations of embryology, McGrawHill.
FORMATION AND DIFFERENTIATION OF GERM LAYERS
• During early differentiation, cells at one pole of the blastocyst, the germ disc give rise to three
separate layers of cells:
Derivation of various body organs by progressive Ectoderm, the outermost layer, forms
differentiation and divergent specialization the anterior pituitary, skin and all its
derivatives ie., CNS, sense organs,
sweat glands, mammary glands and
other skin glands, nails, hair, hooves
and lens of the eye.
Mesoderm, the layer between the
ectoderm and endoderm give rise to
connective tissues, vascular system,
bones, muscles, and as well as the
adrenal cortex, reproductive system,
kidney, urinary ducts.
Endoderm, the innermost layer,
forms the lining of the gut, its glands,
liver, and the bladder.
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• The primary sex cells may be derived from either the mesoderm or the ectoderm.
• The body segment or somites, which develop from the outer somatic layer of mesoderm,
differentiate into three regions and forms different parts of the fetus.
• The first region develops into the vertebrae, which encase the neural tube.
• The second region forms the skeletal muscles, and
• The third region forms the connective tissues of the skin.
• Differentiation of the somite region starts on the 19 th day after ovulation in cattle, the number
increases rapidly to 25 on 23 rd day, 40 on 26 th day and 55 on 32nd day.
DEVELOPMENT OF FETAL MEMBRANES
INTRODUCTION
The fetal or extra embryonic membranes serve as
• Protection of the embryo
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• A means of getting nutrients (from dam to fetus)
• In caring for fetal waste products, and
• Synthesis of enzymes and hormones.
The fetal membranes consists of
• Primitive yolk sac

• Amnion
• Allantois, and
• Trophoblast or chorion (combined with allantois forms the chorioallantois).
The first two structures develop early in the life of the embryo of domestic animals and only function a
short period of several weeks until the chorio allantois develops.
YOLK SAC
• It is a primitive structure.
• Develops early in the embryonic period from the endoderm.
• In ruminants and swine, it disappears after a short period of time. But persists for 4-6 weeks in
horse before it becomes a remnant in the fetal membranes.
• Prior to formation of the amnion, the blastocyst or blastodermic vesicle and then the yolk or
vitelline sac perform limited functions.
• Under the influence of progesterone from the corpus luteum (CL), the uterine glands produce a
secretion called “uterine milk”. This contains fat globules, proteins, organic and inorganic solids
and possibly other nutrients.
• Nutrition for the early embryo is derived by the absorption of uterine secretion by the
blastocyst and yolk sac and for early fetus by the chorioallantois.
AMNION
Source: S.Balasubramanian, TANUVAS, Personal Collection
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• It is an ectodermic vesicle that arises from an outfolding of the chorion or from a space in the
inner cell mass of the blastocyst, as a double walled sac that completely surrounds the fetus
except at the umbilical ring.
• The inner layer of this double-walled sac is the "true amnion" and the outer layer is the "false
amnion", amniotic chorion, or portion of the trophoblast or serosa over the true amnion.
AMNIOTIC FLUID
• Clear, colourless and mucoid in nature.
Source
• In early to mid gestation, it is probably from the amniotic epithelium and from fetal urine as the
fluid is quite watery.
• As gestation advances, the allantoic fluid increase in volume while the amniotic fluid volume
remains fairly static but becomes viscid and glairy because the bladder sphincter prevents
further release of urine in to the amniotic cavity.
• The probable source of mucoid amniotic fluid is then the secretions of the nasopharynx and
saliva of the fetus.
Volume
• Volume of the amniotic fluid is regulated by swallowing of the fetus and does not inhale in to
the lungs.
Amounts present toward the end of gestation
Species Amount (in ml)
Cow 2000 – 8000
Mare 3000 – 7000
Goat 400 – 1200
Ewe 350 – 750
Sow 40 – 200
Dog and Cat 8 - 30
AMNIOTIC PLAQUES
• Most noticeable during 3-7 month of gestation.

• Number varies widely and consists of edematous epithelial cells that are sometimes
keratinized.
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• Amniotic proliferations are found to a lesser degree in horses, sheep and goats but not in swine
and carnivores.
• Etiology and significance is not known and they are apparently not due to infectious agents
either bacterial or viral and there are no inflammatory lesions associated with these plaques.
Amniotic plaques on the inner surface of Amniotic plaques on the umbilical cord
amnion
In the bovine amnion, on the inner surface Also observed in the portion of the amnion
there are small 1/16 -1/2 inch, irregular covering the umbilical cord of bovine fetus
shaped flat, white, elevated epithelial as coarse, elongated villi or papillary
thickenings called Amniotic plaques. elevations.
FUNCTIONS OF AMNION
• Provide a watery medium in which the embryo can develop free from distortions that would
arise from being pressed against rigid surrounding structures.
• Amniotic fluid contains pepsin, a diastatic ferment, a lipolytic ferment, protein, fructose, fat and
salts.
• It is bactericidal and prevents adhesions.
• It prevents adhesions of embryonic skin to the amniotic membrane.
• It may aid in the initial steps of implantation when the expanding chorionic sac is brought in to
close apposition with the endometrium.
• During parturition, lubricant property due to slippery and mucoid consistency facilitates
expulsion of fetus.
ALLANTOIS
• Arises during the second or third week of gestation in bovine fetuses as an outpocketing of the
hind gut and consists of entoderm covered by vascular layer of splanchnopleuric mesoderm.
• As the allantois grows and enlarges it extends between the true and false amnion. The outer
layer of the allantois fuses with the trophoblast, false amnion, or serosa to form the
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chorioallantois. The inner layer, largely devoid of blood vessels, lies against the amnion and
invests the allantoic portion of the umbilical cord.
• In larger domestic animals, it is completely formed by 24–28 days after conception and extends
the entire length of fetal membranes except the undilated apices of the chorionic or
blastodermic vesicle in sheep, pig and cow. Because they are not supplied with blood vessels
these undilated apices atrophy and become necrotic and are called the necrotic tip of the
chorioallantois.
Necrotic tip
ABNORMAL FINDINGS
• In fetal monsters or certain types of fetuses carried overtime the amount of amniotic fluid is
increased up to 8–10 times and is referred to as Hydrops amnii.
• Probably because of perinatal asphyxia or hypoxia in the cow and sheep fetus, there is presence
of meconium in the amniotic fluid, causing staining and smearing of the fetus.
• In rare instances, hair balls may be found in the amniotic fluid, especially in prolonged
gestations associated with fetal giantisms.
ALLANTOIC FLUID
• Clear, watery and amber in colour.

• Contains albumen, fructose and urea.
Source
• Allantoic cavity stores the waste products of the fetal kidneys, which pass to it from the bladder
through the umbilical cord by means of the urachus.
Volume
• Towards end of gestation the volume of allantoic fluid varies.
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Species Amount (in ml)
Cow 4000–15,000
Mare 8000–18,000
Sheep and goat 500–1500
Sow 100–200
Dog 10–50
Cat 3–15
HIPPOMANES
The cow, horse, sheep, goat and pig

allantoic fluid contains amorphous,
semisolid, amber coloured, soft, pliable,
rubber like, irregular shaped masses or
bodies, thinner at the edges and thicker in
the center 2.5–15.0 cm in diameter and
from 0.3–3.8 cm in thickness floating in
the fluid. These bodies are called as
Hippomanes.
• In few cases these masses, resemble fibrin in appearance and consists of a central nucleus of
desquamated cell debrii upon which are deposited a denatured mucoprotein complex and
minerals mainly calcium phosphate in a concentric manner and these have higher specific
gravity than the fluid and will sink to the bottom of the cavity. These are referred to as
“Allantoic Calculi”.
FUNCTIONS OF ALLANTOIS
• Allantoic fluid is composed of hypotonic urine, maintains the osmotic pressure of the fetal
plasma and prevents fluid loss to maternal circulation.
• The pressure of the fetal fluids upon their membranes aids in the dilation of the cervix at
parturition.
ABNORMAL FINDINGS
• Hydrallantois is a condition wherein occasionally excessive amounts of allantoic fluid 40–160

litres or more may accumulate in the allantoic cavity.
• This excessive fluid has the specific gravity and characteristics of a transudate.
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• The cause is most commonly due to the vascular disturbance in the allantois.
• There is some evidence that gonadal hormones may influence the amounts of allantoic fluid.
CHORIOALLANTOIS
• It is formed by the fusion of the outer layer of the vascular allantois and the trophoblast,
chorion or serosa.
• This structure is richly supplied with blood vessels communicating with the fetus and in
intimate contact with the endometrium.
• It is designed to carry metabolic interchanges of gases, nutrients and wastes between the fetal
and maternal circulations.
• Allantois chorion is the fetal placenta, solids and most bacteria ordinarily cannot pass unless
disease of the chorion allows their penetration. Certain bacteria, viruses and parasitic larvae
can pass through the intact placental barrier.
• In the cow, pig and sheep, the allantois is attached to the amnion at various points. This divides
the allantois in to a number of compartments.
• The necrotic tips of the chorion, found at the apices of the chorio allantois, are observed in
sheep, cow and pig and are usually about 1–2.5 cm long and about 0.3 cm in diameter.
BOVINE FETAL MEMBRANES WITH FETUS IN SITU
• The chorioallantoic placentation is characteristic of all farm animals.

• Fusion of the outer layer of the allantois with the chorion, the fetal vessels in the allantois come
in to close apposition to the umbilical arteries and veins located in the connective tissue
between the allantois and chorion.
• The cotyledons are distributed over the chorioallantoic membrane and the amniochorion.
Bovine fetal membranes
A ~ 60 day fetus showing the allantoic and amniotic cavities
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PLACENTA
WHAT IS PLACENTA?
• It is a unique organ that develops in mammalians for the development of the fetus.
• It is an apposition of fetal membranes to the endometrium to permit physiological exchange
between the fetus and the mother.
• The placenta is composed of two parts:
o The fetal placenta or allantois chorion
o The maternal placenta or endometrium.
INTRODUCTION
• The yolk sac or amniotic chorion act as primitive placenta for a few weeks in the early
embryonic period.
• Allantois develop as a diverticulum of hind gut and fuses with the chorion (trophoblastic
capsule of the blastocyst) to form the chorioallantoic placenta.
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• The blastocyst gets attached to the endometrium and the fetal membranes including the
allantois chorion develop during the first month or more of gestation.
• At this time, the villiform projections of the chorion and the maternal crypts in the
endometrium are rudimentary, small and friable, and the nutrition is from the uterine
secretions.
• The easy separation of the two structures i.e., (maternal and fetal placentae) is prevented, not
until the end of the first third of gestation because they do not become sufficiently intimate
and complex.
NON-REJECTION OF PLACENTA IN PREGNANT ANIMALS
• In hemochorial placentas (man and rodents), greater the trophoblastic invasiveness, the greater
the necrosis of both chorionic and endometrial tissue thus resulting in development and
deposition of a mechanical acellular barrier of acid mucopolysaccharide
• In epitheliochorial placentas, (cow, sheep, mare and sow) where the interdigitation of microvilli
of the chorion or trophoblast and endometrial epithelium are closely apposed, no extensive
degeneration or deposition of fibrinoid is present.
• Therefore, in the former (hemochorial placentas) an acellular mechanical barrier and in the
latter (epitheliochorial placentas), the absence of trophoblastic antigenecity offer reasonable
explanations for the retention of the placental homograft.
• The sire contributes half of the genetic makeup of the fetus and placenta and hence there
should be sufficient tissue incompatibility to induce an immune reaction in the dam and
subsequent rejection of the conceptus.
• The inability of the immunologically active maternal cells to penetrate in to fetal circulation
may also be important.
CLASSIFICATION OF PLACENTA
• Anatomical
• General
• Based on the tissues or structures that intervene between the maternal and fetal blood
• Based on sites of chorionic attachment
ANATOMICAL CLASSIFICATION
It is divided in to 4 general types based on their shape as:
• Diffuse
• Cotyledonary
• Zonary
• Discoidal
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GENERAL CLASSIFICATION
Deciduate or conjoined or placenta vera
• Seen in man and rodents and in a slightly modified form in the dog and cat.
• In this type, the decidua composed of portions of the maternal epithelium or endothelium,
submucosa, decidual cells and the fetal placenta are shed at parturition leaving the portion of
the endometrium denuded.
Indeciduate or adeciduate
• Seen in swine, horses and ruminants.

• In this type, the fetal membranes and placenta are expelled at the time of parturition, leaving
the endometrium intact except in ruminants in which only the surfaces of the carcuncles are
devoid of epithelium after the caruncles sloughs about 6–10 days following parturition.
CLASSIFICATION BASED ON THE TISSUES OR STRUCTURES THAT INTERVENE

BETWEEN THE MATERNAL AND FETAL BLOOD
Epitheliochorial type (Horse, Pig, Cow and Sheep)
• In this six structures, the endothelium, connective tissue, epithelium of the endometrium and
the trophoblast or the chorion, mesenchyme and and endothelium of the fetal tissue separate
the maternal and fetal blood.
Syndesmochorial (Ruminants)
• All tissues of the previous type are present with the exception of the maternal epithelium. The
loss of uterine epithelium was previously considered to occur in the placentomes in this type by
phagocytosis and cytolysis by the cells of the trophoblast.
Endotheliochorial (Dog and Cat)
• This has four structures seperating the maternal and fetal blood. i.e., the endothelium of the
uterine vessels and the chorion, mesenchyme and endothelium of the fetal tissues.
Haemochorial (Man and Rodents)
• This has only the fetal tissues of the chorion, mesenchyme and endothelium that lie or bathe in
a lake of maternal blood since all the maternal tissues have been eliminated.
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GROSSER'S CLASSIFICATION OF THE PLACENTAE OF DOMESTIC ANIMALS
Source: Redrawn from S.J.Roberts (1971).
BASED ON SITES OF CHORIONIC ATTACHMENT
• In 1604, Fabricius introduced a classification based on the appearance of the sites of chorionic
attachment to the endometrium.
• The four main placental types, now known as
o Diffuse
o Cotyedonary
o Zonary, and
o Discoidal.
DIFFUSE PLACENTA
22
• It is found in wide range of species, including pigs, horses, camels, lemurs, whales, dolphins,
kangaroos and possums.
• The villi of the chorion are distributed more or less evenly over the entire surface of the
chorionic sac.
• The villi interdigitate with corresponding depressions or villi in the uterine epithelium, and
physiological exchange take across these surfaces.
• The most striking feature of the ontogeny of the fetal membranes in the pigs is that the
membranes undergo a rapid and dramatic elongation between days 6 and 12 of gestation,
during which time the 2 mm spherical vesicle grows in to a filament of up to 1 m in length.
• This elongation is due to a proliferation of trophoblastic tissue.
• Although it is well recognized that the fetal placenta can produce gonadotrophic hormones
during pregnancy in many species, the horse always appeared to be an exception to the general
rule.
• Equine chorionic gonadotrophin was known to be produced by ulcer-like structures on the
inner surface of the uterus, the endometrial cups, and hence it was assumed to be a maternal
hormone.
• Studies of Twink Allen et.al., in cambridge have shown conclusively that endometrial cup tissue
is fetal in origin after all, and its mode of formation and regression are of great fundamental
interest.
ENDOMETRIAL CUPS
• A distinct belt of elongated trophoblast cells forms around the circumference of the chorionic
sac just below the margins of the allantois; this structure is known as chorionic girdle.
• By 42 days of gestation the allantois fuses with almost the entire chorion, and the chorionic
girdle remains below the allantois, now close to the abembryonic pole.
• Starting on about the 35 th day of gestation, cells become detached from the girdle to
penetrate the maternal endometrium and burrow deep in to the stroma, where they enlarge to
form the characteristic “decidual cells” of the endometrial cup.
• On about the 40 th day, the cup tissue becomes visible to the naked eye as a band running
around the circumference of the pregnant uterine horn, and equine chorionic gonadotrophin
first appears in maternal circulation.
• Endometrial cup development and gonadotrophin levels increase to maximum by about day 60,
and thereafter the titres begin to fall as the decidual cells become surrounded by a mass of
lymphocytes.
• Eventually, the cup tissue is sloughed off from the surface of the uterus in to the uterine lumen,
a process that bears a remarkable histological resemblance to a typical graft rejection reaction.
• The subsequent development of the horse fetal membranes is by expansion of the chorionic
sac, which extends in to both the gravid and non gravid horns of the uterus, with the chorio-
allantoic placenta being in contact with the endometrium.
• The complete outer surface of the chorion, with the exception of the area overlying the sites of
endometrial cups and the cervix, is covered in tufts of short villi – Micro cotyledons.
23
Diagrammatic representation of morphogenesis of endometrial cups and their eventual sloughing
and conversion, in some cases, into allanto-chorionic pouches
Source: O.J.Ginther (1992)
COTYLEDONARY PLACENTA
• The cotyledonary placenta is characteristic of the ruminants; instead of being uniformly

distributed over the entire surface of the chorion, the chorionic villi are clumped together in to
well developed circular regions known as cotyledons.
24
• These cotyledons develop only in those regions of the chorion that overlie predetermined
aglandular areas of the endometrium known as the caruncles.
• The fetal cotyledon and maternal caruncle unite to form a placentome, and these placentomes
are the only sites of maternal-fetal exchange, the intercotyledonary chorion being devoid of villi
and unattached to the endometrium.
• The number of caruncles varies greatly among species from as few as three or four per uterine
horn in the roe deer, rein deer and Pere David’s deer up to 180 in the goat and giraffe.
PLACENTOME
• Cotyledon, the fetal placenta produce villi which projects in to the crypts of the maternal
caruncle, that becomes greatly enlarge. These two structures, the maternal caruncle and fetal
cotyledon in ruminants is termed as placentome.
• In pregnant cows, the convex uterine caruncle is elevated above the endometrium like a
button, with the concave fetal cotyledon grasping it.
• In pregnant ewe, the maternal caruncle is also elevated above the endometrium but it is
concave in shape, with the fetal cotyledon fitting in to it.
ACCESSORY PLACENTOMES
25
• The endometrium between the caruncles is called the inter caruncular endometrium and the
fetal placenta between the cotyledons is called the inter cotyledonary placenta.
• This area normall does not take part in placental functions once the placentomes are formed.
• Sometimes due to uterine disease or due to lack of placentomes, primitive placental structures,
simulating a diffuse placenta, develop in this area between the allantois chorion and the
endometrium. These are referred to as adventitious placentae or accessory placentomes.
These may be few in number or they may involve a large portion of the inter caruncular endometrium
and chorion. If extensive and numerous, then pregnancy is usually insecure and the possibility of
subsequent gestation is doubtful.
ZONARY PLACENTA
• It is characteristic of the carnivores, and is the result of an aggregation of chorionic villi to form
a band that encircles the equatorial region of the chorionic sac.
• It may be complete, as in dog and cat, or incomplete, as in bears, seals and mustelids.
• The yolk sac persists as a vestigial structure floating in the allantoic fluid, whilst the
chorioallantois remains as an oblong, fluid filled sac, with its girdle of placental villi.
• Incomplete zonary placenta may resemble the single or double discoid type, but the zonary
placenta always has a central or marginal effusion of the maternal blood (the haemophagous
organ). In dogs, this forms a bright green margin to the vivid red placental attachment zone.
• Zonary placenta is also present in the elephant, and related species. They seem to develop from
a diffuse placenta, in which the chorionic villi at the polar areas of the chorionic sac
subsequently regress.
DISCOID PLACENTA
• It is found in a mixed group of mammals, including man and mouse, bats and rats, rabbits,
hares.
• The chorionic disc may be single (man) or double (monkey).
• However, that not all primates have interstitial implantation resulting in the formation of a
discoid placenta.
26
CLASSIFICATION OF CHORIOALLANTOIC PLACENTAS
Species Classification of Chorioallantoic Placentas
Chorio Villous Pattern Maternal-Fetal Loss of Maternal

Barrier Tissue at Birth
Pig Diffuse Epitheliochorial None (nondeciduate)
Mare Diffuse and Epitheliochorial None (nondeciduate)
Microcotyledonary
Sheep, goat, cow, Cotyledonary Epitheliochorial None (nondeciduate)
water buffalo
Dog, cat Zonary Endotheliochorial Moderate (deciduate)
Man, monkey Discoid Hemochorial Extensive (deciduate)
PLACENTAL FUNCTIONS
• The placenta functions as a multiorgan performing many functions and substituting for the
fetal:
o Gastro intestinal tract
o Lung
o Kidney
o Liver, and
o Endocrine glands.
• In addition, the placenta separates the maternal and fetal organism, thus ensuring the separate
development of the fetus.
27
PLACENTAL EXCHANGE
• The blood of fetus and dam never come in to direct contact. Yet, the two circulations are close
enough at the junction of chorion and endometrium so that oxygen and nutrients can pass from
the maternal blood to the fetal blood, and waste products in the opposite direction.
• The placental membrane controls the transfer of a wide range of substances by several
processes.
• Simple diffusion: The movement of molecules from an area of high concentration to an area of
low concentration.
• Most molecules of physiologic importance are transferred by some active transport, thus they
can be “Pumped” against a concentration gradient allowing the embryo to accumulate higher
concentrations of nutrients that exist in the maternal blood.
CLASSIFICATION OF TRANSFER OF SUBSTANCES
Group Physiologic role Substances Exchange mechanism

I Maintenance of biochemical Electrolytes, water and Rapid diffusion
homeostasis or protection respiratory gases
against sudden fetal death
II Fetal nutrition Amino acid, sugars and Predominantly by active
most water soluble transport system
vitamins
III Modification of fetal growth or Hormones Slow diffusion
</B<> the maintenance of pregnancy
IV Immunologic or toxic Drugs, anaesthetics, Rapid diffusion
importance plasma proteins,
antibodies and whole cells Pinocytosis or leakage
through pores in placental
membranes
RESPIRATION (O2 and CO2 )
• There many similarities between gases exchange across the placenta and the lungs.
• The major difference, however, is that in the placenta it is a fluid to fluid system whereas , in
the lungs it is a gas to fluid system.
• The process of transfer of O2 from maternal to fetal blood involves its dissociation from the
maternal blood, its diffusion through the placental membrane and finally its combination with
fetal haemoglobin.
• The umbilical arteries carry unoxgenated blood from the fetus to the placenta, while the
umbilical veins carry oxgenated blood in the reverse direction.
SYSTEMS OF GAS EXCHANGE
• The gas exchange in the placenta takes place through four basic systems.
28
o Concurrent
o Countercurrent
o Multivillous
o Pool
• The efficiency of oxygen exchange varies with the particular system. It is greatest in the counter
current system and least in the concurrent system. The efficiency of the multivillous system is
intermediate between the above mentioned systems. In the pool system, gas exchange is less
than in the multivillous system but is comparable to a concurrent system.
• It is difficult to ascertain which of these systems is primarily involved in a particular species and
probably some species may contain more than one system.
• The oxygenated blood from the dam is carried to the fetus through the tributaries of umbilical
veins whereas the tributaries of umbilical artery carry the oxygenated blood from the fetus.
• Oxygen and carbon dioxide pass through the membranes by diffusion which is regulated by
blood pressure.
• On account of the low pH in the placenta, the oxygenated haemoglobin from the dam is readily
disssociated thereby releasing oxygen for fetal haemoglobin.
• Carbon dioxide is readily transferred from the fetus to the dam. The placenta thus acts like a
lung.
TRANSPORT OF WATER
• Water moves very freely between the dam and fetus.

• Of the total substances absorbed by the fetus 77% is water.
• However, the water moves from the dam to fetus against the osmotic gradient and low
concentration of plasma proteins.
TRANSPORT OF INORGANIC NUTRIENTS
• Sodium is much restricted in the passage through placenta.

• Iron content is much higher in fetus, which is stored in liver, spleen and bone marrow.
• The transfer of trace elements like copper is readily effected. This element also accumulates in
the liver.
• Calcium and phosphorus enter the fetal blood against the concentration gradient. Depletion of
calcium and phosphorus reserves from the dam occurs in cases of low plane of nutrition.
• Fetal blood comprises of 70–80% fructose whereas glucose predominates in maternal blood.
Probably glucose is formed in the placenta and stored in the fetal liver which serves as a reserve
energy source.
• Placenta is not permeable to fat, but the fatty acids and glycerol pass freely.
• Vitamin A, D and E are obstructed by placenta and hence their concentration in fetus is much
lower. Since water soluble vitamins are synthesized in the rumen their concentration in fetus
has not been studied.
29
• Placenta is also permeable to all hormones, particularly gonadotrophins, steroids and insulin.
The gonadotrophic hormones pass easily through the placenta causing enlargement of fetal
gonads.
• Hormones such as oestrogens, progesterone and gonadotrophins are produced in considerable
amounts by the placenta.
• Fluid waste products like urea of the fetal metabolism escape through the placenta to the dam
which thus has a kidney like function.
30
MODULE-2: PRE-NATAL DEVELOPMENT-HORMONAL CONTROL OF GESTATION -

DURATION OF PREGNANCY
DEFINITION
• The gestation period or pregnancy period is the period from fertilization or conception to
parturition or the birth of young one.
• During this period single cells divide and develop in to highly organized individuals.
INTRODUCTION
• This antenatal period is the least understood and probably one of the most important periods
of life.
31
• The mortality rate of the ovum, embryo or fetus during this period is much greater than for any
other period of equal length after birth.
• Because they are usually unrecognized, early death of the fertilized ovum, or the small embryo
with resulting resorption or abortion is often considered as sterility or infertility.
PRE-NATAL DEVELOPMENT
• The pre-natal development of farm animals may be divided in to three main periods based on
the size of the individual and the development of its tissues and organs.
o Period of ovum or blastula.
o Period of embryo and organogenesis.
o Period of fetus and fetal growth.
PERIOD OF OVUM OR BLASTULA
• In cow it is about 10-12 days.

• It extends from the time of fertilization that usually occurs within a few hours after ovulation,
to the development of the zygotes primitive fetal membranes in the uterus.
• In domestic animals, the size of the ovum not including the zona pellucida is about 120-180 µm
at the time of fertilization and the shedding of the second polar body.
• During this period, division of the fertilized ovum progresses in the region of the ampullary
isthumic junction of the oviduct to the morula stage characterized by the inner and outer cell
masses totalling about 16-32 cells.
• In sows, on the third day and 4 th to 5 th day in other domestic animals the morula enters the
uterus.
• By 6-10 days after fertilization the zona pellucida fragments and a blastocyst is formed
composed of the embryoblast or inner cell mass and trophoblast or outer cell mass and fluid.
• By 11 days in the ewe and 12 days in the cow, the blastocyst is about 1 and 1.5 mm in diameter
respectively and elongation of the blastocyst does not occur.
• During this period, the defective ova die and are absorbed. The corpus luteum (CL) develops
and produces progesterone, a hormone necessary for the growth and preparation of the
endometrium so a favourable environment for the ovum and embryo will be present in the
uterus.
PERIOD OF EMBRYO AND ORGANOGENESIS
• It extends from 12-15 days to about 45 days of gestation in cow, 11-34 days in ewes, 12-55 to
60 days in horse.
• During this period the major tissues, organs and systems of body shape occur so that by the end
of this period the species of the embryo is readily recognizable. This usually coincides with the
development of the eyelids.
• The trophoblast elongates starting at 12 days in the ewe and 14 days in the cow.
• By 18-19 days of gestation in the cow, the trophoblast may extend in to the opposite horn.
32
• In horse, dog, and cat the trophoblast does not elongate but remains oval during this period
causing a localized enlargement in the uterus helpful in early pregnancy diagnosis.
• By 22 days - heart is crudely formed and beating
• By 25 days the neural tube is closed
• The allantois is well developed, anterior limb buds are formed, eye and brain development is
well advanced.
• In the cow, as in other animals, attachment of the fetal membranes is a gradual process that
begins with the formation of the first villi about 30 days of gestation and progresses to a
primitive attachment of the chorioallantois to the endometrium in the caruncular areas about
33-36 days of gestation.
• Until the well developed attachment of the chorion to the endometrium, the nourishment of
the ovum and embryo is provided by the secretion of the uterine glands called "Uterine milk" a
yellowish or whitish, thick, opaque secretion grossly resembling and occasionally mistaken as
for a purulent exudate.
• During this period,
o Severe teratological defects or anomalies of development occur.
o Embryo may die and be expelled unnoticed at the next estrum.
o Becomes macerated and absorbed without external signs.
PERIOD OF FETUS AND FETAL GROWTH
• It extends from 34 days in sheep and goat, 45 days in cattle and 55 days in horse to parturition.
• During this period minor details in the differentiation of organs, tissues and systems occur along
with the growth and maturation of the antenatal individual.
• Changes in the bovine fetus from 70 days to parturition are not radical.
• The increase in the size of bovine and equine fetus takes place very rapidly the last 2-3 months
of gestation.
• From 210-270 days the increase in weight of bovine fetus is equal to 3 times the increase from
the time of fertilization to 210 days.
HORMONAL CONTROL OF GESTATION
• Nervous control of the uterus is not essential during gestation in man and other animals.
• Conception, gestation and possibly normal parturition can occur with complete paralysis and
lack of nerves in the lower portion of the body.
• Gestation and the onset of parturition are entirely under hormonal control.
• In the cow, sheep and pig and probably the mare, about 12-16 days after estrum and fertile
coitus, the trophoblast of the embryo grows very rapidly and its presence causes a persistence
of the corpus luteum (CL) and cessation of the estrous cycle. This is accomplished by the effect
of the trophoblast acting on the endometrium:
o To cause a continuing release of pituitary luteotrophin by means of a neuro-humoral
mechanism acting on the hypothalamus and anterior pituitary gland, and
33
o To prevent the release or formation of uterine luteolysin and thus block the transport of
this substance by the local utero-ovarian pathway to the CL.
• The progesterone from the CL or the fetal placenta during pregnancy is essential for
o Endometrial gland growth.
o Secretion of uterine milk.
o For endometrial growth.
o Attachment of placenta for the later nourishment of the fetus.
o For inhibiting the uterine motility to aid in placental attachment.
• A certain amount of ovarian or placental oestrogen appears to enhance the effect of
progesterone and in later pregnancy to produce udder development, relaxation of pelvic
ligaments, initial uterine tonus and cervical relaxation and to sensitize the uterus to oxytocin.
• Other hormones essential in maintaining pregnancy are the gonadotropic or luteotrophic
hormones from the anterior pituitary gland necessary for the persistence of the CL and its
active secretion of progesterone.
• In the mare, the gonadotropins can be produced by the endometrial cups and in women by the
chorion of the fetal placenta.
• The endocrine glands of the fetus, thyroid, adrenals, gonads, anterior pituitary gland and
possibly others besides the fetal placenta play important roles in maintaining and terminating
the pregnancy.
• The CL of pregnancy is required throughout gestation to maintain a normal gestation period
and permit a normal parturition. It is reported that the normal CL in cows contains about 270
µg of progesterone. Levels below 100 µg were not conducive to embryo survival.
• In sows, ovaries are essential for the maintenance of gestation (pregnancy) throughout most of
the gestation period.
• The ovaries or CL may be removed in the latter half of the gestation in the ewe, mare, woman
and possibly the cat without interrupting or interfering with pregnancy or parturition. In the
latter animals, the placenta assumes the necessary production of the steroid hormones,
progesterone and estrogens.
DURATION OF PREGNANCY
• Duration of pregnancy is the period from implantation of the blastocyst in the endometrium
until termination of pregnancy (pregnancy, gestation or gravidity).
• The length of gestation is calculated as the interval from fertile service to parturition.
Species Duration (in days)

Cow 273 - 296
Horse 327 - 357
Sheep 140 - 155
Swine 111 - 116
34
Dog 60 - 63
Cat 56 - 65
Goat 148 - 156
Water buffalo 316 - 318
FACTORS INFLUENCING DURATION OF GESTATION
• The duration of gestation is genetically determined, although it can be modified by maternal,

fetal and environmental factors.
Maternal factors
• In different species, the duration of pregnancy is influenced by the dam.

• A two day extension from the normal occurs in the 8 year old ewe.
• Young heifers carry their calves for a slightly shorter period than older heifers.
Foetal factors
• In polytoccus species with exception of pig there is an inverse relation between the duration of
gestation and litter size.
• Monotoccus species carrying multiple fetuses also have shorter gestation periods.
• Twin calves are carried 3-6 days less than single calves.
• Interaction between fetal and placental sizes may influence gestation in horse.
• The sex also determines the length of gestation; male calves are carried 1-2 days longer than
females.
• Endocrine functions of the fetus may also influence the duration of pregnancy.
Genetic factors
• The small variations in duration of pregnancy among breeds may be due to genetic, seasonal or
local effects.
• The extreme expression of genetically prolonged gestation is known among dairy cows that
carry fetus homozygous for an autosomal recessive gene.
• Breed of embryo determines the length of gestation in cattle. This has been established by
transferring the embryos from breeds with shorter gestation length than the donor's and vice-
versa.
• Genetic factors are also responsible for differences in gestation length between mutton and
wool breeds of sheep.
Environmental factors
• Season may influence the duration of gestation.
35
• Foals conceived in late summer and autumn have significantly shorter gestation periods than
those conceived at the start of the breeding season in early spring.
SHORT AND PROLONGED GESTATION - TWINS AND MULTIPLE BIRTH
• The gestation period is 3-6 days shorter in cattle carrying twins and is 0.6 days shorter in sheep
and goats
• Adverse disease condition affecting the endometrium and placenta or the fetus may result in
abortion and short gestation
• Other adverse influences include
o Malnutrition
o Chronic debilitating diseases
o Deficiency diseases
o Starvation
o Severe stress, and
o Other conditions favouring abortion.
36
• In inbred Angora goats, genetic involution of the corpus luteum (CL) of pregnancy associated
with hyperplastic adrenal cortices results in abortion.
PROLONGED GESTATION IN DOMESTIC ANIMALS
• In general, the length of gestation period varies depending upon the breed and certain hybrid.
• In domestic animals, the gestation period gets prolonged in a variety of conditions.
Among the domestic animals, prolonged gestation is observed
• In cattle
• In sows
• In ewes
• In mares
PROLONGED GESTATION IN CATTLE
Three types of prolonged gestations have been observed in a number of cattle breeds.
1. Associated with premature, long haired fetal giants in Holstein and Ayrshires and in other breeds
• Due to a homozygous recessive autosomal gene.

• Gestation prolonged by 20-90 days.
• Characteristic features of premature fetuses
o Fetus weight 130-200 lbs
o Long hooves
o Erupted incisors teeth
o Dehydration
o Hypoplastic adrenals.
• Vaginal delivery impossible and results in severe dystocia – Early intervention through C-section
is advisable.
• Affected calves are hypoglycemic and die shortly after delivery.
• Calves delivered by C-section require a continuous regimen of corticosteroids to maintain the
life.
2. Associated with cretin-like immature fetuses with cranial and Central Nervous System (CNS)
anomalies including hydrocephalus, anencephaly or cyclopia and short, deformed loose jointed legs
with aplasia of anterior pituitary gland and a degree of hairlessness.
• Observed in Guernsey, Ayrshires, and Swedish Red cattle.

• Due to autosomal recessive mode of inheritance.
• Gestation gets prolonged from 20 to over 230 days over the normal period.
• Hydramnios is frequently present.
37
• Dystocia may occur, but not a serious problem.
• Characteristic features
o Adrenal glands may be very hypoplastic or absent.
3. Associated with cerebral hernia or catlin mark is an opening of the frontal and parietal bones
• Observed in Holsteins
• Results in dystocia
• Prolonged gestation: 20-60 days overtime.
• Characteristic features
o Severe CNS defects
o A sloping fore head greatly reduced cranial cavity and abnormal brain
o Long hooves and hair, and
o Death before or soon after birth.
• In the above three conditions, no pre-partum or post-partum changes are observed at the time
of parturition and the udder is undeveloped until after the fetus has been removed.
• Parturition does not occur unless the fetus dies in-utero.
• Cattle carrying male fetus had one or two days longer gestation than female fetus.
• Gestation lengths in heifers and in second pregnancy carry one or two days less than parous
cows.
• High doses and continued injection of progesterone or progestins delayed parturition.
• Most fetuses die the following month of normal parturition.
PROLONGED GESTATION IN SOWS
• Iodine deficiency or the administration of thiouracil to produce hypothyroidism results in

prolonged gestation by 4-10 days longer than normal with poorly viable, goiterous, and hairless
piglets.
• Gestation period gets prolonged by 3-4 weeks in inbred sows.
PROLONGED GESTATION IN EWES
• Ingestion of veratrum californicum about the 14 th day of gestation caused severe deformities
of the face, head with hypoplasia of the hypophysis resulted in prolonged gestation up to 230
days with fetal giantism and even rupture of prepubic tendon.
• Deficiency of Vitamin A resulted in prolonged gestation by 1-4 weeks.
• Decapitation of ovine fetuses resulted in overtime small, weak, edematous lambs with adrenals
one fourth to one fifth the normal size.
38
• Destruction of pituitary glands of ovine fetuses by electro cautery at 90-142 days results in
prolonged gestation.
PROLONGED GESTATION IN MARES
• Normal gestation in mares is considered to be 330 days, with a range of 320-340 days.
• Pregnancies that extend well past this upper range have been reported.
• In most cases, the mares progress past the expected foaling date with no signs of impending
parturition such as mammary development or pelvic ligament relaxation. Delivery of these
offspring’s has spontaneously occurred from 365-415 days following ovulation or breeding.
• Fetal oversize has not been typically associated with this condition as it has been in cattle.
• Etiology of prolonged gestation is not fully understood, but it is thought to involve a period of
embryonic diapause. This has been suspected when mares have embryonic vesicles that do not
grow normally in the first month of gestation and endometrial cup formation is delayed. This
delay in endometrial cup formation has been reported to extend for up to 1 month in some
cases. The idea of embryonic diapause is supported by the lack of fetal overgrowth with the
extended gestation length.
• Ingestion of fescue infected with endophyte has also been associated with prolonged gestation.
The average gestation length of mares consuming infected fescue past 300 days of gestation is
2 weeks to 20 days longer than mares not ingesting the endophyte. These mares also do not
have mammary development prior to delivery and on occasion do not even develop the gland
following parturition.
• Parturition in these mares is frequently associated with dystocia. This can result from fetal
malformations, edema of placenta and premature placental separation without rupture of the
chorioallantois at parturition, or "Red Bagging".
• Emaciated status of the fetus may be due to the decrease in the availability nutrients from
across the placenta because of vasoconstriction.
• Vasoconstriction may also be partially responsible for the presence of edema in the fetal
membranes at delivery.
• An ergot alkaloid is thought to be responsible for the associated complications of fescue
ingestion because it causes vasoconstriction and decreased prolactin from increased
dopaminergic activity and decreased serotoninergic activity.
TWINS AND MULTIPLE BIRTH - INCIDENCE AND ETIOLOGY
An uniparous animal when aborts or gives birth to two or more fetuses or young they are called twins,
triplets, quadruplets, quintuplets, or sextuplets.
• In mare, the incidence of twin births is about 0.5 to 1.5 per cent.
• In sheep and goats, the incidence of twinning is greatly influenced by the nutritional status of
the animal at the time of ovulation as well as the hereditary background of twins in the breed.
Primiparous ewes bear twins and triplets much less often than do pluriparous ewes.
39
In cattle, the frequency of multiple births:
o Twins 1 to 96 single births
Bovine twins Bovine triplets

Courtesy: S.A.Asokan et al., (2008)
o Triplets 1 to about 7,500 single births

o Quadruplets 1 to about 700,000 single births.
o Quintuplets 1 to about 60 million single births.
• Twinning is to some extent a breed characteristic, the frequency being 3.3 % in Holsteins, 2.7 %
in Brown Swiss and about 1 % for Jerseys.
• Many multiple conceptions terminate early in the gestation period in embryonic death and
absorption, and later in abortion or premature birth.
• The incidence of monozygous twins to all cattle births: 0.05 to 0.3 %.
• Monozygotic twins arise from one fertilized ovum that divides into two zygotes in the oviduct.
• Dizygotic twins usually arise from the rupture of two follicles, often one in each ovary, or rarely
the rupture of a single follicle containing two ova.
• Monozygotic twins may occur as members of triplet or greater multiple births.
• Monozygotic twins have similar characters in respect to color, color pattern, number of teats,
topline, tail, hair whorls, muzzle pattern, etc. They are always of the same sex and have the
same blood type. Skin or organ grafts survive for an indefinite period when exchanges are
performed between monozygotic twins.
• Dizygotic or fraternal twins bear no greater resemblance to each other than do full siblings.
• Dizygotic twins have different blood types that frequently show blood chimerism due to early
anastomosis of the placental vessels of the two twins and the exchange of primitive
erythrocytic cells that become established in both embryos.
Etiology of twinning
• Environmental causes
o Season
o Age of the dam
o Sires
40
o Hormone injections – Follicle Stimulating Hormone and Pregnant Mare Serum
Gonadotrophin.
• Hereditary causes
o Breed differences
o Differences between dams, sires and families
o Repetition of multiple birth in same cow
o Cystic ovaries.
TERATOLOGY
TERMINOLOGY
Teratology
• It is the division of embryology and pathology dealing with the abnormal development and
malformations of the antenatal individual.
41
Karyotype or Idiogram
• Systematized arrangement of chromosomes in pairs and groups.
Mosaicism
• The occurrence in an individual of two or more cell populations or tissues each with a different
chromosome complement derived from a single zygote.
Chimerism
• The occurrence in an individual of two or more cell populations or tissues each with a different
chromosome complement derived from different zygotes, as in twins with placental
anastomoses.
Cytogenetics
• It is the branch of genetics devoted to the study of the cellular constituents, chromosomes and
genes, which are concerned in heredity.
Pleiotropism
• It refers to certain harmful traits spread widely if they are associated with desirable traits.
Anomaly
• It refers to the malformation involving only an organ or part of the body.
Monster
• It refers to an animal with extensive deformity.
Phenocopies
• It refers to non-genetic anomalies that are similar to genetic anomalies.
Teratogens
• Variety of environmental factors or agents causing non-genetic anomalies or monsters.
INTRODUCTION
• The death or malformations of the antenatal individual arises due to teratologic, abnormal
development arrests in development of the ovum, embryo or fetus. An ovum and a
spermatozoa combine to form a single cell, a new mammalian zygote comprising of all of the
genetic information packaged in to two ten-trillionths of an ounce of DNA in the nucleus
required to form a new enormously complex animal.
• Chromosomes consist of a pair of chromatids held together by a centromere the location of
which together with the size of the chromosome aids in the identification of the chromosomes.
42
INHERITED LETHAL AND SEMI LETHAL CHARACTERS IN CATTLE
Achondroplasia, or dwarf, “comprest” or “bull dog calves”
• All breeds but most commonly in the Hereford, Ayrshire, Angus and Dexter breeds.
• Most common type is, the brachycephalic “snorter” dwarf in Herefords with’ a short, broad
head, bulging forehead, malocclusion of the jaw, prognathism of mandible, pot-belly, low
viability and great susceptibility to bloat and dystocia.
• This type was generally considered to be due to a simple autosomal recessive defect with some
modifiers.
• The “comprest” Hereford is the result of incomplete dominance.
• In Ayrshire, Dexter and other cattle, extreme “bulldog” calves is usually aborted about the fifth
to eighth month of gestation.
• Hydramnios occurs in pregnant Dexter cattle carrying a “bulldog” calf. Normal Dexter cattle are
heterozygotes.
• A type of Aberdeen Angus dwarf characterized by inferior brachygnathism, bulging eyes,
narrow nose, death occurring during parturition or soon after and moderate hydrops amnii
have been observed as an apparent recessive character in several purebred Angus herds.
Affected calves have brittle, easily broken bones that upon examination are solid and devoid of
marrow cavities. If the calf lives a few hours central nervous signs of opisthotonus and
nystagmus are present.
Achondroplasia Extreme Achondroplasia
Courtesy: Drost Project
Epitheliogenesis imperfecta
• It is a condition where skin fails to form.

• It occurs most commonly on the legs below the knees and hocks and
on the muzzle, ears, tongue and mucous membranes.
• It has been described in Holsteins, Ayrshires, Jerseys, Brown Swiss and Shorthorns.
43
Epithelioenesis Imperfecta Epitheliogenesis Imperfecta-Closeup
Hypotrichosis congenita or alopecia is a recessive defect characterized by degrees of hairlessness in

Holsteins, Polled Herefords. It was also described in Swedish Friesian cattle, and Holsteins; in Jerseys
having other defects such as a short lower jaw, short ears and anophthalmia. Streaked hairlessness
reported as a sex- linked lethal in Holsteins.
• Ichthyosia congenita is characterized by a lack of hair and a thick scaly, horny epidermis with
raw fissured skin around the body orifices. It is due to single autosomal recessive genes in
Brown Swiss and Red Polled Cattle.
• Acroteriasis congenita or amelia and hemi melia is seen in Holsteins and Brown Swiss and other
breeds. This is characterized by missing, shortened, deformed, or “amputated” limbs.
• Ankylosis, hydrops, death and mummification of the fetus in the last month of gestation -
reported in Red Danish cattle, due to a pair of single autosomal recessive genes.
• Cerebellar hypoplasia and degeneration is seen in Herefords, Guernseys and Holsteins and is
probably autosomal recessive in nature. This conclusion may be erroneous as BVD-MD virus can
produce this defect in fetuses.
• Sex-linked lethals (Holsteins and other breeds)
• Ataxia with leucodysplasia seen in Angus, Short- horns, Jerseys, Herefords and possibly in
Holsteins ana Hariana cattle at 2 or more weeks of age is due to a recessive condition.
• Doddlers in Herefords, due to a pair of autosomal recessive genes and possibly causing
cerebellar or other brain stem lesions.
• Cerebral pseudolipidosis, ataxia and tremors were reported in Angus cattle in Australia.
• Paralyzed hind quarters have been reported in Red Danish calves at birth due to a pair of
autosomal recessive genes.
• Curved limbs with both rear and forelimbs curved anteriorly, have been observed in Guernseys
as an autosomal recessive trait. Calves are usually stillborn or die promptly.
• Muscle contractures and ankyloses, or arthrogryposis has been reported as a recessive in Dole
cattle in Norway; and a dominant with incomplete penetrance in England.
• Hydrocephalus in Herefords, Ayrshires, Holsteins and other breeds. It is characterized by the
birth of “dummy” or “bawler” calves that are unable to nurse properly and die in several days.
The heads may be enlarged or normal in site but section of the head and brain reveals
distended ventricles. Associated occasionally with hydramnios, dwarfism and high copper levels
in the liver. This is due in an uncomplicated form to a simple autosomal recessive gene. It is
possible that some of these cases of hydrocephalus might be associated with BVD-MD or blue
tongue viruses infecting the bovine fetus.
44
External hydrocephalus Internal hydrocephalus
Courtesy: Drost Project S. Balasubramanian - Personal collection
INHERITED LETHAL OR SEMILETHAL CHARACTERS IN HORSES
• Atresia coli in Percherons is often associated with brain defects.

• Hemophilia
• Fredericksborg lethal, related to sterility in inbred white horses.
• Epitheliogenesis imperfecta, affects lower limbs.
• Sex-linked lethal, ratio of 2 females to 1 male.
• Hereditary ataxia, Oldenberg breed.
• Wobbles or incoordination
o Seen in Thoroughbreds, Standardbreds, American Saddle and other breeds and grade
horses.
o Most common in males by a 3 to 1 ratio.
o Due to a defect of the cervical vertebrae causing compression of the spinal cord.
o Suggested as inherited, a recessive, but not a simple, defect.
o Ataxia in Shetland pony resembling wobbles but the condition was associated with
degeneration of ‘the spinal nerve roots. The condition might be genetic in nature.
o Wobbles due to three distinct types of pathological lesions and listed 6 other disease
entities that may resemble wobbles in horses.
• Cerebellar hypoplasia is possibly a genetic defect in Arabians.
• Absence of a retina is a recessive character.
• Hydrocephalus
INHERITED LETHAL AND SEMILETHAL CHARACTERS IN SHEEP AND GOATS
• Muscle contracture, ankylosis, arthrogryposis, or flexed limbs and wry neck. These are expelled
dead and are due to simple recessive genes. Paralysis of hind limbs is seen in Corriedales as a
simple recessive. Rigid fetlocks are characterized by a deformed body, short wool and hernias.
• Acroteriasis congenita or amputated limbs.
• Lethal gray is seen in gray Karakul lamb with obstruction of the gut and possibly nerve damage.
45
• Lethal myodystrophia, inheritance is questionable.
• Dwarfism or achondroplasia is seen in Ancon sheep due to simple autosomal recessive genes.
• Agnathia is observed in a variety of forms.
• Cerebellar hypoplasia or “daft” lambs, is a simple autosomal recessive character in Corriedales.
• Photosensitization with blindness in Southdown sheep is due to a simple recessive.
• Prolonged gestation.
INHERITED LETHAL AND SEMILETHAL CHARACTERS IN SWINE
• Cerebral hernia, “Catlin” mark

• Hydrocephalus in Duroc Jerseys due to recessive genes.
• Paralysis of hind limbs due to spinal cord lesions. This is a recessive semilethal character.
• Atresia ani
• Thickened forelimbs
• Acroteriass congenita, “amputated” is caused by a single autosomal recessive gene.
• Cleft palate is seen occasionally with harelip in the Large White breed and transmitted as a
single autosomal recessive.
INHERITED LETHAL AND SEMILETHAL CHARACTERS IN DOGS
• Abnormal stenotic larynx in Skye Terriers.

• Failure of the closure of the fontaneiles in Cocker Spaniels.
• Cleft palate in brachycephalic breeds.
• Otocephaly in Beagles with a lack of a lower jaw and ears uniting beneath the head,
hydrocephalus and other defects.
• Cranioschisis in Cocker Spaniels is possibly recessive.
• Esophageal achalasia or megaesophagus is seen in Wirehaired Fox Terriers, German Shepherd
Dogs and other breeds. It is probably inherited as an autosomal dominant.
• Lymphedema of limbs and trunk is inherited as an autosomal dominant condition in Labradors.
• Hemophilias, type A or deficiency of factor VIII, and type B or deficiency of Factor IX (Christmas
disease) are seen in Collies, German Shepherd Dogs, Beagles, Labradors, Cairn Terriers, Irish
Setters, Greyhounds Aberdeen Terriers, Scotch Terriers and others. Both are due to sex- linked
recessive genes on the sex (X) chromosome and characterized by joint and subcutaneous
hemorrhages in male dogs.
• Deficiency of blood factor VII , a mild condition resulting in hemorrhage at the time of surgery
in Beagles is due to an autosomal recessive gene.
• Hemolytic anemia in a chronic form in young Basenji dogs is due to a corpuscular defect causing
a shortened red blood cell life span and is probably genetic.
• Cardiac malformations or anomalies , probably due to a polygenic mode of inheritance.
46
• Patent ductus arteriosis was the most common congenital cardiac defect in dogs. It is a
heritable defect seen most often in female Poodles, Collies and Pomeranians.
• Subaortic stenosis was the cause of 15 per cent of congenital heart disease in dogs and was
possibly genetic in nature as it was seen mainly in German Shepherd Dogs, Boxers and
Newfoundlands.
• Spontaneous byperparathyroidism was apparently caused by an autosomal gene causing renal
cortical hypoplasia in 41 of 47 affected Cocker Spaniels.
• Paralysis with spinal muscular atrophy (Stockard’s syndrome) in crosses between Great Danes,
Bloodhounds and St. Bernards is due to at least 3 genetic factors.
• Spinal dysraphism is a hereditary disease of Weimaraners due to lesions in the caudal spinal
cord causing a hopping gait.
• Hereditary cerebellar ataxia is seen in Smooth Haired Fox Terriers. In Basset Hounds a form of
ataxia and paralysis was due to deformed cervical vertebrae in males similar to wobbles in
horses.
• Progressive cerebellar ataxia starting at 3 months of age in Kerry Blue Terriers. There was a
neuronal degeneration characterized by involvement of the Purkinje cells of the cerebellum and
other nuclei in the brain. It is a possible simple recessive defect.
INHERITED AND GENERALLY NONLETHAL DEFECTS IN CATTLE
• Polydactylism in Holsteins and Herefords is possibly an autosomal dominant character with

incomplete penetrance.
• Syndactylism or “mule-foot” affecting one or both front feet or all four feet has been reported
in Jerseys, Harianale and Holsteins and has a single autosomal recessive mode of inheritance.
Affected Holsteins were unable to withstand stress due to high ambient temperatures and
became hyperthermic. The front feet of the Holstein calves were much more frequently
affected with syndactyly than the rear feet.
• Muscular hypertrophy or “double” muscling is characterized by reduced fat deposits, light bone,
thin skin, and large muscles. It is seen in many breeds of cattle including Herfords, Holstein,
Angus, Charolais. In the latter it may be inherited as an incomplete dominant while in the
former breeds it may be a recessive with incomplete penetrance and variable expression. When
fetuses are affected dystocia often occurs.
Double Muscling in Cattle
Dead fetus Delivered by C-Section Note the thick and large muscles in
neck region
Courtesy: C.Veerapandian Personal Collection

47
• Umbilical hernia was described as being a probable sex-limited dominant character in male
Holsteins but the mode of inheritance in females was uncertain. Umbilical hernia in Holsteins
was caused by one or more pairs of autosomal recessive genes of low frequency. The condition
was seen more often in females but was probably not sex-linked.
• Osteoarthritis and hip dysplasia in Holsteins, Jerseys and Herefords. In dairy breeds the lesions
were noted in the stifle joint at 5 to 13 years of age and were possibly due to a single autosomal
recessive gene. In yearling Herefords the lesions were in the hip joint and it was possiblydue to
an incompletely penetrant dominant character.
• Spastic paresis in Angus, Holstein, Charolais, Shorthorn, Ayrshire, Simmental and rarely Jersey
calves usually 2 to 8 months of age with straight rear legs and a contracted gastrocnemicus
muscle causing the rear leg to be held off the ground and swung rigidly. It is due to an
autosomal recessive condition.
• Spastic syndrome, Krampfigkeit, “Stretches” is a latent recessive condition developing at 2 to 7
years of age and characterized by spastic contractions of the rear limb or limbs and back that
occur intermittently in the standing animal. The condition affects Holsteins, Guernseys,
Charolais, Ayrshires, and occasionally other breeds.
• Epilepsy has been reported in Swedish Red cattle and Brown Swiss cattle characterized by a
sudden loss of consciousness preceded by a convulsion. It may be due to a recessive or
dominant factor.
• Lack of lid pigmentation and ocular carcinoma is seen mainly in Herefords but also Holsteins
and Ayrshires exposed for long periods to sunlight. Pigmentation of the eyelid is strongly
heritable so selection for pigmented eyelids can reduce the incidence of carcinomas.
• Heterochromia irides and albinism in Herefords due to a dominant mode of inheritance. These
cases were more like color dilution rather than true albinism. Some affected cattle had blood
dyscrasias.
• Congenital cataract and blindness (Jerseys and Holsteins).
• Strabismus and exophthalmos “cross-eyed” or “pop-eyed” (Shorthorn, Guernsey and Jersey) are
inherited as recessive characters.
• Hypotrichosis congenita, hairlessness, a non lethal character in Guernseys.
• Red factor is a simple recessive defect in Holstein and Angus cattle where red substitutes for
the normal black color of the hair.
• Congenital porphyria, or pink tooth, in Holsteins, Shorthorns and Jamaican Red cattle, due to a
simple autosomal recessive condition resulting in photosensitivity arid dermatitis of white or
even pigmented skin, pink to brown teeth and bones that fluoresce with ultraviolet light.
• Polycythemia in one- to two-month-old Jersey calves characterized by congested mucous
membranes, lethargy, dyspnea and reduced growth rate was due to a single autosomal
recessive gene.
• Curly coat (Ayrshires and Swedish cattie).
• Deformed limbs or flexed pasterns (Jerseys).
• Wry tail (all breeds).
• Wry muzzle (Jerseys).
• Screw tail (Hoisteins, Jerseys, Shorthorns, Red Polled).
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• Vestigeal tail (Holsteins, Angus, Shorthorns).
• Taillessness (Holsteins and other breeds) possibly inherited.
• Multiple lipomatosis (Hoisteins), a dominant trait with incomplete penetrance.
• Fused teats (Guernseys, Herefords).
• Supernumerary teats (all breeds).
• Notched or short ears : Ayrshires, Jerseys.
• Missing phalanges or “Creeper” calves (Swedish cattle).
• Impacted premolars and “parrot-mouth” (Shorthorns) Short spine (Norwegian cattle).
• Ljutikow lethal.
• Agnathia or absence of a lower jaw (Jerseys and other breeds)
Opacity of the cornea is probably a recessive character in Holsteins.
• Lumpy jaw or actinomycosis and actinobacillosis is characterized by a lack of genetic resistance
in Guernseys to this disease. Ankylosis of the jaw (Norwegian cattle).
• Multiple eye defects (Jerseys, Holsteins).
• Prognathism (Herefords and others).
• Dermoid cysts on cornea, (Herefords and Guernseys).
• Smooth tongue (Holsteins and Brown Swiss).
INHERITED AND GENERALLY NONLETHAL DEFECTS IN HORSES
• Congenital blindness
• Aniridia with cataract was a dominant autosomal character in Belgians.
• Umbilical hernia
• Hypotrichosis cöngenita
• Sidebone
• Cryptorchidism
• Brachygnathism of the mandible
• Subluxation of patella, ponies
• Multiple exostosis is possibly hereditary in Quarter horses.
• Heaves, pulmonary emphysema
• Roaring, laryngeal hemiplegia (?)
• Dysplasia of the hip, (Dole horses)
• “Bleeders,” epistaxis (?)
INHERITED AND GENERALLY NONLETHAL DEFECTS IN SHEEP AND GOATS
• Malocclusion, brachygnathism or prognathism

• Hypotrichosis congenita, Hermaphroditism is common in polled goats, especially Saanen
49
• Cryptorchidism is a recessive character in goats and sheep
• Yellow fat is a simple recessive character
• Acaudate, “no tail” sheep
• Hairy Wool in Romney sheep is caused by an incomplete dominant gene.
• Myotonia congenita or “fainting” goats
• Entropion has probably a complex polygenic inheritance
• Wattles in sheep and goats is due to a single dominant gene
• Hydrocephalus
Caprine Hydrocephalus
Source: S. Balasubramanian (2010)

Personal Collection
• Atresia ani
Atresia Ani in a day old Kid
Source: S. Balasubramanian
(2011) Personal Collection
50
• Sperm granuloma is seen secondary to anomalies of the mesonephric duct in male goats
• Blindness may be due to a simple autosomal recessive gene
• Fleshy outgrowth on the top of the ear in Karakuls is inherited as a simple auosomal recessive
character.
INHERITED AND GENERALLY NONLETHAL DEFECTS IN SWINE
• Epitheliogenesis imperfecta in Berkshires and Yorkshires.

• Wattles, or tassels.
• Testicular hypoplasia
• Screw or kinky tail
• Umbilical hernia
• Inguinal or scrotal hernia; sex-limited and may affect male pseudohermaphrodites.
• Hypotrichosis congenita, Congenital bent legs
• Split ears, deformed rear quarters and occasionally cleft palates
• Diverticulosis, chronic ileitis in Berkshires
• Congenital porphyria, a dominant character
• Cryptorchidism
• Eye defects, micropthalmia, anopthalmia
• Syndactyly and polydactyly
• Sexual impotency
• Hermaphroditism
• Inverted teats
• Hypertrophy of muscle, Pietrain pig in Belgium.
• Subaortic stenosis
• Dermatosis vegetans, is a semilethal autosomal recessive condition of the Danish Landrace
breed and associated with a giant cell pneumononitis, dyspnea and efflorescent skin lesions.
INHERITED AND GENERALLY NONLETHAL DEFECTS IN DOGS
• Proneness to intervetebral disc luxation is inherited in certain long-bodied chondrodystrophoid

types of dogs such as Dachshunds.
• Epilepsy is seen in Fox Terriers, Poodles, Boxers and Keeshonds as a single autosomal recessive
character.
• “Scotch Cramp” or recurrent tetany is a recessive neurosis in Scotch Terriers.
• Polydactyly or double dew claws is due to a recessive character in a number of breeds.
• Elbow dysplasia with osteoarthritis with or without an ununited aconeal process is seen
especially in German Shepherd Dogs, and also Pekinese, Poodles, Cocker Spaniels, Bassett
Hounds, Great Danes, Newfoundlands, Labradors and others. It is probably due to the presence
of 3 dominant genes.
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• Proneness to vaginal prolapse is possibly inherited in Boxers and Bulldogs.
• Patellar luxation is a tibiofemoral deformity in toy breeds and Poodles.
• Hip dysplasia is inherited in a polygenic manner, and is seen in German Shepherd dogs,
Labrador Retrievers, Newfoundlands, Alsatians, and many others.
• Perthes Disease of the hip joint is seen in Fox Terriers, Alsatians and Cairn Terriers.
• Malocclusion or brachygnathism of the mandible is observed in Dachshunds and Cocker
Spaniels and prognathism of the mandible in Bulldogs.
• Shortened spine, “baboon” dogs of S. Africa is characterized by a humped back, very short neck
and short tail.
• Hydrocephalus may be hereditary in Chihuahuas, Boston Terriers and others.
• Achondroplasia and other related skeletal abnormalities in Scotch Terriers, Bulldogs,
Sealyhams, Bassets, and Beagles.
• Prolongation of soft palate and laryngeal collapse is seen in brachycephalic dogs as Boxers and
Bulldogs.
• Crooked tails is inherited in Fox Terriers.
• Taillessness or anury or brachyury is inherited in Cocker Spaniels and other breeds.
• Inguinal hernia is seen most commonly in female Cocker Spaniels and Dachshunds. Umbilical
hernia has a complex polygenic inheritance and is seen in Pekinese, Cocker Spaniels, Collies,
Bull Terriers and others.
• Diaphragmatic hernia may possibly be inherited as an autosomal recessive character.
• Cystinurea , causing soft, yellow urinary calculi in Dachshunds and other breeds, is apparently
an autosomal recessive character and possibly sex-limited as it has been seen only in males.
• High uric acid excretion in Dalmatians is inherited as a simple recessive autosomal character.
• Epitheliogenesis imperfecta , ichthyosis, alopecia, acanthosis nigrans are congenital, possibly
hereditary, defects of the skin in dogs.
• Hairlessness: The hairless breeds, such as the Mexican hairless dogs, are heterozygous for this
defect. In the homozygous state the fetuses are expelled dead or have an occlusion of the
esophagus.
• Merle or harlequin coloring is seen in heterozygotes, while in homozygotes the animals are
white, show deafness and eye defects, such as microphthalmia. It is seen in Collies, Great
Danes, and Bull Terriers.
• Nasal solar dermatitis or “Collie nose” is seen in Collies and Shetland sheep dogs.
• Proneness to dermatitis and skin diseases such as demodectic mange occurs in Dachshunds and
Great Danes; alopecia in Chows and Boxers; and eczemas in Chows.
• Dermoid sinuses on the back are seen in Rhodesian Ridgebacks.
• Trichiasis and distichia are seen in Poodles, Spaniels, Pekinese and Toy breeds.
• Ectropion and entropion is genetic in a number of breeds such as: Spaniels, Bloodhounds, St.
Bernards, and Chows
• Ocular fundus anomaly, ectasia syndrome or chorioretinal dysplasia is seen in nearly one-third
of Collies and is a simple autosomal recessive character with variable expressivity.
52
• Cataract is a dominant defect in Beagles and Alsatians.
• Microphthalmia is seen in homozygous “merles” or “harlequins”. In Australian Sheperd dogs
this is an autosomal recessive character.
• Retinal detachment is a recessive character in Bedlington Terriers.
• Persistent pupillary membrane is possibly inherited as an autosomal, non-sex-linked type of
inheritance with variable expression in Basenjii.
• Progressive retinal degeneration and atrophy in Irish Setters, Gordon Setters Laborador
Retrievers. Norwegian Elkhounds, Miniature and Toy poodIes and others usually progressing to
blindness at adulthood to middle age, is usually an autosomal recessive character but other
modes of inheritance are possible.
• Luxation of the lens and secondary glaucoma is seen in many breeds especially Wirehaired Fox
Terriers, Hodgman; and in Norwegian Elkhounds and Sealyhams.
• Hemeralopia is reported in Alaskan Malamutes and Poodles as a simple autosomal recessive.
• Dermoid cysts of the cornea are seen in St. Bernard and New foundlands and the mode of
inheritance is not known.
• Proneness to disease of the ear canal is seen in breeds such as Poodles, Bedlingtons, Sealyhams
and Wirehaired Fox Terriers with an excessive hair growth in the external ear canal.
• Deafness is seen in Bull Terriers, Dalmatians and Sealyhams and is often linked with the white
coat color.
• Cryptorchidism is seen commonly in brachycephalic breeds and has an irregular mode of
inheritance, probably a modified recessive mode. In Cocker Spaniels it is apparently a sex-linked
autosomal recessive character.
• Hydrocephalus is seen in Bulldogs and Beagles and is due to recessive genes.
• Abnormal maternal behaviour is seen most commonly in toy breeds.
• Aggressive behaviour is seen in German Shepherd Dogs and others.
• Proneness to neoplasia such as: Mastocytoma in Boxers and pituitary tumors in Boston Terriers
is observed.
INHERITED SEMILETHAL AND NONLETHAL DEFECTS IN CATS
• Porphyria is due to a simple autosomal dominant character.

• Taillessness is noted in true Manx cats. It may be associated with a rabbity or hopping gait.
• Strabismus or cross eyed ness is seen in Siamese cats.
• Polydactyly is a dominant, autosomal character with a variable expression. All four feet or just
the front feet, but never just the hind feet, may be affected. The extra toe may hang loosely
from the skin or be attached with normal bones.
• Hydrocephalus is a simple recessive gene in Siamese cats.
• Deafness is associated with white or albino color in cats, as in dogs. It is associated with
agenesis o1 the organ of Corti, the spiral ganglion and the cochlear nuclei.
• Retinal atrophy was reported occasionally in Siamese and Persian cats and might be hereditary
as in dogs.
53
• Cerebellar hypoplasia has been described by Innes and Saunders and others as a possible
genetic lesion since it is familial in nature.
• Osteogenesis imperfecta is not a genetic defect although it has been described as one in cats
and dogs for many years because litter mates were often affected. A nutritional disease caused
by all meat diets high in phosphorus and low in calcium.
INTRODUCTION
• In domestic animals, there are innumerable types and degrees of non-genetic anomalies, or
monsters.
• Anomaly refers to malformation of only an organ or part of the body.
• Monster refers to an extensive deformity is extensive.
• Suspect genetic role, if a similar defect appears quite frequently in related individuals or those
tracing back to a common ancestor. It would be impossible to differentiate some of these
defects appearing in families or related animals in a herd due to environmental causes without
a carefully controlled experiment.
Susceptibility
• The period of early differentiation in the embryo or about the time germ layers and organs are
rapidly developing - Highly susceptible.
• The zygote is not as susceptible to teratogens during the period of the ovum or blastula or the
period of the fetus as it is during the period of the embryo and organogenesis, especially the
first half of that period.
TERATOGENIC AGENTS OR FACTORS
Nutritional deficiencies in the dam
• Vitamin A and E, riboflavin, folic acid, pantothenic acid, niacin and other vitamin deficiencies,
minerals such as iodine and possibly manganese, and amino acids such as tryptophane may
cause congenital defects. Hypervitaminoses A and D will also cause anomalies.
Endocrine disturbances of the dam
• Diabetes, thyroid malfunction, and large exogenous doses of glucocorticoids, ACTH, insulin,
androgens, progestagens, estrogens, thyroxine and thiouracil will cause defects of the embryo.
Large doses of glucocorticoids in pregnant animals at the proper stage of gestation may cause
cheilo or palatoschisis. Progestagens given during pregnancy may cause masculinization of the
genitalia of female fetuses.
Physical factors
• Reduced atmospheric pressures, hypothermia, hyperthermia and, anoxia cause anomalies.
Radiation
• X-ray or radioactive substances induces congenital defects.

54
Drugs or chemicals
• Thalidomide, quinine, sulphonamides, tetracycline, streptomycin, salvarsan, lead, mercury,

nicotine, malathion, carbon tetrachloride, apholate, selenium, fluorine, cytotoxic agents
including aminopterin in sheep, nitrogen mustard, actinomycin D, 6 mercaptopurine, azoserine,
azo dye, trypan blue and other dyes, salicylates, histamines, ergot, “Diamox,” reserpine,
phenylmercuric acid, galactose, E.D.T.A. and certain plant compounds as in Veratrum
californicum and locoweeds possibly containing lathyrogens, all produce fetal anomalies in
animals under certain conditions.
Infections
• Blue tongue in sheep, hog cholera in swine, feline panleucopenia in cats, bovine virus diarrhea-
mucosal disease virus, and toxoplasma can cause anomalies in the embryo.
Ageing of ova
• By delaying ovulation 24-48 h was characterized by a three-fold increase in chromosomal

anomalies with a higher incidence of embryonic death in rats. Similarly ageing of rabbit
spermtozoa before permitting them to fertilize eggs resulted in normal fertilization but greater
embryonic death losses. Thus age affects the genes and chromosomes as does other agents.
MALFORMATIONS DUE TO ALTERATIONS IN TISSUE DIFFERENTIATION

THAT ARISE FROM A SINGLE AREA IN THE EMBRYONIC DISC
Most of these are due to the local arrest in the normal process of tissue development and produce
• Defects due to excessive division: polydactylia, polythelia, polydontia.

• Defects due to failure of structures to fuse normally: palatoschisis, cheiloschisis, cranioschisis,
spina bifida, and schistosomus.
• Defects due to arrest in division: cyclopia, ren arcuatus or horseshoe kidney; and syndactyly.
• Defects due to complete local failure of tissue growth: amelia or lack of limbs; ectrodactyly or
absence of phalanges; vertebral or costal abnormalities; epitheliogenesis imperfecta; acrania;
agnathia; and anophthalmia.
• Defects due to arrest in assumption of final form or position: ectopia cordis, hypognathia, and
dextro-position of the aorta.
• Defects in the persistence and disappearance of contiguous structures that normally follow a
certain pattern: the aortic arches, foramen ovale, urachus, ductus arteriosus and persistence of
the median wall of the paramesonephric or Mullerian duct.
• Defects due to overdevelopment of’ local tissues: polycystic kidneys; tumors such as sarcomas,
hemagiomas and teratomas.
• Defects due to displacement of tissue: teratomas and dermoid cysts
• Defects due to fusion of sexual characters: true hermaphrodites, false hermaphrodites, and
freemartins.
• Defects due to miscellaneous causes: ichthyosis, chondrodystrophies, osteogenesis imperfecta,
and porphyrinuria.
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ANOMALIES OF THE ORGANS OR TISSUES INVOLVED
• Heart and blood vessels

• Digestive and alimentary system
• Urinary system
• Sexual organs and gonads
• Head and central nervous system
• Skeleton
• Trunk
• Limbs
ANOMALIES OF HEART AND BLOOD VESSELS IN DOMESTIC ANIMALS
• Relatively common.
• Many animals with cardiac defects die soon after birth, a few survive a long period due to
compensatory factors. Eg. Subaortic septal defects in some cyanotic calves and in cervical
ectopia cordis.
• In cattle a subaortic septal defect was in 18 of 37 cattle with cardiac aberrations.
o Seen mainly in Guernseys
o Commonly associated with anopthalmus or micropthalmus, and
o a twisted shortened tail.
Clinical symptoms
• Shortness of breath on exercise

• Rapid pulse rate
• Increased cardiac area
• Cyanosis, and
• A marked systolic bruit especially over the right side of the thorax where a thrill was, often
palpable.
• Another very common defect, observed in 12 out of 37 cases in cattle, was the transposition of
the aorta into the dextroposition or Eisenmenger complex, where it arose from the right
ventricle or over the right ventricle and interventricular septum.
o Left ventricle was usually very small or nonfunctional, and
o Persistence a foramen ovale or a subaortic septal defect or both were necessary so that
blood from the left atrium could get into the right ventricle.
o Often the ductus arteriosus was persistent.
o Systolic bruit was more pronounced on the left side of the thorax and a thrill was not
palpable.
56
Other cardiac anomalies
• Atresia of the aorta with persistence of the ductus arteriosus

• Cor triloculare biatrium
• Tetratology of Fallot
• Ectopia cordis, either cervical, pectoral or abdominal
• Persistence of the right aortic arch with absence of the left causing stenosis of the esophagus,
and
• Various types of acardiac monsters.
In dogs
• Congenital heart anomalies are quite common

• Incidence about 1 %.
• Many neonatal pups die without a postmortem examination, some deaths could be due to
cardiac defects.
• Some of these are genetic.
• Most common congenital heart defects are:
o Pulmonic stenosis
o Aortic stenosis
o Patent ductus arteriosus
o Interventricular septal defect
o Tetratology of Fallot, and
o Persistent right aortic arch with a left ductus arteriosus resulting in compression of the
esophagus and pericardial defects.
• Cardiovascular anomalies in the cat and sheep are uncommon
• Other anomalies of the thorax and lungs are uncommon in domestic animals.
• Occasionally congenital diaphragmatic hernias have been described in the dog and cat.
• Anomalies of the lungs are rare in animals.
MAMMARY GLAND ANOMALIES IN DOMESTIC ANIMALS
• Virgin animals may enlarge and secrete a small amount of milk during gestation due to the
effect Fused teats and supernumerary glands and teats.
• Some of the supernumerary teats, polythelial may be fused to the normal teat. The mammary
glands in of hormones from the placenta or from the ovary, or from granulosa cell tumors.
• Congenital atresia, or stenosis of one or more teats or glands, may occur but this is difficult to
differentiate from pathological processes that may have occurred prior to or after parturition.
• A rare case of total mammary gland aplasia has been reported in a fertile cow.
57
Four Functional Mammary Hypothelia in a Buffalo
Gland in a Goat
Source: S. Balasubramanian et Courtesy: Ravi Sunder George
al. (1994) - Personal collection
HEAD AND CENTRAL NERVOUS SYSTEM ANOMALIES
Anomalies
• Microcephalus
• Cyclopia or Cebocephalus
• Hydrocephalus
• Meningnocele
Microcephalus-Description
• Characterized by a small cranial cavity and brain.
Cyclopia or cebocephalus
• Cyclopia is seen most commonly in the pig and, sheep but may be present in all species.
In Sheep
• Characterized by a single orbit in which global tissue is absent or rudimentary or which the
eyeballs vary from a single apparently normal eye through all degrees of doubling to one
consisting of two complete but small adjacent globes.
58
• Eyelids are rudimentary or absent and the nose is usually absent or in the form of a tubular
appendage placed above the centrally located eye.
• This rudimentary nose does not communicate with the pharynx.
• The skull is usually small and the lower jaw, being longer than the defective upper jaw, is curved
dorsally at its cranial end.
Hydrocephalus
• Occurs due to an abnormal accumulation of fluid in the cranial cavity.

• Internal hydrocephalus is due to excessive fluid in the ventricular system.
• External hydrocephalus is rare and due to excessive fluid between the brain and dura mater.
• Internal and external hydrocephalus may be combined.
• In marked cases, the dorsal portion of the brain is encompassed only by the skin, the
subcutaneous tissues, and the brain coverings.
In Buffalo
Meningnocele
Cranioschisis or crania bifida
• Defects of the skull that may result in meningoencephalocele or meningocele .

• In the later instance the skull defect is large, so that parts of the brain and the meninges are
extruded.
In Buffalo
59
ANOMALIES OF THE HEAD
Facial fissures
• Palatoschisis, cheiloschisis, macrostomia, and schistoprosopus or divided face.
Lack of cranial or facial structures
• Acephalia, or absence of a head; acrania; hemicrania; astomia; microstomia, arhinencephalia or

absence of a nose, agnathis, hypognathia, anophthalmus, microphthalmia, aprosopia or partial
or complete absence of a face, anotia or absence of ears, polyotia and polydontia or anodontia.
Congenital defects of the head and ears of ovine fetuses are common. Anophthalmus and
microphthalmia may possibly be related to a severe vitamin A deficiency.
Cerebellar hypoplasia and allied defects
• Possible genetic or congenital abnormality in all domestic animals. Cerebellar hypoplasia or

aplasia can be produced in newborn kittens by infecting the pregnant dam with feline
panleucopenia virus. It can be produced in newborn calves by infecting the pregnant dam
around the fifth month of gestation with BVD-MD virus.
Hydranencephaly and arthrogryposis or muscle contractures
• Hydranencephaly and arthrogryposis or muscle contractures in newborn calves of various

breeds. Blindness was also a part of this syndrome in some calves. The agent causing the
anomalies was believed to have been active between 2 and 6 months of gestation.
Crooked calf disease
• Characterized by arthrogryposis, torticollis, scoliosis and occasionally cleft palate.
These anomalies of the central nervous system are often characterized externally by ankylosed joints,
deformed fetlocks or “club feet” and other defects including-hydramnios in some severely affected
fetuses. As with other markedly defective fetuses their size is usually smaller than normal.
SKELETAL ANOMALIES
Achondroplasia, Chondrodystrophy or Dwarfism
• Several types and degrees and most, or all, are hereditary.

• In achondroplastic fetuses the long bones are abnormally short. The trunk is of normal length
and the abdomen is large. The head is moderately enlarged and flattened.
• “Bulldog” head and brachygnathism of the maxilla, “undershot,” or prognathism of the
mandible, “overshot,” are common.
• In Herefords, the recessive gene for dwarfism is found commonly in the heterozygous
“comprest” animal.
• Most dwarfs are the result of a complex mode of inheritance.
60
Spina bifida or rachischisis
• Absence of the dorsal portions of the vertebrae or vertebral arches often in the lumbar or
sacral region with defective rear limbs and tail and paralysis of the rear parts.
• Observed in Angus, Holsteins, Bull terriers and other animals.
• May resemble the Perosomus elumbis monster.
Tailessness, anury or Perosomus acaudus
• Common defect in dairy and beef cattle.

• Characterized by a lack of coccygeal vertebrae and deformed sacral vertebrae with a sunken
perineal region and in some cases a characteristic hopping gait.
• Condition could not be proven to be genetic in nature.
Hemivertebrae
• Most commonly in English bulldogs and Boston terriers

• Characterized by failure of the centers of ossification to unite.
• Scoliosis, kinked tails and a shortened spine are present if many vertebrae are involved.
SCHISTOSOMUS REFLEXUS
Condition
• Schistosomus reflexus is seen most commonly in cattle, but in rare cases may be observed in
sheep, goats, and swine.
In Bovine
Description
• It is characterized by a marked ventral curvature of the spine so the occiput of the head lies
near the sacrum.
• The body and chest walls are bent laterally and the thoracic and abdominal viscera are exposed.
61
• The pelvis is deformed.
• The liver is abnormal in shape and cystic.
• The rumen is occasionally distended with fluid.
• The limbs are usually ankylosed and rigid.
• In rare cases the limbs and head may be enclosed in a complete sac of skin.
CAMPYLORRACHIS SCOLIOSA
Condition
• Campylorrachis scoliosa is a fetal monster, rarely seen in cattle and swine.
Description
• It is characterized by a lateral curvature of the spine.

• The limbs are usually deformed and ankylosed.
PEROSOMUS ELUMBIS
Condition
Lateral View Dorsal View
Source: Balasubramanian et.al., (1991). Indian Vet. J. 68: July 677-678
Description
• Seen occasionally in cattle and swine.

• It is characterized by a lack of vertebrae and spinal cord caudal to the thoracic region.
• The monster has a small, flattened, deformed pelvis with strongly ankylosed and flexed hind
limbs and atrophy of the muscles of the rear quarters.
62
PEROSOMUS HORRIDUS
Condition
Caprine Perosomus Horridus
Source: Balasubramanian et. al., (1995). Indian Vet. J. 72: Sept. 985-986.
Description
• Perosomus horridus is a bovine fetal monster with general ankylosis and muscle contractures.
• This is due to a marked double S-shaped lateral twisting of the vertebrae.
• It is characterized on external examination by a short spine.
LIMB ANOMALIES
• Include amelia, missing or “amputated” extremities.
Amputated Limbs in a Buffalo Calf
• Micromelia; hemimelia, or absence of the distal half of the limb; sirenomelus, or fusion of the
hind limbs with varying amounts of hypoplasia and deformity of the pelvis and pelvic organs;
hypoplasia of the extremities; polydactyly, or the increased number of digits or claws in cats,
dogs, cattle, horses and swine; syndactyly or the union of digits or claws, especially in cattle and
swine; and ectrodactyly or absence of phalanges.
• Ectopia of the patella has been reported in cattle, dogs and horses.
63
• Miscellaneous anomalies due to displacement of tissues include teratomas, dermoids, and
dentigerous cysts.
o Dentigerous cysts
Characterized by a displaced dental follicle containing fluid and teeth, is seen
most commonly in the horse.
May be located beneath the ear and are called an “ear tooth.”
o Dermoids
Seen occasionally on the cornea, third eyelid or on the neck in cattle and other
species.
In horses dermoid tumors may rarely involve the ovary or testis, especially the
retained testis.
o Teratomas
Occasionally seen in all species.
DEFINITION
• Embryonic duplications are malformations due to abnormal duplication of the germinal area
giving rise to fetuses whose body structures are partially but not completely duplicated.
FREE MONOZYGOTIC OR DIZYGOTIC TWINS OR TRIPLETS
• Symmetrical twins are either monozygotic or identical, or dizygotic or fraternal.

• Asymmetrical twins consist of a normal and an acardiac or monster individual. These may
include three types:
o Hemicardius
A very imperfect individual but parts are recognizable, and
A rudimentary heart is present.
o Holocardius acephalus
The cranial part of very imperfect individual is lacking.
No heart is present.
o Holocardius amorphus or Amorphus globosus
The general body form is unrecognizable.
It may occasionally be seen, most commonly in the cow, but also in the mare,
ewe and goat, attached to the placenta of the normal monozygotic or dizygotic
twin.
These very imperfect zygotes are parasitic upon the placenta of the normal twin
and are never observed in single births.
64
AMORPHUS GLOBOSUS
In Bovine
• Usually appears as a round or oval, edematous structure weighing 1/2 to 7 lbs.

• Covered with skin and hair and containing connective tissue, fat and other soft tissues and
occasionally cartilage and bone.
• However, in cattle one acardiac monster was female and its normal cotwin was male. This
confirmed Williams theory’ that the Amorphus globosus was an imperfect zygote of dizygotic
twins.
• It was demonstrated that the leucocytes of the normal male calf only contained the XY or male
chromosome complement and no blood cell chimerism occurred.
• The monster composed mainly of stomach and intestinal tissues were enclosed in its own
amnion.
• In another case, two acardiac monsters were attached to the placenta of a normal bovine calf.
In Mare
• In the mare this structure usually consists of a round, thin, fenestrated ball of cartilage 3 to 5
inches in diameter.
• It is covered with mucous membrane.
• The interior of the equine amorphus monster is jelly-like tissue.
In Human
• Observed in the chorion in about 1 in every 100 single births.

• Based on karyotypic studies of chromosomes, human acardiac monsters were found to be the
same sex as their normal twin supporting the theory of their monozygotic origin.
In Goat
Fig.1: Gross morphology of

amorphus fetus with
pigmented skin and a few
hairs.
65
Gross Features
• The anomalous fetus was covered with pigmented skin with a few hairs (Fig.1). It was slightly
flattened and roughly spherical, measured 9.3 x 6.1 x 3.4 cm, and weighed 786 g.
• One pole of the anomalous fetus had a soft tissue protuberance and the other had 2 unequal
and undifferentiated limbs. The cranial and caudal ends could not be identified and no oral or
anal openings were discernible.
Radiographic Features
Fig.2: Radiograph of anomalous

fetus showing irregular soft round
tissue mass with soft tissue
protrusion on one side.
• The radiographic image showed an irregular round soft tissue mass with soft tissue protrusion
on one side and a partly developed appendicular structure with undifferentiated bone and a
rudimentary appendicular protrusion on the other side (pole, Fig. 2).
• The tissue mass was divided into 2 zones by a radio dense soft tissue layer near the periphery.
• Two unequal linear radio-opaque structures in the center were made of bone that resembles
the pelvic girdle.
• An irregular oval mass between the linear bony structure and the soft tissue protrusion
resembled undifferentiated fused spines.
• A medial linear incision was made to identify the development of various anatomical structures.
• Undifferentiated muscle and prominent blood vessels were observed, but there was no
recognizable organ system.
• The bony mass could not be differentiated as forelimb or hind limb. Achordia was evident.
Histological features
• Histologically there were numerous lymphoid aggregations and blood filled capillaries.
• Capillary endothelium showed oval to elongated nuclei. Some areas showed epithelial type of
cells with eosinophilic granular cytoplasm. Arteries were present (Fig.3).
• Some areas showed scattered mononuclear cell infiltration, whereas, other areas revealed
dense fibroblasts (Fig.4) arranged in various directions.
66
Fig.3: Histological section of Fig.4: Histological section
amorphus globosus showing showing mononuclear infiltration
prominent artery. with dense fibroblast.
Reference
• Md. Taslim Anwar, Athar Iman Khan, S.Balasubramanian, R.Jayaprakash, T. A. Kannan,

S.Manokaran, S.A.Asokan and C.Veerapandian (2009). A rare case of globosus Amorphus in
goat. Candian Vet. J . Vol 50: Aug p854-856
CONJOINED TWINS
Conjoined twins in which the components or component parts are symmetrical are called Diplopagus
monsters or “Siamese” twins.
• Triplopagus is extremely rare.

• Conjoined twins arise from a single ovum and are monozygotic.
• Occurrence: about once in 100,000 bovine births.
• Most common in cattle but are seen rarely in sheep, pigs, dogs and cats and are exceedingly
rare in horses.
Those conjoined twins in which each component is complete or nearly so include
• Thoracopagus, sternopagus, or ziphopagus twins are joined at or near the sternal region. The
internal organs are usually duplicated. The components are face to face.
• Pygopagus monsters are connected at the sacrum and the components are back to back.
• Craniopagus twins are united at the heads. Components may be facing in the same or in the
opposite direction.
• Ischiopagus fetuses are joined at the lower pelvic region and the bodies extend in a straight
line and the heads in the opposite direction.
The two components equal one another in this group but each is less than an entire individual.
• Usually associated with lateral fusion.
67
• May vary from single normal individuals to those of two normal but superficially joined
individuals.
• Duplication may lead to doubling of the cranial end of body while the caudal end remains
single; or the caudal part may be doubled and the cranial part single.
• Duplication can occur at both cranial and caudal ends with the middle area of the monster
remaining single.
• Duplication, of the cranial part of the fetus is more common than that of the caudal portion.
DUPLICATION IN THE CRANIAL REGION
Monocephalus
• Monsters with partial duplication of the frontal region, nose and mouth are referred to as
Diprosopus or double face.
• Either face may be complete or one eye of each may be fused into a common medial orbit. Di-,
tri- or tetraophathalmus and di-, tri- or tetraotus may be present.
Feline Double Monster: Monocephalus,

tetrapus tetrabrachius
Dicephalus or two heads, with distomus or monostomus occasionally is seen.
In Cow In Cow In Buffalo
Source: Antonie and Balasubramanian personal collections
• Tricephalus is very rare.

68
• A Dicephalus dipus dibrachius monster has two forelimbs and two hind limbs with partial
duplication of the spine and one or two tails, dicaudatus.
• Dicephalus dipus tribrachius has 3 forelimbs
• Dicephalus dipus tetrabrachius has 4 forelimbs.
DUPLICATION IN THE CAUDAL REGION
Duplication in the caudal region is designated as Dipygus. Tripygus is very rare.
• Monocephalus tripus dibrachius has 3 rear limbs.

• Monocephalus tetrapus dibrachius has 4 rear limbs.
• Cephalothoracopagus has a single neck and more or less complete fusion of the heads to form
an almost single face.
• Syncephalus has one face, four ears, and a single or partially doubled cerebrum.
• Janiceps is a monster with two faces on opposite sides of the head.
DUPLICATION OF CRANIAL AND CAUDAL REGIONS
• Duplication of both cranial and caudal regions is Dicephalus dipygus.

o Dicephalus tripus tribrachius
o Dicephalus tetrapus tetrabrachius
o Dicephalus tripus tetrabrachius, or
o Dicephalus tetrapus tribrachius
UNEQUAL AND ASYMMETRICAL CONJOINED TWINS
• Unequal and asymmetrical conjoined twins are composed of one very imperfect and
incomplete twin, called the parasite, dependent on the other twin, the autosite. This is called a
heteropagus monster. The autosite is nearly normal and the parasite is attached to it as a
dependent growth.
o The parasite may be attached to the visible surface of the autosite. Common junction
sites are the back, thorax, sacrum or pelvis, and in rare cases the abdomen, head, or
palate. The latter is called epignathus. Some of the smaller, more imperfect parasites
may be called teratomas.
o A parasite can rarely develop within the autosite usually in the abdominal, thoracic,
pelvic or cranial cavity, or in the spinal canal or scrotum.
o Teratomas in the abdominal cavity and between the mandibles have been described in
two calves.
DEFINITION
• Intersexes are individuals in which the diagnosis of the sex is confused because of congenital
anatomical variations.
69
OCCURRENCE AND CONDITIONS
Occurrence
• In goats and pigs: Most common

• In horses and dogs: Less common
• In sheep and cattle: Occasional
• In cat: Rare
Conditions in intersexes
• Hermaphroditism
• Abnormalities of the accessory genital organs
• Gonadal dysgenesis, and
• Freemartinism.
CLASSIFICATION
• Intersexes may be separated into males or females based on

o Their genetic sex, either chromosomal or nuclear sex,
o Their gonadal sex or presence of ovaries or testes
o Their phenotypic sex or the morphology of their accessory genital organs
o Possibly their hormonal or behavioural sex.
• Hermaphrodites are usually classified on the basis of gonadal sex as
o True hermaphrodites: Presence of both testes and ovaries or ovotestes.
o Pseudohermaphrodites: Presence of gonads of only one sex.
Male pseudohermaphrodites: Phenotypically resemble females but have testes.
Female pseudohermaphrodites: Phenotypically resemble males but have ovaries.
• Caprine pseudohermaphrodites, even though they have testes, are females according to the
sex ratio, sex chromatin studies and chromosome analyses.
• In goats this condition is a simple recessive sex-limited character associated with hornlessness
or the polled condition. Horned hermaphrodites are extremely rare. In swine, a similar
recessive type of hermaphroditism, some may be non genetic.
• Crew and others prefer to consider the terms true hermaphroditism and
pseudohermaphroditism as misnomers indicating they should be regarded as degrees of
intersexuality.
• Almost all male and female pseudohermaphrodites are genetic or chromosomal females (XX)
and are positive on nuclear sexing as indicated by the presence of the sex chromatin mass or
Barr body in the nucleus.
70
TRUE HERMAPHRODITE
• Rare
• Has internal genitalia resembling both sexes and external genitalia of an intermediate type that
may tend either toward the male or female.
• Most frequent in swine.
• In most cases the genetic sex is female (XX) but it is likely that on further study many of these
cases may prove to be mosaics or chimeras produced by nondisjunction and/or other mitotic
errors during mitosis early in embryogenesis or dispermic fertilization of an ovum by an X-
bearing sperm and a non extruded polar body by a Y-bearing sperm resulting in tissues with
variable sex chromosome complements such as: XX/XY, XXY, XXYY or XXXY.
PSEUDOHERMAPHRODITE
Female pseudohermaphrodite
• Rare: Intersexes with female gonads and external genitalia resembling the male may be
produced by exposure to androgens during embryonic life.
• Cause
o Lesion of the adrenal gland or
o A biochemical lesion of steroidogenesis.
• Female or true hermaphrodites with fairly normal external and internal female structures may
rarely be fertile since ovulation may occur.
Male pseudohermaphrodite
• Very common
• Symptoms
o Testes in the abdominal cavity or beneath the skin in the scrotal region.
o Scrotum seldom develops, due to the anomalous growth of the external genital organs
which usually resemble the female.
o Often a greatly enlarged clitoris is present, which with the vulvar configuration, called
“fishhook” vulva.
• In swine, often, when urinating, leads to direct the stream in a greater dorsal arc than does the
normal female.
• Location of the urethral opening may be anywhere from that of the normal female to one in a
penis-like structure with hypospadias in the scrotal or abdominal region.
• May be detected by their failure to show signs of estrum.
• Body appears as a male castrate.
• Hermaphrodites commonly resemble cryptorchid males or nymphomaniacs in their male
actions and attitudes.
71
• In the male pseudohermaphrodite, the internal genitalia resemble both sexes and a uterus like
structure is nearly always present. Hermpahrodites are invariably sterile, especially males with
intra abdominal or subcutaneously located testes.
• In swine, male pseudohermaphrodite, and probably the same would be true in goats where this
condition is also genetic, that cells have only an XX chromosome complement. Hypoplastic
testicular development with modification of the external genital tract occurs in the absence of
the Y chromosome.
Male pseudohermaphrodite in a Goat Male pseudohermaphrodite in cattle
Enlarged Clitoris "Fish Hook" Vulva
Courtesy: Balasubramanian Personal Collection Courtesy: Drost Project
HYBRIDS
• Hybrids are an extreme outcross

• A cross of the ass on the mare to produce the mule or the sheep on the goat, the dog on the
coyote, and the bison on the cow.
• The ass with a diploid chromosome number of 62 when mated with the horse with a diploid
chomosome number of 64 produces a mule with the chromosome number of 63.
Female mule
• Undisturbed ovarian hormonal function.

• Produce normal follicles and corpora lutea.
• Exhibit estrum, and occasionally show mammary development with the production of milk.
• The female and male mules are sterile, probably due to a failure of gametogenesis caused by
asynapsis during the first meiotic division.
• A number of alleged fertile female mules examined were found to be donkeys rather than
mules when chromosome studies of their body cells were made.
72
DEFINITION
• Freemartin is an infertile female with a modified genital tract born cotwin, or in greater
multiples, with a bull with which it has exchanged whole blood.
• The freemartin is one of two dizygotic individuals that are of different sexes and do not
resemble each other.
CLINICAL SIGNS IN CATTLE
• Ovaries usually fail to develop and remain small, about the size of a flattened barley grain, and
undifferentiated.
• In rare cases some differentiation toward the female or male gonad may occur.
• The genital tract, especially the portion arising from the paramesonephric duct, is markedly
arrested in development.
• Often in the region of the cervix, two tubular structures or remnants of the mesonephric duct
resembling seminal vesicles are present.
• The vagina is undeveloped.
• The vulva is fairly normal, except for the occasional presence of a prominent clitoris and a large
tuft of vulvar hair.
• In the yearling animal, failure of estrous cycle; the udder and teats remain very small and the
external characteristics resemble a steer.
DIAGNOSIS IN CATTLE
Fincher’s Test tube Test
• Insert a test tube or glass speculum of 3/8- to 1/2-inch with lubrication into the vulva of the
suspected heifer.
In freemartin
• Tube will go no farther than the hymen, or the caudal portion of the vagina or about 7.5 to 10
cm, 3 to 4 inches, in a young calf, as there is no normal vagina.
• Use of a light will reveal, the no vaginal opening anterior to the urethral opening on the floor of
the vulva.
In normal
• Some resistance may be encountered when the test tube passes through the vulvovaginal
region but it then will pass 12 to 18 cm, 5 to 7 inches into a freely dilatable vagina.
• Use of a light will reveal a normal small cervix.
73
The only chance for error in this technique is in heifers with an imperforate hymen.
Rectal examination
• Perform after the freemartin female becomes 8 to 14 months of age.

• Marked arrest in the development of the vagina, cervix, uterus, and gonads.
• Usually these structures cannot be found on rectal examination or they are very minute.
Male cotwins to freemartins are usually considered to be fertile.
IN OTHER DOMESTIC ANIMALS
• Freemartins are rare.

• It has been reported in sheep, pigs and possibly goats.
• The chorions of twins or greater multiples in these species will often fuse but anastomosis of
blood vessels is rare.
74
MODULE-3: FETAL MUMMIFICATION - MACERATION - EXTRA UTERINE PREGNANCY
DEFINITION
• Fetal death during the middle or last one third of gestation with failure of regression of the
corpus luteum and abortion of the fetus within a week or 10 days or decomposition or
maceration of the fetus within the next several months, followed by autolytic changes in the
fetus, absorption of placental and fetal fluids, and involution of maternal placenta leads to
MUMMIFICATION.
INCIDENCE
• In cattle, the incidence of fetal mummification is low and sporadic.

• In some herds the incidence may be higher and in few instances apparent epizootics of
mummified fetuses may occur.
75
TYPES OF MUMMIFICATION
Hematic mummification
• Observed in cattle
• Maternal placenta or caruncle undergoes involution
• Between endometrium and fetal membranes, variable amount of hemorrhage occurs
• Plasma gets absorbed and leaves a reddish-brown, gummy, tenacious mass of autolyzed red
cells, clots and mucus, and
• Imparts reddish-brown colour to fetus and fetal membranes.
Papyraceous mummification
• Observed in mares, sheep, goats, dogs and cats.

• Resorption of fetal fluids
• Shriveled and dried fetal membranes, and
• Resemble a parchment paper.
HEMATIC MUMMIFICATION
• Incidence low and sporadic.

• Affects cattle of all ages.
• Occur at 3–8 th month of gestation but most common in 4, 5 and 6 th months.
• Usually affects single fetus but may occasionally involve one or both fetuses in twin
pregnancies.
ETIOLOGY
• In cattle, cause of fetal death and mummification are same as for fetal death and abortion.
• Genetic factors.
• Torsion or compression of umbilical cord.
• Fetal death due to Infectious causes includes V. fetus, moulds, leptospirosis and BVD-MD virus.
• Administration of progesterone or progesterone like compounds if continued beyond 210 days
of gestation.
• It is often difficult or impossible to ascertain the cause, since the time of fetal death is unknown
and due to autolysis and mummification of fetus and membranes.
CLINICAL SIGNS
• Failure of oestrum.
• Not suspected until late in gestation when normal development of the fetus, body changes
related to parturition and calving fail to occur.
76
• Mummy remains in semi-moist state without odour or pus until spontaneous abortion in 1-2
months to 1-2 years, or until diagnosed, treated or corrected or slaughtered.
• Rectal examination reveals
o Persistent corpus luteum (PCL)
o Uterine walls contracted and tightly enclose the conceptus
o Uterine walls fairly thick
o Absence of fetal fluids
o Absence of cotyledons, and
o Uterine artery small and absence of fremitus.
o In early case
Uterus feels doughy due to large, soft blood clot
Difficult to palpate the fetus.
o In long standing case
Dry, firm and more leather – like fetus (In cow).
Bovine Fetal Mummy
• Vaginal examination reveals a closed cervix with a mucous seal of pregnancy.
PAPYRACEOUS MUMMIFICATION
Caprine Fetal Mummy Ovine Fetal Mummy
77
• Observed in the sow, bitch and cat, as well as in the biparous ewe and goats
• Ayyappan et.al., (1993) have reported a case of normal kid with three papyraceous mummified
fetuses in a non-descript doe.
In Swine
• Occurs most frequently.

• Important cause of prenatal losses.
Porcine Fetal Mummies
• Economic importance by lowering the fecundity.

• In-utero death of fetuses between 40–90 days of gestation, undergo mummification and are
expelled at parturition.
Mummifying fetus Uterus with Mummified Fetus Multiple Mummies
• High incidence in five viral diseases

o Aujezsky’s disease or pseudorabies
o Japanese encephalitis B virus
o Japanese hemagglutination virus
78
o Modified hog cholera virus, and
o A number of picorna, entero- or SMEDI viruses.
• No clinical sign of mummification during pregnancy.
• Draws attention at parturition, when among the normal piglets small mummified fetuses,
surrounded by parchment-like membranes, are expelled.
In dogs and cats
Canine Fetal Mummy
• Uncommon
• Sporadic
• Tendency to be associated with uterine inertia, particularly if only one normal fetus is present.
Ganesh et.al., (1996) have also reported a case of fetal mummification in canine.
• In cats, relatively frequent occurrence.
• Often noticed in large litters with expulsion of liver-like, partially resorbed placentae along with
normal fetuses.
• Close inspection may reveal an attached, small, resorbed fetus.
• It may represent overcrowding in the uterus and relative underdevelopment of the placenta,
leading to fetal death.
DIAGNOSIS
• Based on History and Clinical examination

• Prognosis is guarded.
TREATMENT
• Two treatment options are available.

o More rational approach is to initiate parturition.
o Perform hysterotomy.
79
Termination of pregnancy
• Manual
o Enucleation of Persistent corpus luteum (PCL)
o Danger of trauma and damage to ovary
o Following removal of CL
The cervix dilates and secretes fluid mucous.
The uterus contracts and forces the fetus outwards, and
At the same time the cow shows oestrus.
• Medical
o Use of oestrogen and prostaglandin preparations.
o A similar chain of events may be caused by therapeutic luteolysis using stilboestrol or
prostaglandin F2 alpha.
o With the advent of prostaglandin F2 alpha, the above approaches have lost importance
mainly due to their less precision and reliability.
o Since mummification is characterized by a PCL, it can be treated with prostaglandin F2
alpha preparations.
• Balasubramanian et.al., (1990) have reported a case of mummification of fetus in a crossbred
jersey heifer and its successful treatment with single injection of Lutalyse (25 mg i/m).
• Lefebvre et.al., (2009) have reported that hysterotomy represented an effective approach for
extracting mummified fetuses from cows that did not respond to prostaglandin F2 alpha
treatment.
MUMMECTOMY
• When expulsion with the aid of prostaglandin fails the colpotomy approach for removal of a
mummy is feasible. It is performed under epidural anesthesia. Exposure varies with the
flexibility of the broad ligaments hence is better in older cows.
Source: Hopper RM (2007)
80
INSTRUMENTS REQUIRED
• Homemade stainless steel shaft with a

sharp beveled cutting end [length 50
cm, diameter 2 cm], patterned after
the Kimberling-Rupp instrument below.
• A bloat trocar (top), after sterilization,

can be used to make a stab incision in
the fornix. In the middle, a home made
spear with a pointed V-shaped tip. At
the bottom, a homemade stainless
steel shaft with a sharp beveled cutting
end [length 50 cm, diameter 2 cm];
made from the shaft of a defunct IV
stand. The legs of a retired small
animal examination table can also be
used for this purpose.
COLPOTOMY STEPWISE PROCEDURE (Fig. a-e)
Fig.a
• Prior to the transvaginal procedure the cervix

and vagina are examined with a speculum for
evidence of pus or contamination. Here, a
cylindrical glass speculum [length 24 cm,
diameter 4 cm] is used Drost M, 2009).
81
Fig.b
• View of the cervix through a cylindrical glass

speculum. A small piece of bone can be
identified in the external os (it turned out to be
the tip of a claw). King AC (2009).
Fig.c
• The anterior cutting end of a sterile stainless

steel shaft [length 50 cm, diameter 2 cm] is
shown prior to insertion into the vagina (Drost
M,2009).
Fig.d
• Placement of the tip of the colpotomy spear is

at the 2 0'clock position in relationship to the
cervix and aimed slightly ventrally. This
minimizes the risk of puncturing a distended
rumen (Lunsford ND, 2008).
Fig.e
• The cutting end of the shaft is advanced into

the fornix, at a 2 o'clock position in relationship
to the external os of the cervix. The wall of the
fornix is pushed forward and with a quick
thrust the shaft enters the peritoneal cavity.
After removal of the shaft the incision is
enlarged by inserting first one finger, then two,
and subsequently the entire hand (Drost M,
2009).
Courtest: Drost Project
82
COLPOTOMY STEPWISE PROCEDURE (f-j)
Fig.f
• The uterus is exteriorized by retracting it into

the vagina and exposing it at the vulva (Drost
M, 2009).
Fig.g
• Exposure of the uterus via colpotomy under

epidural anesthesia (Drost M, 2009).
Fig.h
• The enlarged uterine horn (containing a small

mummy, or in this case several macerated
bones) is positioned for the removal of its
contents. The mass was curved and felt dry
without crepitus (King AC, 2009).
Fig.i
• An 8 cm incision has been made along the

greater curvature (Drost M, 2009).
Fig.j
• Several bones and small hooves are removed.

There was no odor, no pus, nor fluid (Drost M,
2009).
83
REMOVAL OF MUMMIFIED FETUS
Several bones , small hooves and teeth After cleansing, a femur, five claws, a carpal
covered with some inspissated tissue, were bone and three small teeth compatible with
removed. There was no fetid odor. 7-month old fetus ere identified.
Drost M (2009) Drost M (2009)
CLOSURE OF UTERINE INCISION
Positioning of the uterine horn with a Closure of the uterine incision with the utrecht
uterine pattern. After rinsing with sterile saline the
forceps for cloure of the inision. uterus was returned to the abdominal cavity.
Drost M (2009) The incision in the fornix was not sutured.
Drost M (2009)
SELECTED REFERENCES
• Ayyappan,S., S. Balasubramanian, Srijayanth,R., R.S.George., K.B.P.Ragavendra and P.H.Tank

(1993). Papyraceous mummification in a doe. Indian Vet. Med. J., Vol. 17, Sept-Dec, P-169-170.
• S.Balasubramanian, T.G.Devanathan, A.Subramanian and V.N.Seshagiri (1990). Use of lutalyse
for bovine fetal mummification. IJAR : 11 : 2 : 168 - 169.
• S.Balasubramanian and P.Sridevi (1999). Unpublished data.
84
• Ganesh,T.N., (1996) IVJ.
• Rejean C. Lefebvre, Emilie Saint-Hilaire, Isabelle Morin, Gabriel B. Couto, David Francoz and
Marie Babkine (2009). Retrospective case study of fetal mummification in cows that did not
respond to Prostaglandin F2 alpha treatment. Can. Vet. J., 50:71-76
FREQUENTLY ASKED QUESTIONS
Will fetal death in all cases end up in mummification?
• No. In early pregnancy, following fetal death total resorption or abortion usually occurs.
Whereas, fetal death from mid gestation onwards, unaccompanied by failure of abortion or
parturition mechanism and autolytic changes in fetus, absorption of fetal and placental fluids
and involution maternal placenta leads to mummification.
Can we determine the cause of fetal mummification?
• No. Since the time of fetal death is unknown and due to autolysis and mummification of fetus
and membranes, it is often difficult or impossible to ascertain the cause.
Is removal of the corpus luteum advisable to terminate pregnancy in bovine fetal mummification?
• No. Should seldom be used due to possible danger of trauma, bleeding, damage to ovary
leading to ovaro-bursal adhesions, and sterility.
Can we administer corticosteroids to terminate pregnancy in bovine fetal mummification?
• No. Use of corticosteroids will be effective only when the fetus is alive.
INTRODUCTION - FETAL MACERATION
• Occur at any stage of gestation.

• Observed in all species, most often in cows.
Macerated Fetus in Goat
85
• When fertilized ovum or embryo succumbs to bacterial or viral infection or other diseases or
abnormality early in gestation it is usually absorbed in the uterus or a slight and often
insignificant purulent uterine or vaginal discharge may be present.
• The interval between the estrual periods may be prolonged if the embryo did not succumb until
20-50 days after conception.
• Early embryonic death and maceration are probably caused by a variety of miscellaneous
organisms that may be found in the uterus and are of common occurrence in cows affected
with trichomoniasis or vibriosis.
• Occasionally cases of pyometra seen in trichomoniasis, fetal shreds and placental remnants are
often found floating in the pus.
• In cases of early fetal maceration, the cervix may be tightly sealed or some pus discharge may
be evident in the vagina or from the vulva.
• These cases are usually diagnosed and treated as pyometra or endometritis; in the former,
estrum is not present; in the latter estrum may occur.
FETAL MACERATION IN COW
• Occurs after 3 months of gestation, by which time fetal bones are fairly well developed.
• Caused by similar wound infection bacterial agents.
• Septic metritis of pregnancy, resulting in the death, emphysema and maceration of the fetus in
a closed uterus is uncommon.
• Symptoms of septic metritis of pregnancy are similar to septic metritis after parturition.
• Condition may be more serious and fatal due to the presence of decomposing fetuses, failure of
cervix and genital canal to dilate normally and a uterine inertia.
• More commonly fetal emphysema and maceration follow fetal death and beginning abortion in
which the cervix had dilated, but the fetus was not expelled due to:
o Failure of the genital tract to dilate sufficiently or
o Failure to contract normally or
o Because of fetus was dead and in an abnormal position and posture.
• In rare instances, fetal emphysema and maceration may be associated with uterine torsion
during gestation.
• Fetal emphysema and maceration follows when 2 factors are present:
o Open cervix
o A dead fetus at body temperature
o Both cause a rapid bacterial invasion of the fetus and fetal membranes of organisms
already present in the uterus or from the more caudal portions of the reproductive
tract.
• If the bovine fetus is beyond the 3 rd month of pregnancy and if the usual expulsive efforts are
not observed or are unsuccessful, the fetus develops emphysema in 24-48 h and in 3-4 days
maceration begins.
86
• Because of relatively smaller size of the fetus, those cases of fetal emphysema and maceration
accompanying an abortion during the middle period of gestation are treated differently.
SYMPTOMS AND DIAGNOSIS IN COW
• History of intermittent straining for several days associated with foul, fetid, reddish-grey vulvar
discharge
• Temperature and pulse often elevated
• Anorexia
• Drop in milk production, and
• Occasionally diarrhoea.
• Palpation per vaginum or rectum
o Distended, swollen fetus with gas crepitating in the tissues is diagnostic of fetal
emphysema.
In long standing cases
• Acute emphysematous stage has passed

• Straining is seldom observed
• Cervix is quite contracted
• Generalized symptom of elevated temperature, pulse and anorexia are usually not present
• There is often history of chronic, fetid, mucopurulent discharge from the vulva over a period of
several weeks or months
• Rarely cervix may be sealed
• History of gradual drop in milk flow
• Loss of weight, and
• Presence of diarrhoea.
RECTAL EXAMINATION FINDINGS IN COW AND MARE
• Fetal bones may be palpated in the uterus either floating in the pus or crepitating against each
other with little pus around them.
• Uterine wall is thick and heavy.
• Cervix usually large and hard.
• Severe degenerative and sclerotic changes in the endometrium.
SYMPTOMS AND DIAGNOSIS IN DOG AND CAT
• In most cases no external symptoms of illness are seen except possibly a uterine discharge
appearing occasionally in the vulva.
• Diagnosis is aided by abdominal palpation and radiographs besides observing symptoms.
87
PROGNOSIS
• Poor
• Treatment in the cow is difficult
• If much pus is present, treat as for pyometra
• Laparohysterotomy is difficult because of the small size of the uterus and its infected contents
and seldom indicated
• Future breeding life is questionable
• Longer the condition, the greater the damage to the endometrium, poorer the prognosis
• Most cases, slaughter is recommended
• In multiparous animals, hysterectomy or hysterotomy may be performed depending upon the
circumstances.
TREATMENT
In bovine
• In abortion from 3-7 months with fetal emphysema:

o If the cervix is sufficiently dilated and lubrication is used, fetus usually may be removed
by careful and gradual traction.
o In those cases in which the cervix is contracted and the fetus cannot be removed, heroic
treatment is not indicated.
In mare
• Cervix may be carefully dilated manually prior to removal of the decomposing fetus
• After removal, the uterus should be re-examined to make certain another fetus is not present
and remove the placenta if possible.
Supportive treatment
• Administration of antibiotics and sulphonamides parenterally along with large doses of

oestrogens: 50-100 mg of stilboestrol or 5-10 mg of oestradiol daily or every other days for 4-7
days.
• Until the cervix is relaxed enough or the fetus is macerated sufficiently to effect its removal
entirely or in pieces without injury to the cow.
• With this type of treatment, the danger of excessive traction or embryotomy causing
lacerations or rupture of the cervix and uterus is avoided.
• Because the uterus and its contents are relatively small, the development of septic metritis and
severe toxemia is prevented by supportive therapy.
• Cesarean section should be considered as a last resort in the cow.
• Cow should not be rebred for at least 3-4 months, and the outlook for her reproductive life is
guarded.
88
TYPES OF EXTRAUTERINE PREGNANCIES
• Extra uterine pregnancies are of two types

o True extra uterine pregnancy
o False extra uterine pregnancy
• In humans, some long existing extra uterine fetuses become quite firm and encapsulated with
calcium laid down in the capsule, causing them to be spoken as "Lithopedions"
• These well encapsulated extra uterine fetuses in animals may occasionally be referred as “Extra
uterine fetal mummies".
TRUE EXTRA UTERINE PREGNANCY
It is characterized by a fertilized ovum, embryo or fetus that has established nutritive relations with
organs or tissues other than the endometrium and has undergone in this location a degree of
embryological development.
• In humans, ovarian and tubal pregnancies may occur, latter being fairly common.
• True abdominal pregnancies with the placenta attaching to the mesentry and omentum are
rare in humans.
• In ovarian, tubal and abdominal pregnancy, embryonic development proceeds only for a short
period and then the fetus succumbs.
• In human tubal pregnancy, the oviduct ruptures usually accompanied by severe haemorrhage.
• No authentic case has been observed so far in domestic animals.
• This difference is apparently related in the manner in which the development of zygote
establishes nutritive relationship with the dam.
• In humans and rodents, the developing zygote erodes the mucosa and buries itself in the
maternal tissues while in domestic animals, the villi of the trophoblast attach themselves in the
maternal crypts formed in the endometrium.
FALSE EXTRA UTERINE PREGNANCY
In this condition the fertilized ovum, embryo or fetus develops normal placental relationship with the
endometrium and the fetus reaches recognizable size. It then escapes from the uterine cavity either
into the abdominal cavity or vagina.
• Seen occasionally in all domestic animals, and very rarely in mares.

• Occurs in last 2/3 rd of gestation.
• Almost all secondary extra uterine pregnancy fetuses are dead by the time the condition is
diagnosed (Fig.1).
89
Fig.1: Secondary extra uterine goat fetuses
• In so called vaginal pregnancies, it is obvious on examination that the fetus came through the
cervix from the uterine cavity.
• The cause of uterine rupture is frequently unknown.
• Occurs in uterine torsion, fetal emphysema, chronic peritonitis and following dystocia, and
administration of oxytocin in bitches.
• Occur spontaneously or possibly associated with violence in advanced pregnancy.
• In multipara, uterine torsion may involve a part of one horn or the entire horn with the
enclosed fetus being separated from the rest of the uterus.
• The adhesion that take place may cause the condition to be diagnosed as an extra uterine
pregnancy or fetus.
• In many cases in domestic animals in which a sterile fetus is released in to the abdominal cavity
with little or no external symptoms.
• The fetus dies and with its membranes becomes walled off as a sterile foreign body in the
ventral portion of the abdominal cavity and remains there as an inert mass for months.
• Often extensive adhesion develops between it and other viscera.
• Site of rupture may be small or invisible scar after the uterus involutes (Fig.2).
Fig.2: Scar in goat uterus
• Mild digestive disturbance may be present.
90
• Occasionally large extra uterine pregnancy may be diagnosed by rectal examination in cow, if
the fetus was near term when it escaped from the uterus.
DIFFERENTIAL DIAGNOSIS
• Extrauterine pregnancies should be differentiated from:

o Mummification
o Tumors, and
o Fat necrosis
PROGNOSIS
• Guarded.
• Advise Slaughter.
• Laparotomy to remove the fetus in large animals may be difficult because of extensive
adhesions whereas in dogs and cats, operation may be considered.
DROPSY OF FETAL MEMBRANES/FETUS - ABDOMINAL HERNIA
91
INTRODUCTION
• A pathological condition of the pregnant animal characterised by excessive accumulation of

fluid within the amniotic or allantoic cavity is referred to as
o Hydramnios (Hydrops amnii) or
o Hydrallantois (Hydrops allantois), respectively.
• Earlier this condition was termed as hydrops amnii but observations have established that the
excess of fluid is usually in the allantoic sac and hence should be referred to as hydrallantois
(Arthur, 1989).
• Dropsy of the fetal sacs usually occurs in bovine, but also seen in mares of 10-20 years, few
cases recorded in sheep, and also observed in canines.
• In cattle, it is mostly seen in the last three months of gestation.
ETIOLOGY
• Cause unknown; but Arthur has postulated a placental dysfunction consequent upon
incompatibility of mother and fetus.
• Cow bearing twins is more likely to develop hydrallantois.
• Normally, in cattle, there is markedly accelerated production of allantoic fluid at 6-7 months of
gestation and it is suggested that, where placental dysfunction exists, this increase may become
uncontrolled and lead to massive accumulation.
CLINICAL SIGNS
Hydrallantois in goat • All cases of hydrallantois are progressive but they vary in time of
clinical onset (within the last 3 months of pregnancy) and in their
rate of progression.
• Distended abdomen (In goat).
• Allantoic fluid volume varies up to 273 litres and such large
amounts cause a serious strain on the cow and greatly interfere
with respiration and appetite.
• Gradual loss of condition, and at an unspecified later time leads
to recumbency and death.
Rear view
• Occasionally the animal becomes relieved by aborting.
Hydrallantois in cow • Less severely affected animals reach term in poor condition and
because of uterine inertia frequently require help at parturition.
• Dislocation of the hips or backward extension of the rear limbs
may occur and the cow lies on her sternum looking like a
"Bloated bull frog appearance" (In cow).
92
SPECIFIC FEATURES
• Abnormally low number of functionary cotyledons.

• Non gravid horn usually does not take part in placental formation.
• In the gravid horn, a compensatory accessory caruncular development occurs.
• Histologically features
o A non-infectious degeneration, and
o Necrosis of the endometrium.
• Fetus may be small sized.
DIFFERENTIATION OF HYDRALLANTOIS AND HYDRAMNIOS
ITEM HYDRALLANTOIS HYDRAMNIOS
Incidence 85 - 95 % 5 - 15 %
Rate of development Rapid, within 1 month Slow, over several

months
Shape of abdomen Round and tense Piriform, not tense
R/E of placentomes Cannot be palpated Can be palpated

and fetus
Gross characteristics Watery, clear, amber coloured, Viscid, may contain

of liquid transudate meconium
Fetus Small seldom malformed Malformations present
Placenta and Allantois chorion diseased and Placenta, allantois

placentomes abnormal with placentomes chorion and
hypertrophied and reduced number placentomes normal
Refilling of cavity after Rapid Does not occur

removal of excess fluid
Occurrence of Common Uncommon

complications
Outcome Abortion or maternal death common Parturition at

approximately full term
93
DIAGNOSIS
• Based on the easily appreciable fluid distension of the abdomen with its associated symptoms
in the last third of pregnancy.
• Confirmation by rectal palpation of markedly swollen uterus, and failure to palpate the fetus
either per rectum or externally.
TREATMENT
• In mild cases, when dropsy develops shortly before term, restricted water intake,
administration of diuretics and cardiovascular stimulants may be tried.
• Resort to two stage cesarean operation.
• Corticosteroid (20 mg of dexamethasone or 5-10 mg of flumethasone) in conjunction with
oxytocin by intravenous drip for 30 minutes.
• A single intramuscular dose of 40 mg of dexamethasone is recommended (Sloss & Dufty, 1980).
• Administration of glucocorticoids leads to severe stress on bone marrow function, leukopenia
develops and persists for several days. Metritis, pneumonia and enteritis may follow this.
• An intramuscular injection of 0.5 to 0.7 mg of PGF2 alpha analogue (Cloprostenol) can be used
at any stage of pregnancy with satisfactory results.
• Recumbent cases - Slaughter.
INTRODUCTION - DROPSY OF FETUS
• Dropsical conditions affecting the fetus are of several types.

• The conditions of importance from obstetrical stand point of view are:
o Hydrocephalus
o Meningocele
o Ascites
o Anasarca
• Location and amount of the excess of fluid dictates the form of the fetus and the degree of
obstetrical problem.
• Increased diameter of the fetus leads to dystocia.
FETAL HYDROCEPHALUS
• It involves a swelling of the cranium due to an accumulation of fluid which may be in the
ventricular system or between the brain and the dura (Arthur et al., 1989).
• Affects all species of animals and is seen most commonly by veterinary obstetricians in pigs,
puppies and calves .
• Generally described as being either internal or external and CSF collects passively inside or
sometimes outside the ventricles, causing pressure atrophy of cerebral tissues (Gilman, 1956).
94
• Inherited internal hydrocephalus is recognized as a clinical entity by the animal breeding
specialists and the veterinary profession.
• Probably many cases go undiagnosed because of lack of knowledge or thorough examination.
• It is important for the practitioner to realize that internal hydrocephalus and other cranial
abnormalities can exist without a gross distortion of the skull.
ETIOLOGY
• There are probably several etiological factors including dietary deficiency (Vitamin A in lab
animals), infectious agents (Swine fever vaccine in pigs) and genetic factors (accompanies
achondroplasia in cattle and dogs).
• In cattle practice, it usually occurs sporadically and the cause is then not determined.
• In broad etiological sense, the so-called congenital brain hernias (meningeocele and
encephalocele) may be included with congenital hydrocephalus, as these also are associated
with an extensive prenatal accumulation of cerebrospinal fluid (CSF) with or without a
protrusion of the cerebral tissues.
• In all these cases, CSF collects passively inside or sometimes outside the ventricles, causing
pressure atrophy of the cerebral tissues.
• Such accumulations of fluid may be due to obstruction of the foramen of Monroe, the cerebral
aqueduct, or the foramina of the roof of the fourth ventricle, resulting in internal
hydrocephalus (Gilman, 1956).
CLINICAL FEATURES
Visible distortion of the cranium • Balasubramanian et.al., (1997) have reported a case of
congenital internal hydrocephalous in a calf resulting in
dystocia and its management.
• The male fetus weighed 29 kgs with visible distortion of
the cranium.
• The muscles in the fore and hind limbs showed atrophy.
Excessive thinning of the • Radiograph revealed failure of fusion of the flat bones in
cerebral tissues the cranium leaving an opening of 10.5 cms diameter.
• The skin in the area was gently dissected and there was
excessive thinning of the cerebral tissues.
• Trocarization resulted in serous fluid of 1.6 litres and
subsequent collapse of the cerebral tissues.
95
TREATMENT
• In more severe form, due to marked thinning of cranial bones trocarization and compression of
the skull facilitates vaginal delivery.
• In cases where trocarization and compression cannot be performed, dome of the cranium may
be sawn off with an embryotomy wire or chain saw (Arthur et.al., 1996).
• In severe cases, c- section may be performed.
MENINGOCELE
• Reported in ovine, its occurrence in bovines is very rare (Abid et.al., 1988).
• Morphogenesis of these defects is not simply a problem of defective ossification with
secondary protrusion of meninges, but instead depends on a primary defect of neural tube
leading to local failure of development of the skeletal encasement (Jubb and Kennedy,1970).
• The meningocele varies in size from few to several inches in diameter and mostly associated
with suture line, frequently involving frontal region (Leipold et.al., 1983).
• Sarma et.al. (1993) successfully carried out surgical removal of congenital meningocele in a
bovine calf.
Meningocele • Ayyapan et.al. (1996) have reported a case of

congenital meningocele in a 10 day old buffalo
calf.
• Clinical examination revealed a bilobed soft
fluctuating swelling attached to the frontal
region of the head.
•
The calf was presented with the history of swelling in

the cranial region and recumbent since birth.
FETAL ASCITES
• Ascites or dropsy of the peritoneum is a common accompaniment of infectious diseases of the

fetus and of developmental defects such as achondroplasia.
In Caprine In Bovine
96
• Occasionally it occurs as the only defect.
• Aborted fetuses are often dropsical; when the fetus is full term ascites may cause dystocia.
• This can usually be relieved by incising the fetal abdomen with an embryotomy knife.
Bovine Fetal Hydroperitoneum
FETAL ANASARCA
• Fetal anasarca of Ayrshire cattle is a hereditary condition and is determined by autosomal

recessive genes (Donald et al., 1952) it may also affect sheep (Roberts, 1971) and goats (Tamuli
et al., 1987 and Balasubramanian et al., 1990).
Caprine Fetal Anasarca
• Cases of subcutaneous edema are present in the oldest obstetric literature but in recent years a
peculiar form in the Ayrshire breed has caused many instances of severe dystocia.
• The trait has been disseminated by the widespread use of bulls certain popular strains and
subsequent close breeding within herds has caused it to appear.
• Affected fetus is usually carried to term and concern is caused by the lack of progress of second
stage of labour.
97
• This is due to the great increase in fetal volume caused by the excess of fluid in the
subcutaneous tissues, particularly of the head and hindlimbs.
• Interesting point – An undue proportion of these fetuses are presented posteriorly, enormous
swelling of the presenting limbs is very conspicuous.
• Peritoneal and plueral cavities - excess fluid with dilatation of the umbilical and inguinal rings as
well as hydrocele.
• Fetal membranes are also edematous and occasionally there is a degree of hydrallantois.
• Fetal weight varies from 39–102 Kg
• In less severe cases, delivery may occur spontaneously or by traction, others require partial
fetotomy or multiple incisions of the subcutaneous tissues.
• In more severe cases, perform C- section.
SELECTED REFERENCES
• Ayyappan, S., S.Balasubramanian, A. Subramanian and P. Dhanaplan (1996) congenital

meningocele in a buffalo calf- A case report. Cherion 25:5-6.
• Ayyapan, S., S.Balasubramanian C.Veerapandian and S.R.Pattabiraman (1993). Bovine fetal
dropsy with bilateral lymphatic cyst. Indian Vet. J. 70:171-172.
• Ayyappan, S., S.Balasubramanian and Archibald David (1993). Fetal hydroperitoneum with mild
anasarca in a doe – A case report. Indian Vet. J. 70:273-274.
• Balasubramanian, S., A. Subramanian and C. Veerapandian (1990). Normal kid cotwinned with
an anasarcous fetus. Vet. Rec. Oct 27:436.
• Balasubramanian, S., S.A.Asokan, V.N.Seshagiri, and S.R.Pattabiraman (1997). Congenital
internal hydrocephalus in a calf. Indian Vet. J. 74 :May: 446- 447.
DEFINITION-ABDOMINAL HERNIA
• Abdominal hernia refers to protrusion of any organ from the abdominal cavity through an
accidental or physiological opening in its walls.
INCIDENCE
• The incidence of hernias in cattle and goat has not been widely studied.
• Abdin-Bey and Ramadan (2001) collected data from 59 hernias in goats studied at the
Veterinary Teaching Hospital, King Faisal University, Al-Hasa and reported that umbilical,
ventral abdominal, scrotal, inguinal and perineal hernias were common.
• The content of hernias was predominantly omentum followed by the intestines, abomasum,
the rumen and the gravid uterus.
• Umbilical and scrotal hernias were more frequent in young animals of less than 1 year of age,
while ventral abdominal and inguinal hernias were observed more in adults.
• Adhesion between the internal hernial sac and hernial content was observed in majority of
cases and tended to increase with chronicity of lesion.
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NORMAL SHAPE AND LOCATION OF UTERUS
• In the cow and mare, beyond fourth or fifth month of pregnancy the gravid uterus usually lies
on the abdominal floor beneath the intestines.
• In cow, sheep and goat, since the rumen is situated on the left side of the abdomen, the uterus
is usually pushed towards the right side.
• The length of bovine and equine fetuses during advanced pregnancy may exceed the distance
from the diaphragm to the pelvis.
• Consequent to this, in the mare, the uterus and fetus in the abdominal cavity assumes a
diagonal position.
• Whereas in the cow, the nose and the forelimbs of the fetus along with the fetal membranes
and the uterine wall may enter the pelvic cavity and extend caudally over the cervix.
• In dog, cat and sow, the entire length of the gravid horn is tubular and is of same diameter.
• In sow, the gravid horns are very long and lie folded as like that of the intestines on the
abdominal floor.
PARTS OF HERNIA
• A hernial ring, or opening in the muscular wall of the abdomen, which may have been brought
about as the result of an accident or may have been present at birth.
• A hernial swelling below the skin composed of the “hernial sac”.
• Ring may be of any shape, but often it is round or oval.
• Ring size varies; a small hole with difficulty permitting one finger to pass through, to a large
opening permitting the gravid uterus to escape from the abdominal cavity and get localized
under the skin (Ventral hernia).
• Hernial sac is composed of:
o skin on the outside
o few strands of fibrous tissue
o some bundles of muscular fibres below the skin
o more fibrous tissue
o layer of peritoneum
• According to the situation, size and nature of hernia, the contents vary.
CLASSIFICATION OF HERNIA
• A reducible hernia is one which is freely movable that its contents may be pushed back into the
abdominal cavity through the hernial ring. When the retaining pressure is released, the
contents once again return back through the same opening.
• An irreducible hernia is one which cannot be pushed through the opening, either because of:
o adhesions with adjacent area,
o enlarged after emerging probably be due to interference with blood supply,
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o fat deposition in place of the herniated organs.
VENTRAL HERNIA
Synonyms
• Ventral meterocele (gravid)

• Ventral hysterocele
ETIOLOGY
• Serious trauma to the muscular portion of the abdominal wall.

• In cow, sheep and goats, it is often due to horn-gores from other animals.
• If it occurs accidentally during the advanced pregnancy, then the increased weight of the gravid
uterus, fetus along with the fetal membranes and fetal fluids, and possibly other changes would
lead to weakening of the abdominal floor.
SYMPTOMS
Ventral hysterocele
In Cow In Buffalo In Goat
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Symptoms
• Generally commences as a local swelling about the size of a football but rapidly enlarges to
form an enormous ventral swelling extending from the pelvic brim to the xiphisternum.
• In cow, buffalo, sheep and goat, swelling is usually observed on the right side and in mare on
the left side of the abdominal floor.
• In extensive cases of unilateral ventral hernia, the swelling is most prominently noticed in the
posterior aspect, where it may sink to the level of the hocks. The sagging of the abdominal floor
may be 6 to 8 inches or more lower than that of the normal side.
• The author has made an interesting observation in a cow, in which there was an extensive and
massive ventral hernia resulting in an uniform and bilateral sagging of the abdominal floor.
• During this period, the entire gravid uterus along with its contents escapes out of the abdomen
and occupies a subcutaneous focus. Radiography in goat, sheep, sow, bitch and queen will
often reveal the presence of fetus in the subcutaneous focus.
• In cows and goats, the udder gets deflected to one side of the abdomen since the bulk of the
swelling is usually situated between the hind legs.
• Generally this condition gets complicated by development of gross edema of the abdominal
wall due to pressure on the veins.
• Palpating the edges of the ruptured site or fetus becomes impossible in cases where there is
extensive edema of the abdominal wall.
GENERAL CONSIDERATIONS
• As a rule there is no interference in the progression of gestation, but when parturition

commences it becomes grave for both the mother and the fetus, particularly in the case of
mare (Noake’s et al., 2001).
• Despite of severe ventral hernia, cows and ewes may give birth spontaneously. But in such
animals, labour should be closely monitored so that artificial assistance could be extended in
the event of any emergency.
TREATMENT
• Empirically, cows and goats with severe ventral hernia may deliver spontaneously.
• However, in case of the mare, from the dam’s welfare point of view, the veterinarian has to
decide
o Whether pregnancy should be allowed to continue, or
o To euthanize the dam.
• In the mare, as soon as the expulsive forces begin,
o Artificial interference should be immediately extended in order to save the life of the
foal.
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o Traction can be attempted to deliver the fetus.
o But in some cases, where the fetus may be far from reach, it is advisable to anesthetize
the dam and place in dorsal recumbency.
o By applying pressure, the hernia is reduced and delivery of the fetus should be
attempted in this position.
LAPAROTOMY AND HERNIORRAPHY
• Radhakrishnan et.al., (1993) have successfully performed surgical intervention in a goat with
unilateral ventral hysterocele.
Unilateral Ventral Hysterocele
Before Surgery After Surgery
Procedure
• Operative site was prepared aseptically.

• Analgesia was induced by local infiltration with 2% xylocaine.
• Skin incision was made over the swelling.
• Intact peritoneum was opened.
• Hernial ring was enlarged.
• Displaced gravid uterus was reduced and replaced in to the abdominal cavity.
• Abdomen was closed using No.1 catgut for peritoneum, muscle and fascia.
• Skin incision was sutured with No. Silk.
• Treated with antibiotics for seven days.
• Skin sutures were removed on day 10.
• Animal recovered uneventful and kidded 35 days after surgery.
APPROACH IN NEAR TERM ANIMALS
• Balasubramanian et.al., (1991) have reported a case of extensive ventral hysterocele and its
successful surgical correction in doe.
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Procedure
• Adopting aseptic precautions the surgical site was prepared.

• Local infiltration of 2% lignocaine HCl was administerd.
• An oblique cutaneous incision was made on the hernial sac.
• A longitudinal incision was made over the greater curvature of the gravid uterine horn.
• The fetus and fetal membranes were removed.
• The uterine incision was closed by inversion suture.
• The uterus was replaced in to the abdominal cavity.
• The edges of the hernial ring were freshened with scalpel blade, and opposed with chromic
catgut (No.2) by overlapping (sliding) mattress pattern suture.
• Suture line was reinforced with a row of simple continuous pattern
• Skin incision was closed by horizontal mattress suture.
• Treated with parentral and intrauterine antibiotic and fluid therapy.
• Skin sutures removed on day 10.
• Animal made an uneventful recovery.
NOVEL OBSTETRICAL APPROACH IN CATTLE
• A novel, conservative obstetrical approach was successfully attempted in a cow with extensive
unilateral ventral hysterocele (Balasubramanian et.al., 1998).
Novel obstetrical approach Procedure
• The animal was well secured in the trevis.

• A wooden plank of 10 feet length, nine inches wide and
one inch thickness was placed beneath the abdomen
just in front of the mammary gland with the left end of
the plank held resting on the ground while the right end
was raised gently and firmly by two assistants.
• Meanwhile one of them carefully guided the mass into
the abdomen.
• The application of the plank facilitated the compression resulting in the correction and
retention of the mass in the abdomen as well as raises the level of fetus.
• At this point, the fetal extremities were now easily accessible, fetus alive and p1, p2 and p3 were
anterior, dorso–sacral and lateral deviation of head and neck with unilateral shoulder flexion.
• The postural abnormality was corrected and by gentle traction directed upwards the fetus was
lifted from the uterus in an arc fashion and a live female calf was delivered.
• The entire process was carefully monitored and guided by the operator performing per
vaginum examination; and required only about 15 minutes.
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Advantages
• Can be performed while the animal is in standing position.

• Minimal stress and trauma to the animal.
• Requires only few assistants, and
• Beneficial under field conditions where facilities for laparohysterotomy are limited.
SELECTED REFERENCES
• Balasubramanian, S., B. Ramesh Kumar., S. Ayyappan., and S.R.Pattabiraman (1991). Ventral

hysterocele in a Doe- A case report. Indian J Anim Repr. 12: 2: 206-207.
• Balasubramanian, S., Ravi Sunder George and A.Subramanian (1998). Maternal dystocia due to
ventral hysterocele in a cow: A novel obstetrical approach. Paper presented at the 8 th World
Conference on Animal Production, during June28 – July 4, 1998 held at Seoul National
University, Seoul, KOREA.
• Radhakrishnan, C., S.Balasubramanian and S.Thilagar (1993). Repair of ventral metrocele
(gravid) in a goat. Vet. Rec. Jan 23, vol 132, p-92.
• Abdin-Bey, M R. and Ramadan, R O. (2001). Retrospective study of hernias in goats. Scientific
Journal of King Faisal University (Basic and Applied Sciences) Vol 2 No.1, p77-88.
FREQUENTLY ASKED QUESTIONS
Why in ruminants, ventral hernia usually occurs more commonly on the right side?
• In ruminants (cow, sheep and goat), since the rumen is situated on the left side, it prevents the
gravid uterus from slipping towards the left side.
Will the gestation process be interfered in a pregnant animal which develops ventral hernia?
• NO. As a rule, gestation process is uninterrupted.
Do we need to monitor labour in a cow or mare suffering from severe ventral hernia?
• YES. When labour begins, the condition becomes grave for the dam and fetus, particularly in
mare, due of the inability of the abdominal muscles to contract equally and strongly and force
the fetus toward and through the birth canal. Hence, close monitoring during labour is
important, so that artificial assistance could be extended, if required. However, some cows and
ewes may give birth spontaneously despite severe ventral hernia.
Will there be recurrence of ventral hernia in subsequent pregnancies?
• YES. Usually after calving, in some animals, the abdominal floor of the affected side would
retract so that the abdominal contour is regained and occasionally remain normal during
subsequent pregnancies. But, it usually recurs during the latter stages of each gestation period.
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MODULE-4: VAGINO-CERVICAL PROLAPSE - VAGINAL PROLAPSE
DEFINITION
• Vagino-Cervical prolapse usually involves a prolapse of the floor, the lateral walls and a portion
of the roof of the vagina through the vulva with the cervix and the uterus moving caudal, not
infrequently the entire vagina and cervix are prolapsed through the vulva.
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Vagino-Cervical Prolapse in Cow
INCIDENCE
• Seen commonly in all species of domestic animals, but most commonly in the cow and ewe.
In Sheep In Goat In Pig
• In late pregnancies it is less than 1% of all obstetrical cases.

• Prolapse of the vagina and cervix will invariably recur and become more severe during
subsequent pregnancies.
• Incidence of ovine vagino-cervical prolapse is 0.5%; it may reach 20%.
• Commonly seen in young brachycephalic dogs during oestrum.
• In cats, it is practically unknown.
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ETIOLOGY
• Probably multiple.
• Observed during last 2-3 months of gestation, when large amounts of oestrogenic hormone
being secreted by the placenta.
• Intra-abdominal pressure.
• Due to hereditary or genetic factors.
• More common in pluripara than in primipara, injuries or stretching of the birth passage at the
first or subsequent parturitions may predispose to prolapse.
• Favoured by close confinement; in which the cow's rear quarter projects over the gutter.
• Sheep confined on lush pastures and carrying twins.
• Over distension of the abdomen or excessive amounts of loose pelvic fat favour the condition
by increasing the intra-pelvic pressure.
• In cattle occasionally observed following parturition, but often associated with cystic ovaries.
PATHOGENESIS
Vagino-Cervical Prolapse in • Due to a combination of some factors, when

Cow an animal becomes recumbent on an inclined
plane with its hind quarters positioned
downward will lead to prolapse.
• Spontaneous reduction occurs in initial cases
when the cow rises.
• Recurrent prolapse often causes bruising,
soiling and infection, and in turn leads to the
development of inflammatory swelling of the
mucosa.
• As a result of inhibited venous blood return
there is an increase in the swelling of the
mass.
• Progressive circulatory embarrassment results
in thrombosis and finally leading to necrosis.
• The mass reaches a size which precludes
spontaneous reduction so that the condition
becomes permanent.
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DIAGRAMATIC REPRESENTATION OF STAGES OF DEVELOPMENT OF VAGINAL PROLAPSE
A - Slack vaginal wall, B - Prolapse following recumbency, C - Spontaneous

reduction of prolapse on standing, D - Swelling of the vaginal wall after
recurrent prolapse, E - Irreducible prolapse, and F - Devitalized vaginal wall
after reduction of prolapse.
STAGES OF DEVELOPMENT OF VAGINAL PROLAPSE IN A COW
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SYMPTOMS
• The symptoms of vagino-cervical prolapse are obvious and the condition is often spoken of by
the farmer as “Casting of the wethers".
Severe necrotic vagino-cervical Traumatized mucous Intact cervical seal

prolapse membrane
• The symptoms may vary from

o A mild protrusion of the vaginal mucous membrane through the vulval lips when the
animal lies down, to a severe necrotic vagino-cervical prolapse containing a greatly
distended bladder and complicated by a prolapse of the rectum due to constant
tenesmus.
o Edema of the prolapsed vagina and cervix occurs because of the irritation and trauma to
the exposed mucous membrane, and because this portion drops over the ischial arch
thereby causing a passive venous congestion.
o The cervical seal usually remains intact; although if the cervix is prolapsed and inflamed,
the external portion of the seal may be absent.
o Occasionally the cervix relaxes, the seal is lost and abortion or premature parturition
occurs within 24-72 h.
o In neglected, severe cases the exposed mucous membrane may be necrotic resulting in
a toxemia and septicemia. Necrosis and gangrene may even involve the cervix and the
caudal portion of the uterus secondary to severe vascular insult and thrombosis.
o Usually the size of the prolapsed vagino-cervical mass varies from approximately 10 cm
to over 30 cm in diameter (Sloss and Dufty, 1980). Whereas, Gnanasubramanian et.al.,
(2000) have reported an unusually very large (45 cm in diameter) vagino-cervical
prolapse with partial uterine prolapse in a she buffalo.
TREATMENT: GENERAL CONSIDERATIONS
• Method of treatment varies with the

o Species and breed of the animal
o Severity of the condition
o Stage of pregnancy
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o Ability of the owner to care for, and observe the animal until after parturition.
• Early prompt treatment often permits the use of simple conservative methods and obviates the
necessity of using more heroic techniques.
• Operator should select the most conservative method possible under the circumstances and
caution the owner that as pregnancy progresses other methods may need to be used to control
the condition.
• Combinations of methods may be used.
PROCEDURE FOR MANUAL REDUCTION
• In replacing the prolapsed bovine vagina and cervix, epidural anesthesia is very helpful and
usually is necessary in more severe cases where tenesmus is present.
• It is advisable to have the animal standing, preferably with the hind quarters elevated to
facilitate easy replacement of the prolapsed mass.
• Methods to elevate rear quarters
• Portable rear quarter elevator device
• Wash the prolapsed portions free of dirt and debris with a mild, non-irritating antiseptic
solution or physiological saline.
• If irritation, infection, or straining is present, a bland antiseptic oil, such as 1 oz. of bismuth
formic iodide in a pint of mineral oil; or sulfonamides or antibiotics in oil or ointment might be
helpful when applied to the prolapsed mass before replacing.
• If difficulty is encountered in replacement of the prolapsed vagina due entrapment of a
distended bladder, gently raise the prolapsed portion dorsally in order to reduce the sharp kink
in the urethra, thus permitting the escape of collected urine.
• Palpate the bladder before replacing the uterus, if distended, catheterize (Fig 1 and 2) so that it
does not interfere with the replacement process.
Fig.1: INSERTION OF URINARY Fig.2: RELIEVING OF URINE

CATHETER
• However in exceptional cases, it may be necessary to trocarize the bladder through the
prolapsed vaginal wall with a large gauge needle.
• Following replacement of floor and walls of the prolapsed mass, normal circulation is restored
and and the edema in the vaginal walls and mucous membrane is rapidly reduced.
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• Carefully introduce into the vagina sulfonamides or antibiotics in oil or ointment once or twice
daily for several days or more after replacement.
• If the vagina is badly infected the animal may have an elevated body temperature. In such
cases, and in those where the cervix is relaxed and dilated and abortion is likely, a course of
antibiotics or sulphonamide therapy is indicated to control infection and septicemia, and if
abortion does occur to prevent septic metritis.
DIFFERENT TREATMENT APPROACHES
• Elevation of the rear quarters is the most practical method in cattle

• Hormone: Inj. Progesterone: 50-100 mg i.m. daily or 500 mg once every 10 days - rationale not
clear
• Unilateral pudental neurectomy is unsatisfactory
• Vulvar truss is of practical value
• Pessaries are popular in Europe but not in USA.
• Vulvar tape retention sutures.
• Buried or "hidden" purse string type suture, Buhner's method.
• Modified Caslick operation
• Minchev's method: Surgically fastening the cranial portion of the vaginal wall through the lesser
sciatic foramen to the dorso-lateral wall of the sacrosciatic ligament, muscles and skin of the
croup.
• Winkler's method: fixation of the cervix to the prepubic tendon.
• Farquharson method: submucous resection of the edematous and devitalised mucous
membrane.
• Guard and Frank technique.
• In chronic prolapse in postpartum cows treatment with a gonadotrophic hormone rich in the
luteinizing factor is indicated, if cystic ovaries are present.
VULVAR TAPE RETENTION SUTURES
Indications
• It is one of the simplest, most common and effective method to retain a simple or recurrent
vaginal, cervical or uterine prolapse in cattle.
• It is a temporary measure to control prolpase.
Restraint
• If the animal is standing, it is retrained in a trevis.

• If recumbent, the hind quarter should be elevated using either conventional methods or a hind
quarter elevator device.
• Administer sufficient amount of epidural anaesthesia using 2% lignocaine HCl to produce
analgesia of the perineal skin to about 3 cm below the ventral commissure of the vulva.
111
Materials required
• Gerlach's perivaginal needle
• Sterile cotton umbilical tape

• Povidone iodine
• Scissors
Procedure
• Clean and thoroughly disinfect the anus, vulva, prolapsed parts, perineal skin and the tail.
• Return the prolapsed part to its proper position.
• Locate the vulvar hairline on one side (located at least 2-3 inches lateral to the vulvar lips) and
swiftly pass the needle subcutaneously from the dorsal commissure parallel through the entire
vulval lip out of the ventral commissure.
• This affords a much tougher and thicker skin for the suture, which does not tear out as readily
nor cause as much irritation as one in the vulvar lips.
• Place one hand in the vagina for proper orientation of the needle and to maintain it at a depth
of about 5-6 cm until the eye of the needle emerges through the ventral commissure.
• A piece of sterile cotton umbilical tape, 30 cm long, dipped in povidone iodine is threaded
through the eye of the needle and in one stroke pulled out through the dorsal commissure.
• Likewise repeat the procedure on the other side.
• Both the ends are tightened and securely tied towards one side. The excess ends of the tape
are cut short.
• It is desirable to use a type of suture that can be untied or released.
Correct Method Incorrect Method
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BURIED OR "HIDDEN" PURSE STRING TYPE SUTURE, BUHNER'S METHOD
• It is used for the vulva following replacement of a prolapsed vagina described by Pierson,
Arthur (1966) and Woelffer.
• This technique may be used in chronic post partum prolapse as well as prepartum prolapse.
• Under epidural anaesthesia and with a near sterile procedure, two one-half inch incisions are
made one to two inches above the upper commissure and below the lower commissure of the
vulva.
• With a long eye point needle, a Gerlach's perivaginal needle, similar to a seton needle, an 18
inch piece of one-eighth inch nylon cord or heavy vetafil is passed within the tissues from one
incision to the other lateral to one vulvar lip.
• The needle is withdrawn and reinserted in the opposite direction lateral to the opposite vulvar
lip to the lower incision site and again withdrawn.
• The purse string suture around the vulva is tightened sufficiently to allow 4 fingers in the vulva,
and the knot is tied and buried beneath the skin of the upper incision by suturing the skin over
the heavy purse string suture leaving it buried within the vulvar tissues until parturition when it
is removed.
A - Insertion of perivaginal needlefrom the dorsal to ventral incision. B -Insertion of needle

on the opposite side for completion of loop. C - Completed loop before tightening and tying.
NARASHIMAN TECHNIQUE - A MODIFICATION OF BUHNER'S METHOD
• Before reduction of prolapse , at the level of the vestibular fold in the submucosa apply a
buried purse string suture
• Exercise care not to occlude the urethra
• After reduction of prolapse, tighten the suture to the desired degree and apply knot.
Source: Narashiman, K.S., S.A.Quayam and K.L.Gera (1971). Indian Vet. J. 52:311
113
MODIFIED CASLICK OPERATION
• A vulva closing technique modified from the Caslick operation in mares is useful in the
treatment of chronic prepartum (2 months) prolapse or in post partum prolapse.
a - Vulvar skin ; b - Area of a - Stainless steel wire doubled a - 1/4 " umbilical tape doubled
vaginal mucous membrane to be
cut. An interrupted vertical matress If the animal is straining, a deep
suture is used to draw the wound matress suture is placed through
Under epidural or local edges gently together. both vulvar lips cranial to the
anesthesia, a three-quarter inch suture line.
strip of mucosa is removed from
just inside the vulvar lips.
MODIFIED MINCHEW METHOD
• Surgically fastening the cranial portion of the vaginal wall through the lesser sciatic foramen to
the dorso-lateral wall of the sacrosciatic ligament, muscles and skin of the croup.
Indication
• Recurrent prolapse of dorsal or dorsolateral walls of vagina.
Restraint
• Low caudal epidural anesthesia.
Instruments
• Gerlach’s perivaginal needle

• Non-absorbable, monofilament, heavy gauge suture – 1 metre
• Small gauze plugs (5 cm long x 2 cm diameter) – 4 Nos.
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Procedure
• Clip and surgically prepare on one or both sides, a 10 cm square area of skin, 11 cm lateral and
anterior to the base of the tail
• Along the course of anchor suture, infiltrate local anesthetic (2% Lignocaine; 20 ml) of all layers
of pelvic and vaginal wall
• Form a loop with the suture material doubled and threaded through the eye of the gerlach’s
needle
• With one hand, push the needle and loop threaded through the anesthetized path of the skin,
muscles, and sacrosciatic ligament in to the vaginal cavity, with the other hand guide the needle
from the vagina.
• When the needle eye and loop enter the vagina, insert a gauze plug into the loop to anchor the
loop while the needle is withdrawn
• Tie the suture outside over another gauze with enough tension to hold both the plugs in
position
• Too tight sutures may lead to inflammatory swelling – lead to embedding of gauze into
perivaginal tissues and result in abscess
• Sutures are left in situ for at least 14 days to allow adhesion formation between the vagina and
pelvic wall
• Remove sutures later.
WINKLER'S METHOD
(Fixation of the cervix to the prepublic tendon)
• Relatively easy to perform in young cows

• Difficult to insert the needle in to the tendon in old cows, due to a pendulous abdomen.
Indication
• In recurrent vagina prolapse of ventral vaginal wall or cervix
Restraint
• Epidural Inj. 2 % Lignocaine HCl sufficient enough to cause analgesia of perineal skin ~ 3 cm
below the dorsal commissure.
Instruments
• Suture needle (size 1), half circle, cutting edge bent to a U shape
• Non-absorbable, monofilament, extra heavy suture material – 100 cm
• Metal urinary catheter.
115
Procedure
• Clean and reduce the prolapse

• Per vaginally locate the attachment of the pre pubic tendon to the anterior border of the pubis
• The tendon is about 5 cm wide on each side of the symphysis and extends downward at an
angle of 90°.
• Laterally, a short accessory band of tendon is attached to the ileopectineal protruberance
• Insert a metal urinary catheter in to the urethra and pushed away from the operation site
• Pass the needle with suture material through the ventral vaginal wall immediately posterior to
the cervix and through the triangular space formed by the main tendon and accessory band
• Now pass the needle medially and dorsally through the prepubic tendon and back through the
ventral vaginal wall about 5 cm from the original point of insertion
• Direct the needle through the ventral wall of the posterior cervix without entering the lumen
• Tie the ends of the suture such that a loop is formed, short enough to prevent recurrence.
FARQUHARSON'S METHOD
(Submucous resection of the edematous and devitalized mucous membrane)
Indication
• In recurrent vagina prolapse unresponsive to other methods

• In conjunction with Buhner’s method.
Instruments required
• Scalpel
• Straight scissors
• Minumum 6 hemostats
• Large Vulsellum -Albrecht or Glock’s forceps
• Needle driver
• Chromic catgut – Size 2, and
• Curved, round bodied suture needles – Size 10.
Restraint
• Epidural Inj. 2 % Lignocaine HCl sufficient enough to cause analgesia of perineal skin ~ 3 cm
below the dorsal commissure.
Procedure
• After correction of prolapse , exteriorize the devitalized portion
116
• At the widest portion of devitalized vagina wall, make a transverse, crescent shaped incision on
the mucosa
• Excise the mucosa using a scissors
• Easily accomplished, if mucosa is edematous and some separation from underlying structures
• Perform stripping of mucosa in small section
• Appose the edges of each section by simple, interrupted catgut sutures
• Tie sutures with great tension than normal, to prevent suture tension slackening following
decrease in size
• Subsequent fertility and parturition unaffected.
GUARD AND FRANK TECHNIQUE
• Removal of large amounts of perivaginal fat by incising the dorsal wall of the vagina
Hormone therapy
• In cows suffering with chronic postpartum prolapse , treatment with a gonadotrophic hormone
rich in the luteinizing factor is indicated, if cystic ovaries are present.
ANTE-PARTUM VAGINAL PROLAPSE
• In most flocks the great majority of cases requiring treatment are of this typical form.
• Initially the pink mucosa of the vagina may be noticed protruding slightly between the lips of
the vulva in a ewe lying down, only to disappear from view when she stands up.
• Later the vagina fails to return to its normal position when the ewe stands and the prolapse
progresses until the vagina is completely everted and the cervix is visible. Initially the vaginal
mucosa is pink, moist and smooth but, if not treated, the vagina becomes swollen, oedematous
and congested.
• It is very susceptible to injury.
• After prolonged exposure, the dried vaginal mucosa becomes rough and haemorrhagic and
gangrene may develop.
• Straining becomes a feature of the condition when the mucosa is irritated or obstruction of the
urethra leads to severe distension of the bladder.
POSTPARTUM VAGINAL PROLAPSE IN EWE
• Occasionally presented as a flock problem.

• In most cases it occurs within a few hours of lambing, while in some cases it may occur up to 15
days post partum.
• The uterus is involved in the prolapse and its exposed surface is readily traumatized.
• Most affected ewes die from haemorrhage and shock within few hours.
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CLASSIFICATION OF SEVERITY
Stage 1: Vaginal mucosa Stage 2: Protruding vaginal Stage 3: Vagina protrudes

protrudes from the vulva when mucosa remains visible and cervix is visible.
recumbent, but disappears even when the ewe stands,
when she stands. the cervix is not visible.
PREDISPOSING FACTORS IN EWE
• Hormonal excesses and imbalances

• Hypocalcemia
• Twins or triplets
• Fat condition
• Thin condition
• Inadequate exercise
• Short tail docking
• Bulky food
• Excess dietary fibre
• Dietary estrogens and their precursors
• Sloping terrain
• Vaginal irritation
• Previous dystocia
• Inherited predisposition.
TREATMENT
• Administer low caudal epidural anesthesia.

• Reduce and reposition the prolapsed mass, and
• Retain the mass using either Plastic retainer or Buhner’s purse string sutures using
monofilament nylon.
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Plastic Retainer
PROGNOSIS
• Depends upon the

o Severity of the condition, and
o Length of time it has existed.
• Except in extreme or severe cases, the prognosis is generally fair to good for the life of the
animal and the fetus, if treatment is prompt and after care is good.
• Cows usually calve without any assistance in nearly all uncomplicated cases.
• After parturition, the prolapse is usually immediately relieved.
SELECTED REFERENCES
• Brian Hosie (1989). Vaginal prolapse and rupture in sheep. In practice 9 : 215-218.
• Gnanasubramanian, T., S.Balasubramanian, Cecilia Christopher and D.Kathiresan (2000).
Vagino cervical prolapse with partial uterine prolapse in a she buffalo. IJAR., 21 (2) :161.
VAGINAL PROLAPSE IN DOGS
Definition
• Vaginal prolapse/Vaginal hyperplasia is referred to as the edematous enlargement of the

vaginal tissue that occurs during oestrus or proestrus. Both usually cranial to the urethral
papilla.
Vaginal prolapse in a Vaginal hyperplasia in a

German Pug Doberman
Involves the 360° May originate from a stalk
protrusion of vaginal of mucosa on the floor of the
mucosa. vagina.
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Synonyms
• Vaginal hypertrophy
• Vaginal oedema
• Estrual eversion
• Estrual hypertrophy
PATHOPHYSIOLOGY
• Normal oestrogenic stimulation results in hyperemia, oedema and keratinization of vaginal

mucosa.
• During proestrus/estrus, occassionally at the end of diestrum or parturition, these normal
effects are accentuated to result in vaginal prolapse.
• Hyperoestrogenism or weakness of vaginal connective tissue may also lead to prolapse.
• Extent of oedema and eversion are variable.
• Vaginal tissue protrudes through the vulval lips in case of severe oedema.
• Protruding mass may be large, but the origin is usually small and located on the vaginal floor
cranial to the urethral orifice.
• Width of mass: stalklike to involving the circumference of vaginal floor.
• Prolapsed tissue promotes straining and further increase in the size.
• Edematous tissue causes mechanical obstruction and interference in normal breeding.
• Abrasion, licking or drying cause tissue trauma and leads to bleeding.
• Compression of surrounding structures may lead to stranguria, hematuria, or tenesmus.
• Following reduction in oestrogen levels, spontaneous resolution occurs, but may recur in
subsequent oestrus.
DIAGNOSIS
Diagnosis is based on
• History
o Protrusion of mass from the vulva
o Vulvar discharge or bleeding
o Refusal to intromission during breeding
o Signs referrable to fecal or urinary difficulties.
• Clinical signs
o A mass protruding between vulval lips
o Perineal enlargement and swelling
o In acute and non protruding prolapse: Glistening, edematous, pale pink vaginal mucosa.
o In chronic prolapse: Appear leathery, corrugated, and sometimes ulcerated or fissured.
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o Perineal licking
o Pollakiuria
o Dysuria.
• Physical examination
o Carefully examine the mass to locate
Origin
Size at the base
Locations of vaginal lumen and urethral opening
Extent of tissue damage.
o On vaginal palpation
Should identify the mass arising from ventral vaginal floor, if it is not protruding.
Vaginal areas other than those just cranial to the urethral orifice should feel
normal.
• Laboratory findings
o Vaginal cytology reveals RBCs in the absence of cornified vaginal epithelial cells.
• Uterine prolapse
• Vaginal tumors
o Fibroleiomyoma
o Lipoma
o Leiomyosarcoma
o Squamous cell carcinoma
o Transmissible veneral tumour
• Non-Neoplastic differentials
o Vaginal cysts
o Septa
o Congenital malformations
TREATMENT
Medical Management
• Spontaneous resolution of vaginal prolapse occurs following decline in oestrogen levels,

provided the protrusion is not circumferential.
• Administer gonadotrophin releasing hormone (GnRH, 50 µg/40 lbs, IM) to cause shortening of
oestrus.
• Administer human chorionic gonadotrophin (HCG, 500-1000 IU, IM) to cause ovulation.
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• Do not use for breeding, since the disease is familial.
• In valuable bitch that does not allow intromission, but owner's insist breeding, artificial
insemination may be considered.
Surgical Management
• To prevent recurrence and injury to the everted mass, ovariohysterectomy (OHE) is

recommended.
• Perform episiotomy and manually reduce the large, protruding mass and apply vulvar sutures,
to prevent recurrence until oedema reduces.
• Resection of protruding tissue without OHE is not recommended as it
o Results in severe hemorrhage, and
o Does not prevent recurrence during subsequent oestrous cycles.
• Resection is recommended, if protruding tissue is severely damaged or necrotic.
• Reduction without OHE may require hysteropexy, cystopexy, and/or colopexy to prevent
recurrent prolapse and herniation, respectively.
PRE-OPERATIVE MANAGEMENT
• Lavage the protruding mass with warm saline or water to remove the debris and necrotic
tissue.
• Apply an antibiotic or antibiotic/steroid ointment to the exposed tissue.
• Replace the mass within the vagina or vestibule.
• To prevent self mutilation, apply Elizabethan collar, bucket or side bars.
SURGICAL CORRECTION OF VAGINAL PROLAPSE
• Perform an OHE
• Replace the protruding mass into the vagina or vestibule
• Lavage, lubricate and reduce the mass by digital manipulation
• Apply 2-3 horizontal mattress sutures between the vulvar lips using 2-0 nylon or polypropylene.
If resection of necrotic or severely traumatized tissue is necessary
• Position the animal in a perineal position

• Perform an episiotomy to expose the mass
• Place and maintain a urethral catheter during the procedure
• In stages, incise the base of the edematous tissue
• Control hemorrhage with pressure, ligatures, and electro-coagulation
• Appose adjacent mucosal edges with interrupted or continuous approximating sutures using 3-
0 or 4-0 polydioxanone, polyglecaprone 25 or polyglyconate.
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Stepwise Surgical Procedure
Positioning and Incision Placement of urethral After complete resection After complete recovery
catheter
Courtesy: Md. Shafiuzama (2009)
• Edema should resolve within 5-7 days of OHE.
POST-OPERATIVE CARE AND PROGNOSIS
Post-operative care
• Administer fluids and analgesics.

• Immediately after episiotomy, apply cold compress and on the next day warm compress to
reduce inflammation and swelling.
• Apply Elizabethan collars to avoid self mutilation of episiotomy and/or vulvar sutures, which
otherwise may lead to dehiscence.
• Examine the vagina 5-7 days following the reduction of mass.
• Remove the vulvar sutures if there is no reccurrence of prolapse.
• Amputation of edematous protruding tissue may lead to hemorrhage - Self limiting, if good
surgical technique is adopted.
Prognosis
• Excellent following OHE

• If OHE is not performed, recurrence during subsequent estrus and conception problem
• At the end of estrus, edema subsides following decrease in estrogen levels.
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MODULE-5: UTERINE TORSION
DEFINITION
• Uterine torsion is commonly referred to as the twisting or revolving of the gravid uterus on its
longitudinal axis.
INCIDENCE
• European study: 3-4 %

• North American study: 3-7 %
• British study: 5-6 %
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• Reported in all domestic species
• Most commonly prevalent as a cause of dystocia in cattle and usually develops during the late
first stage or early second stage of labour
• Most cases involve only the uterus but some may be complicated by incarceration of other
organs eg. Jejunum and bladder
• Common in cows and buffaloes; relatively high in surti buffaloes
• Occasionally in ewe and goats; rare in mare, bitch, cat and sow
• Occurs in both uniparous and multiparous animals
• In uniparous animals, both gravid and nongravid horns are involved in torsion because of the
strong intercornual ligament and the distension of the uterine horns and body with placenta
and fluid
• In multiparous animals, only a portion of one uterine horn containing usually only one fetus
may be twisted or rotated (at the point of its junction with the body, the horn entire rotates)
• Common in pluriparous (large abdominal cavity together with decreased uterine tone and
mesometrial stretching) than in primiparous animals (Frazer, et al., 1996).
ETIOLOGY
• Predisposing causes
• Environmental causes, and
• Exciting causes.
CLINICAL SIGNS
• Torsion with degree of 45-90 lacks clinical symptoms; if 180° or more definite clinical symptoms
are noticed
o Colicky pain
o Teeth grinding
o Restless
o Anorexia
o Lack of rumination
o Rapid pulse
o Tachycardia
o Treading and tail switching, and
o Displacement of dorsal commissure (Fig.a and b)
o Tucked up udder
o Vulval edema, and
o Slight depression of the lumbo-sacral vertebrae (Fig.c and d).
125
Fig.a: In Normal cow Fig.b: In Uterine torsion cow
Fig.c: Laeral view in buffalo Fig.d: Dorsal view in buffalo
DIAGNOSIS
• Pregnant animals which exhibit the clinical signs must be subjected to both per rectal and per
vaginum examinations to arrive at a confirmative diagnosis for
o Direction of torsion
o Degree of torsion, and
o Position of torsion.
126
DIRECTION OF UTERINE TORSION
• Normal Position of Broad ligaments and

vagina.
• Clockwise (Right side torsion).

• On rectal examination: The ligament and
middle uterine artery (MUA) on the right side is
stretched and pulled vertically downward
under the uterus, whereas the ligament on the
left side is stretched and pulled tightly across
the top of the uterine body.
• Counter clockwise (Left side torsion).

• On rectal examination: The ligament and MUA
on the left side is stretched and pulled
vertically downward under the uterus, whereas
the ligament on the right side is stretched and
pulled tightly across the top of the uterine
body.
Vaginal examination
• Abrupt stenosis of the vagina with the vaginal wall spirally twisted and external Os of the cervix
not palpable depending on the degree of torsion.
DEGREE OF UTERINE TORSION
• The degree of uterine torsion may be 45°, 90°,180°, 360°, and 540°
Per Vaginum examination
• In Post cervical uterine torsion: Cervix is not palpable with abrupt closing of the vagina.
127
o In less than 90°: Hand could be passed to palpate the external Os of the cervix with
some resistance.
o In 90°-180°: One or two fingers can be passed.
o In more than 360°: Abrupt stenosis.
• In Pre cervical uterine torsion: Cervix is palpable and fetus is not palpable.
POSITION OF UTERINE TORSION
Based on the site of occurrence it is either

Post cervical: Involvement of vagina Pre cervical: Involvement of uterus
• Uterine torsion should be differentiated from conditions such as

o Indigestion
o Pyelonephritis
o Traumatic gastritis, and
o Internal intussusceptions.
PROGNOSIS
• Prognosis of uterine torsion depends on the

o Degree of torsion
o Severity of torsion, and
o Length of time of existence of torsion.
Prognosis
• In cattle
o Good: If the condition is diagnosed early, before the occurrence of fetal emphysema,
secondary contraction of the cervix, uterine rupture and peritonitis.
128
o Poor: In torsion of uterus with extensive rupture of uterus, hemorrhage, or severe
uterine edema and gangrene secondary to thrombi in the large uterine vessels.
• In other species
o Guarded to poor: Because an early diagnosis is difficult or impossible to make without
an exploratory laparotomy operation.
Prognosis with respect to life of fetus
• Poor. In most cases, it is presented too late with the fetus having reduced oxygen supply
leading to death due to asphyxiation.
• In most cases, unrelieved uterine torsion result in death of the dam.
• In rare cases, the fetus remains in the uterus and macerates, with extensive adhesions
developing around the uterus; the condition may not be diagnosed for several months.
Mortality
• Mortality in mares may be equal to or probably greater than that in cattle.
TREATMENT APPROACHES
• Various methods have been described for relieving uterine torsion in bovines (Sloss and Dufty,
1980).
• The choice of method depends on:
o The degree of uterine torsion
o Stage of gestation
o The condition of the dam, fetus and the uterus.
Different approaches
• Manual detorsion per vaginum

• Manual detorsion per vaginum in combination with external pressure on the abdomen
• Stimulation of vigorous fetal movements
• Abdominal ballotment
• Suspension of the cows body
• Detorsion by simple rotation
• Schaffer’s method (Modified rolling technique)
• Intra abdominal manipulation / Flank laparotomy
• Cesarean section, and
• Medical termination of pregnancy.
DETORSION BY SIMPLE ROTATION
• Oldest and simplest method

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• Requires assistance of 3-6 men depending on the size of the animal
• Rolling should be done out- of – doors, on a sand pit (Fig.a)
Fig.a : Uterine correction in ow - Rolling on a sand

pit
• If the animal is large and vigorous – Give tranquilizers – Intra venous or intra muscular as a
sedative 20 minutes prior to rolling.
OBJECTIVE OF SIMPLE ROLLING
• Rotate the body of the animal in the same direction as the torsion of the uterus, rapidly enough
to rotate the body around or faster than the inert uterus and fetus.
• The rapidly rotating body of the animal thereby overtakes the more slowly rotating inert gravid
uterus.
TECHNIQUE OF SIMPLE ROLLING
• Assess the side of uterine torsion and cast the animal on the same side as the direction of
torsion
• Cast the animal adopting squeeze method
• The two hind legs of the cow are fastened together and two front legs are tied together
• The animals head is held extended
• The front and hind feet should not be tied together, because this compresses the abdominal
cavity and tends to make the gravid uterus rotate with the animal
• Animal should be rapidly rotated in the same direction of uterine torsion, by strong co-
ordinated pulling
• After the animal has been rapidly rolled 180 degrees, her body must then be either rolled back
slowly to the original position or be pushed, usually slowly, over her legs and sternum so that
she is once more in lateral recumbency on the same side as the direction of the torsion, ready
to be rapidly turned over again.
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CORRECTION OF UTERINE TORSION
(Right side - Post Cervical - Less than 90 degree)
IN COW USING SIMPLE ROTATION
Cow is cast on the same direction Cow is rapidly rotated on the After completion of one rapid
of torsion and positioned in same direction of torsion. rotation.
sternal recumbency.
CLINICAL EVALUATION
• Some clinicians advise the operator to keep the hand in the vagina or even to grasp the fetus, in
order to hold the gravid uterus in place. This is a very awkward position to assume or maintain
as the animal is being rolled and is unnecessary unless the operator is uncertain as to the
direction in which the uterus is rotated.
• Place the hand in the cranial portion of the vagina, if rolling is in wrong direction, then spiral
folds in the vagina will tighten.
• After each 2 or 3 rapid rotations of the animal’s body, the birth canal should be examined to
determine if uterine torsion is corrected.
• If so, the spiral folds and stenosis disappear, if cervix is dilated, the fetus may be palpated with
ease.
• Occasionally, there may be gush of fetal fluids from the uterus as torsion is relieved.
• If uterine torsion is not relieved, repeat the rolling procedure 4-5 or more times before failure is
admitted and another technique is attempted.
• Rolling might result in rupture of the uterus, especially when the uterus is edematous.
SCHAFFER'S METHOD (Modified rolling technique)
• Described by Arthur (1966).

• Requires less assistance.
OBJECTIVE OF ROLLING
• The animal is rolled slowly instead of rapidly.

• The uterus and its contents are held in place by the plank and the weight of man standing on it
while the animal is rotated around them.
131
TECHNIQUE OF ROLLING
• Cast the animal on the same side as the direction of uterine torsion
• Tie in a manner similar to that described in rolling technique
• Place the plank (9–12 feet length and 8–12 inches wide) on the animal’s abdomen with the
lower end of the plank on the ground (Fig.a).
Correction of uterine torsion (right side) in cow

by Schaffer's method. Note the placement of
plank
• An assistant stands on the plank and the animal is slowly rolled in the same direction as the
torsion by pulling on the ropes around the front and hind feet (Fig.b).
Correction of uterine torsion (right side) in cow

by Schaffer's method. Note an assistant
standing on the plank
• The plank creates pressure first on the upper abdominal wall, then the floor and finally the
opposite side of the abdomen resulting in a correction of the uterine torsion that can be
determined by examining the genital tract
• If there is any question concerning the direction of the uterine torsion, the operator, by placing
his hand in the canal, can readily determine whether the torsion is being relieved or not as the
animal is slowly rolled
• As in the initial rolling technique, if uterine torsion is not relieved the first time the animal is
rolled, the procedure may be repeated several times
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• In most cases, the uterine torsion is corrected on the first rolling.
MEDICAL TERMINATION OF PREGNANCY
• Medical termination of pregnancy may be attempted to mimic the first stage of labour with
prostaglandin expecting spontaneous correction due to uterine contractions and fetal
movements.
• Kathiresan et.al., (2001) have concluded that fresh cases of pre-cervical uterine torsion (<180°)
in cows with live fetus and no adhesions can be corrected successfully by medical termination
of pregnancy.
SELECTED REFERENCE
• D.Kathiresan, S.Balasubramanian, Cecilia Joseph, T. Gnansubramanian, C. Veerapandian and

S.R.Pattabiraman (2001). Medical management of pre-cervical uterine torsion in a heifer. Indian
Vet.J., Jan: 78; 55-56.
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MODULE-6: PYOMETRA - MUCOMETRA
DEFINITION
• In cattle, pyometra is defined as progressive accumulation of a variable amount of purulent

exudates within the lumen of the uterus and associated with the presence of persistent corpus
luteum (PCL) in one of the ovaries.
ETIOLOGY
• Mostly occurs as sequelae to chronic endometritis

• The corpus luteum (CL) persists due to the infection of the genital tract, abnormal uterine
contents prevents the release of prostaglandin from the endometrium or sequester it within
134
the uterine lumen. Thus uterus is under the continuous influence of progesterone; in turn
further depresses phagocytic activity of uterine neutrophils and allow persistence of infection.
Because the cervix remains fairly tightly closed the purulent exudate accumulates within the
uterine lumen, although occasionally there is a slight purulent discharge.
• Occasionally occur in the presence of a luteal cyst.
• Death of the fetus, invasion of the uterus by A. pyogenes and retention of the CL of pregnancy,
a relatively infrequent cause of pyometra.
• Venereal infection with organisms such as Trichomonas fetus (T.fetus), which cause embryonic
death, also causes pyometra.
CLINICAL SIGNS
• Cows show few or no signs of ill health; the main reason for them being examined is the
absence of cyclical, activity, or, perhaps, the presence of an intermittent vaginal discharge
• Uterine horns are enlarged and distended, an unequal degree, owing to incomplete involution
of the previously gravid horn or to recent conceptus death
• In some cases, purulent vaginal discharge may be noticed
• Common presenting sign is anoestrus due to persistent corpus luteum
Pyometra associated with T. foetus infection presents different features
• Pus is more copious and may attain a volume of many litres

• Pus is more fluid and is grayish white or white
• Greater distension of uterus
• Mucus occupying the cervix is moist and slippery, rather than sticky and tenacious, and
• Motile trichomonads can generally be found in the mucus.
Postcoital pyometra is pathognomonic for

trichomoniasis in cattle.
135
DIFFERENTIATION OF PYOMETRA AND NORMAL PREGNANCY
• Uterine wall is thick, flaccid and atonic (In pregnancy, it is thinner and more resilient)
• Uterus has a more ‘doughy’ and less vibrant feel.
• Positive signs of pregnancy (Fetal membrane slip, amniotic vesicle, placentomes, fremitus and
fetus) are not present.
• Transrectal ultrasonography will demonstrate the absence of a fetus and the presence of a
‘speckled’ echotexture of the uterine contents compared with the black anechoic appearance
of normal fetal fluids.
• If diagnosis is doubtful, the cow should be left untreated and reexamined 2 weeks later for
evidence of change.
PROGNOSIS
• In early cases: Fair to good

• In long standing cases: endometrium is destroyed and uterine wall becomes fibrotic – complete
recovery and conception difficult
• Pyometra associated with perimetritis: Hopeless
TREATMENT
• Drainage of pus from the uterus using horse catheter followed by infusion of antibiotics may
produce recovery in some cases.
• Best treatment is the use of PGF2alpha or its analogues.
• Administration of PGF2alpha results in
o Regression of the corpus luteum
o Dilatation of the cervix
o Expulsion of the purulent fluid, with
o Oestrus occurring 3-5 days later.
DEFINITION
In bitches,
• Pyometra refers to the accumulation of purulent material within the uterus

• Hydrometra refers to uterine distension with sterile fluid (watery secretions)
• Mucometra refers to uterine distension with sterile fluid (mucoid secretions).
INTRODUCTION
• Pyometra is a life threatening condition associated with cystic endometrial hyperplasia.

• Cystic endometrial hyperplasia and pyometra both develop during diestrus.
136
• Administration of estrogen increases the risk of pyometra during diestrus.
• The risk of an intact bitch developing pyometra before 10 years of age is 23% to 25%.
• Infection causes the morbidity and mortality associated with pyometra.
• Concurrent abnormalities in animals with pyometra may include
o Hypoglycemia
o Renal dysfunction
o Hepatic dysfunction
o Anemia
o Cardiac abnormalities, and
o Coagulation abnormalities.
• Pyometra is often associated with systemic inflammatory response syndrome caused by
production and release of inflammatory mediators with systemic effects.
• Hypoglycemia is common in canine pyometra.
PATHOPHYSIOLOGY
• In normal nongravid bitch, the diestrual period lasts approximately 70 days.

• Progesterone produced by ovarian corpora lutea exerts its influence on the uterus and:
o Stimulates the growth and secretary activity of the endometrial glands, and
o Reduces myometrial activity.
• Cystic endometrial hyperplasia is an abnormal uterine response that develops during diestrus
(luteal phase of cycle) when there is high or prolonged ovarian production of progesterone or
exogenously administered progesterone.
• Excessive progesterone influence or an exaggerated progesterone response causes the uterine
glandular tissue to become cystic, edematous, thickened and infiltrated by lymphocytes and
plasma cells.
• Fluid accumulates in endometrial glands and the uterine lumen with cystic endometrial
hyperplasia.
• Progesterone inhibition of myometrial contractility interferes with the uterine drainage.
• This abnormal uterine environment allows bacterial colonization to cause pyometra.
DIAGNOSIS
• The diagnosis of pyometra in bitches is based on

o Clinical presentation
o Physical examination
o Diagnostic imaging
o Laboratory findings
137
CLINICAL PRESENTATION
Signalment
• Affects intact dogs more commonly than cats.

• No breed predisposition in dogs although some indicate a modestly increased risk in various
breeds (golden retrievers, miniature schnauzers, Irish terrier, rough St. Bernard, Leonberger
Airedale terrier, Cavalier King Charles spaniel, rough collie, Rottweiler, Bernese Mountain dogs
and English cocker spaniels).
• Domestic shorthair and Siamese cats are affected more commonly than other breeds.
• Generally occurs in older (6 to 11 years, median 9 years) intact bitches and queens
• May occur in younger animals that have been given exogenous estrogen (dogs) or progestins
(cats).
• Nulliparous bitches are at moderately greater risk for pyometra than are primiparous and
multiparous bitches.
History
• Usually occurs several weeks (i.e. in cats 1-4, in dogs 4-8) after estrus or following mismating
injections or exogenous administration of estrogens or progestins.
• May have a purulent or bloody vaginal discharge.
• Obvious abdominal distension
Severely dsitended abdomen in closed cervix pyomtra
• Fever
• Partial-to-complete anorexia
• Lethargy
• Polyuria
• Polydipsia
• Vomiting
• Diarrhea, and/or
138
• Weight loss.
• Animals with closed pyometra more commonly have vomiting and diarrhea.
PHYSICAL EXAMINATION FINDINGS
• In open cervix pyometra, a purulent blood-tinged vaginal discharge may be observed.

• On abdominal palpation, uterine distension may be detected.
• Dehydration is frequent.
• If endotoxemia or septicemia is present, the bitch may be in shock, hypothermia, and/or
moribund.
• Fever is infrequent.
DIAGNOSTIC IMAGING
• A fluid-filled uterus should be detected on abdominal radiographs and / or ultrasonography
Canine pyometra
Radiographic image of pus filled Ultrasound image of uterine sacculations

and distended uterus
Courtesy: K.Thirumurugan and R.C.Rajasundaram (2011).
• The enlarged uterus is located in the caudal abdomen and may displace intestines cranially and
dorsally
• Open pyometra or uterine rupture may cause enough drainage so that the uterus is not
radiographically detected
• Displacing the intestines with a wooden spoon or abdominal bandage may improve uterine
visualization, but should be performed with caution if the uterus is significantly distended
because it may induce rupture
• Signs of uterine rupture and peritonitis (i.e., poor visceral detail) should be noted
• It is important to rule out pregnancy
• Radiographic confirmation of pyometra may not be possible until 41 to 43 days after ovulation
• Radiographically, fetal calcification can be identified after approximately 45 days of gestation
139
• Ultrasonography can identify fetal structures, assess fetal viability, identify uterine fluid and
determine uterine wall thickness and irregularities
• Pyometra, hydrometra, mucometra or hematometra may appear similar ultrasonographically
and radiographically. However, although mucometra and hydrometra typically are associated
with anechoic fluid within the uterine lumen on ultrasound, the fluid associated with pyometra
is typically echogenic.
LABORATORY FINDINGS
• Metabolic clinicopathologic abnormalities may occur.
Most common hemogram findings
o Neutrophilia with a left shift

o Monocytosis, and
o White blood cell toxicity.
• White blood cell numbers usually exceed 30,000/ ml, with closed pyometras and may be as
high as 100,000 to 200,000/ ml. However, normal numbers of white blood cells are often seen
with open pyometras.
• Leukopenia may indicate overwhelming infection and septicemia or uterine sequestration of
neutrophils.
• Increased leukocyte count and decreased lymphocyte count are directly proportional to the
disease severity.
• The high percentage of bands in most pyometras helps differentiate them from cystic
endometrial hyperplasia with mucometra.
• Mild normocytic, normochromic, nonregenerative anemia or nonregenerative, microcytic,
hypochromic anemia may occur.
• Clotting abnormalities and disseminated intravascular coagulation may occur in severely
affected patients.
Common biochemical abnormalities - It includes
• Hyperproteinemia
• Hyperglobulinemia, and
• Azotemia.
• Hyponatremia and hyperkalemia may occur with severe vomiting or diarrhea, mimicking
hypoadrenocorticism.
• Less common abnormalities include
o Increased alanine aminotransferase, and
o Alkaline phosphatase activities (secondary to toxemia-induced hepatocellular damage
or dehydration).
• Hyperglycemia or hypoglycemia may be associated with concurrent diabetes or sepsis.
140
• Although C-reactive protein elevations help differentiate pyometra from cystic endometrial
hyperplasia with mucometra, the test is not readily available.
• Urinalysis may reveal isosthnuria, proteinuria, and/or bacteriuria.
• To prevent uterine puncture and abdominal contamination, cystocentesis should not be
performed if pyometra is suspected.
• Vaginal cytology confirms a septic exudate with open pyometra and is abnormal (i.e.,
predominantly neutrophils with some degenerative bacteria), even when the cervix is closed.
• Bacterial culture and susceptibility are essential for selection of appropriate antibiotics.
• Canine pyometra should be differential diagnosed from that of the following conditions
o Pregnancy
o Mucometra
o Hydrometra
o Pyovagina
o Metritis
o Uterine torsion, and
o Peritonitis
MEDICAL MANAGEMENT
• In critically ill patients, use of prostaglandin therapy to evacuate the uterine contents is not
ideal because evacuation is neither immediate or complete.
• In metabolically stable, valuable breeding animals, medical therapy with antibiotics for 2-3
weeks and with PGF2 alpha or preferably aglepristone (antiprogestin) combined with
cloprostenol (synthetic PG) can be considered.
• In open cervix pyometra, medical therapy is most preferred.
• In such cases, PG may be need in more than one series of injections.
• While resorting to PG therapy, the veterinarian should clearly discuss and inform the owner
about the serious complications such as uterine rupture or leakage of intraluminal contents in
to the abdomen and sepsis are possible.
• Transient (30-60 minutes) side effects include
o Panting
o Salivation
o Emesis
o Defecation
o Urination
o Mydriasis
o Nesting
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o Tenesumus
o Lordosis
o Vocalization, and
o Intensive grooming
• High dose of PG may lead to
o Ataxia
o Collapse
o Hypovolemic shock
o Respiratory distress, or
o Death
• Fertility may get reduced with the use of PG treatment.
• Combination of aglepristone and cloprostenol over 15 days has been reported to be safe and
effective with few side effects.
• Vulvar discharge increases and clinical signs begin to improve within 24-48 h of initial
aglepristone injection.
• Including an anti-lipopolysaccharide to reduce endotoxins may be beneficial.
• It is advisable to breed the animal during following oestrus cycle.
• Chance of recurrence is 20% during subsequent oestrous cycle.
Drugs Dose Route
Antibiotics for 2- - -
3 weeks
or PGF2 alpha 0.1 0.25 mg/kg; BID, 3-5 days SC
or PGF2 alpha 12.5 - 25 mg/kg Intra Vaginally, raise

hind quarters for 3-5
min
with 10 mg/kg; Days 1,3,8 and 15 (if not cured based on SC

Aglepristone ultrasonography)
with 1 µg/kg;Days 3 and 8, "far from feeding"; alternatively SC

Cloprostenol administer on days 3,5,8,10, 12, and 15 (if not cured
based on ultrasonography)
SURGICAL TREATMENT
• Surgical treatment [ovariohysterectomy (OHE)] should not be delayed more than is absolutely
necessary. Morbidity and mortality are associated with concurrent metabolic abnormalities and
organ dysfunction.
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• Surgical drainage of the uterus without OHE is not recommended, but has been successful in a
few cases.
• The corpus lutea are removed and each horn lavaged and suctioned.
• Indwelling drains are placed through the cervix to allow daily lavage with diluted antiseptics
• Surgery should not be delayed more than a few hours while medical therapy (i.e., fluid therapy)
is instituted especially in patients with closed pyometra.
• Urine output, glucose and arrhythmias should be monitored preoperatively.
• Hydration, electrolyte and acid-base imbalances should be corrected before surgery, if possible
(the prognosis is improved when azotemia is corrected before surgery).
• A broad-spectrum antibiotic effective against E.coli (e.g., cefazolin, cefoxitin, enrofloxacin and
ticarcillin plus clavulanate; should be given IV while awaiting antibiotic susceptibility results.
Aminoglycosides are nephrotoxic and not recommended because of the prevalence of renal
dysfunction with pyometra.
• In addition to fluid volume replacement, severely endotoxic or septicemic patients may also be
given corticosteroids (15 to 30 mg/kg prednisolone sodium succinate IV).
• Fluid input and uterine output should be monitored to help assess renal function.
• Low-dose dopamine (0.5 to 1.5 mg/kg/min IV) may be used to improve renal function or
diuretics (e.g., furosemide, 2 to 4 mg/kg IV, IM or SC or 20% dextrose IV) may be administered
in volume-overloaded patients with reduced urine production.
• Administration of antiarrhythmics may occasionally be necessary.
SELECTED ANTIBIOTICS TO TREAT PYOMETRA
Antibiotics Dose Route
Cefazolin 22 mg/kg; TID IV or IM
Cefoxitin 30 mg/kg; TID IV
Amoxicillin plus Clavulanate 12.5 - 25 mg/kg; BID PO
Ampicillin 22 mg/kg; TID to QID IV, IM, or SC
Ticarcillin plus Clavulanate 50 mg/kg; TID to QID IV
Enrofloxacin 7- 20 mg/kg; once a day PO or IV
Source: T.W. Fossum (2007)
ANAESTHESIA
• Anesthetic protocols vary greatly depending on patient status.
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• Animals that are systemically ill need to be closely monitored during anesthesia. They may be
induced with an opioid plus a benzodiazepine, given in incremental doses as necessary to
intubate.
• If intubation is not possible, etomidate or reduced dosage of thiopental or propofol may be
given. If etomidate is not available, arrhythmic dogs may be premedicated with
hydromorphone and induced with thipental and lidocaine. For the latter, 9 mg/kg of each is
drawn up and half is given initially, IV. Additional drug is given to allow the dog to be intubated.
To prevent toxicity, usually no more than 6 mg/kg of lidocaine is given IV.
• Isoflurane and sevoflurane are the inhalants of choice because they cause minimal cardiac
depression, and induction and recovery are usually rapid.
• The anaesthetic depth should be monitored closely in these patients.
• Hypotension should be corrected before and prevented during and after surgery in animals
with pyometra.
• The patient should be monitored for arrhythmias or tachycardia.
• Hypertonic saline with a colloid (e.g., dextran or hetastarch) improves hemodynamics and
oxygenation in animals with septic shock.
• Animals with total protein less than 4 g/dl or albumin less than 1.5 g/dl may benefit from
perioperative colloid (e.g., hetastarch) administration. Hetastarch may be given preoperatively,
intraoperatively, and / or postoperatively for a total dose of 20 ml/kg/day in dogs and 10-15
ml/kg/day in cats. If colloids are given during surgery (7-10 mg/kg) acute intraoperative
hypotension should be treated with crystalloids.
• Dobutamine (2-10 mg/kg/min IV) or dopamine (2-10 mg/kg/min IV) may be given during
surgery for inotropic support. Dobutamine is less arrhythmogenic and chronotropic than
dopamine and is preferred if the patient is hypotensive and anuric.
• In dogs that are anuric and normotensive, low-dose dopamine (0.5-1.5 mg/kg/min IV) plus
furosemide (0.2 mg/kg IV) may be preferable. In cats, mannitol (0.25-0.5 g/kg/IV slowly over 20
minutes) may be used for diuresis.
SELECTED ANAESTHETIC PROTOCOLS
Selected Anaesthetic protocols for Debiliated/Shocky animals with Pyometra
Premedication and • Hydromorphone (0.02-0.2 mg/kg; IV or IM) plus Diazepam (0.2

Induction mg/kg IV).
• Give incremental doses.
• Intubate if possible.
• If necessary, give etomidate (0.5-1.5 mg/kg IV).
• Alternatively, if no vomition, mask induction can be used or
give thiopental or propofol at reduced doses.
Maintenance • Isoflurane or Sevoflurane
Source: T.W. Fossum (2007)
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SURGICAL ANATOMY OF THE FEMALE REPRODUCTIVE TRACT
• The female reproductive tract includes

o Ovaries
o Oviduct
o Uterus
o Vagina
o Vulva
Ovaries
• Ovaries are located within a thin walled peritoneal sac, the ovarian bursa located just caudal to
the pole of each kidney.
• Right ovary lies further cranially than the left.
• Right ovary lies dorsal to the descending duodenum, and the left ovary lies dorsal to the
descending colon and lateral to the speeln.
• Medial retraction of the mesoduodenum or mesocolon exposes the ovary on each side.
• Each ovary is attached by the proper ligament to the uterine horn and via the suspensory
ligament to the transversalis fascia medial to the last one or two ribs.
• The ovarian pedicle (mesovarium) includes the suspensory ligament with its artery and vein,
ovarian artery and vein, and variable amounts of fat and connective tissue.
• Canine ovarian pedicle contains more fat than feline ovarian pedicles, making it more difficult
to visualize the vasculature.
• Ovarian vessels take a tortuous path within the pedicle.
• Ovarian arteries originate from the aorta.
• The left ovarian vein drains in to the left renal vein; the right vein drains in to the caudal vena
cava.
• The suspensory ligament is tough, whitish band of tissue that diverges as it travels from the
ovary to attach to the last two ribs.
• The broad ligaments (mesometrium) is the peritoneal fold that suspends the uterus.
• The round ligament travels in the free edge of the broad ligament from the ovary through the
inguinal canal with the vaginal process.
Oviduct
• The uterine tube or oviduct courses through the wall of the ovarian bursa.
Uterus
• The uterus has a short body and long narrow horns.

• Blood supply: uterine arteries and veins.
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• Cervix is constricted caudal part of the uterus and is thicker than the uterine body and vagina. It
is oriented in a nearly vertical position with uterine opening dorsally.
Vagina
• Vagina is long and connects with the vaginal vestibule at the urethral entrance.
• The clitoris is broad flat, vascular, infiltrated with fat, and lies on the floor of the vestibule near
the vulva.
• The clitorial fossa is depression on the floor of the vestibulethat is sometimes mistaken for the
urethral orifice.
Vulva
• Vulva is the external opening of the genital tract.

• The vulvar lips are thick and form a pointed commisure.
• The constrictor vulvae and vestibule muscles encircle the vulva and vestibule.
SURGICAL TECHNIQUE
Positioning
• Position the patient is dorsal recumbency for a ventral midline celiotomy

• The entire ventral abdomen should be clipped and prepared for aseptic surgery
Surgical Technique
• Expose the abdomen through a ventral midline incision beginning 2-3 cm caudal to the xiphoid
and extending to the pubis
• Explore the abdomen and locate the distended uterus.
• Observe for evidence of peritonitis (i.e., serosal inflammation, increased abdominal fluid, and
petechiation)
• Obtain abdominal fluid for culture
• Evacuate the urinary bladder by cystocentesis and collect a urine specimen for culture and
analysis if not previous submitted
• Carefully exteriorize the uterus without applying pressure or excessive traction
• A fluid-filled uterus is often friable; therefore lift rather than pull the uterus out of the abdomen
• Do not use a spay hook to locate and exteriorize the uterus because it may tear
• Do not correct uterine torsion because this will release bacteria and toxins
• Isolate the uterus from the abdomen with laparotomy pads or sterile towels
• Place clamps and ligatures as previously described for OHE except that the cervix may be
resected in addition to ovaries, uterine horns and uterine body.
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• Ligate the pedicles with absorbable monofilament suture material (i.e., 2-0 or 3-0
polydioxanone or polyglyconate) and transect the junction of the cervix and vagina.
• Thoroughly lavage the vaginal stump.
• Culture the contents of the uterus without contaminating the surgical field.
• Remove laparotomy pads and replace contaminated instruments, gloves and drapes.
• Lavage the abdomen and close the incision routinely unless peritonitis is present.
• Submit the uterus for pathological evaluation.
Site of incision Skin incision Incision of external oblique

muscle
Incision of internal oblique Exteriorization of uterus Clamping and ligation of ovary
Ligation of utero-ovarian artery Skin sutures
Courtesy: S.Ayyappan, Dept. of Veterinary Surgery and Radiology, MVC, TANUVAS.
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Pus filled canine uterus removed Cut open uterus after drainage of pus
surgically
POST-OPERATIVE CARE
• Administer post-operative analgesics
Analgesic Drugs Dose Route Frequency
Oxymorphone 0.05-0.1 mg/kg IV, IM Every 4 h (as needed)
Butorphanol 0.2-0.4 mg/kg IV, IM, or SC Every 2-4 h (as needed)
Buprenorphine 5-15 µg/kg IV, IM Every 6 h (as needed)
• Closely monitor for 24-48 h for sepsis and shock, dehydration, and electrolyte/acid-base
imbalances.
• Severe hypoproteinemia or anemia may require plasma or blood transfusions.
• Fluid therapy should be continued until the animal resumes normal feed and water.
• Antibiotic therapy should be continued based on culture and sensitivity results for 10-14 days.
• Low dose dopamine (of questionable value) or diuretics may be given if urine production is
reduced.
COMPLICATIONS
• Complications associated with elective ovariohysterectomy (OHE) may also occur following OHE
for pyometra.
• Death (5-8%) despite of appropriate therapy, especially following uterine rupture (57%).
• Septicemia, endotoxemia, peritonitis, and cervical or stump pyometra may occur.
• Stump pyometra may be associated with residual ovarian tissue. In such cases, excise the
remaining stump and remove the residual ovarian tissue.
• Other complications include anorexia, lethargy, anemia, pyrexia, vomiting, icterus, hepatic
disease, renal disease, and thrombo-embolic disease.
• Most complications resolve within two weeks of surgery.
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COMPLICATIONS
• Complications associated with elective ovariohysterectomy (OHE) may also occur following OHE
for pyometra.
• Death (5-8%) despite of appropriate therapy, especially following uterine rupture (57%).
• Septicemia, endotoxemia, peritonitis, and cervical or stump pyometra may occur.
• Stump pyometra may be associated with residual ovarian tissue. In such cases, excise the
remaining stump and remove the residual ovarian tissue.
• Other complications include anorexia, lethargy, anemia, pyrexia, vomiting, icterus, hepatic
disease, renal disease, and thrombo-embolic disease.
• Most complications resolve within two weeks of surgery.
INTRODUCTION
• In general, mucometra and hydrometra are similar

• Difference is only the degree of hydration of the mucin in the uterus, may vary from a watery
fluid to a semisolid mass
• Secondary to cystic ovaries and cystic endometrial hyperplasia usually associated with an
anestrus period of 6 months or more
o Small cysts, 1 - 1.5 cm
o Usually two to four cysts on each ovary
o Resists rupture by manual pressure due to thick cyst wall
o In addition, characterized by cystic degeneration of the endometrium and atrophy of
the uterine wall, with an ounce to ~4500 ml of thin to viscid mucus in the uterus.
ETIOLOGY
• Observed in heifers or cows with arrests in the development of the Mullerian duct system or
segmental aplasia of the paramesonephric ducts in which part of the vagina, cervix, or uterus
may be missing or defective
• Persistence of the hymen causing mucometra and mucovagina has been previously described
• These genetic or congenital defects may result in a distention of both horns with watery,
viscous, or even rather solid coagulated masses of mucus and cellular debris that may be
confused with pregnancy
• In these affected cattle the ovaries and endometrium are normal, and estrum therefore usually
occurs normally
• Rare cases of mucometra may be associated with a retained corpus lutem
• In the cow, as in the dog, mucometra can apparently be produced by prolonged hormonal
stimulation by estrogens and/or progesterone.
• Secondary to trauma and a line adhesion obstructing the lumen of the cervix at the region of
the internal os
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• In cases of mucometra, no infection is usually present unless introduced accidentally by trauma,
service, or treatment.
• Mucometra should be differentiated from pregnancy

• This can be accomplished by a careful examination of the genital tract
o Failure to slip fetal membranes
o Presence of anomalies in the uterus, vagina, and cervix
o Ovaries palpable with a single or multiple small cysts 0.5 - 0.75 inch in diameter
o Persistent corpus luteum on repeated examinations
o Lack of enlargement or whirring of the uterine artery
o Inability to palpate the fetus or cotyledons
o Although some cases with firm, gum- like-mucus in one horn or an apex of one horn
may simulate a fetus or mummified fetus
o Presence of a uterine wall that is usually thin and lacks tone as compared to the normal
pregnant uterus, and
o Absence of regular developmental changes that occur in a normal pregnancy are the
clinical findings on rectal examination of cattle.
PROGNOSIS
• Use as breeding animals is questionable from a hereditary standpoint

• Cows with mucometra, or hydrometra due to defects of the genital tract are often sterile
• In case of uterus unicornis, pregnancy occurs in the normal horn
• In simple imperforate hymen, it can be opened.
TREATMENT
In cows with mucometra and anestrum due to cystic ovaries
• Large dose of LH 20,000 IU of HCG or more intravenously may occasionally bring about
recovery.
In rare cases of mucometra with a persistent corpus luteum
• Old approach
o Injection of estrogens to involute the corpus luteum (CL) or
o Manual removal of CL may be successful in correcting the condition.
• Current approach
o Injection of Prostaglandin F2 alpha 25 mg i/m.
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MODULE-7: ABORTION IN DOMESTIC ANIMALS
DEFINITION
• Abortion is the expulsion from the uterus of a living fetus before it reaches a viable age, or
more commonly the expulsion of a dead fetus of recognizable size at any stage of gestation.
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Abortion in a cow Aborted fetus
INTRODUCTION
• Economically, abortions are of great concern to the farmer, because

o The fetus is lost
o A prolonged period of uterine disease and sterility may follow
o Unproductive female must be maintained for a long period or sold
o If the cause of abortion is infectious, it threatens the rest of the herd.
• Agents which affect the fetus or its placental membranes or both results in abortions.
• The etiological agent of abortions determine the degree of damage to fetal membranes and
endometrium and frequency of placental retention and sterility.
• Disease of the fetal placenta closely reflects in the maternal placenta due to their intimate
contact.
• In dam, agents causing severe stress reaction can lead to abortion.
• Any abnormal genital discharge noticed should be investigated and closely monitored during
subsequent estrus periods.
• In the cow, abortions after 4th month of gestation frequently results in placental retention.
SUMMARY OF CAUSES OF BOVINE ABORTION
Infectious Causes Non-Infectious Causes
Bacterial Chemicals, Drug and Poisonous plants
Brucellosis (Br. abortus), Leptospirosis Nitrates, chlorinated napthalenes, arsenic,

(Leptospira pomona and others), Listeriosis (L. locoweeds, perennial broom- weed, pine
monocytogenes), Tuberculosis (Mycobacterium needles.
bovis) and Vibriosis (V. fetus venerealis).
Miscellaneous Bacterial Hormonal
Streptococci, diplococci, staphylococci, E. Coli, Estrogens, glucocorticoids, progesterone
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Alcaligenes fecalis, Pseudomonas aeruginosa, deficiency.
Corynebacterium pyogenes, Erysipelothrix
insidiosa, Hemophilus, Vibrio fetus intestinalis,
Mycobacterium avium, Pasteurella multocida,
Salmonella paratyphi B, S. cholera-suis and S.
dublin, B. anthraci Nocardia asteroides, and
Mycoplasma.
Viral Nutritional
Infectious bovine rhinotrachitis (IBR-IPV), Starvation, malnutrition, vitamin A

Epizootic bovine abortion (E.B.A. or Chlamydia). deficiency, iodine deficiency.
Miscellaneous Viral Physical
Foreign diseases such as: foot and mouth Douching, infusing or insemination of the
disease, rinderpest, Rift Valley fever, bovine pregnant uterus, rupture of the amniotic
infectious petechial fever and tick borne fever; vesicle and/or trauma to embryo, removal
Native diseases as bovine virus diarrhea— of the corpus luteum, torsion of the uterus
mucosal disease (BVD-MD) Myxovirus or umbilical cord, marked stress due to
parainfluenza—3, malignant catarrhal fever and severe fatigue due to transport, work,
pseudorabies. severe systemic diseases, or major
operations.
Mycotic or Fungal Genetic or chromosomal
Aspergillus spp., Mucorales Spp. (including Certain defects of the embryo or fetus.
Absidia, Mucor, Rhizopus), and yeasts.
Protozoal Miscellaneous
Trichomoniasis, toxoplasmosis, besnoitis or Twinning, allergies and anaphylactic

globidiosis, trypanosomiasis, anaplasmosis, reactions, tumors and etc.
babesiasis or piroplasmosis.
BRUCELLOSIS
(Contagious or infectious abortion or Bang's disease)
INTRODUCTION
• First described by Bang (1897) in Denmark.

• Most important worldwide cause of abortion in cattle, except in countries like USA.
• In cattle, abortion occurs during the last trimester of pregnancy and a subsequent period of
infertility.
• Mainly infective for cattle, but occassionally in sheep, swine, dog and horses.
153
INCIDENCE AND CAUSATIVE AGENT
Incidence: Varies from 5-90% in a herd depending upon
• The number of susceptible pregnant animals

• Rate of transmission
• The virulence of the organism, and
• Other factors.
Causative agent
• Small gram-negative rod, Brucella abortus

• Grows intracellularly.
TRANSMISSION AND PERSISTENCE OF INFECTION
Transmission
• Introduction of infection in to susceptible herds by purchase of an infected cow

• Occasionally carried by dogs or persons from one farm to another or contact of infected and
susceptible animals across a line fence
• Frequently by ingestion of infected genital discharges of aborting animals that contaminate
feed and water
• Through the mucous membrane of the eye and by intrauterine artificial insemination of
infected semen
• Calves nursing infected cows may spread by fecal contamination of food ingested by
susceptible animals
• Once infection is established in sexually mature animals, it tends to persists indefinitely
• By contaminated trucks/at fairs or shows.
Transmission of brucellosis is Suspected cows should be isolated

primarily by ingestion of Brucella to prevent contact with the aborted
organisms which typically occurs in fetus and fetal membranes- Six
this setting by snoopy cows month old fetus is shown here.
"inspecting" an aborted fetus.
154
Persistence of infection
• Organism is found in the chorion of the placenta.

• Perisitent infection in the udder nd the supermammary, retropharyngeal and internal and
external iliac lymph nodes of adult cows and in the testes, epididymides, vasa deferentia and
seminal vesicles of bulls.
• After abortion, the organism does not perisits in the uterus and disappears in 1-5 months.
• Occasionally organisms persists in joints and bursae.
CLINICAL SIGNS
• Abortions usually occur from 6-9 months of gestation
Autolytic aborted fetus - 5.5 months Autolytic aborted fetus - 6 months

• Premonitory signs of udder enlargement and vuvlal edema are often absent.
• Fetal membranes:
o Edematous
o Hemorrhagic
o Leathery and necrotic
o Brownish yellow pasty exudate in the uterochorionic space
• Retained placenta and metritis with a following period of genital discharge and infertility.
• After recovery, most cows carry their subsequent calves normally but a few cows may abort
two or three times.
• Occasionally fetuses may be born alive but most are weak and premature and die within a few
hours.
• Dead fetus may exhibit some autolytic changes of edema and hemorrhages of the tissues and
body cavities and may be stained with meconium.
DIAGNOSIS
• Isolation of organism from fetal lungs, stomach or placenta
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Aspiration of abomasal contents for the
purpose of recovery and isolation of Brucella
abortus from an aborted fetus.
• In adult animals, organisms may be recovered from the milk or serum or from lymph nodes
after slaughter
• Serological test for agglutinins in the blood
o Tube and plate agglutination test
o Heat inactivation test
o Acidified plate antigen (APA) test
o Acridine compound (Rivanol) precipitation test
o Complement fixation test (CFT)
o Two-Mercaptoethanol (ME) test.
In non-vaccinated cow
1:50 reaction is a suspicious reaction
1:100 reaction is positive.
In officially calfhood vaccinated cow

1:100 reaction is suspicious
1:200 reaction is positive.
• Agglutination test on milk include the milk ring test (MRT) or Brucellosis ring test (BRT)
• Agglutination test may be conducted on seminal plasma from bulls in which it is highly effective
in detecting an increased local antibody level and on vaginal mucus from cows when a virulent
infection is present in uterus.
PREVENTION AND CONTROL
• Effective means of eradicating bovine brucellosis is by operation of test and slaughter policy,
inconjunction with effective measures for controlling the movement of animals
156
• If disease is prevalent, reduce the spread of infection and lower the prevalence by intensive
vaccination. A test and slaughter policy may then be adopted.
• Hygiene and sanitation
• Vaccination of calves with strain 19 from 3-7 months of age
• Testing and disposal or elimination of reactors
• Aborted fetuses and placentas should be buried or burnt and contaminated areas should be
disinfected with 4% compound solution of cresol or similar disinfectant.
• RB 51 vaccine: the newer live-attenuated vaccine strain used currently. This is a "rough" variant
of B.abortus that lacks the O-side chain on its LPS.
o Vaccination should occur during calfhood (4-12 months for RB51) so as to minimize the
induction of antibodies that might be interpreted as evidence of actual infection. (This is
much less of a problem with RB51 than it was with S-19 because of the lack of the O-
chain on RB51).
o Vaccination was mandatory in the past when the incidence of brucellosis was greater.
Today, the most common reason for vaccination is that vaccinated animals command a
higher value at sale. However, some countries will not accept vaccinated animals for
export.
o Vaccination should not conducted in pregnant animals because of the risk of vaccine-
induced abortion.
LEPTOSPIROSIS
INTRODUCTION
• First described in cattle in USA by Jungherr (1944)

• Agent recovered by Baker and Little (1948)
• In cattle, outbreak of leptospirosis is characterised by abortion, still birth and weak calves
• Outbreak in cattle herd may be sporadic
• L.Pomona is the most common and serious of the five serotypes, as a cause of disease and
abortion in cattle
• Incidence of abortion may vary from 5-40% of the herd depending upon the number of
susceptible cattle in the last third of gestation, the numbers and virulence of the infective
organisms and the opportunity for the spread of infection.
CAUSATIVE AGENT AND TRANSMISSION
• Small filamentous spirochete with about 40 serotypes, the most common of which are
Leptospira pomona, Leptospira hardjo, Leptospira grippotyphosa and Leptospira canicola
• Organisms are readily destroyed by heat, sunlight, drying, acid and chemical disinfectants
• Survive for days or weeks in a moist environment at moderate temperatures as in stagnant

ponds, streams or wet soil
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Leptospira pomona, a spirochete is a common cause of
abortion in catte
• Enter by penetration of the abraded skin of the feet and legs when wading and by passage
through the mucous membranes of the mouth and pharnyx, nose and eyes by contact with
contaminated water and feed or urine.
Optimal setting for the (interspecies)

transmision of leptospirosis via urine, by
running cattle and pigs together in an area with
stagnant water.
CLINICAL SIGNS
• Anorexia
• Drop in milk flow with a slack udder containing slightly thick "gargety" milk
• Marked drop in milk with thick, slightly bloody secretion, a flaccid udder
• Loss of condition
• Anemia
• Hemoglobinuria
• Dyspnoea
• Icterus, and
158
• Often death in 1-3 days
• In all forms: abortions occur in the last half of gestation, may occur from 1-3 weeks after
recovery from the acute febrile stage
• Not all susceptible infected cows in advanced pregnancy will abort
• Occasionally an infected cow will give birth to a live, weak calf that dies within few days
• Retained placenta and its sequelae of metritis and infertility are common.
DIAGNOSIS
• More difficult than those due to brucellosis

• Based on clinical symptoms together with necropsy findings of widespread petechia indicative
of a severe septicemia.
• Culture of fetus/ fetal membranes for leptospira in lab animals/media is seldom successful.
• Silver staining of liver and kidney sections.
• Use of fluorescent antibody technique to stain leptospires in infected urine from aborting cows;
culturing of urine may also be successful.
• A variety of serological tests have been recommended.
TREATMENT
• Since eradication of leptospirosis is not possible, control and treatment of bovine leptospirosis
may be accomplished by:
o Hygiene and sanitation
o Vaccination
o Antibiotic therapy
• Treatment of acute stage:
o Parenteral administration of large doses of antibiotics including penicillin 3 million units
and streptomycin 5 gm twice daily or tetracyclines 2.5 -5.0 gm daily /450 kg animal for 5
days.
• Treatment of carrier state: similar
o A single injection of dihydrostreptomycin at a dose level of 25 mg /kg would eliminate
the carrier state.
VIBRIOSIS
INTRODUCTION
• A venereal disease of cattle caused by Vibrio fetus venerealis spread at the time of coitus or at
the time of artificial insemination with improperly handled and treated semen, and
characterized by infertility with an increased number of services necessary per conception.
• First described by Mc Fadyean and Stockman in sheep (1910) and cattle (1913).
• Organism was called Vibrio fetus by Theobald Smith (1918-1923).
159
CAUSATIVE AGENT
• Vibrio fetus venerealis.

• Organism may appear as motile, or non-motile, gram-negative, short, comma-shaped rods, or
as double spiral shaped filaments.
TRANSMISSION
• V. fetus venerealis is found only in the female genital tract and its contents, fetus and placenta,
and in the prepuce and semen of the bull.
• Organism usually invades the uterus about 7 days after natural service to an infected bull.
• It remains there for about 13 weeks until a local immunity develops and the infection is
eliminated.
• Infection may remain in the cervix and vagina for 8-18 months or more.
• Rarely a cow may carry infection through a normal geatation period.
• Young bulls of under 5 years of age are difficult to infect.
CLINICAL SIGNS
• Insidious in manner in which it enters the herd.

• Until signs of infertility with failure of conception occurs in large number of cows, the condition
may not be recognized for several months or more.
• Acute type of infertility
o Introduced by an infected bull in to a clean or susceptible herd.
o Marked drop in conception rate, occasionally to less than 10%.
o Infertility may a last for 2-6 months or more.
o Immunity develops by this time and conception will follow breeding to an infected or
uninfected bull.
• The chronic or subacute type
o Characterized by a history of an acute infertility problem.
o In some herds the infertility may be limited to the portion of a herd served by a single
bull, or it may involve all cows bred naturally, while cows being bred artificially with
antibiotic treated semen conceive normally.
o Examination of bull and its semen usually reveals no abnormalities or explanation for
the infertility.
o Abortions may occur in both the acutely and chronically affected herds, but more
frequent in acute outbreaks.
o Some heifers have a natural immunity or develop it promptly and conceive within 2
months. Other conceive promptly but remain carriers of the organism for months. While
other remain infected for months, have many services or abort.
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• Specific signs
o Vibriosis may fail to become established in a susceptible animal after coitus with an
infected bull, either due to natural resistance or because of low number of organisms.
Conception and normal gestation may occur. Occasionally the infection fails to establish
itself in the uterus and cause the early death of ovum or embryo. Gestation continue for
some months and then terminate in 3-8 months in abortion.
o Endometritis.
o Infertility or failure of conception.
o Long estrous cycles.
o Abortions
Occur from 4 months to 7 months of gestation.
Some indication of impending abortion after 4-5 months with presence of vulvar
dischare and slight vulval edema.
Some enlargement of udder.
In late abortions, placental retention occurs.
Pyometra rarely observed.
Intercotyledonary spaces filled with thick , purulent viscid material.
Cotyledons - greyish white in colour with much chessy exudate between the
maternal caruncle and the fetal cotyledon.
The membranes may be thickened and edematous.
Amniotic fluid turbid due to fetal diarrhoea.
Aborted fetus - autolytic changes of subcutaneous edema, thin, blood fluid in the
body cavities, and in the stomach a thick, yellow, flocculent turbid material that
usually contains many vibrio.
o Lack of libido in bulls.
DIAGNOSIS
• On the basis of the herd history or symptoms.

• A careful review of breeding records.
• Careful physical examination of the individual animals in the herd, including the bull.
• Cultures of vaginal, cervical or uterine mucus.
• Culture of V.fetus from semen and preputial smegma.
• Culture of aborted fetuses.
TREATMENT
• Genital contact between infected and non-infected animals should be prevented.

• Control of V.fetus in frozen semen is more difficult than in the extended liquid semen because
the glycerol interferes with the effect of the antibiotics on the organism.
161
• Intrauterine infusion of 1 gm of streptomycin together with penicillin in an aqueous or oil base.
Elimination is most efficient if administered within 24 h after service to an infected bull.
• Infusion of dihydrostreptomycin 5 gm in 10 ml of a 50% aqueous solution into the preputial
cavity and massaged through skin for 5 minutes while the orifice is closed. Repeat for 5 days. At
the time of first and third treatments, administer dihydrostreptomycin 22 mg/kg bw
subcutaneous.
INFECTIOUS BOVINE RHINOTRACHEITIS (RED NOSE) - INFECTIOUS PUSTULAR VULVO

-VAGINITIS (IBR-IPV) VIRUS
INTRODUCTION
• Common cause of abortion in cattle in USA and other countries.

• This is a herpes virus and has many features similar to rhinopneumonitis virus, a herpes virus in
horses, and herpes simplex virus in humans.
• Clinical morbidity may vary from 10 - 100 % and mortality is generally under 10 %.
• Deaths in prenatal fetus and neonatal calves may be high.
• Although generalized viremia develops in nearly all IBR-IPV infections, localized manifestations
of the disease occur that confuse the diagnosis.
CLINICAL FORMS OF THE DISEASE
• Upper respiratory form: characterized by fever (104-107F), anorexia, depression, reddened

nasal mucous membrane, and nasal discharge, pustules and ulcers in the mucosa of the nose,
pharynx and trachea, infrequent coughing and drop in milk production lasting for 2- 7 days.
• Conjuctival form: exhibits marked lacrimation changing to a mucopurulent profuse discharge
from the eyes along with septicemic signs exhibited in (1). The conjunctiva is reddened, swollen
and contains necrotic pustules and ulcers.
Ocular lesions associated with bovine herpes

virus infection (BHV1) or infectious bovine
rhinotracheitis (IBR).
Roberts SJ (1973)
162
• Neonatal digestive form: in young calves from birth to 2-3 weeks of age is associated with a
high mortality and is characterized by severe signs of septicemia resembling that associated
with E.Coli but exhibit necrotic lesions in the mouth, pharynx, larynx, esophagus and fore-
stomachs with diarrhea and death within 1-3 days.
• Meningo - encephalitic form: seen occasionally in young cattle 4-10 months of age.
Characterized by dullness, in-coordination, tremors, amaurosis, opisthotonus, coma and death
within 3-4 days.
• Vulvo-Vaginal form: Generalized septicemia, pustules and ulcers of the vaginal and vulvar
mucosa and purulent discharge (previously called as coital vesicular exanthema or
blaschenausschlag). occasionally small abscess beneath the mucus membrane are observed.
• Preputial form: In bulls is characterized by pustules and ulceration of the penis and prepuce,
severe degenerative changes of the seminiferous epithelium and a period of infertility or
sterility lasting upto 3-4 months.
• Prenatal or abortive form: characterized by infection and intra-uterine death of the fetus and
abortion 2-5 or more days later may occur in all 3 trimesters most common from mid gestation
to term. Incidence in a herd vary from 5-60% depending on virulence of the organism and
number of susceptible cows in advanced pregnancies. RFM occurs in 50% of abortions.
• Intra-uterine form: caused by necrotizing endometritis when IBR - IPV virus is present in semen
at the time of AI. Results in erect edematus uterus and short cycle of 9-15 days length.
o Abortions may occur from 2 weeks to 2-3 months after any form of disease in pregnant
animals but is rarely observed in vulvo-vaginal form.
o Signs of impending abortion are usually not observed. Aborted fetuses are invariably
expelled dead with a degree of autolysis.
o Placenta shows autolytic non-distinctive lesions characterized by edema and presence
of yellow brown amniotic fluid. Hemorrhages and petechiae are often widespread in the
fetus.
o Culture of fetal organs and fluids especially fetal cotyledons may recover the IBR-IPV
virus.
CLINICAL SIGNS
• Signs of impending abortion not observed.

• Aborted fetuses are invariably expelled dead with a degree of autolysis.
• Premature births or living fetuses or calves at term not reported.
• Calves normal at birth may become infected and die in 24-48 h of infection.
• Lesions in aborted fetus is of diagnostic value.
• No evidence of uterine disease.
• Placenta: autolytic non-distinctive lesions characterized by edema, and presence of yellow,
brown amniotic fluid.
• Autolysis of fetus always present to a varying degree with reddish-brown subcutaneous edema
and dark red watery fluid in the body cavities.
• Widespread hemorrhages and petechiae are observed in the fetus.
163
• Microscopic characterisitic lesions
o Focal necrosis in the liver, lymph glands, kidneys, other organs and placenta.
o Most striking gross change occur in kidneys: Marked hemorrhagic edema.
o Severe hemorrhagic necrosis confined largely to the cortex and often severe that the
medulla and part of the cortex floats in dark red fluid.
o Adrenal glands: pin-point necrotic and white foci.
o Intranuclear inclusion bodies are seen infrequently in the autolysed fetuses.
DIAGNOSIS
• Culture of fetal organs and fluids and especially the fetal cotyledons.
• Serological testing using serum neutralization test: Best conducted on double serum samples
taken at the time of the acute illness, when most samples are negative, and again 2-6 weeks
later.
• In cases of abortion, the serum titers are usually elevated in the dam at the time of the
abortion, but a second sample taken 2-3 weeks after abortion may reveal a rising titer.
• In herd out break: Representative samples should be taken from normal, recovered, aborting or
acutely ill. Samples should be taken in as near sterile manner as possible in sterile vacuum vials.
CONTROL AND TREATMENT
• Blood testing and isolation of new arrivals in to the herd with a second sample taken 1-2
months later.
• Animals with positive titer should be considered as potential carrier.
• In an outbreak, contact between animals should be kept at a minimum.
• In vulvovaginal or preputial form of the disease, breeding should be stopped for 3-4 weeks.
• In severe cases, apply oily antibiotic preparations locally to the ulcerated mucous membranes
of the genital tract.
• In valuable animals suffering from the respiratory form, administer antibiotics to prevent
pneumonia or secondary respiratory complications.
• In abortions:
o Destroy the fetus and fetal membranes.
o Isolate the cow from other pregnant susceptible animals for 3-4 weeks.
o If calves are infected and ill, prevent contact with pregnant animals.
• IBR-IPV vaccines are available either alone or in combination with BVD-MD (Bovine virus
diarrhea-mucosal disease) virus or parainfluenza virus. Keep vaccines well refrigerated to
maintain potency.
• Pregnant cows at any stage of gestation should not be vaccinated with IBR-IPV vaccine.
164
EPIZOOTIC BOVINE ABORTION (EBA)
INTRODUCTION
• Abortions are confined to the habitat of the argasid tick Ornithodoros coraceus.
• Early studies suggest that it is caused by an agent of the psittacosis lymphogranuloma,
chlamydia or migawanella group of organisms (Storz et al 1960).
• Authenticity of the the isolation of organism and its role in pathogenesis is debatable.
• These organisms differ from most viruses in that they are susceptible to antibiotics, they grow
well in the yolk sac of chick embryos and they have developmental cycles during which large
elementary bodies are formed.
• Abortions occur 6-8 months of gestation.
• Incidence vary from 30-40%, occasionally up to 75% or more of susceptible females aborting.
• In susceptible herds, all ages would abort, thereafter largely limited to heifers.
CLINICAL SIGNS
• Outbreaks occur without any premonitory signs of illness or impending abortion.

• Primarily affects the fetus, no clinical evidence of infection in cow.
• Abortions occur from 4 months to term; most common at 7, 8 and 9 th months.
Epizootic bovine abortion, or Foothill Abortion, appears to be Epizootic bovine abortion, or

geographically limited to the western United States. Live fetuses Foothill Abortion, appears to be
may be aborted, and most dead fetuses are fresh. Fetal lesions geographically limited to the
include granulomatous hepatitis and lymphoid hyperplasia in the western United States. Live
lymph nodes. Once a heifer or a cow aborts and remains in the area fetuses may be aborted, and most
she will be immune. dead fetuses are fresh. Fetal
lesions include granulomatous
hepatitis, which is generally
periportal, and central veins are
dilated.
165
• Fetuses are expelled dead at term or calves born alive and weak, succumb later.
• Aborted fetuses are not autolysed.
• Aborted fetus exhibit characterisitc lesions of anemia, and extensive petechial hemorrhages of
the conjunctival and oral mucosa and skin.
• Subcutaneous tissues edematous, especially those of the head.
• Body cavities usually contain straw coloured fluid.
• Striking lesion: Swollen, coarsely nodular yellow coloured liver, develops secondary to chronic
vascular lesions and chronic passive congestion.
• Petechial hemorrhages in most organs and tissues.
• All lymph glands enlarged and edematous.
• Basic histological change: granulomatous inflammatory process or a diffuse or focal reticulo-
endothelial hyperplasia irregularly involved in all organs.
• Fetal membranes edematous: Not of diagnostic value if entire placenta is not expelled.
• Entire placenta if expelled: Inter-cotyledonary tissue of the apices of the placenta often tough,
leathery and reddish white in colour and the edges of the cotyledons contain small round focal
areas of necrosis.
DIAGNOSIS
• Complement fixation test on paired samples taken at the time of abortion and 2-3 weeks later -
If rising titre is observed - Diagnostic value.
CONTROL
• Attempted by ensuring that susceptible animals are exposed to ticks before they become
pregnant.
BOVINE VIRAL DIARRHOEA (BVD)
INTRODUCTION
• BVD was initially recognized to cause diarrhoea, and more recently shown to cause infertility.
• Due to the importance of fetal infection, to be considered primarily as a disease of
reproduction.
• BVD was first recorded as a cause of bovine abortion in UK in 1980.
CAUSATIVE AGENT
• BVD virus is a pestivirus.

• Related to the viruses of Border disease of sheep and classical swine fever.
• Two main biotypes
o A cytopathic strain
o A non-cytopathic strain.
166
TRANSMISSION AND PATHOGENESIS
• Infection with non-cytopathic strain in utero between days 30-125, results in birth of calf
persistently infected with virus.
• Infection of cows at other stages of pregnancy causes early embryonic death and abortion, with
aborted fetuses exhibiting abnormalities of the CNS and ocular systems.
• Infection in last third of pregnancy does not cause immunotolerance, but results in birth of calf
that is immune to the disease.
• Bulls excrete virus in their semen following spontaneous, persistent and chronic infection.
• Seen in young animals (6-24 months)
• Disease characterised by
o Pyrexia
o Anorexia
o Watery diarrhoea
o Nasal discharge
o Buccal ulceration, and
o Lameness.
DIAGNOSIS
• Introduction of persistent infected cows or heifers in to susceptible herd should be viewed with
concern.
• First signs are abortions and birth of congenitally deformed calves.
• Fetuses may be fresh, autolysed or mummified.
• Virus can be isolated from fetus, particularly lymphoid tissue such as spleen.
• Immuno-cytochemical identification of BVD viral proteins in fetal tissue, especially kidney, lung,
or lymphoid tissue.
• A substantial rise in neutralizing antibodies in herds experiencing abortions and the presence of
antibodies in serum of new born calves or thoracic fluids of abortuses.
CONTROL
• Extensive culling of persistently infected animals.

• Do not breed from persistently infected cows.
• Screen all newly purchased animals before introduction in to the herd.
• A sero-positive animal would be safe to purchase but a sero-negative one requires to be free of
virus to assure freedom from risk.
• In pregnant cows, killed vaccines can be used but not modified live virus vaccines.
167
MYCOTIC ABORTIONS
INTRODUCTION
• Frequent and consistent cause of abortion in cattle.

• Sporadic abortions.
• Incidence: 5-10%.
CAUSATIVE AGENT
• Frequently isolated fungi are

o Absidia spp
o Rhizopus spp
o Mucor spp, and
o Aspergillus spp
• Other fungi implicated are
o Mortiella wolfii, and
o Petriellidium boydii
CLINICAL SIGNS
• Infection does not always cause abortion.

• Infected live calves can be born.
• Abortions occur between 4-9 months; mostly bewteen 7-8 months.
• Appearance of characteristic lesions on the placenta and calf.
• Whole or part of the placenta appears discoloured when shed - either grey, yellow or reddish
brown
Mycotic lesions on a 6.5 month old fetus. The Mycotic infection of the placenta grossly
incidence of fetal lesions is 30 %; 75-80 % are resembles that of brucellosis and
caused by Aspergillus sp. (septate) and 10-15% campylobacteriosis. Abortion occurred around 6
by Mucorales sp. (nonseptate)Roberts SJ (1973). months of gestation. Roberts SJ (1973).
168
Aspergillus fumigatus, the mold responsible for Histologic section of the placenta with mold
75-80 per cent of fungal abortions in cattle. infection. Roberts SJ (1973).
Roberts SJ (1973).
• Inter-cotyledonary areas of the allantochorion are thickened, wrinkled or leathery

• Cotyledons with attached portion of the caruncle appear thickened and have a cup-like or
coffee bean appearance
• Fetal skin lesions: circumscribed, greyish white thickened patches similar in appearance to skin
ringworm in calves and young cattle.
DIAGNOSIS AND CONTROL
Diagnosis
• Appearance of placenta is fairly typical.

• Fetal skin lesions are almost pathognomonic.
• Laboratory confirmation requires submission of placental tissue, preferably whole organ.
• Culture from placental tissue no value, as placenta is usually contaminated after expulsion.
• Culture from fetal lungs and abomasum more reliable, but contamination can occur.
• Reliable and traditional method: Identification of fungal cells in histological sections of
placenta.
• Potassium hydroxide "crush" mount of non-fixed tissue.
• Conclusive diagnosis of mycotic placentitis (Kirkbride,1990)
o Characterisitic lesions of placentitis present in association with presence of mycotic
elements.
o Characterisitc lesions of fetal dermatomycosis present in association with presence of
mycotic elements.
o Fetal bronchopneumonia associated with mycotic elements.
• Serological tests at present, unreliable and cannot be used for routine diagnosis.
Control
• Feeding of mouldy forage or the use of mouldy bedding material should be avoided.
169
TRICHOMONIASIS
ETIOLOGY
• Protozoan, Trichomonas fetus.

• Piriform, 10-25 mm in length by 5-10 mm in width (structures with * can be seen without
staining).
Causative organism of trichomoniasis, Scanning Electron Micrograph of

Tritrichomonas foetus, a protozoon. Tritrichomonas foetus, a protozoon.
Three flagella are distinguishable. The Three flagella are distinguishable
live organism has a tumbling motion
BonDurant RH (2008).
Drost M (1980).
PATHOGENESIS
In cow/heifer - method of spread is venereal.
• Infection (localizes in the vagina, uterus and oviduct) following initial exposure (breeding) does
not interfere with conception.
• Mucopurulent discharge present in some cases usually small quantities and therefore seldom
observed.
• Embryonic wastage is attributed to inflammatory changes (uterus and fetal membranes).
• Average stage of gestation at the time of abortion is 3 months.
• Subsequent susceptibility to reinfection and severity of reinfection depends on(delay in calving)
depends on the infection-free interval preceding re-exposure.
• Cow may carry infection thorough a normal gestation, rarely, raises the possibility of carrier
cows.
• Palpable postcoital pyometra and abortion after 5th month gestation are sporadic.
• Bull - Asymptomatic.
o Localizes in the secretions and epithelium lining the penis, prepuce and anterior portion
of the urethra.
o Low incidence of infection in bulls of less than 4 years of age however can be chronically
infected.
170
DIAGNOSIS
• Tentative diagnosis is based on clinical signs after eliminating other common cause of herd
infertility.
• Definitive diagnosis is based on the presence of T. fetus.
HERD CONTROL
• Prognosis for infected herd is generally good, provided control measures are adequately
implemented.
• Details involving the implementation of control measures for a specific herd will vary.
• Control measures should be based on the epidemiology of the disease and the particular herd.
• Proven control methods are
o Depopulation
o Artificial insemination
o Quarantine
o Removal of infected bulls and sexual rest, and
o Selective culling combined with the use of young bulls.
TREATMENT
Cow/heifer - Due to temporary nature of the infection, treatment of individual cows has not been
thoroughly investigated.
Bull - Prognosis in an individual bull - excellent. As young bulls of less than 4 years of age recover
spontaneously, they do not need any treatment.
• Three 5-nitroimidazoles (Dimetridazole, Ipronidazole and Metronidazole) are all effective as

systemic treatment agents.
• Dimetridazole (1,2-dimethyl-5-nitroimidazole) EMPTRYL, Salsbury labs, USA.
o 50 mg/kg orally, daily for 5 days.
o 10 mg/kg i.v daily for 5 days to 50-100 mg/kg in single dose.
• Ipronidazole (1-methyl-2isopropyl-5-nitroimidazole) IPROPRAN, Hoffman-la Roche, USA.
• First pretreat with procaine penicillin 7000 IU / kg IM for 2 days.
• Ipronidazole 30 gm in 60 ml sterile water IM on day- 1, followed by 15 gm in 30 ml of sterile
water on days 2 and 3.
• Metronidazole (1-b-hydroxyethyl-2-methyl-5-nitroimidazole).
• FLAGYL: 75 mg/kg for 3 successive injections at 12 h intervals to 10 mg/kg once daily for 2 days.
171
GENERAL CONSIDERATIONS OF ABORTIONS
• It is important that the appropriate specimens for diagnostic laboratory assistance are properly
collected, handled and submitted so that they arrive promptly in good conditions for
examination.
• The best specimens include the aborted fetus and fetal membranes and maternal serum, urine
and vaginal discharge.
• If it is impractical to submit the whole fetus, perform a necropsy and submit the tissues and
specimens listed below.
• Weigh the fetus or estimate the weight and determine the age by crown-rump measurement.
• For histopathological examination, place 1/2 to 1/2 inch thick sections of tissues and whole
cotyledons in 10% buffered neutral formalin (BNF): 10 volumes of BNF to 1 of tissue.
• Send directly or keep overnight at room temperature.
• Transfer fixed tissues to a small, wide-mouth, screw-capped jar or sealed plastic bag containing
1 to 2 volumes of fresh BNF.
• All specimens for microbiological examination should be placed in separate small containers,
eg. Whirl bags, then placed together in a larger container, and packed with enough ice,
insulation, and packing to provide refrigeration and to prevent leakage until arrival at the
diagnostic laboratory.
• Specimens should be forwarded to the laboratory without delay.
• Preferably have someone take the fetus or specimens directly to the laboratory.
• As the time interval between collections and laboratory examination increases, chances for
diagnosis diminish.
MATERIALS AND HANDLING PROCEDURES
Origin Fresh or refrigerated 10% BNF
Fetal • 2-3 infected cotyledons • 2-3 infected cotyledons and

membranes surrounding ICA
Fetus • Abomasal contents 3-5 ml • Lung, Liver, Kidney, Intestine

• Lung, Liver, Kidney - 1/2 to 1/2 and other organs with
• Spleen, blood sample or lesions.
peritoneal or pleural fluid - 5
ml
Aborting cow • Serum 4-5 ml* -

• Vaginal discharge or cervical
swab, Urine: 3-5ml
172
In contact • Serum sample from 10 cows or -
cows 10% of the herd*
*Paired samples, 10-14 days apart, If necessary.
UNIQUE DIAGNOSTIC PROCEDURES
• Direct microscopic examination

o This can be performed in the practitioner's office for quick screening and diagnosis.
o Smears of infected cotyledons and abomasal contents, dried and heat-fixed, stained by
Gram and modified acid fast methods -- Campylobacters (characteristic morphology)
and Brucellae (small red coccobacilli, blue background).
o Wet preparations examined by direct, phase contrast or darkfield microscopy.
Abomasal contents -- trichomonads, campylobacters, leptopspire and fungal
hyphae
Cotyledonary smears -- campylobacter and fungi (clear with 10% KDH first)
Placental and uterine fluids -- trichomonads and leptospires
Fetal peritoneal fluid -- leptospires
Maternal urine -- leptospires
• Immunofluoresence
• Bacterial culturing
• Viral examination
• Histopathology
• Toxins
• Plant-induced abortions.
NO DIAGNOSIS PROBLEM
• Failure to diagnose the cause of abortion may result from:

o Inadequate specimens: maternal and fetal membrane samples tend to be neglected.
o Specimens arriving at the diagnostic laboratory in poor condition.
o Marked fetal autolysis: the longer the time interval between fetal death, abortion and
laboratory examination, the less the chance of making a diagnosis.
o Lesions present but no pathogen identified: undiagnosed infectious.
o Non-infectious cause.
o More specimens required: submit as many aborted fetuses and fetal membranes and
maternal specimens as possible until a diagnosis is reached.
173
• Incidence of equine abortion is higher than that of cattle and usually ranges from 5 to 15 %.
• Many of these abortions are not associated with infectious agents.
• The causes of equine abortion can be broadly divided into:
o Non-infectious (70%)
o Infectious (15%), and
o Unknown (15%).
• Abortions usually occur after the 4th month of gestation.
174
SUMMARY OF CAUSES OF ABORTION IN MARES
Bacterial Chemicals, drugs and poisonous plants
Streptococcus zooepidemicus (genitalium), (No material or substance confirmed as a

Salmonella abortus equi and leptospirosis cause for equine abortion) (Phenothiazine?)
(Leptospira pomona and possibly other
leptospira)
Miscellaneous Bacterial Hormonal
Anaerobic, motile (Lancefield Group D) and Estrogen, oxytocin (?), progesterone

other streptococci, E. coli, Pseudomonas deficiency (?) and cortisone excess (?)
aeruginosa, Corynebacterium equi,
Actinobacillus (Shigella) equi, Streptococcus
equi, Staphylococci, Klebsiella pneumoniae var
genitalium, Brucella abortus, Mycoplasma,
Diptheroids, and Sarcina
Viral Nutritional
Rhinopneumonitis or Equine Herpes I virus, Reduced energy intake

Arteritis virus
Miscellaneous viral Physical
Equine infectious anemia virus Manual dilation of the cervix and douching
of the uterus, natural service during
pregnancy (?), trauma or injury to the very
young blastodermic vesicle, torsion and
strangulation of the umbilical cord and
torsion of the uterus or strangulation of the
uterus by a lipoma
Mycotic or fungal Genetic or chromosomal
Aspergillus fumigatus, Mucorales, and Fetal anomalies and early embryonic deaths
Allescheria boydii
Protozoan Miscellaneous causes
Trypanosome equiperdum (dourine) and Twinning and early embryonic deaths.

Babesia equi and caballi (piroplasmosis)
Source:S.J.Roberts (1971)
175
STREPTOCOCCUS GENITALIUM OR ZOOEPIDEMICUS
INTRODUCTION
• It is the most common pathogen of genital infections and its incidence ranges from 10 to 20%
and may reach upto 40% in poorly managed farms.
• The causative organism is a hemolytic streptococcus of Lancefield’s group C found ubiquitously
on external genitalia of mares and stallions.
• Pathogen is commonly associated with metritis, cervicitis and vaginitis secondary to pneumo-
vagina or wind sucking.
• Incidence is more in mares with lowered resistence, trauma or disease, lesions of the genital
tract, breeding on 9th day after foaling, pneumo-vagina, localized dilation of uterine wall and
cystic degeneration of the endometrium.
• Infection is limited to the genital tract and is not spread by ingestion or any other agents.
CLINICAL SIGNS
• Mucopurulent discharges may precede abortions that usually occur from 2 to 6 months of
gestation.
• Abortions over half to last third of gestation lead to retention of placenta and persistent uterine
infection.
• Aborted fetuses show autolytic changes that vary from slight to complete maceration.
DIAGNOSIS AND PREVENTION
Diagnosis
• Organisms can be demonstrated from the fetus, fetal membranes and genital discharges.
• No serological tests are available.
Prevention
• Proper management, and

• Breeding of healthy mares only.
• Culture tests should be undertaken in barren mares, and suitable antibiotic therapy should be
initiated.
SALMONELLA ABORTUS EQUII
INTRODUCTION
• Incidence may reach up to 50 to 90% in the susceptible mares and the organism is inhabitant of
the intestinal tract of apparently normal horses.
• Transmission is by ingestion of contaminated feed and water by feces and genital discharges of
aborting mares.
176
• Incubation period ranges from 10 to 28 days.
CLINICAL SIGNS
• Before impending abortion mare exhibits:

o General reaction
o Depression
o Anorexia, and
o Fever.
• Abortion occurs between 6th to 9th month of gestation, and may occur as early as 4th month,
and as late as 11th month of gestation.
• Infected foals born at term are weak and often die within several days.
• Allanto-chorion show non-specific edema, necrosis and hemorrhage.
• Fetus exhibits autolytic lesions with presence of reddish serous fluid in the body cavities.
• Future fertility of the mare is unaffected.
Diagnosis
• Organisms can be cultured from fetal organs and tissues, fetal membranes and uterine
exudates.
• Positive serum agglutination test has titers ranging from 1:500 to 1:5000 in aborted mares.
Prevention
• Use of bacterins for yearly immunization of mares.

• Pregnant mares are vaccinated with 1-2 ml of bacterin subcutaneously at 4th month of
gestation at three weekly intervals and repeated after 3 to 4 months.
• Isolation, quarantine and strict sanitation procedures help in limiting the spread of infection.
CONTAGIOUS EQUINE METRITIS
ETIOLOGY AND CLINICAL SIGNS
• Taylorella equigenitalis is a highly contagious gram negative coccobacillus.

• Transmitted venereally by stallions, contaminated equipment, instruments and personnel.
• Mares exhibit shortened diestrus periods and copious mucopurulent vulvar discharges lasting
up to 14 days.
DIAGNOSIS
• Diagnosis is confirmed by isolation of organisms from samples taken during early estrus from
endometrium or cervix.
177
• Swabs should also be obtained from clitoral fossa and three clitoral sinuses; these can be
obtained during any phase of the estrous cycle including pregnancy.
• Enzyme-linked immunosorbent assay and passive hemagglutination tests are superior for
detection of mares with active infection.
TREATMENT
• Daily intrauterine infusion of penicillin (5-50 million units) for 5-7 days, ampicillin, neomycin
and nitrofurazone have been reported to be successful.
• Clitoral fossa and sinuses must be thoroughly scrubbed daily for 5 days with 4% chlorhexidine
solution and packed with nitrofurazone or chlorhexidine ointment.
LEPTOSPIROSIS
• Leptospira pomona, grippotyphosa and bratislava occasionally causes abortion in mare from 7th
- 11th month of gestation.
Clinical signs
• Elevated temperature of 102-103º F

• Slight icterus
• Anorexia, and
• Depression that lasts for 3-4 days.
• Abortion occurs 1-3 weeks after onset of clinical signs.
• Aborted fetus is slightly icteric with some degree of autolysis.
• Periodic opthalmia occurs 12-14 months after abortion.
Diagnosis
• By significant rising titers associated with abortion.

• Recovery of organisms from autolysed aborted fetus is difficult
• Special staining of fetal organ sections and Fluorescent antibody technique - Diagnostic value.
• Immunofluorescence for spirochetes in aborted fetal tissues (kidney, liver, and placenta).
Prevention
• Vaccine approved for use in mares does not exist.

• By isolation, instituting strict sanitation measures, and through disinfection of equipment and
troughs.
178
• Contact with infected urine, aborted fetuses or contaminated feed and water must be
eliminated.
MISCELLANEOUS BACTERIAL ABORTIONS
• Associated with sporadic abortions that range from 5 to 10%.

• Agents include anaerobic bacteria like Streptococcus viridans, Streptococcus equi, Motile
Streptococci, Escherichia coli, Actinobacillus (Shigella) equi, Corynebacterium equi, Klebsiella
pneumoniae var genitalium, Pseudomonas aeruginosa, Brucella abortus, and Mycoplasma.
• Diagnosis is by pure cultures of organisms from the organs of aborted fetuses.
EQUINE HERPES VIRUS I or RHINOPNEUMONITIS VIRUS
ETIOLOGY
• Commonly causes abortion and influenza viruses are classified as EHV-I to EHV-5.
• Disease is transmitted by infected foals and horses by infective material carried by persons,
dogs, foxes or carrier birds.
• Virus is spread by inhalation, droplet infection or by ingestion.
CLINICAL SIGNS
• Mild febrile respiratory disease observed in young horses at 4-8 months of age.
• Incubation period is 2-3 days.
• Infection is characterized by four distinct syndromes:
o Respiratory
o Abortigenic
o Neonatal mortality, and
o Neurological.
• Temperature is elevated to 102-104º F with serous rhinitis and congestion of nasal mucosa and
conjunctiva associated with coughing, inappetence and depression with leucopenia.
• Neurotropic form of Equine Herpes Virus I exhibits dragging of the toes of the rear foot as the
first sign which progresses into ataxia, paresis, prostration and death in up to 60% of the
horses.
• After a febrile period mucopurulent rhinitis; “the snots” develop along with cough that persists
for several weeks that is followed by an abortion.
• Abortions usually occur from 8th to 11th month of gestation and retention of placenta is
uncommon.
• Spread of EHV-1 occurs transplacentally to fetuses by infected leucocytes, and abortion occurs
within 120 days, with the majority occurring in 7-20 days.
• The longer period may result from persistence of the virus in leucocytes in the endometrium or
chorioallantois before it invades the fetus and causes death and abortion.
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• Virus damages the endometrium and the chorioallantois causing local edema at fetomaternal
junction, leading to separation of the chorioallantois from the endometrium and death of the
fetus due to anoxia.
DIAGNOSIS
• Gross examination of aborted fetus reveals

o Edematous amnion
o Yellow amniotic fluid
o Slightly yellow or icteric coloured fetal tissues
o Straw coloured fluid in thoracic cavity
o Edema and small hemorrhages in the lung
o Petechial and ecchymotic hemorrhages in the epicardium, and
o Small whitish pin head sized foci of necrosis in liver.
• Microscopic examination of stained tissue sections reveals
o Intra-nuclear inclusion bodies in liver, bile duct, lymph nodes, thymus and bronchial cells
of the fetus.
• Complement fixation test or serum neutralization test to determine the antibody levels.
PREVENTION
• No permanent immunity against the virus.

• Live vaccine prepared from hamsters is administered intra-nasally in a 3 ml dose by a flexible
catheter late in june or early in july and repeated in october.
• Vaccination should be avoided in pregnant mares in late gestation, sick animals, those under
stress and simultaneous administration of other viral vaccines.
• Both modified live and killed vaccines are available.
• Controlled studies have showed that both are effective and both had failures.
• Recommendations are to vaccinate pregnant mares with 3 doses, given at 5, 7 and 9 months of
gestation.
EQUINE ARTERITIS or EPIZOOTIC CELLULITIS

(PINK EYE SYNDROME)
Etiology
• Caused by arterivirus of the family Togaviridae that produces severe general respiratory disease
including abortion.
Transmission
• By droplet or aerosol infection and contracted by inhalation when in close contact with an
infected or convalescent horse.
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• Horses of all ages are affected with an incubation period of 3-9 days and the course of the
disease ranges from 2-15 days.
CLINICAL SIGNS
• Clinical signs include

o Elevated temperature of 103-106º F
o Leucopenia with panlymphopenia
o Conjunctivitis
o Lacrymation and occasional keratitis
o Photophobia, and
o Palpebral edema.
• Other signs include
o Anorexia
o Severe depression
o Rapid loss of weight
o Serious nasal discharge with congested nasal mucus membranes
o Increased respiratory rate
o Generalized weakness and stiffness
o Frequent colic, and
o Diarrhea
o In a few horses edema of limbs and ventral abdominal wall are noticed.
• The virus is pathogenic to endothelial cells and causes panvasculitis. The inhaled virus replicates
in the macrophages of the lungs and spreads to the local lymph nodes.
• Abortion results from severe necrotizing myometritis, placental detachment, decreased
progesterone ad local prostaglandin release.
• Mortality is 30-50% in experimentally infected old pregnant mares.
• Abortions occur up to 50% in susceptible mares from 5th to 10th month of gestation and
placental retention is uncommon.
• Fetal lesions include petechial hemorrhages on the peritoneal and pleural surfaces, epicardium
and endocardium with pleural effusions.
• No inclusion bodies are found but virus can be demonstrated in fetal tissues like liver and lungs.
PREVENTION
• Prolonged immunity to infection is noticed following recovery.

• Control is by use of a live attenuated vaccine.
• Mares should not be vaccinated during the last 3 months of pregnancy. Once vaccinated, a
stallion cannot be distinguished from a naturally infected animal by serology; therefore there is
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some reluctance towards widespread use of the vaccine. However, virus isolation from the
semen can distinguish carriers from vaccinates.
• Proper segregation, isolation and quarantine along with other sanitary procedures are adopted
in preventing the spread of the disease.
EQUINE INFECTIOUS ANEMIA
• It is occasionally characterized by abortion in infected pregnant mares.

• Pathogenesis of the abortion has not been established.
MYCOTIC OR FUNGAL ABORTIONS
• Aspergillus fumigatus, Mucorales and Allescheria boydii.

• Sporadic abortions in mares by inhalation or ingestion of mould spores.
• Mycotic agents may cause up to 5-10% abortions.
• Abortion occurs due to severely diseased necrotic, yellowish, leathery, thickened allanto-
chorion that interferes with fetal nutrition and causes fetal death.
• Amnion may have necrotic plaques in about 10% of mucor infections.
• Initially infection begins in the chorion adjacent to the cervical star then progresses cranially up
the uterine body that causes progressive placental insufficiency that interferes with fetal
nutrition and growth and results in intrauterine growth retardation.
• Abortions usually occur from 8th to 11th month of gestation.
• Aborted fetuses are usually fresh, emaciated and small for their gestational age.
• Liver is pale enlarged, and mottled.
• Lungs reveal 1-3 mm grayish white granulomas in mucor infections.
DIAGNOSIS AND CONTROL
Diagnosis
• By culturing the fungi from placenta and occasionally from fetal liver, stomach, lungs and skin.
Control
• Depends on good management and hygiene procedures by avoiding use of moldy hay and
straw.
• Aborting mares should not be bred at foal heat.
TRYPANSOMA EQUIPERIDUM
• Transmitted by sexual contact.

• Rarely a cause of abortion in mares.
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• Diagnosis is by complement fixation test, and
• Eradication is by destroying the positive mares.
BABESIA EQUII AND CABALLI OR PIROPLASMOSIS
• Spreads by blood sucking ticks.

• May cause abortion in severely affected horses.
• Diagnosis: Fluorescent fixation test in RBC of fetus or foal.
• Complement fixation test: specific for Babesia caballi and the infection persists for 1-5 years.
NON-INFECTIOUS CAUSES OF ABORTION
Chemicals, drugs and poisonous plants
• Phenothiazine, thiabendazole, lentin, purgatives such as arecoline, aloes, sudan or sorghum

pastures, organophosphate insecticides, ergot and fescue toxicity.
• Abortions are sporadic.
Hormonal causes
• Estrogens administered at 50-150 mg caused abortions in few mares.

• Progesterone deficiency is the common cause for abortion from 1 ½ to 8th month of gestation.
• Oxytocin or pituitrin administered to pregnant mares has not been proven to cause abortion,
but may induce parturition in mares after 345 days of gestation.
Nutritional deficiencies
• Poor quality pastures produced early embryonic deaths at 18 days of gestation.
PHYSICAL CAUSES OF ABORTION
Manual dilation of cervix
• Manual dilation accompanied with infusion of several liters of normal saline, dilute lugols iodine
or iodized oil produced abortion within 3-10 days.
• Not recommended in the last trimester of pregnancy as complications may arise from a large
sized fetus.
Natural service during pregnancy
• Abortions after a natural service are rare.
Trauma or Injury
• Rough manipulation of blastodermic vesicle from 20-50 days of gestation should be avoided.
• Twin pregnancy diagnosed prior to 30 days of gestation.
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• Severe stress, prolonged difficult slipping, hard sustained work, difficult and complicated
operations, vigorous struggling and trauma during casting may cause abortions in pregnant
mares.
Torsion or strangulation of umbilical cord
• Responsible for 1% of fetal deaths and abortion during the later half of gestation.
• Normal long umbilical cord has 1-3 rotations. It may get extremely twisted or rarely get
wrapped around a fetal extremity occluding the lumen of the vessels.
Fetal anomalies
• It is a probable cause in 1.3% of abortions.

• It includes chromosomal defects of zygote which are due to aged spermatozoa or ova prior to
fertilization.
MISCELLANEOUS CAUSES OF ABORTION
Twinning
• Very common cause of abortion.

• Majority of fetuses abort from 5th month of gestation to term.
• Failure of anastamosis of the placental vessels of allanto-chorion of the two blastocysts and lack
of sufficient placental area for nutrition results in fetal death and abortion.
Early Embryonic Death
• Incidence varies from 5-24%. Between days 14 to 40 the rate varies between 10 and 17%.
• Poor conformation of vulva, vagina and cervix.
• There is a probable relationship between early embryonic deaths with lactation, malnutrition,
improper breeding hygiene, genetic or chromosomal defects and breeding with infertile
stallions.
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INTRODUCTION
• In swine industry, the economic losses consequent to reproductive failure are very high thus
exerting great pressure for sustaining the profitability.
• Infertility and abortions can result from many factors such as bacteria, viruses, protozoa, and
fungi, and non infectious factors such as nutrition, genetics, environment, management
practices, and husbandry procedure.
• Reproductive losses may be due to early embryonic deaths and abortions or absorptions or
fetal deaths of the entire litter or mummifications and stillbirths or weak piglets with an
incidence of 5 -10% still births and 1-5% of fetal mummification.
SUMMARY OF CAUSES OF SWINE ABORTION
Bacterial Chemical, Drug and Plant
Leptospirosis (L. pomona, L. grippotyphosa, L. Dicoumarin, aflatoxin B (moldy corn),

hardjo and L. canicola), Brucellosis (Br. suis) pentochlorophenols and creosote
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Miscellaneous bacterial Hormonal
Streptococci, Staphylococcus aureus, E. coli, Estrogen, glucocorticoids (?)

Salmonella enteriditis, avian tuberculosis,
Listeria monocytogenes (?), B. anthracis, C.
pyogenes and Erysipelothrix rhusiopathiae
Viral Nutritional
Hog cholera, pseudorabies (Auesky’s disease), Deficiencies of iodine, vitamin A, iron, and
picorna (S.M.E.D.I) (?) viruses calcium
Miscellaneous viral causes Physical
Foot and mouth disease, Japanese B. Stress and exhaustion coincident to

encephalitis, hemagglutination virus, transportation, fighting and injury
influenza, African swine fever
Mycotic or fungal Genetic or chromosomal
Aspergillus fumigatus and other molds Anomalies, early embryonic deaths
Protozoan Miscellaneous
Toxoplasma gondi (?), eperythrozoonosis (?) Poor management, increased stillbirths

associated with large or small litters and in
older sows.
Source: S.J.Roberts (1971)
LEPTOSPIROSIS
ETIOLOGY
• Leptospirosis is caused by a variety of motile, aerobic spirochetes from the Leptospira genus.
• It is the most common cause of abortion with varied incidence from 3 - 25% caused usually by
Leptospira pomona and occasionally by L. grippotyphosa, L. hardjo, L. canicola, L. hyos, L.
bratialava and L. sajroe.
TRANSMISSION
• Organisms are localized in the kidney tubules and are discharged in urine for varied amount of
time with greatest number of organisms being shed at 20-30 days after exposure.
• Organisms spread directly by the urine or indirectly by contaminated feed and water to
susceptible pigs and also through ingestion of milk from infected dams. Infected boars might
infect susceptible sows at coitus or by artificial insemination.
• Transmission is through abraded skin, mucus membranes of the nasal conjunctival, digestive or
reproductive tracts.
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CLINICAL SIGNS
• Bacteremia and a generalized infection that lasts for 5-10 days after which period serum
antibodies can be detected with highest titers at 3-4 weeks after exposure and persist for a year
or more.
• Leptospiral infections of swine are inapparent, except for abortions that occurred in sows
infected late in the 2nd month or during the 3rd month or early in the 4th month of gestation.
• Abortions occur 1-4 weeks prior to term.
• Some or all the fetuses may be infected and fetal death is due to leptospiral septicemia.
DIAGNOSIS
• By serum titers that range from 1:800 to 1:3200 or higher in aborting sows which is determined
by agglutination lysis test.
• Organisms can be isolated from fetal liver, kidneys, peritoneal and pericardial cavities.
• Histopathological examination of silver-stained sections of fetal kidney revealed the organisms.
• Direct field examination of pericardial or peritoneal fluid or kidney scrapings may reveal small
fine filamentous, motile organisms.
• Fluorescent antibody test may also be used.
• Microscopic agglutination test (MAT) is the most accurate test that measures immunoglobulin
M antibodies with titers as high as 1:12800 following infection.
PREVENTION
• By sanitation, vaccination and antibiotic therapy with feed grade tetracyclines used at the rate
of 800 gm per ton of feed.
• Providing sanitary environment free of water holes, swampy areas and mud puddles aid in
preventing the spread of disease.
• Covering feed and water troughs to prevent contamination.
• Proper sanitation and management, frequent testing, segregation and isolation are the
methods adopted to produce specific pathogen free herd.
BRUCELLOSIS
ETIOLOGY
• Caused by Brucella suis.

• Overall infection rate < 1.5% and occasionally by Br. abortus with no clinical signs.
TRANSMISSION
• Organism gains entry through mouth by ingestion of contaminated feed and water by uterine
discharges, urine or feces of infected animals.
• Major source of infection in the sow is mating with an infected boar.
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• Intermittent bacteremia occurs up to 8 months and may last up to 3 years.
CLINICAL SIGNS
• Abortion, stillbirth or weak piglets, infertility due to early embryonic death and less commonly
orchitis, posterior paralysis and lameness due to vertebral lesions.
• Boars infected with brucellosis had lesions in epididymis and seminal vesicles and produced
normal but infected semen with normal fertilization.
• Following service abortions occur as early as 17 days after breeding and return to estrus in 30-
45 days. Infections after 30-40 days of gestation result in abortions ranging from 46-105 days.
• Organisms may persist in granulomatous lesions and in mucosal cysts of the endometrium and
catarrhal endometritis may occur.
• Granulomatous lesions may also be found in lymph glands, spleen, liver, kidneys, testes, ovaries
and accessory sex glands.
• Unilateral testicular enlargement that is hard on palpation with undulating pyrexia is a common
sign.
DIAGNOSIS
• Serum antibody titers develop in 10-21 days.

• Organisms are recovered by cultural methods from organs of infected sow or boar and from the
stomach contents of aborted fetuses or from the chorion of the placenta.
• Tube or plate agglutination tests with positive titers greater than 1:100.
• Supplemental tests to identify carriers include
o Acidified plate antigen test
o Heat inactivation test
o Rivanol test
o Complement fixation test and card test.
PREVENTION
• Selling the stock for slaughter.

• Cleansing and disinfecting the premises or moving to clean environment and restocking with
validated herds.
• Repeated blood testing at 30 day intervals coupled with slaughter of reactors is successful.
• Antibiotics have proved to be ineffective in treatment of infected swine.
• Natural resistence or immunity to Br. suis is present in about 30% of swine.
MISCELLANEOUS BACTERIAL CAUSES
• Sporadic abortions occur due to

o Staphylococcus aureus
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o Mycobacterium avium
o Listeria monocytogenes
o Salmonella enteriditis
o E. coli
o Corynebacterium pyogenes
o Erysipelothrix rhusiopathiae
o Pseudomonas spp, and
o Pasteurella.
• Use of oral antibiotics during last 30 days of gestation greatly increased the number of live
piglets per litter and number of weaned piglets per litter.
CLASSICAL SWINE FEVER (Hog Cholera)
Etiology
• Caused by pestivirus classical swine fever virus (CSFV) also referred to as hog cholera virus
(HCV) which differs markedly in virulence.
Transmission
• Intra uterine transmission of the virus did not occur in immune sows with virulent strains.
Signs
• Vaccines of field strains of low virulence or attenuated or modified strains inoculated to
pregnant sows during first 10-20 days of gestation resulted in abortion of embryos and fetal
malformations.
• Infection in sows from 30-90 or more days of gestation resulted in fetal mummification,
stillbirths or weak piglets. Only 30% of the piglets are affected in intra uterine route of
infection.
• Natural exposure to low virulence virus or vaccination with attenuated virus resulted in birth of
piglets with cerebellar hypoplasia, hypomyelinogenesis and congenital tremors or myoclonia
cogenita.
• Stillborn piglets often revealed subcutaneous edema which is probably an autolytic change.
• Fetuses that are infected during pregnancy and those that survive after birth become immune
and tolerant carriers.
Diagnosis
• By culturing the virus from infected fetuses, stillbirths or live new born piglets, and
• Fluorescent antibody technique.
Prevention
• Based on programs based on testing, and

• Slaughter of the reactors.
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PSEUDORABIES OR AUJEZSKY'S DISEASE
Etiology
• Herpes virus and the infection results in high mortality in young piglets from birth to 30 days of
age.
Clinical signs in adult pigs
• Dullness
• Anorexia
• Constipation, and
• Occasionally posterior paresis with low mortality.
• Virus invades pregnant uterus and causes fetal death, mummification, stillbirths and poorly
viable piglets.
• Pinpoint to poppy seed sized necrotic foci are noticed on the liver of aborted or stillbirth
fetuses
Diagnosis
• By isolation of the virus from vagina and prepuce.

• Identification of the virus from stillborn or weak and dying piglets.
• Serum neutralization test in the serum of sows.
PICORNA VIRUSES, ENTERO VIRUSES OR SMEDI VIRUSES
• Cause occassional abortions.

• Spread by contact with infected pigs.
• In susceptible pregnant gilts inoculated with SMEDI viruses at 25 days of gestation
o Embryonic deaths
o Mummification
o Stillbirths to birth of weak piglets that die within 6 h after delivery.
o Fetuses of the same sow may be infected and may die at different stages of gestation.
• Absorption results in embryos that die before 30 days of gestation and mummification or
stillbirths in fetuses dying after 30 days of gestation.
• Recovered immune sows have normal gestation during the next breeding season.
• The boar may act as temporary carrier.
• Diagnosis is by virus isolation from internal organs of stillborn fetuses or weak, poorly viable
newborn piglets.
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MISCELLANEOUS VIRAL CAUSES
• Agents include Japanese B encephalitis and Japanese hemagglutinating viruses which produce
signs similar to pseudorabies and SMEDI viruses, influenza virus and transmissible
gastroenteritis virus.
• Abortions late in the gestation are also noticed in vesicular stomatitis, foot and mouth disease
and African swine fever.
MYCOTIC OR FUNGAL ABORTIONS
• Aspergillus fumigates or Nocardia asteroids have been demonstrated on very rare occasions.
• Two moulds associated with reproductive disorders
o Fusarium graminnearum (Fusarium roseum)
o Claviceps purpurea (ergot)
• In pregnant sows, ergot in rations is not generally a cause of abortion.
• Swine exposed to ergot during late gestation routinely suffer agalactia but rarely abortion.
TOXOPLASMOSIS
Etiology
• Toxoplasma gondii
Symptoms
• New born piglets occasionally show illness.

• In coordination and tremors due to CNS lesions that should be differentiated from other viral
diseases.
Diagnosis
• Microscopic examination of infected tissue indicates presence of cysts.

• Serological diagnosis is by Sabin-Feldman dye test.
Treatment
• Not available
Prevention
• By proper cat and rodent control, and

• Proper disposal of dead pigs and aborted tissues.
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EPERYTHROZOONOSIS
Causative agent
• Eperythrozoon suis, which attaches to the surface of the red blood cells and destroys them,
leading to anemia and icterus.
Transmission
• By hog louse and other blood sucking insects.
Clinical signs
• Apathy and fever with temperatures more than 40°C

• Anemia
• Icteroanemia
• Embryonic death
• Stillbirths, and
• Abortion.
Diagnosis
• By demonstration of the organism at onset of clinical signs in stained blood smears taken with
Diff-Quik/Wright-Giemsa stains/Acridine orange.
• Detection of antibodies by indirect hemagglutination and indirect immunofluorescence testing.
• ELISAs using whole organisms.
Treatment
• Affected herds are fed with diet containing arsenilic acid at the rate of 90 gm/ton, and
• Also use of feed grade tetracyclines at the rate of 400 gm/ton of feed.
• Inj. tetracycline at the dose rate of 20-30 mg/kg of body mass is the treatment of choice.
• Symptomatic treatment with iron (200 mg iron/dextran/piglet).
Prevention
• By proper lice control and proper needle management.
CHLAMYDIAL INFECTION
Chlamydia psittaci
• Can also cause abortions in pregnant sows.

• Major route of infection is by inhalation, ingestion and venereal contact.
• Clinical signs include
192
o Poorly viable piglets at birth
o Late term abortions
o Endometritis,
o Orchitis
o Epididymitis, and
o Urethritis.
• Organisms have been isolated from aborted fetuses and boar semen.
• Laboratory diagnosis is by complement fixation test.
• Treatment is by using feed grade tetracyclines at the rate of 400 gm/ ton of feed with a 21 day
feeding schedule to prevent relapses.
• Prevention is by proper hygiene and disinfection by quaternary ammonium compounds or
fumigation.
NON-INFECTIOUS CAUSES OF ABORTION
Chemical, drug or plant poisonings
• These agents are seldom causes for abortion which includes agents like dicoumerol,
pentachlorophenols, creosote.
• Moldy corn toxicosis due aflatoxin B is associated with bloody diarrhea, anorexia, depression,
ataxia and abortion.
• Ingestion of legume Leucaena leucocephele resulted in early embryonic deaths and fetal
mummification.
Hormonal
• Abortions of this nature are rare.

• Spoiled moldy corn or barley by Gibberella zea produced estrogen that resulted in abortion.
Nutritional
• Deficiencies of Iodine, Vitamin A, Iron and Calcium.

• Iodine deficiency is characterized by hairlessness, goiter, and edema of the fetus with slightly
prolonged gestation.
• Vitamin A deficiency resulted in birth of weak, moribund new born or stillborn piglets with
edema, ascitis, cleft palate, anophthalmia, microopthalmia, hydrocephalus and cardiac defects.
• Iron deficiency results in birth of piglets with severe anemia.
Physical
• Stress and exhaustion due to transport.

• Fighting between sows, and
• Injury inflicted by boars.
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Genetic or Chromosomal
• In normal sows, about 10-20% of the blastocysts have chromosomal defects like polyploidy that
may account for 30% of total pregnancy losses.
Miscellaneous abortions or neonatal loss
• Due to poor management at farrowing resulting in smothering, crushing or chilling of new born
piglets.
• Infectious causes of abortions play an important role and could be a major source of economic
loss.
• In sheep and goat, the incidence of 1-5% abortions and stillbirths are considered as average or
acceptable.
• Higher incidences should be carefully investigated by collecting fresh fetuses and placenta from
aborting ewes in a sterile container, chilled and promptly transported to a well equipped
diagnostic laboratory.
194
• Placentitis is the lesion common in all infectious abortions.
• Due to placentitis, the fetus either dies due to inability to exchange nutrients through the
placenta, or becomes infected and dies.
• A prolonged period of uterine disease and infertility may follow.
• In infectious abortions, the disease threatens rest of the herd.
SUMMARY OF CAUSES OF SHEEP AND GOAT ABORTION
Bacterial causes Drugs, chemical and plant

poisonings
Vibrio fetus var. intestinalis; Listeria monocytogenes;
Brucella melitensis, abortus, and ovis; Salmonella phenothiazine, carbon
abortus ovis, dubiin, typhimurium and others; tetrachloride, lead, nitrate,
Leptospira pomona and others; Corynebacterium locoweeds, lupines, sweet
pyogenes, pseudotuberculosis and others; and clover, Veratrum and onion
Pasteurella tularensis, pseudotuberculosis and grass.
others.
Miscellaneous bacterial causes Hormonal
E. coli and other coliforms, streptococci Estrogens, progesterone

staphylococci, Clostridlum feseri and Bacteroides deficiency, cortisol and ACTH
fragilis. excess.
Viral and rickettsial causes Miscellaneous
Enzootic abortion in ewes (EAE) due to Chlamydia Chromosomal or genetic

lethals. Severe physical stress,
Miscellaneous viral and rickettsial causes dystocia due to
malpresentation and small
Tickborne fever, Wesselbron virus, Rift Valley fever, birth canal, possibly twinning.
Nairobi sheep disease, rinderpest, foot and mouth
disease, bluetongue and Coxiella (Rickettsia) burneti
(?)
Mycotic causes
Aspergillus fumigatus
Protozoan causes
Toxoplasma gondi
Source:S.J.Roberts (1971).
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VIBRIOSIS
ETIOLOGY
• Campylobacter jejuni and C. fetus subspecies fetus, a microaerophilic gram negative rods lead
to epizootic abortions causing serious economic losses.
• Incidence of abortions varies from 5-70% with an average of 10-20 %.
TRANSMISSION
• By ingestion of infective material from aborting ewes, intravenous injection of organisms and
carrier sheep that harbour the organisms in intestine and gall bladder which shed the organisms
in feces.
• Carrier birds like magpies and crows carry the organism in their gut and transmit the disease
from one herd to another.
• Ram does transmit the disease by coitus but may harbour the organism in its intestine.
• Following ingestion incubation period is 7 to 25 days with a period of bacteremia during which
the organism enters the maternal placenta and causes inflammatory changes and then
infection extends to the fetal placenta and chorion.
• The organisms gain entry into fetal circulation and cause fetal bacteremia and death.
• Abortions occur 1-3 days after death and continue for 6-12 weeks in the flock.
CLINICAL SIGNS
Premonitory symptoms include
• Occasional swelling of the vulva and a slight reddish discharge and fetuses are expelled in the
last 4-6 weeks of pregnancy.
• At abortion, fetuses are fairly fresh and rarely decomposed or mummified.
• They may exhibit subcutaneous edema and reddish serous fluid in the body cavities due to
autolytic changes.
• Liver may show 1/4th to 1 ½ inch infracts.
• Fetal cotyledons show inflammatory changes characterized by edema and necrosis.
• About 5 % of aborting ewes die due to uterine sepsis.
DIAGNOSIS
• By isolation of organisms from fetal liver infracts, stomach, lungs and placenta.
• Serological identification is by Agglutination test or Fluorescent antibody test for rapid
diagnosis.
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TREATMENT AND CONTROL
• Aborting ewes should be immediately segregated and isolated for 2-4 weeks until the genital
discharges cease.
• Fetus and placenta should be buried or destroyed after through disinfection of the infected
pen.
• Incidence of abortions can be reduced by injecting 3 lakh units of penicillin and 1 gm of
dihydrostreptomycin intramuscularly twice daily or feeding tetracycline @ 250 to 300
mg/head/day or treated with long acting oxytetracycline @ 20 mg/kg.
• Vaccination is by bivalent alum adjuvant killed vaccine injected twice at 15-30 day intervals
before the breeding season or during the first half of pregnancy produced excellent immunity
that lasted for 3 years.
LISTERIOSIS
ETIOLOGY AND INCIDENCE
• Caused by Listeria monocytogenes sensu stricto and Listeria ivanovii that manifest septicemic,
encephalitic, reproductive or abortifacient form of the disease.
• Incidence of abortions ranged from 1-25 %.
• Reproductive form occurs naturally as an epizootic outbreak in pregnant ewes and does.
• The disease can be carried by clinically normal sheep with abortions occurring in late gestation
and may occur over several months.
PATHOGENESIS
• L. monocytogenes may be found in soil, water, plant, litter, silage and the digestive tract of
ruminants and humans.
• Organisms can survive in soil and feces for a very long period and grows in poorly fermented
silage (pH 5.5).
• In some farms, feeding of silage is attributed as cause for abortion.
CLINICAL SIGNS
• Fetuses have been dead for several days before expulsion hence exhibit autolytic changes with
decomposition of fetus and fetal membranes.
• Retained placenta is common with metritis.
Postmortem examination of the fetus reveal
• Grey/white focal necrosis of the fetal liver hence termed as “sawdust liver” with edema and
congestion of meninges.
• Chorion is covered with brownish red exudates and heavy brown vaginal discharges are
noticed.
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• Some lambs near term may be born alive but die within several days with keratitis and liver
necrosis.
• Genital tract of the infected ewes sheds organisms in the uterine discharge for several days and
is free of infection by 2-3 weeks.
DIAGNOSIS
• Organisms can be cultured from the placenta, brain, abomasum, meconium and most of the
fetal organs.
• High serum antibody titre to L. monocytogenes in goats that have aborted is indicative of
abortion due to listeriosis.
• By dividing the flock into smaller units.

• Isolation of aborting or convalescent ewes with proper sanitation and disinfection of the
premises.
• Discontinue silage feeding and eliminate environmental stress.
• Further abortions can be prevented by administering long acting oxytetracycline @ 20 mg/kg.
• Theoretically, a live vaccine should be more effective than killed preparation.
BRUCELLOSIS
ETIOLOGY
• Caused by Brucella melitensis, Br. abortus and Br. ovis, a gram negative intracellular organism.
• Br. melitensis causes enzootic abortions in goats with an incidence of 40 -60%.
• Abortions occur in the last third of gestation.
TRANSMISSION
• By ingestion of feed and water contaminated with aborted fetuses, placenta or genital
discharges or transfer of organisms between genital mucus membranes of ram and ewe.
• Organisms enter the mucus membrane and become localized in the lymph nodes, udder,
uterus, testes and spleen.
• In the placenta, they produce severe lesions of edema and coalescing areas of necrosis in the
placentomes and intercotyledonary placenta to interfere with fetal nutrition that causes fetal
death and abortion.
CLINICAL SIGNS
• Abortion during late pregnancy.

• When the disease is introduced, may be as abortion storm, followed by a period of resistance
abortions do not occur.
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• Systemic reaction characterized by
o Fever
o Depression
o Loss of weight
o Diarrhoea
o Mastitis
o Lameness
o Hygroma, and orchitis in males
• Placentitis with necrosis of placentomes in advanced stages.
• The fetus is also infected with inflammatory and necrotic foci on liver and other organs.
DIAGNOSIS
• Based on culture of organisms from stomach contents of aborted fetuses, placenta and
cotyledons or vaginal discharges.
• Serological diagnosis is based on agglutination, precipitation, and complement fixation tests.
• No treatment.
• Isolation or quarantine and slaughter of infected animals.
• By sanitation.
• Aborted fetuses and placentas should be burned or buried deeply.
• Period blood testing of all new animals imported in to the farm.
• Simultaneous vaccination with Br. abortus strain 19 and a formalin killed oil adjuvant Br. ovis is
used to immunize young rams.
• Alum precipitated Br. ovis vaccine injected 30-60 days apart followed by yearly once
vaccination prevented Brucellosis.
SALMONELLOSIS
ETIOLOGY
• Caused by Salmonella abortus ovis with varied incidence of 8-33%.

• Other organisms that cause ovine abortions are Salmonella dublin, S typhimurium, S melagridis,
S. menston, S. martevideo and S. arizonae.
TRANSMISSION
• Infection is spread by ingestion of contaminated feed and water with aborted material or other
animal sources.
• Rams may transmit infection to ewes at coitus.
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• The organisms invade the mucosa of small intestine and through the general circulation are
carried to the placenta pass through the chorionic villi and fetus.
CLINICAL SIGNS
• The septicemic fetus is aborted, stillborn or born alive depending on the gestational age of the
fetus exposed to infection.
• Diarrhoea is noticed in few cases but in most outbreaks no clinical signs other than abortion in
the last third of gestation or stillbirths at term are noticed.
Diagnosis
• Organisms are isolated from internal organs of the fetus, placenta and the uterine discharges
within a few days after abortion.
• Serodiagnosis is based on serum agglutination test in susceptible rams and ewes.
Prevention
• By segregating the aborting ewes and destroying the placenta and aborted fetuses.
• Contamination of feed and water should be prevented.
LEPTOSPIROSIS
ETIOLOGY
• Caused by Leptospira pomona and L. hardjo with a less incidence in sheep and goat as
compared to cattle and swine as the former seem to be more resistant to infection.
• The disease is more common in young lambs than in older ewes.
• L. grippotyphosa caused abortions in goats.
• Abortions ranged up to 20%.
CLINICAL SIGNS AND DIAGNOSIS
Clinical signs
• Icterus
• Hemoglobinuria, and
• Death of ewes.
Diagnosis
• By isolation of organisms from fresh fetuses, placenta or by histological examination.

• Serodiagnosis includes Fluorescent antibody technique or Microscopic agglutination test.
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Treatment
• By administering dihydrostreptomycin @ 25 mg/kg as a single dose or tetracycline @ 200-400

mg/head/day for 2-3 weeks reduces the incidence of abortions.
Control
• By vaccination of all susceptible animals with adjuvant inactivated vaccine of L. hardjo

“VAXALL”.
PASTEURELLA, CORYNEBACTERIA AND MISCELLANEOUS
Pasteurella tularensis and Pasteurella pseudotuberculosis
• Cause abortions in later part of the gestation and show white necrotic foci on the fetal liver.
• Enzootic outbreaks have been recorded due to spread of infection by wild rodents,
Dermacentor andersoni and other ticks.
• Affected sheep show depression, anorexia, elevated temperature, increased pulse and
respirations, cough, premature birth, stillbirth and abortion.
• Tick paralysis is a complicating sign with high mortality.
• Treatment includes administration of streptomycin or oxytetracycline for prompt recovery.
• Tick infestation is controlled by dipping the sheep.
Corynebacterium pyogenes, C. pseudotuberculosis, C. renale and C. equi
• Cause ovine abortions and also cause mortality in new born lambs.
Miscellaneous bacteria
• Causing abortion in ewes include E. coli and other coliforms, streptococci and staphylococci.
BORDER DISEASE VIRUS (BDV)</<>
• Caused by a pestivirus closely related to Bovine Viral Diarrhea.

• Infected sheep exhibit viremia in less than 7 days and shed the virus in urine, feces and saliva.
• Virus attacks the maternal-fetal junction and destroys nutrition and oxygen transfer.
• Myelination of nerve cells is disturbed, particularly in the cerebellum.
• Hair follicles are affected and produce hair rather than wool.
• Clinical signs
o Abortions or congenital defects or weak lambs with shortened facial and leg bones.
o Wool is hairy with dark pigmentation over the shoulders and head.
o The lambs are termed as “hairy shakers” as they may show severe tremors.
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• Diagnosis is by virus isolation from aborted fetuses from the buffy coat of the blood collected
from congenitally affected lambs. Lambs show cerebellar hypoplasia, hydranencephaly with
hypomyelination and microgliosis.
• Control
o Affected lambs should be slaughtered.
o Cattle and sheep should be housed separately.
MISCELLANEOUS VIRAL CAUSES OF ABORTION
Tick borne fever
• Caused by Cytoecetes phagocytophilia spread by sheep tick Ixodes ricinus.

• Abortions occur in late gestation with an incidence up to 50% and mortality up to 20% when
pregnant ewes are reared in tick infested pastures.
• Inoculation of infected blood leads to pyrexia up to 107º F in 4-8 days and lasted for 10 days
during which period abortions occurred.
• Inclusion bodies are demonstrated in the neutrophils and large monocytes.
Wesselsborn virus
• Cause of abortion in sheep and mortality in new born lambs.

• Virus is transmitted by mosquitoes and apparently affects and kills the fetus in the uterus.
Rift valley fever virus or Enzootic hepatitis
• A major cause of abortions in Kenya and South Africa, until effective immunization programmes
were undertaken.
• Disease is also spread by insects.
Nairobi sheep disease virus
• Causes abortion in sheep where the disease is prevalent.
Blue tongue virus
• Spread by midge or gnat (Culicoides veriipennis).

• Live vaccine preperations if administered to pregnant ewes between 4th to 8th week of
gestation caused fetal losses characterized by stillbirths or spastic lambs and lambs with a
variety of defects.
• Losses with natural infection are not reported.
• Cattle harbour the virus and spread it to sheep.
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ENZOOTIC ABORTION OF EWES(EAE) OR OVINE ENZOOTIC ABORTIONS OR KEBBING
• Caused by Chlamydia psittaci immunotype 1 (Chlamydophila abortus) with predilection to

pregnant uterus.
• Transmission is by wild foxes, gulls and crows, sheep to sheep by contact, ingestion or
inhalation of infectious particles from placenta, uterine discharges and fetuses.
• Infection contacted by an open ewe is dormant and gets reactivated in pregnancy.
• Rapid replication of the organism leads to local necrosis.
• Spread of infection cotyledonary and intercotyledonary placenta and apposing endometrium
results in abortion occurring in the last 2 weeks of pregnancy.
• Placenta is edematous thickened and leathery with necrosis of fetal cotyledons and a thick
yellow deposit on the chorion.
• Aborted lambs are well developed, fresh and show no autolytic changes and live lambs are
weak and fail to survive after good nursing.
• Rams may develop epididymitis.
• Smears from intercotyledonary areas, wet skin of the fetus stained with Ziehl –Neelson method
to detect intracellular inclusion bodies.
• Serodiagnosis is by Fluorescent antibody technique or Compliment fixation test a titer greater
than 64 is considered as a positive result.
• Enzyme linked immmunosorbent assay and immunofluorescent antibody test are also available.
• Treatment is given at 95-100 days of gestation with long acting oxytetracycline @ 20 mg/kg
every 10-14 days until lambing.
• Prevention is by isolation, proper disposal of aborted material and disinfection of lambing pens.
• Enzovac is a live attenuated 1B strain vaccine administered at 5 months of age to lambs used
for breeding or at 4 months before tupping in older ewes.
COXIELLA BURNETI OR QUERY OR QUEENSLAND OR Q FEVER VIRUS
• Incidence of abortions that range from 20-50%.

• Transmission is by inhalation, contact with aborted material, vaginal secretions or fluids.
• Placentitis leads to abortion thickened yellow cotyledons and intercotyledonary zone.
• Virus particles have been demonstrated in the placenta of ewes and does by Ziehl –Neelson
staining.
• Serodiagnosis by antibody titers in several abortions.
• Treatment is by administration of long acting oxytetracycline.
TOXOPLASMA GONDII
• It is a common and serious cause of abortions.

• Incidence of abortion may vary from 3-30%. Heavy rainfall favors the spread of the disease.
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• Stress may cause latent infection to become active. Lifecycle of the parasite is completed in
domestic and wild cats.
• The sporozoites are released from the oocyst in the host intestines as tachyzoites that invade,
multiply within and rupture the host cells. In pregnant sheep these tachyzoites infect the
cotyledons and fetus.
• Fetuses of all ages are susceptible.
• Infection prior to 40 days of gestation results in resorption, between 40 to 120 days results in
maceration, mummification or abortion, after 120 days results in stillbirths or birth of weak or
healthy lambs.
• Infection is characterized by placentitis with multiple small 1 to 3 mm soft white nodules on
fetal villi in the dark red cotyledon with edematous intercotyledonary placenta.
• Organism is readily identified either free or in cysts in the fetal liver, lungs and brain. Sabin–
Feldman dye test of ewe’s blood detects antibodies that are usually present at the time of
abortion and continue to rise for several weeks. Serology is by complement fixation test and
skin sensitivity tests.
• Treatment of the flock with Monensin @10–20 mg/head/day or Decoquinate @2 mg/kg
throughout the gestation increased the percentage of live births.
• Vaccination is by “Toxovax” a live vaccine containing tachyzoites of the S48 strain of
Toxoplasma gondii.
DRUGS, CHEMICALS OR PLANT POISONINGS
• Phenothazine administered in late pregnancy caused abortion within 4 days with dead
emphysematous, macerated fetus that caused dystocia, metritis and death.
• Carbon tetrachloride may cause abortions when given to pregnant ewes.
• Nitrate feeding in excess caused severe methmoglobinemia leading to abortions in ewes.
• Locoweeds caused abortions in all stages of gestation.
• Lupine ingestion caused chronic lupinosis and resulted in abortion and fetal death.
• Veratrum caifornicum consumed by pregnant ewes caused early embryonic deaths, abortions
and deformed lambs.
• Sweet clover hay rich n dicoumarol fed to pregnant ewes resulted in abortions.
• Onion grass (Romulea bulbocodium) ingested by pregnant ewes caused abortions.
HORMONAL CAUSES OF ABORTION
• Estrogens: Ingestion of subterranean clover rich in estrogens resulted in uterine inertia,

dystocia ad stillborn lambs with persistent uterine damage.
• Progesterone deficiency and excess of cortisol or ACTH resulted in abortions in goats and ewes
occurring from 2 weeks of gestation to term with over 60% of them occurring from 100-120
days of gestation.
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NUTRITIONAL CAUSES OF ABORTION
• Lack of TDN or energy lead to high incidence of abortions and maternal deaths with pregnancy
toxemia.
• Copper deficiency is associated with stillbirths.
• Cobalt deficiency is associated with high mortality of neonatal lambs.
• Vitamin A deficiency produced high incidence of still births or poorly viable new born lambs.
• Iodine deficiency resulted in congenital goiter, abortions or stillbirths.
• Selenium deficiency is reported to cause abortions or stillbirths with congenital white muscle
disease affecting the heart.
CHROMOSOMAL, PHYSICAL AND MISCELLANEOUS
• Lethal genetic defects associated with fetal deaths, abortions and stillbirths.
• Severe physical stress, fright and exhaustion caused by dogs chasing a flock of ewes in
advanced pregnancy have occasionally caused abortions.
• Malpresentation with dystocia is a common cause of stillbirths.
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INTRODUCTION
• Abortions are much less common than in the larger domestic animals.
• Most of the abortions are sporadic except for enzootic or epizootic outbreaks due to Brucella
canis.
SUMMARY OF CAUSES OF CANINE AND FELINE ABORTION
Bacterial causes Drugs, chemical, poisons
Br. canis. 0- diazoacetyl- L- serine, N- desacetyl

chiocolchicine, malucidin.
Miscellaneous bacterial causes Hormonal
Br. abortus (?), staphylococci, streptococci Progesterone deficiency.

and coliform organisms, paratyphoid,
leptospirosis (?).
Viral Causes Physical
Distemper viruses, infectious canine Severe trauma.

hepatitis virus (?), and feline coryza and
panleukopenia viruses (?)
Other infections Miscellaneous
Toxoplasma gondi in dogs and cats. Anemia and pregnancy toxemia (?) in cats,
hyperactivity of sympathetic nervous
system (?) and others.
Source:S.J.Roberts (1971).
BRUCELLOSIS
Etiology
• Brucella canis is the most common cause of abortion in dogs caused by gram negative
coccobacillus affecting domestic and wild canids.
• A highly contagious disease commonly observed in Beagles although observed in other breeds
of dogs including Pointers, Greyhounds, Foxhounds, Old English Sheepdogs, Mongrels and
others.
• The disease resembles brucellosis of swine, but is relatively mild.
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Transmission
• Occurs mainly across mucous membranes by inoculation.

• Ingestion of contaminated food and water, and to a lesser extent.
• By infected male to the bitch at coitus by infected seen with the organisms being shed from
epididymis, testes and prostate. Male dog may rarely spread infection by his urine.
Clinical signs
• Fever is uncommon with generalized lymph node enlargement as a result of diffuse lymphoid
and reticular cell hyperplasia
• Spleen is firm and nodular with inflamed liver
• Discospondylitis of the thoracic and lumbar vertebrae
• Endopthalmitis and recurrent uveitis
• Arthritis or polyarthritis
• Poor hair coat
• Listlessness, and
• Exercise intolerance.
In bitches
• Abortion occurs between 30-57 days of gestation with 85 % of them noticed between 45 and 55
days of gestation.
• Failure of conception is also a common sign and is due to early embryonic deaths between 10
and 35 days of gestation. Early embryos are largely unobserved as the affected bitches would
ingest the expelled membranes and embryos.
• Incidence of abortions may reach up to 80 percent without retention of placenta and prolonged
vaginal discharges that lasted for 1-6 weeks after an abortion.
• Aborted fetuses are both dead and alive, live pups often die and some fetuses exhibit degree of
autolytic changes. Few pups that survive were infected with bactremia although they appear
healthy.
In adult male dogs
• Orchitis is a consistent sign with swollen and hyperemic scrotum.

• Epididymides enlarged and firm with testicular degeneration and atrophy.
• Following exposure bactremia developed within 1-3 weeks with generalized lymphadenitis and
spleenitis with detectable antibodies by serum agglutination test.
• Brucella organisms may persist in all the organs of the body for several months or indefinitely.
Diagnosis
• By readily culturing the organisms from aborted fetuses, placental tissues and vaginal
discharges. Blood cultures are often positive.
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• Agglutination titers after a month or more after exposure may vary between 1:100 to 1:1600
and may persist for long periods.
• Other serological tests include
o Tube agglutination test (TAT)
o Slide agglutination test (SAT)
o Rapid slide or card agglutination test (RSAT)
o Agar gel immunodiffusion test (AGID), and
o Modified mercaptoethanol tube agglutination test.
Treatment
• Administration of Tetracyclines @ 10 mg/kg orally for 14 days or

• Gentamicin @ 2.2 mg/kg intramuscularly for 1 week or
• Doxycycline or Minocycline @ 55 mg/kg BID orally for 2 weeks or
• Streptomycin @ 4.5 mg/kg intramuscularly for 7 to 14 days.
MYCOPLASMA AND UREAPLASMA
• These microorganisms are normal inhabitants of canine vagina and abortions caused by them
are rare.
• Dogs are exposed to large concentration of these organisms in crowded kennels.
• Pathological situation is noticed when pure cultures are isolated from discharges of
metritis/vaginitis.
• Treatment involves administration of chloramphenicol or tetracycline for 10-14 days in
neonates or nursing bitches while pregnant bitches are treated with erythromycin.
MISCELLANEOUS BACTERIAL ABORTIONS
• Br. abortus, suis and melitensis can cause occasional sporadic abortions in pregnant bitches
when they ingest infected materials like milk, meat, aborted fetuses an placenta. These
conditions are diagnosed by culture of aborted, infected fetuses or membranes and by serum
agglutination test.
• Non specific organisms like coliforms, staphylococci, streptococci and parathyphoid are
frequently associated with sporadic abortions especially in older bitches and queens often
accompanied by cystic endometrial hyperplasia.
• Abortions are associated with infertility, persistent vulval discharge, chronic metritis and
repeated abortions.
• Treatment involves injection of large doses of penicillin and streptomycin during the early post
estrus period reported to have prevented abortions in dogs and cats.
CANINE HERPES VIRUS (CHV)
• It is fairly ubiquitous in dogs with lifelong state of latent infection.
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• Transmission occurs venereally, transplacentally via fetal contact with virus filled vesicles that
rupture during birth or through respiratory route.
• In adult dogs, usually subclinical or mild with signs of conjunctivitis, serous or mucopurulent
ocular and/or nasal discharges and vaginal/vestibular/vulval lesions that are vesicular early in
the course of the disease and later become circular and pock-like.
• Infection results in fetal resorption or mummification in infected early in the gestation, abortion
if infected in mid gestation or premature birth if infected late in the gestation.
• Placenta is typically underdeveloped and congested with several grayish white foci ranging
from miliary to rice grain sized in the placental labyrinth.
• Diagnosis is by virus isolation and serum neutralization test.
• Prevention is by segregating the infected animals especially during the last 3 weeks of gestation
and first 3 weeks of neonatal life. No vaccine is available.
MISCELLANEOUS VIRAL CAUSES
• Abortions have been reported following an acute attack of distemper but incidence is rare as
many bitches at puberty are immune to distemper.
• Sporadic abortions in cats have been reported due to infectious coryza and panleucopenia
virus.
TOXOPLASMA GONDII
• It is uncommon, as dogs are only an intermediate host while cats are definitive host.
• Transmission is by ingestion of oocysts in cat feces or ingestion of infected meat or congenital
exposure.
• Infection may cause abortions, premature birth, dead or moribund pups or kittens or live pups
or kittens with congenital toxoplasmosis.
• The organisms are recovered from fetal organs especially from the brain. Sabin-Feldman dye
test on the blood of the dam detects the organisms. Serological testing is by compliment
fixation test.
ABNORMAL MATERNAL ENVIRONMENT
• Systemic Disease
o Any factor causing significant stress or damage to uterus or fetus can cause fetal death.
o Severe cardiac disease during pregnancy is likely to have compromised uterine blood
supply leading to fetal death.
o Hypothyroidism can lead to abortion or fetal death.
o Diabetes mellitus is associated with inability to carry litter to term or abortion.
• Uterine Disease
o Abnormal uterus that is unable to support pregnancy like
Cystic endometrial hyperplasia
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Chronic uterine infection
Uterine neoplasia, and
Uterine adhesions.
• Trauma
o A significant blow to the abdomen has the potential of causing damage to the uterus or
fetus which could lead to abortion.
NON-INFECTIOUS ABORTIONS
Drugs that caused abortions include
• N-deaceylthiocolchicine
• O-diazoacetyl-L serine, and
• Malucidin a yeast extract that caused resorption of fetuses and abortion in pregnant cats.
Hypoluteoidism
• May cause abortions around 5-6 week of gestation in bitches and cats due to premature
regression of corpus luteum or faulty development of corpus luteum.
• Abortion can be prevented by administering progesterone @ 5-25 mg intramuscularly for 2-3
times a week until 8th week of pregnancy.
Other causes include
• Severe anemia and pregnancy toxemia in cats that is characterized by subnormal temperature,
malaise, running fits and tremors.
• Autonomic sympathetic hyperactivity caused vasoconstriction of sub placental decidual vessels
of the uterus causing fetal death and abortion.
• Genetic defects of the developing embryo or fetus may result in fetal death.
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MODULE-8: SYMPTOMS - INITIATION - INDUCTION OF PARTURITION
DEFINITION
• Parturition refers to those events which take place at the end of a normal gestation period,
leading to the expulsion of the fetus and the fetal membranes.
INTRODUCTION
From the Veterinarians stand point of view
• One must be familiar with the normal process of parturition in various domestic animals and be
able to immediately recognize any deviation and extend artificial interference in order to save
the life of the dam and fetus.
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From the farmers stand point of view
• Parturition is considered to be a specially important juncture, wherein highest death rate

occurs. Furthermore, there may be severe damage or injury to the fetus, and also the dam thus
compromising its future reproductive and productive efficiency.
TERMINOLOGY
• Eutokia or a safe, easy, natural, or physiological parturition is completed spontaneously without

any complications that might affect the health, viability and subsequent productivity of the dam
and it’s off spring.
• Dystocia refers to difficulty in birth especially when the first or usually the second stages of
parturition gets prolonged, becomes difficult or impossible for the dam to deliver without
artificial interference.
Terminologies referred to act of parturition in farm and pet animals
Cow Calving
Mare Foaling
Ewe Lambing
Doe Kidding
Sow Farrowing
Bitch Whelping
Queen (Cat) Kittening
SIGNS OF APPROACHING PARTURITION
• In domestic animals, signs of approaching parturition are somewhat similar but vary in certain
important aspects.
• Between individual animals and between consecutive parturitions, symptoms are inconsistent,
making it difficult for accurate prediction.
• Veterinarians should refrain from making too positive or definitive statement concerning the
exact time of parturition. Breeding date, if known, would be helpful in predicting the
approximate time of parturition.
• Towards the end of pregnancy, the preparation stage to parturition commences and may last
from a few days to several weeks.
• During this period, the dam undergoes many changes and prepares herself for the delivery of
the young and provide for it subsequent nourishment.
• During most of the gestation period in monotoccus species (cow, mare and ewe), the fetus
usually lies on its back with its feet pointing upwards. The first sign of parturition may start with
the “rotation of the fetus to birth position” wherein the fetus lies on its thorax or abdomen,
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head resting between the forelimbs and pointing towards the cervix. In this position, parturition
proceeds easily, except in pigs where both anterior and posterior delivery proceeds with equal
ease.
SIGNS FEW DAYS PRIOR TO PARTURITION
• The clinical signs observed within few days prior to parturition are categorized as follows
o Maternal behaviour
o Changes in pelvis and genital organs
o Changes in mammary gland
o Changes in body temperature
MATERNAL BEHAVIOUR
• In all species, as parturition approaches, the dam seeks seclusion.

• Mostly in herds, the expectant dam leaves the herd and prefers quiet surroundings in
preparation for the process of parturition.
• Mares greatly prefer solitude and calm environment, and are more capable than other animals
to control or suppress parturition until the night hours.
• The nesting behaviours are strong in queens, bitches and sows, but is nearly absent in ewes,
cows and mares.
CHANGES IN PELVIS AND GENITAL ORGANS
As parturition approaches
Relaxed sacrosciatic ligaments in a buffalo
Relaxation of pelvic tissues and ligaments
• May occur up to 10 days prior to

calving.
• Changes are most obvious in the
sacrosciatic ligaments of pluriparous
animals.
• In cows and buffaloes, results in slight
sinking of the gluteal muscles,
hollowing of the croup and an elevation
of the tail.
• Relaxation of pelvic ligaments and the structures around the perineum is due to the changes in
the collagen fibres of the connective tissue, probably caused by an increase in estrogen.
• In young females, the pubic symphysis undergoes sufficient demineralization or dissolution of
connective tissue to allow some separation at the time of parturition.
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• In most cows, presence of very relaxed ligaments indicates that parturition will probably occur
in 24-48 h.
• In mares, sinking of the sacrosciatic ligaments is not so pronounced due to the heavy croup
muscles.
Vulval lips of a buffalo
Vulval opening increase in size between the dorsal and

ventral commissure.
• In all species, as the labiae enlarge and soften it

becomes more mobile and pendulous.
• In mare, the vulval edema is not so pronounced as in
cows.
• In the bitch, the vulva becomes flaccid, enlarged and
edematous.
CHANGES IN MAMMARY GLAND
• In all animals, noticed few days prior to parturition.
In cow
• The mammary gland becomes distended and swollen that the overlying skin cannot be easily
picked up between the fingers and thumb.
• In heifers, the changes in the udder may commence during mid-gestation, whereas in older
pluriparous cow they may not become evident unit a few weeks before parturition.
Distended mammary gland
In heifer In cow In buffalo
Source: S.Balasubramanian (TANUVAS) Personal collection
• Just prior to parturition, the udder secretions changes (in cow and in buffalo) from a honey-like
dry secretion to yellow, turbid, opaque cellular secretion called colostrum.
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• During this time, the udder and teats are so distended with colostrum, and in “easy milkers” it
may leak out through the teat orifice.
• Occasionally, edema of the subcutaneous tissues surrounding and adjacent to the udder may
also develop.
In mare
• Two days before foaling, the colostrum oozes from the teats, called “waxing” usually noticed in
95 % of mares 6-48 h before foaling.
In bitch, sow and cat
• The mammary glands become enlarged and edematous and milk may be present in the udder
several days before parturition.
In the sheep and goat
• The development and udder is not so marked.
CHANEGS IN BODY TEMPERATURE
• Body temperature changes are a signal of impending parturition.

• In the cow, during the last 7-10 days of pregnancy, a slight decrease in the rectal or vaginal
temperature takes place maximum values being attained 2-4 days before commencement of
labour. However, this sign for predicting the onset of parturition is limited.
SIGNS WITHIN FEW HOURS OF PARTURITION
• In all species, inappetance, distress and anxiety are observed.

• The dam may move about in circles.
In cows
• Anorexia and restlessness
In heifers
• Kicking the abdomen

• Treading
• Switching of the tail, and
• Frequent lying down and rising.
In mares
• No vaginal mucus discharge prior to foaling

• Sweating in the flank region and frequently behind the elbows.
• Anorexia 1-2 h before foaling
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• Restless
• Slight colicky symptoms
• Switching of the tail, and
• Frequently lying down and getting up.
The nature of the mucus and volume of mucus produced by the cervical glands increase and they may
become so copious that strings are found to be hanging from the vulva, soiling the tail and hocks.
In bitches, during the 6-25 h before birth of the first pup, behaviour changes
• Seeking of seclusion
• Digging and scratching at the floor
• Chewing
• Panting
• Anorexia
• Vomiting, and
• Shivering.
• Copious greenish mucoid vaginal discharge before, during and after parturition.
INITIATION PROCESS
• Fetal stress causes stimulation of hypothalamus to release adrenocorticotrophin releasing

hormone (ACTRH) which in turn stimulates the anterior pituitary to release
adrenocorticotrophin hormone (ACTH). ACTH acts on the adrenal cortex causing release of
cortisol. Cortisol acts on the placenta stimulating the enzymes 17 alpha hydroxylase and
converts progesterone to 17 alpha hydroxy progesterone which is converted to
androstenedione which in turn is converted to oestrogen by the enzyme aromatase.
• Oestrogen acts on the cotyledonary caruncular complex to release PGF2 alpha. PGF2 alpha in
turn cause regression of CL, lower the progesterone level and release of relaxin. Relaxin causes
stretching of pelvic ligaments. Increased oestrogen causes stimulation of myometrial
contractions which causes the fetus to engage in the cervix thereby stimulating oxytocin which
potentiates myometrial contractions. Oestrogen also increases the secretions of the cervix
lubricating the birth passage.
• The initiation of parturtion process is represented in the form of flow chart for the following
domestic animals:
o In cow and goat
o In sheep
o In mare
o In swine
o In bitch
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INITIATION OF PARTURITION IN COW AND GOAT
(CL dependent Species)
217
INITIATION OF PARTURITION IN SHEEP
218
INITIATION OF PARTURITION IN MARE
219
INITIATION OF PARTURITION IN SWINE
220
INITIATION OF PARTURITION IN BITCH
221
THEORIES ON THE INITIATION OF PARTURITION
• Parturition is triggered by the fetus and is completed by a complex interaction of endocrine,

neural and mechanical factors, but their precise roles and interrelationships are not fully
understood.
Theory Possible Mechanism
Fall in progesterone Blocks myometrial contractions during pregnancy, near term

concentration the blocking action of progesterone decreases.
Rise in estrogen Overcomes the progesterone block of myometrial

concentration contractility and/or increases spontaneous myometrial
contractility.
Increase in uterine volume Overcomes the effects of progesterone block of myometrial

contractility.
Release of oxytocin Leads to contractions in an estrogen sensitized myometrium
Release of prostaglandins Stimulates myometrial contractions; induces luteolysis

leading to a fall in progesterone concentrations (corpus
luteum-dependent species).
Activation of fetal Fetal corticosteroids cause a fall in progesterone, a rise in

hypothalmic-pituitary- estrogen, and a release of PGF2 alpha. These events lead to
adrenal axis myometrial contractility.
MECHANISM OF INITIATION
• Both fetal and maternal mechanisms play roles in initiating parturition. The fetal endocrine
system dominates in ruminants (eg. sheep, goat and cattle) whereas; it plays a minor role in
other species (eg. horse and human).
• The mechanisms that follow the release of cortisol differ among species depending on the
source of progesterone maintaining the pregnancy.
o In sheep, fetal cortisol induces the placental 17 alpha enzyme to catalyse the conversion
of progesterone or pregnenolone to estrogen. The elevated levels of estrogen stimulate
secretion of prostaglandin and development of oxytocin receptors.
o In CL dependent species, cortisol in addition to the synthesis of estrogen causes a
release of prostaglandin from the endometrium, which in turn causes regression of the
corpora lutea.
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PREFACE
Possible mechanisms of initiation of parturition in farm animals
Species Mechanism
Pig PGF2 alpha is the luteolysin that induces CL regression. The increase in
estrogen reflects increase pituitary-adrenal axis; estrogens increase
oxytocin and PG release.
Sheep Fetal cortisol acts on the placenta to induce the enzyme 17 alpha and in
goat, hydroxylase to decrease plasma P4, while increasing estrogen
levels. The increase in E:P ratio enhances the sensitivity of PGF2 alpha
and oxytocin.
Cattle PGF2 alpha induced luteolysis initiates parturition. Fetal cortisol

stimulates the release of PGF2 alpha, probably from the uterus. Other
endocrine changes are similar to those of sheep and goat.
Horse Oxytocin rises progressively towards the end of pregnancy, and then a
massive release triggered by a mechanical stimulus stimulates the
synthesis of PGF2 alpha. The combined actions of these two hormones
result in expulsion of fetus.
MECHANICS OF PARTURITION
• Successful parturition depends on two mechanical processes

o The ability of the uterus to contract and
o The capacity of the cervix to dilate sufficiently to enable the passage of the fetus.
• The activity of the uterine muscle (myometrium) is under the influence of progesterone, which
ensures an environment conducive to the developing fetus.
• Myometrial contractions of low amplitude and frequency occur during the major part of the
gestation.
• At term the uterus switches from a progesterone dominated to an estrogen dominated state.
• As a result two parallel molecular/biochemical pathways are mobilized within uterine tissues.
o The first pathway is similar to those in smooth muscle and transforms the uterus from
its "relaxed" state during pregnancy to an "activated" state.
o The second pathway that results from an increase of the E/P ratio increases the
synthesis or release of uterotonins (eg. PGF and Oxytocin).
• These two pathways acting jointly initiate the intense, synchronous myometrial contractions
needed to dilate the cervix and effect delivery of the fetus(s).
223
ROLE OF UTERUS AND CERVIX
224
ENDOCRINE CHANGES
• Endocrine changes that occur before and during parturition in sow, ewe and cow
225
INDICATIONS
• Parturition may be desirable in animals suffering from a severe illness in that pregnancy as a
means of salvaging a live young from her.
• To save the animal in severe disease condition like traumatic reticulo peritonitis, cardiovascular
disease, bronchopneumonia etc.
• Pre parturient cervico vaginal prolapse in cow and Downer cow syndrome
• Pregnancy toxemia and Prolonged gestation
• As a management tool to concentrate calving in day light hours and on week days for increased
foetal survival and reduced maternal death.
INDUCTION OF PARTURITION IN CATTLE
Dexamethasone (or) Betamethasone: 25-30 mg and Flumethasone: 10-15 mg
• Parturition is induced within 2-3 days of injection

• Disadvantages
o Retained placenta occurs up to 90% of treated cows.
o The onset of milk production is somewhat slower than normal
o Delayed uterine involution.
• PGF2 alpha can be used successfully from 275 days of gestation onwards.
• Dose
o Natural: 25mg
o Synthetic: 500-700 mcg.
• Parturition is induced within 2-3 days of PGF2 alpha injection.
Corticosteroid and prostaglandin combination
• Advantage - The interval from the time of induction to calving was reduced.
INDUCTION OF PARTURITION IN EQUINE
• Corticosteroids
o 100 mg at 24 h interval until parturition occur.
o The average induction time is 4 + 1.6 days.
o Injections of corticosteroid can be started at 321 days of gestation with satisfactory foal
survival and subsequent growth rate.
o Disadvantage
Repeated steroid treatments create the potential for lowered resistance in the
foal.
• PGF2 alpha - Only synthetic prostaglandins are recommended.
226
o Dose: 2.2 mg/kg bw.
o Foaling occurs in approximately 4 h.
o Natural prostaglandins cause strongest smooth muscle contractions which lead to early
placental separation and increased foetal weakness and mortality.
• Oxytocin
o The dosage and administration varies with the degree of cervical relaxation.
o If the cervix is relaxed, 40-60 units of oxytocin are administered as an intravenous bolus.
o If the cervix is closed, oxytocin can be administered in increments of 10 units at 15-30
minute intervals.
o Cervical relaxation can be evaluated prior to each additional increment.
o Birth is usually induced by the time four to five of the 10 unit dose have been given.
• Combination of prostaglandin and oxytocin
INDUCTION OF PARTURITION IN SHEEP AND GOAT
In Sheep
• Glucocorticoids: 5–10 mg, i/m
In Goat
• Glucocorticoids: Dose: 5-10mg, i/m

• PGF2 alpha
o Natural: 5-10 mg, i/m
o Synthetic: 62.5 to 125 µg, i/m
The induction time varies between 30-35 h
INDUCTION OF PARTURITION IN SWINE
PGF2 alpha
o Natural:10 mg
o Synthetic: 175 µg
alpha
• Pregnant animals should not be treated with PGF2 a until day 111 or later to avoid
compromising piglet birth, weight and viability.
• Parturition is induced in majority of the sows from 24-30 h after PG treatment
Corticosteroid
• 75-100 mg (i/m) on day 101–104 of gestation.
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MANIPULATIONS FOR DAY LIGHT CALVING
• The majority of parturition in bovines takes place during the hours of darkness and it has been
suggested that this is a response to variations in the intensity of light of an adaptive mechanism
evolved to provide some protection for the new born.
• Various management techniques have been employed to minimize wastage at calving time.
Synchronization of oestrus
• It has significantly shortened the calving period, but around the clock observation should still be
employed during the calving season.
Induction of parturition
Night feeding
• The easiest and most practical method of inhibiting night calving at present is by feeding cows
at night. The physiologic mechanism is unknown, but some hormonal or anti prostaglandin
effect may be involved. Rumen motility studies indicate that the frequency of rumen
contraction falls a few hours before parturition. Intraruminal pressure begins to fall in the last 2
weeks of gestation, with a more rapid decline during calving. It has been suggested that night
feeding causes intraruminal pressure to rise at night and decline in the day time.
• Cows were started on night feeding the week calving started or 2-3 weeks earlier. Late evening
feeding of cattle seems to be the most effective method of scheduling parturition so assistance
can be available during day light hours.
Tocolytic drugs
Isoxsuprine
• 0.4-2.0 mg/kg. Tocolysis develops within 15 min, and last for 2 h, if required its action can be
suspended at any time by administration of oxytocin.
Clenbutrol
• A β2 stimulant has been used successfully for short term postponement of parturition in cows,
sow and ewe. A rapid tocolysis occurs after administration of clenbutrol in cattle, within 10-15
min and in Swine within 5 min. The parturition was delayed in cattle 5-8 h without any ill-effects
on the cows or calves.
Dose
• Cattle: 300 µg
• Sheep: 240 µg
• Swine: 150 µg
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STAGES OF PARTURITION
INTRODUCTION
• In all species of domestic animals, parturition usually takes place with the dam in lateral
recumbency.
• The essential components of parturition are:
o The expulsive forces
o The foetus(es), and
o The birth canal
• When the expulsive forces are sufficient to cause normally and correctly disposed fetuses and
(fetal membrane) to negotiate a birth canal of adequate width, leads to normal birth.
• The parturition process is continuous and for purpose of better understanding it is usually
divided into three stages or phases.
FIRST STAGE OF LABOUR (Stage of cervical dilation)
• Usually last from 3-6 h, but there is often difficulty in determining its beginning.
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• Apparent for longer periods in primiparous than pluriparous animals.
• Cow exhibits
o Restlessness
o Anorexia
o Colic pain
o Lying down and getting up
o Tail switching
o Repeated stretching as if to urinate
o Frequent small bowel evacuations, and
o Looking at the flank.
• In mares
o Patchy sweating behind the elbow and flanks is noticed.
• In bitches
o Restlessness
o Panting
o Nesting
o Shiver
o Vomit, and
o Chew.
• During this stage, even though there are no visible external changes, preparation of the birth
canal and the fetus for expulsion takes place.
• This stage marks the onset of parturition and is characterized by
o Progressive relaxation and then dilation of the cervix,
o Onset of uterine contraction, and
o Orientation of the fetus.
DILATATION OF CERVIX
• Dilation first occurs at the external os and proceeds inward.

• There is initial wide dilation of the external cervical os, which becomes palpable as a frill at the
cranial end of the vagina.
• The cone shaped cervix so produced under goes a simultaneous shortening and the last part to
dilate is the internal os.
• When the internal os is fully dilated, the vagina and uterus form a continuous canal, which
becomes engaged by distended allantochorion.
• The firm texture of the pregnant cervix is transformed into a soft yielding consistency.
• The propulsion of the conceptus into the cervix widens that organ to the limits of its
extensibility.
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• The changes in the cervix are presumably effects of various hormones, including
o Oestrogens
o Adrenal corticoids
o Relaxin, and
o Prostaglandins.
MYOMETRIAL CONTRACTIONS
• Active contractions of both the longitudinal and circular muscle fibers of the uterine wall occur.
• Uterine contraction occurs regularly with intermissions, they are at first weak but they progress
in intensity.
• Contraction starts in the apices of the uterine horn and proceeds along the horn towards the
cervix.
• In polytocous species especially in bitches, only that part of the uterine containing the
conceptus adjacent to the cervix first becomes active.
• This contractibility in the uterine musculature allows the parturient cervix to be gradually
dilated by the tension of the contractions of the longitudinal muscles of the uterus.
• The contractions of the uterus also cause other changes.
• In the placenta, the attachments to the endometrium become less intimate and with a
deciduate placenta, separation of the margins with hemorrhage.
ORIENTATION OF FETUS
• As regards to the equine and canine foetus, there is a progressive rotation from the ventral to
the dorsal position, while the fore limb, head and neck become extended.
• In case of bovine and sheep fetus, only extension is necessary to change the foetus from its
gestational posture to that of parturition.
SECOND STAGE OF LABOUR (Expulsion of fetus)
• In the monotocous species, that part of the birth process in which the foetus is expelled is
called the second stage of labour.
• In polytocous species, the fetal membranes as well as fetuses are delivered during the expulsive
phase, the second and third stages being merged.
• This stage is characterized by
o Entrance of the foetus into the dilated birth canal
o Rupture of the allantoic sac
o Abdominal and uterine contractions, and
o Expulsion of foetus through the vulva.
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SECOND STAGE OF LABOUR
In cow
• The entrance of the foetus into the birth canal (pelvic inlet) is brought about initially by uterine
contractions on which are superimposed bouts of abdominal contraction.
• Each of these bouts consists of a series of abdominal contractions. Consecutive bouts of
straining coincide with succeeding uterine contractions which recur at a rate of 4-8 times/10
minutes in cow. The co-ordination between the two is due to the fact that the myometrial
contractions force the fetus into the pelvic inlet which activates the pelvic reflex and stimulates
straining.
• The straining forces the fetus against the cervix and anterior vagina thus initiating Ferguson’s
reflex, so that oxytocin which is released causes further contractions of the myometrium. As a
result of these contractions the chorioallantois membrane nears the vulva and during the
abdominal contractions the chorioallantois ruptures.
• In most cases the allantois ruptures, when the animal is standing. In others, rupture may occur
after the animal lies down. Due to its highly vascular nature it appears as bluish sac. The extent,
to which the chorioallantois protrudes from the vulva, however will depend to some extent on
the degree of cotyledon separation.
• Following rupture of chorioallantois there may be a temporary weakening or cessation of
abdominal straining which recommences as the amnion near the vulva. This membrane is an
opaque, white and relatively avascular structure. The amnion is progressively expelled and
become ruptured by a fetal foot with escape of some of the lubricant amniotic fluid.
• The fetal head next occupies the vulva and at this time the contractions of the uterine and
abdominal muscles reach a climax of expulsive effort coinciding with the birth of the fetal head.
• When the head is born the mother may rest for a while but soon a further bout of straining
causes the fetal thorax to pass through the vulva.
• Usually birth of the hips quickly follows and the hind limbs may be expelled at same time.
• Almost all animals lie down as soon as straining commences. Occasionally the foal or calf may
be born with the dam standing. The mare and sow usually lie on lateral recumbency, whereas
the cow, bitch and ewe are more likely to lie on their sternum.
• The off springs are often born with intact umbilical cords and some minutes may elapse before
the cord in ruptured by the movement of the off spring or mother.
• It is important to allow this to happen naturally, since artificial or premature rupture of the cord
may deprive the new born of a large volume which would normally pass to it from the placenta.
When rupture occurs the two umbilical arteries and urachus retract towards, or into the
abdomen and this prevent hemorrhage.
• During its passage from the uterus to the exterior the foetus of the monotoccus species follows
an arched route. This tends to reduce the dorsoventral diameter of the fetal pelvis and also
tends to keep the fetal pelvis high in the brith canal where the maternal bisiliac diameter is
widest.
In ewe and goat the second stage is similar to that of cow.
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In bitch
• The amnion appears at the vulva and is usually broken by the bitch as she licks the vulva.
• The delivery of the head through the vulva requires the greatest expulsive force and once this is
born the remainder of the fetus follows easily.
• The stage of expulsion of foetus is most irregular; one bitch may have her first puppy and then
rest for several hours, then deliver two or three more in quick succession and then rest again
before expelling several more.
• The fetal membranes are generally voided of in 10-15 min. They may come individually or in
other instances a puppy may be born with the membrane of its predecessor around its neck.
• A feature of parturition in the bitch is that much of the uterine discharge is dark green in colour
due to the presence of pigment called uteroverdin. This is due to bile like change which was
taken place in the blood.
In mare
• One fore limb precedes the other by a distance of 6 inches and this position is maintained until
the head is born.
• The point of significance is that one elbow passes through the bony pelvic inlet before the other
and in this way nature has provided that the foal shall present the minimum obstructions to
pelvic inlet.
In swine
• Parturition effort is expended over the first pig let.

• The birth of foetus is followed by the passage of small quantity of fetal fluid.
• The fetal membranes tend to be expelled as two of three masses of joined allantochorion.
DURATION OF SECOND STAGE OF LABOUR
• In cow, it is 2 h.
• In mare it is 5-40 min (15 min).
• In ewe and goats, it is 0.5-2 h or slightly longer if twins or triplets are present. In multiparous
animals the length of the second stage of birth is variable, often depending upon the number of
fetuses in the uterus.
• In the bitch, the average total time for the second stage of parturition in a bitch is 3-6 h. Twelve
hours would certainly be the maximum.
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MATERNAL BEHAVIOUR AFTER EXPULSION OF FETUS
• After delivery, the licking and grooming response of the new born is strong in all domestic dams
except the sow.
• The grooming response is important since licking the nasal area after removes placental tissue
and mucus which may obstruct respiration, since the sow does not groom, piglets often
suffocate from nasal obstruction.
• Queen, bitches and sows nurse their liter in recumbency whereas cow, mare and ewe, nurse
their young while standing.
• Within the first few hours after delivery, a strong bond develops between dam and neonate
which last until weaning. The imprinting of the bond depends primarily upon olfaction, which
depends on pheromone.
THIRD STAGE OF LABOUR (Expulsion of fetal membranes)
• During this stage, rapid and progressive separation of cotyledons from the caruncles occurs so
that the entire fetal membranes are eventually expelled form the uterus. The activity of uterine
musculature is almost entirely responsible for third stage of labour. This stage consists of
dehiscence and expulsion of fetal membranes.
• In cow, dehiscence is not confined to this stage alone but can occur to a limited extent during
first and second stages.
• In mare, the chorion separates completely from its uterine attachment during the second stage
of parturition.
• Expulsion of the chorioallantois and attached parts of amnion usually take place in two phases,
first being expulsion of the membranes from the non-gravid uterine horn which appears
immediately after delivery of the foetus, and remains hanging from the vulva and the gravid
horn portion of placenta delivered some time later.
• Following rupture of the umbilical cord, there is a decrease in the amount of blood to the
uterus. This causes collapse of the placentomes and separation of the cotyledons from the
caruncles due to a decrease in size of the villi and expansion of crypts. Further separation is also
brought about by the uterine contractions on which are superimposed bouts of abdominal
straining and finally the membranes are expected from the posterior genital tract.
• In polytocous species, the dehiscence and expulsion of fetal membranes are interspread with
the fetal birth.
• In the mare, the resumption of substantial contractions of the uterine musculature in the third
stage causes mild abdominal pain and it is common for expulsion of the membrane to be
preceded by mild symptoms of colic.
DURATION OF LABOUR IN DOMESTIC ANIMALS
Average duration of labour in domestic animals (in hours)
Species I stage II Stage III stage
Mare 1-4 0.2 - 0.5 1.0
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Cow & Buffalo 2-6 0.5 - 1.0 6 - 12
Ewe 2-6 0.5 - 2.0 0.5 - 8.0
Sow 2 - 12 2.5 - 3.0 1.0 - 4.0
Dogs 6 -12 3 - 6 (12) -
DEFINITION
• Pureperium refers to the post-parturient phase including the third stage of labour, during
which the reproductive organs gradually return to a structurally and functionally normal non-
gravid state.
MAIN AREAS OF ACTIVITY
In cow, mare and sow
• Puerperium should be normal.

• Extension of the puerperium may have a detrimental effect on the reproductive performance of
the individual.
• It is important to remember that following the first gestation, some changes are not completely
reversible, thus the reproductive system does not return to original non-gravid state.
Four main areas of activity
• Uterine involution.
• Restoration of endometrium.
• Return of ovarian cyclical activity, and
• Elimination of bacterial contamination.
STIMULUS IN COW
• Primary stimulus is due to the removal of the fetus.

• In addition, oxytocin and prostaglandin F2 alpha (PGF2 alpha) are also involved.
• Following parturition, an increase in PGF2 alpha, peak values occur 3 days postpartum and do
not return to basal levels until 15 days postpartum.
INVOLUTION
• It is referred to as the reduction in the size of the genital tract. Reduction in size occurs in a
decreasing logarithmic scale, the greatest change occurring during the first few days after
calving.
o Uterine contractions continue for several days, although decreasing in regularity,
frequency, amplitude and duration.
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o The atrophy of the myofibrils is shown by their reduction in size from 750 to 400 μm on
the first day to less than 200 μm over the next few days.
o Associated with the rapid involution is uterine discharge.
o In primipara and pluripara, entire uterus is usually palpable per rectum by 8 and 10 days
postpartum, respectively.
o Depending on the degree of involvement in placentation, the speed of involution of the
non-gravid horn varies.
o Cervix constricts rapidly postpartum.
o Within 10-12 h of normal calving, it becomes almost impossible to insert a hand through
it into the uterus, and by 96 h it will admit just two fingers.
o Prostaglandins may have a role in controlling uterine involution, although the
postpartum rise in the metabolite of PGF2 alpha may be a reflection of the process of
involution rather than the cause.
RESTORATION OF ENDOMETRIUM
• In cows, during the first 7-10 days after calving there is a considerable loss of fluid and tissue
debris, inspite of a non-deciduous type of placentation.
• The presence of such a discharge in cows is normal.
• It is referred to as the ‘second cleansing’ or ‘secundus’ by herdsmen.
• In human gynaecology, the postpartum vaginal discharge is referred to as lochia.
LOCHIAL DISCHARGE
• The lochia are derived from the remains of fetal fluids, blood from the ruptured umbilical
vessels and shreds of fetal membranes, but mainly from the sloughed surfaces of the uterine
caruncles. Due to the degenerative changes and necrosis of the superficial layers, the slough
occurs (Rasbech,1950).
o Usually yellowish brown or reddish brown.
o Volume voided varies greatly from individual to individual.
o Pluripara can void up to a total of 2000 ml, more usually about 1000 ml.
o In primipara, it rarely more than 500 ml and in some animals it is occasionally nil, owing
to the complete absorption of the lochia.
o During the first 2-3 days, increased flow of lochia occurs, reduced by 8 days and it
virtually disappears by 14-18 days postpartum. At about 9 days it is frequently
bloodstained, whilst before it ceases it becomes lighter in colour and almost ‘lymph-
like’.
o Normal lochial discharge does not have an unpleasant odour.
SEQUENTIAL CARUNCULAR CHANGES IN COW (up to day -8)
• After the placenta is shed, the caruncle is about 70 mm long, 35 mm wide and 25 mm thick.
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• The endometrial crypts frequently contain remnants of the chorionic villi which were detached
from the rest of the allantochorion at the time of placental separation.
Post Changes Caruncle

Partum
Period
Within Evidence of early necrotic changes in
48 the septal mass of the caruncle; the
Hours caruncular blood vessels become rapidly
constricted and are nearly occluded.
A - Septal mass(early evidence of

necrosis of septums)
B - Epithelial lining of endometrium
C - Stratum compactum
D - Myometrium
Day 5 Rapid necrosis results in a leucocyte-

laden necrotic layer on stratum
compactum. Some of this necrotic
material starts to slough and contributes
to the lochia. protrusion of small blood
vessels, mainly arteriols from the
surface of the caruncle, leads to oozing
of blood, causing a red coloration of the
lochia.
A - Necrotic septal mass.

Day 8 Complete regenaration of the
epithelium occurs in the intercaruncular
areas.
SEQUENTIAL CARUNCULAR CHANGES IN COW (from day 10-60 post partum)
Most of the necrotic caruncular tissue sloughs and

Day 10
undergoes some degree of liquefaction
Sloughing is complete, leaving only stubs of blood

vessels protruding from the exposed stratum
compactum.
Day 15
A - Necrotic septal mass now sloughed.
B – Vascular stubs
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Due disappearance of the vessels, the surface
becomes smooth.
Day 19
A – Smooth surface of stratum compactum
Complete re-epithelialisation of the caruncle; which

Day 25 onwards is largely derived from centripetal growth of cells
from the surrounding uterine glands
Caruncles become smaller and consist of small

Day 40-60
protrusions 4-8 mm in dia and 4-6 mm high.
RETURN OF CYCLICAL ACTIVITY (Ovarian rebound)
• In this period, the ovaries usually have numerous large anovulatory follicles which quickly
become atretic. In some instances, it may be incorrectly diagnosed as cysts.
• In the immediate postpartum period: Both oestradiol and progesterone are low.
• During the first few days postpartum: Anterior pituitary is capable of releasing FSH, so that with
the sporadic release of endogenous GnRH there is a gradual and sustained rise in plasma FSH.
• After about 7-10 days: Sufficient to result in the emergence of the first follicular wave:
o In dairy cattle- occurs at about 4 days.
o In beef cattle- occurs at 10 days.
• The ability of the pituitary to release luteinising hormone (LH) is much slower, early release of
GnRH causes some rise in LH, it quickly returns to basal levels.
• The first sign of oestrus is not always a true reflection of the onset of cyclical activity, because
the CNS requires prior exposure to progesterone to elicit behavioural signs; a similar
phenomenon occurs in ewes at the beginning of the breeding season.
• Milk progesterone assay can be employed to determine the onset of cyclical activity.
Other endocrine organs involved
• The adrenal cortex plays an important role.

• Adrenocorticotrophic hormone (ACTH) and corticosteroid administration suppress the
secretion of LH.
• Stimulation of the teat and milk removal causes a rise in glucocorticoids.
• Suckling may exert its effect by modifyng the tonic release of GnRH and LH by the release of
opioid peptides, thereby leading to delay in the return of cyclical ovarian activity.
• The role of prolactin is equivocal, there appears to be a reciprocal relationship between the
hypothalamic control of LH release and prolactin release.
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ELIMINATION OF BACTERIAL CONTAMINATION
• At calving and immediately thereafter, bacteria gain entry into the vagina, then the uterus
through the relaxed vulva and the dilated cervix.
• A wide range of bacteria may be isolated from the uterine lumen; most frequently isolated
being Arcanobacterium Actinomyces Corynebacterium pyogenes, Escherichia coli, streptococci
and staphylococci.
• Due to spontaneous contamination, clearance and recontamination during the first 7 weeks
postpartum, the flora fluctuates.
• Blood, cell debris and sloughed caruncular tissue provide an ideal medium for bacterial growth;
however, in most cases the bacteria do not colonize to produce a metritis endometritis.
Mechanism of bacterial elimination
• Phagocytosis by migrating leucocytes.

• Persistence of uterine contractions.
• Sloughing of caruncular tissue, and
• Uterine secretions all assist in the physical expulsion of the bacteria.
Early return to cyclical activity is probably important since the estrogen dominated uterus is more
resistant to infection.
FACTORS INFLUENCING THE PUERPERIUM
Uterine involution
• Age: Involution is more rapid in primipara than pluripara.

• Season of year: Most rapid in spring and summer.
• Suckling vs. milking
• Climate: Heat stress can accelerate and inhibit the speed of involution.
• Perparturient abnormalities:
o Dystocia
o Retained fetal membranes
o Hypocalcaemia,
o Ketosis
o Twin calves, and
o Metritis delay involution.
• Delayed return to cyclical ovarian activity.
Restoration of the endometrium
• Retained fetal membranes and metritis inhibit healing, whilst ovarian rebound to cyclical
activity may have an influence.
239
Return of cyclical activity (ovarian rebound)
• Periparturient abnormalities
• Milk yield
• Nutrition
• Breed
• Parity
• Season of the year
• Climate
• Suckling intensity and milking frequency.
Elimination of bacterial contamination
• Magnitude of bacterial contamination

• Nature of bacterial flora.
• Delayed uterine involution.
• Retained placenta.
• Calving trauma to the uterus.
• Return of cyclical ovarian activity.
In mare
• The regression of uterus proceeds at a rapid rate.

• Exercise appears to hasten involution.
• The rapid involution of endometrium is probably related to the simple diffuse placental
attachments.
• By about 13-25 days the endometrium is fully restored back to normal.
• A slight amount of lochia may be present for about a week post-partum.
In bitch
• The uterine horns are back to nearly normal size in 4-5 weeks.
• The bitch discharges dark, mucoid, green lochia after parturition. This green colour is due to
pigment uteroverdin and is produced by the breakdown of hemoglobin.
In Ewe
• The uterus completely involutes by 30 days post partum.
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POSTPARTUM CARE OF DAM AND NEWBORN
IMMEDIATE POSTPARTUM CARE
• Check for evidence of another fetus

• Check the entire birth passage to rule out any damage
• Check for signs of hemorrhage
• Check the udder for signs of mastitis
• Check for signs of metabolic disorders
• Protect the dam against infection by administration of antibiotics, and
• Administration of oxytocin 60–100 I.U. following calving depending on the size of the cow.
EXAMINATION OF NORMAL POSTPARTUM MARE
• Initial examination should be simple, as intervention beyond absolute necessity may disrupt the
adaptation processes that are under way during this time.
• Examination should consist of
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o Evaluation of the mare’s behavior including attitude and interaction with her foal, and
o Her general condition including:
Character of pulse and respiration
Color of mucous membranes
Degree of alertness, and
Responsive reaction to stimuli.
• Examine the udder for consistency of mammary secretions and patency of the teats.
• Evaluate the systemic condition, such as rectal and vaginal examination, blood counts, and
clinical chemistry tests, are indicated when a specific problem is suspected based on the
general examination.
Examination of placenta
• Placenta should be thoroughly examined and weighed once it is passed.

• A normal equine placenta weighs approximately 14% of the mare’s body weight or between 10
and 18lb.
• A placenta weighing greater than 18lb is edematous and indicates that the foal may not have
received adequate gas exchange in utero.
• Foals from excessively heavy placentas need to be considered at high risk for neonatal
problems.
• The chorioallantoic and allantoamnionic surfaces and the umbilical cord need to be examined.
• Irregularities in color, thickness, length of villi, and the presence of any secretions should be
noted.
• If placental abnormalities are found or the foal is born before 325 days of gestation, a blood
sample from the foal should be obtained and a complete blood count performed.
• Foals with in utero stress
o If the stress was of short duration leading to premature delivery
A low white blood cell count (<5000 cells/µl), and
Low fibrinogen level (<200 mg/dl).
o If the stress was prolonged
A high white blood cell count (>8000 cells/µl), and
A high fibrinogen level (>400mg/dl).
• Premature foals or foals that experience in utero stress have a greater chance of survival with
appropriate nursing care.
CARE OF NORMAL POSTPARTUM MARE
• Mares should foal in a clean, dry, draft-free area that has protection from excessive sun and
wind. If the climate permits, a small, clean grass paddock is best; otherwise, a well-bedded dry
stall that is at least 12 ft by 12 ft will do.
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• Mares housed in paddocks can be grouped with either one or two mares or be left by
themselves. The number of mares in the paddock should be minimal to decrease competition
among the mares for food and space and to allow the mare to bond with her foal.
• During the postpartum period mares need exercise to promote uterine involution and to
stimulate appetite and gastrointestinal function. Leaving a mare in a stall for prolonged periods
is detrimental, as the mare may accumulate intrauterine fluid leading to metritis or septicemia.
If the mare must remain in the stall because the foal is ill, the mare’s uterus should be
evaluated daily for its accumulation. If fluid accumulates, lavaging her uterus with large
volumes of warm saline until the efflux clear followed by administration of 10 to 20 units of
oxytocin has been helpful in preventing metritis.
• For the first few days after foaling, feeding should be light to moderate, and laxative feeds such
as bran mashes are appropriate to reduce the incidence of constipation.
• Routine care of the mare post partum should include essential preventive medicine procedures.
• In the ideal situation, mares will have received routine vaccinations for the common infectious
diseases during the last month of gestation. This allows maximum protection for the foal by
way of colostrum. When vaccination history is vague or absent, the mare should be
simultaneously vaccinated with tetanus antitoxin and toxoid, at different sites.
• Most broodmares on well-managed farms are on a parasite control program whereby
antiparasiticals are given every 45 to 60 days. If the mare is not on a bimonthly program and
has not been dewormed during the last 2 months of gestation, she should be dewormed within
a few days of foaling. Broad-spectrum antiparasitical compounds such as ivermectin are best.
Then, an intensive parasite control program, preferably deworming every 45 days, should be
implemented.
• Mares with a history of a Caslick’s operation as an essential part of infertility management
should be resutured as soon as practical. If performed within 15 minutes of parturition, local
anesthesia is not required. If the mare tears the dorsal commissure of her vulva and it is not
sutured immediately, it is best to keep the area clean until it is sutured in 3 to 4 days. If it is
sutured when inflammation is maximal, 24 to 48 h after parturition, it will likely dehisce.
COLOSTRUM MANAGEMENT
• Assessment of quality and quantity of colostrum is essential as the foal depends on absorption
of adequate quantities of colostral immunoglobulin for protection against disease during the
first month of life.
• Colustrum with a high immunoglobulin concentration is thick and sticky with either a yellow or
gray tinged appearnance.
• Immunoglobulin content can be estimated by measuring the clostral specific gravity.
• Equine colostrometer (Lane manufacturing, Loveland, Co) developed for measuring specific
gravity is difficult to obtain commercially.
• A colostral specific gravity of 1.06 or greater correlates with a colostral IgG content of greater
than 3000 mg of IgG/dl (30G/L).
• Foals that suckle colostrum with specific gravity over 1.06 rarely exhibit failure of passive
transfer and have serum IgG concentrations of above 400 mg/dl at 24 h of age.
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• Colostral quality can also be estimated with a sugar or an alcohol refracometer. The alcohol
refractometer is used to measure the percentage of alcohol in wine by wine makers and is
readily available.
• Colostrum with a level of 6000 mg of IgG (60G/L) read 16% with the alcohol and 23% with the
sugar refractometer.
• Colostrum with a specific gravity above 1.07 or with a 16% reading from alcohol refractometer
or 23% with sugar refractometer may be saved for colostrum bank.
• Colostrum (250 ml) from the udder after the foal first sucks can be collected and tested for
isoantibodies to ensure that the foal receives the banked colostrum does not develop neonatal
isoerythrolysis.
• Colostrum can be stored in clean labeled containers in a refrigerated freezer (-5 °C) for
approximately 18 months without degradation of the IgG.
• Frozen colostrum can be thawed in warm water or in a microwave on the defrost cycle.
POSTPARTUM CARE OF DOE
• Carefully perform routine abdominal ballottement of the doe immediately after parturition for
the presence of additional fetuses.
• On abdominal palpation, a retained fetus may be detected as a firm mass, and can be
confirmed by ultrasonographic examination.
• Exercise great care to visualize the fetus once the fluid contrast is lost after the chorioallantoic
membrane has ruptured.
• Examine the birth canal for any signs of trauma or hemorrhage.
• After parturition, assess the doe’s vital signs and muscle tone to detect hypocalcemia, as it may
predispose to uterine prolapse.
Placenta
• The placenta is shed often within 1 h of delivery of the last kid, but it is not considered retained
until 8 to 12 h post partum.
• During this period, gentle manual traction, inj. oxytocin (if within 48 h post partum), and
systemic or local antibiotics can be administered.
Lochia
• In normal does, lochia can be discharged for up to 4 weeks.

• Before milking, carefully clean the lochia from the udder.
• Lochia from normal births may contain Chlamydia psittaci, Coxiella burnetii, or other pathogens
that are infectious to humans and other goats.
• Normal reddish brown lochia must be distinguished from the brownish, watery, malodorous
discharge that accompanies postpartum metritis.
• In metritis, does are usually febrile and partially anorectic and have depressed milk production.
It should be treated with local or systemic antibiotics and non-steroidal anti-inflammatory
drugs, and may require supportive therapy.
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Colostrum
• Does should be milked soon after parturition and hand- feeding of kids ensures maximum first
feeding ingestion of colostrum by all kids.
• Udder should be palpated for evidence of mastitis and to evaluate sufficiency of milk
production, and milk should be expressed from each teat to assess the patency of the teat and
to detect abnormal secretions.
• Does with good milk production that give birth to a single kid should be considered as
candidates for cross-fostering another kid.
• Assure that both udder halves are being nursed and monitor for the presence of mastitis and
adequacy of milk production. This also facilitates the doe bonding with all members of the litter
and aids in decision-making as to whether a doe can raise her entire litter or whether one or
more kids should be hand-reared or fostered to another dam.
• Watch closely the postpartum does for signs of hypocalcemia or ketosis.
• Maximizing dry matter intake of fresh does will help to prevent metabolic disease and ensure
maximal peak milk production.
• Monitor their ability to compete at feeders (and moved if needed), and provide fresh supplies
of water and high-quality forage immediately to encourage early return to normal feed intake.
POST-FARROWING CARE
• Farrowing is assumed to be complete, when the sow stops straining and begins to demonstrate
an interest in her litter.
• Complete expulsion of the fetal membranes and placentas is the final phase of parturition,
however the time required for expulsion of the fetal membranes may range from 20 min to 12
h after the last pig is born.
• Retained placenta occurs rarely in sows. Failure to find the placentas in the farrowing crate 4 to
12 h post partum suggests the presence of another pig in the birth canal, and a vaginal
examination is indicated.
• Sows that continue to strain, have a malodorous and discolored vulvar discharge, or show signs
of depression or weakness also should be vaginally examined for retained pigs.
• Many sows are anorectic during parturition and may refuse to eat for the next 48 h. Feed
should be withheld from sows (or only a very small amount provided) the day of farrowing.
Then feed can be increased to 4 pounds daily, plus 1 pound per pig per day for the first week,
with an average intake of 10 to 12 pounds of feed per day. Water intake is essential for
optimizing feed intake and milk production during lactation. Lactating sows will drink 4 to 5
gallons of water per day, and the recommended flow rate for nipple waterers is 2 quarts/min.
• The sow is continually available for suckling by the newborn pigs for the first few hours after
parturition. This constant mammary stimulation results in a high level of circulating oxytocin
and facilitates the piglet’s ability to readily obtain colostrum.
• The sow generally is exhausted from parturition and demonstrates little interest in the piglets.
During this time, however, some sows are observed to savage their newborn pigs. This
condition tends to occur more often in primiparous sows, and the aggressive behaviour is often
directed toward the first-born piglet. Separation of the piglets from the sow until farrrowing is
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completed usually is all that is required to calm a sow that is savaging her piglets. On some
occasions a sow may require sedation before accepting her piglets or fostered piglets.
• Inspect the sow’s udder for
o Color
o Consistency
o Heat, and
o Lesions likely to be associated with pain at this time to determine if the sow is suffering
from mastitis or any other puerperal disease condition.
• Approximately 24 h after birth the sow will begin to actively encourage the pigs to nurse by
grunting and positioning her mammary glands so that the nipples are available for suckling.
Cyclic nursing begins at this time, and milk letdown occurs approximately every hour for a
period of a few minutes.
IMMEDIATE CARE AND MANAGEMENT OF NEWBORN
INTRODUCTION
• The fetus during its development inside the uterus is maintained under constant, regulated and
well protected stress free environment.
• Under the influence of hormonal changes during the latter part of gestation, a number of
maturation changes occur in the fetus so as to prepare it for survival in a free state.
• Inspite of this in utero preparation, following delivery, the fetus has to quickly get adapted to
the sudden change in its immediate environment.
• Generally, when the parturition is normal, the fetus easily overcomes this transition.
• However, from birth to variable period of time afterwards, a number of important events must
occur.
• It is imperative that, the personnel supervising or assisting the parturition process has to
exercise great care to recognize the changes in the new born so that it could be rectified quickly
to enhance its survival.
• The following aspects have to be taken care of
o Onset of spontaneous respiration
o Acidosis
o Thermoregulation
o Care of umbilicus
o Feeding of colostrum
o Protect the new born from an excitable or viscious dam.
ONSET OF RESPIRATION
• In normal calving, spontaneous respiratory movements of the offspring occur within 60

seconds. If there is a delay in calving, sometimes respiratory movements occur before expulsion
of the fetus.
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• During the birth process the PO2 and blood pH are falling and PCO2 is rising due to start of
placental separation, occlusion of the umbilicus, thus restricting gaseous exchange. These
changes stimulate chemoreceptors in the carotid sinus for initiation of respiration.
• Tactile and thermal stimulation are also important for initiation of respiration.
• Licking and nuzzling of the dam provides some stimulus (In cow and goat).
• Immediately after delivery of the fetus, clear the upper respiratory tract of fluid and attached
membranes using fingers.
• Elevating the rear of the calf will help in escape of copious volume of fluids. Some fluid may also
come from the stomach.
• Brisk rubbing of the chest with straw and towels frequently, provide necessary tactile stimulus
for respiration.
• If spontaneous respiration is not present it may be stimulated by pinching the fetal nose,
tickling the nasal mucosa or by splashing cold water.
• Respiratory stimulants like coramine and adrenaline may be tried.
• Oxygen cylinder and resuscitator are useful. Oxygen therapy may be supplied by face mask. If
resuscitation does not result in spontaneous respiration in two or three minutes, it is unlikely
that new born will survive even though there is a strong pulse and heart beat.
ACIDOSIS
• During normal calving, fetus will usually have a mild metabolic acidosis, corrected within a few
hours, and respiratory acidosis, which may last up to 48 hours.
• Dystocia is likely to cause a severe respiratory and metabolic acidosis and result in adverse
effect on both respiratory and cardiac function, and in the case of the calf will reduce vigour,
the suck reflex resulting in reduced colostrum intake and impaired passive immunity (Grove-
White, 2000).
• Metabolic acidosis is primarily due to the production of lactic acid by tissues. When sodium
bicarbonate is used to neutralize the acid, CO2 and H2O are produced; the former will
exacerbate any respiratory acidosis. Thus it is important that the calf is breathing normally so
that it can expire this additional CO2.
METHODS OF ASSESSMENT
• Presence of good muscle tone and a pedal reflex: a well-oxygenated calf with fairly normal acid-
base status.
• Presence of scleral and conjunctival haemorrhages: hypoxia and acidosis - poor prognosis;
similar lesions are present extensively at necropsy in calves that die at birth (Grove-White,
2000).
• Simple method of assessing the degree of acidosis (Schuijt and Taverne, 1994).
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Based on the time to the calf assuming sternal recumbency
Sl.No Feature Time taken to assume sternal

recumbency (in minutes)
1 Normal calving 4.0 ± 2.2
2 Traction 9.0 ±3.3
3 High predictive value for death >15

of the calf
TREATMENT
• A calf requiring resuscitation is likely to be suffering from both a metabolic (low plasma
bicarbonate concentration) and a respiratory (high PCO2) acidosis. The PCO2 will be reduced
with improved alveolar gas exchange and tissue perfusion.
• Metabolic acidosis may be treated with sodium bicarbonate (Grove-White, 2000).
• Assess the degree of metabolic acidosis using blood gas analysis.
• Under field conditions this is seldom possible.
• A newborn calf with the history and clinical signs suggestive of acidosis, sodium bicarbonate at
a dose rate of 1-2 mmol/kg as a bolus intravenous injection of 50-100 ml (35 gm in 400 ml of
lukewarm water) can be used quite safely (Grove-White,2000).
THERMOREGULATION
• Thermoregulation is controlled in two ways:

o By increased metabolic rate for which adequate glycogen reserve is required.
o Reduce heat loss:
The new born has little subcutaneous fat and hence insulation is poor.
Ensure that there is adequate food and arrange for birth to occur in at least a
thermally controlled environment.
Reduced heat loss by ensuring that the coat is adequately and quickly dried.
The neonates should be placed in a warm environment until they can be
returned to the dam.
• The new born puppy should be placed:
o In the first week at 95-100 0F
o In second week at 850 F, and
o In the third week at 70-85 0 F.
CARE OF UMBILICUS
• The haemostatic clamp is removed from the umbilical cord, which is checked for haemorrhage.
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• Should bleeding occur the cord may be ligated with a suitable suture.
• It is important not to cut the cord too close to the abdomen, first to allow the placement of a
further ligature if needed in case of bleeding and for spontaneous vasoconstrictions of the cord
after birth to allow for the blood included in the cord to be reused by the neonate thus
reducing the amount of blood loss.
• The umbilical cord should also be disinfected with mild antiseptic.
o Umbilical care in a kid
o Umbilical care in a calf
FEEDING OF COLOSTRUM
• The new born should recieve colostrum from the dam.

• Generally, the new born gets to identify the udder and consumes the colostrum.
• If new born is delivered by assistance or through c-section, then it has to be assisted.
• Colostrum should be made available to the new born during the first 24 h of delivery, after
which time its absortion is greatly reduced.
• Feeding of colostrum to the young one provides antibodies.
PROTECTION FROM AN EXCITABLE OR VICIOUS DAM
• In some instances, the dam may attack the new born. In such cases it needs to be provided with
physical protection.
IMMEDIATE CARE OF NEW BORN FOAL
• During immediate postnatal period, the veterinarian role will vary with training and experience
of the foaling attendants.
• Veterinarian should review with the foaling attendant, the normal foal behavior and emergency
procedures.
• Guidelines indicating when veterinary assistance is needed should be discussed with the foaling
assistant.
• If parturition proceeds normally, the first veterinary examination is conducted between 8 and
24 h after birth.
• A foal that is not breathing at birth needs immediate assistance.
o Attendant can attempt to resuscitate foal by clearing the nostrils and mouth, by pacing
blunt objects into the nostrils to stimulate breathing by holding the head upright so that
fluid may in through the nostrils.
o Mouth-to-nose resuscitation may “buy time.” The veterinarian should be contacted
immediately.
o Large farms frequently have a source of humidified oxygen that may be delivered to
foals.
o Farm personnel must be trained in its use.
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• The navel of the foal should be disinfected immediately after birth and again in 4 to 6 h to
reduce the nu mber of microorganisms that colonize the umbilical stump.
o An iodine based disinfectant, preferably 3.5% solution, is preferred.
o Avoid stronger solutions such as 7% tincture of iodine as it may cause tissue damage.
o Chlorhexidine diacetate solution (0.5%) is more effective in reducing bacterial numbers
than 2% povidone iodine and does not cause tissue destruction.
• To facilitate passage of the meconium,warm water enemas or soap-based enemas are
commonly administered.
o Enema tube should be lubricated before its placement in the rectum.
o Small amounts of enema fluid, 60 to 120 ml, should be administered slowly, and
repeated until the meconium is passed.
o If there is resistance during delivery of the enema, the procedure should be stopped and
seek veterinary assistance.
• If the dam has not been vaccinated against tetanus during the last 30 days of gestation, her foal
should receive tetanus antitoxin at birth.
o Tetanus toxoid should be given at 6 weeks of age and repeated at 12 weeks.
• In normal foals, antibiotics are not indicated at birth.
• First veterinary examination of the foal
o Usually between birth and 24 h.
o Observe the foal from a distance to determine its behavior, ability to rise, coordination
and strength, ability and willingness to nurse, and attitude and response to external
stimuli.
o Perform a brief, but complete physical examination.
o A serum sample for measuring IgG concentration and, if a problem is detected in either
the foal or the placenta, a blood sample for a complete blood count needs to be drawn.
Foals with serum IgG concentrations above 800 mg/dl are considered to have
adequate transfer of maternal immunity.
Foals having serum IgG concentrations below 400 mg/dl are considered to have
failure of passive transfer.
Serum for measuring IgG can be obtained as early as 8 h after birth.
o By measuring serum IgG concentrations in foals at 8 to 12 h of age the veterinarian has
time to supplement orally foals with low IgG concentrations prior to gut closure.
o Foals younger than 18 h of age with IgG concentrations between 200 and 400 mg/dl and
foals whose dams have colostral specific gravities less than 1.06 (alcohol refractometer
reading <16%; sugar refractometer reading <23%) should be supplemented with at least
250 ml of colostrum that has a specific gravity greater than 1.06.
o Orphan foals, foals whose dams prematurely lactate, and foals with lgG concentrations
below 200 mg/dl may need up to 1 L of colostrum.
o On a weight basis, foals require approximately 1 g of colostral IgG/kg of b.wt to attain an
IgG concentration of 800 mg/dl serum. Therapies for foals older than 24 h of age with
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failure of passive transfer include intravenous plasma, purified lgG products, and
antibiotics
o Specificity of IgG administered may be more important in preventing infection than the
total concentration of IgG attained in the foal’s serum.
o Some commercial products may not contain antibodies to the potential pathogens in
the foal’s environment. The ideal plasma donor is an adult horse with serum IgG
concentrations greater than 1500 mg/dl that has been blood typed and found free of
isoantibodies to the equine major blood types (universal donor).
PARAMETERS OF NORMAL FOALS IMMEDIATELY AFTER BIRTH
Parameter Time frame

Time to suck Within 2-20 minutes; stimulated by placing finger in mouth
Sternal recumbency 1-2 minutes
Time to stand 1-2 hours; longer than 2 hours is abnormal
Time to nursing 2 hours; longer than 3-4 hours is abnormal
Temperature 99-101.5º F
Heart rate 1-5 minutes post foaling >60 bpm; 6-60 min; 80-130 bpm
Respiration rate First 30 minutes post foaling: 60-80 breaths/min; 1-12 hours: 30-40 breaths/min
Blood glucose >80 mg/dl
• Reproduced from Current Therapy in Large Animal Theriogenology by Youngquist R.S. and W.R.
Threlfall (2007). P-137.
POSTNATAL CARE OF KIDS
• At the time of birth, kids should be observed for normal respiration, evidence of respiratory
acidosis, and other evidence of fetal distress such as meconium staining.
• Clearing of nasal passage: Mucus and fluids should be immediately removed from the nose and
mouth of newborn kids.
• Aspiration of meconium should be suspected in kids with extensive meconium staining that
demonstrate respiratory difficulty. For cases under intensive clinical management, oxygen or
doxapram hydrochloride, or both, may be needed to support or stimulate respiration, especially
in premature kids. Mild to moderate acidosis can be treated with intravenous HCO at
1.OmEq/kg or as determined after the base deficit is analyzed.
• Kids and placentas are examined for abnormalities that would suggest placentitis or other signs
of in utero infection that might warrant submission for necropsy. If the owner plans to rear kids
using pasteurized colostrum methods to prevent transmission of pathogens such as caprine
arthritis-encephalitis virus (CAEV) or Mycoplasma spp., the kids should be removed from the
doe at birth, before the doe has been allowed to lick them.
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• Care of umbilicus: The umbilicus of all kids should be inspected for hemorrhage or herniation,
and the umbilical stump disinfected with tincture of iodine or chlorhexidine solution. Treatment
of the umbilicus should be continued for several days is preferred.
• Kids should be examined for the presence of congenital defects such as
o Pseudohermaphroditism
o Teat anomalies
o Cryptorchidism
o Atresia ani
o Cleft palate
o Brachygnathia
o Prognathia, and
o Congenital goiter.
• In herds using pasteurized kid-rearing methods, kids are removed at birth and hand-fed heat-
treated goat colostrum or cow colostrum (heat-treated preferred) by nipple bottle.
• A sucking reflex can be stimulated by stroking the kid’s face behind its muzzle. Weak kids can be
given colostrum with the use of a soft rubber catheter as a stomach tube and the barrel of a 60-
ml catheter-tip syringe as a reservoir for gravity flow.
• Depression caused by respiratory acidosis may reduce suckling and result in decreased
colostrum intake.
• Delayed colostrum intake, inadequate colostrum ingestion, and ingestion of poor- quality
colostrum are common reasons for failure of passive transfer.
• Palpation of kids’ abdomen after nursing serve as indicators of colostrum consumption.
However, hand-feeding of colostrum to all kids is the most definitive means of ensuring
adequate colostral intake.
• Failure of passive transfer can be confirmed by screening serum immunoglobulins using zinc
sulfate turbidity, sodium sulfite precipitation, and other screening techniques.
o Serum immunoglobulin G levels greater than 1600 mg/dl are most desirable.
o Serum immunoglobulin G levels less than 600 mg/dl indicate failure of passive transfer,
and partial failure of passive transfer is suggested by serum immunoglobulin G levels
between 600 and 1600 mg/dl.
• Transfusion of 20 to 40 ml/kg caprine plasma intravenously may be indicated for valuable
neonatal kids with failure of passive transfer.
• If the use of goat colostrum is planned, or if the cow colostrum is from a predictable source,
vaccination of the donor dam 1 month before parturition against Clostridium perfringens types
C and D, tetanus, and other appropriate pathogens will maximize specific immunoglobulin
concentration in colostrum. Regardless of source, colostrum must be of high immunoglobulin
concentration and have good nutritional quality. Does that leaked colcstrum or were milked
because of premature distention of the udder will have colostrum of low immunoglobulin,
vitamin, and fat content. Colostrum with immunoglobulin content greater than 6g/dl and
specific gravity of at least 1.050 is most desirable.
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• Microbial contamination can be minimized by the use of hygienic milking practices. Clipping the
doe’s udder and thighs before parturition and cleaning the teats before milking or allowing kids
to nurse will minimize bacterial contamination of colostrum and prevent ingestion of
environmental organisms by kids. If stored, colostrum should be refrigerated or frozen in small
containers to allow rapid cooling and to minimize bacterial growth.
• Removal of kids at birth may also reduce their likelihood of exposure to Johne’s disease and
other organisms. Heat treatment of colostrum for 1 h at 56°C has been demonstrated to
prevent CAEV transmission in colostrum. Feeding heat-damaged colostrum, even if filtered,
usually results in osmotic diarrhea.
• Frozen colostrum is best thawed in a warm water bath. Repeated freezing of thawed colostrum
and storage of frozen colostrum for longer than 1 year are not recommended. Cow colostrum
can be used instead of goat colostrum; however, goat owners must take steps to ensure that
the colostrum quality and freedom from Mycobacterium paratuberculosis or other enteric
pathogens meet the same standards that they would demand from goat colostrum. Neonatal
isoerythrolysis has been reported following ingestion of cow colostrum, but appears to be quite
rare.
• Large cardboard boxes with clean bedding material work well for housing newborn dairy goat
kids, especially in large herds. A doe’s kids can be placed in one box, and the dam’s
identification written on the box as a means of identifying kids until they can be labeled with
paper collars and permanently identified by tattoo. Disposable boxes are a useful means of
preventing build-up and spread of enteric pathogens. Kids can be kept in these boxes for about
2 weeks, after which the box can be destroyed and kids housed in larger groups.
POST-FARROWING CARE OF NEONATE
• Newborn pigs require immediate energy intake and must be provided a microenvironment that
is draft free and dry with a temperature of at least 30° C. Heat loss can be reduced if piglets are
dried at the time of birth or shortly after by temporary placement of an additional heat lamp at
the rear of the crate.
• Piglets acquire immunoglobulins from colostrum. It is imperative that newborn pigs suckle
within the first few hours after birth. Colostral immunoglobulin G (lgG) levels drop by 50%
within 6 h of the first nursing; late-born piglets may receive significantly lower levels of passive
immunity than littermates born earlier in the farrowing order. When the piglets are 24 h old,
the small intestine loses its ability to transport immunoglobulins (macromolecules) to the
lymphatic system, and “gut closure” occurs. It is a good practice to collect excess colostrum
from newly farrowed sows and store it in the freezer for the purpose of supplementing weak or
orphaned piglets.
• As piglets are born, an effort should be made to dry each animal and dip the umbilical cord into
a mild disinfectant solution.
• Clipping of needle teeth usually is performed to reduce damage to the sow’s underline and to
minimize wounds sustained by piglets when fighting to establish dominance. The decision to
clip needle teeth will vary according to farm-specific conditions. Piglets should be allowed to
suckle colostrum before their teeth are clipped.
• Further piglet processing usually occurs at 3 to 5 days of age. Processing tools should be sharp
and should be disinfected in between litters. Sick litters should be processed last.
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• Pigs have a limited iron supply at birth, and sow’s milk provides very little iron. Without iron
supplementation, piglets will develop a microcytic anemia within 2 weeks of birth. To prevent
microcytic anemia in piglets, it generally is recommended to administer an intramuscular
injection of 200mg of iron dextran in the neck of each piglet within the first 5 days after birth.
• Tail docking often is performed at the same time the iron is administered so that any pigs that
have not received an iron injection can be easily identified. Tails can be trimmed with side-
cutting pliers to a length of about 2cm from the body. Tail docking is performed to reduce the
incidence of tail biting in the grow-finish stage of production.
• Ear notching or tattooing also can be performed before the pig reaches 5 days of age.
• Male pigs should be castrated between 5 and 14 days of age.
• Cross-fostering is the practice of moving pigs between litters to achieve uniform weight and to
ensure that adequate functional teats are available to the number of pigs suckling. This practice
is particularly important for sows with pendulous udders, which may not be able to expose the
bottom row of teats to their piglets. Pigs should be moved from one litter to the next within the
first 24 h after birth so that the fostered pig can receive colostrum from its new dam. Care
should be taken to avoid placing all small pigs on primiparous sows because the small pigs may
not provide the young sow with aggressive-enough stimulation to ensure oxytocin release Pigs
can be bottle-fed, or mechanical feeding systems can be used. Feeding pigs milk replacers
requires a great deal of additional labor to maintain a high level of sanitation of the equipment.
• Providing additional attention to individual pigs can be rewarding. Warming individual pigs that
become chilled or have limited mobility and providing nourishment by means of a stomach
tube can give them a head start before they are placed with their littermates.
• Splay-legged piglets can be assisted by providing support tape between their two rear legs. This
tape should allow the animal to walk with short steps and can b removed in 2 days, allowing the
pig to stand without assistance.
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MODULE-9: TERMINATION OF PREGNANCY
INDICATIONS IN CATTLE
• Therapeutic abortion may be indicated during normal or abnormal pregnancy.
During normal gestation
• Misidentification of a breeding female

• Accidental breeding of a very young heifer, and
• Unwanted pregnancy in feedlot heifers.
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During abnormal gestation
• Fetal maceration,
• Fetal mummification
• Hydramnios, and hydrallantois.
PHYSIOLOGY OF PREGNANCY MAINTENANCE
• Gestation period extends from 270 to 292 days after breeding.

• Once conception has occurred, progesterone is essential for pregnancy maintenance.
• Both luteal and extraovarian sources of progesterone must be eliminated for successful
induction of abortion.
• Although the maternal endocrine events of the first 15 days of cycle and of pregnancy are
similar, the conceptus secretes a range of products, including steroids, prostaglandins, and
proteins, beginning at 12 to 13 days of gestation.
• At least one of these products, interferon results in maternal recognition of pregnancy by
inhibition of luteolysis and prolonged luteal lifespan.
• These effects are mediated by attenuation of endogenous prostaglandin F2 alpha (PGF2α)
secretion.
• The functional life of the corpus luteum (CL) is controlled by a balance of luteotropic factors,
including luteinizing hormone, and luteolytic factors, including PGF2α.
• PGF2α is the naturally occurring luteolysin, acting both directly and indirectly on the CL.
• PGF2α may cause local vasoconstriction of luteal blood flow; however, PGF2α, receptors are
present on luteal cells, and PGF2α has a direct effect on luteal progesterone secretion.
• Endogenous luteolysis occurs in response to a cascade of hormonal events that result in
pulsatile PGF2α secretion. It has been proposed that as a part of this cascade, oestradiol induces
oxytocin receptors on endometrial cells.
• Oxytocin activates those receptors, resulting in the synthesis and secretion of PGF2α.
Role of Progesterone
• Throughout gestation: Fluctuate between 6 and 15 ng/mL

• Two to four weeks preceding parturition: A gradual decline.
• The adrenal gland may contribute 1- 4 ng/mL of progesterone.
• Progesterone is luteal in origin for the first 150 days of gestation.
• Between 150 and 250 days, the placenta acts as additional source of progesterone.
• In the final month of gestation, placental progesterone declines and pregnancy is again
dependent on luteal progesterone.
• Successful treatment to induce abortion must lower circulating progesterone below 1 ng/mL,
which is the threshold necessary to maintain pregnancy, and must be directed specifically at
the source of progesterone appropriate for the stage of gestation at the time of treatment.
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PROSTAGLANDIN F2 ALPHA
• The corpus luteum (CL) is sensitive to PGF2α beginning 5 to 7 days after ovulation.
• In both normal and abnormal pregnancy, administration of PGF2α after that time results in
luteolysis at any stage of pregnancy; however, PGF2α treatment alone induces abortion only up
to 5 months of gestation.
• Rarely, luteolysis is incomplete, in which case luteal progesterone remains above the threshold,
and partial cervical dilation and abdominal straining may occur before the cow resumes normal
gestation.
GLUCOCORTICOIDS
• Reduce placental progesterone secretion from 150 days of gestation. Luteal progesterone is
unaffected, however, and abortion does not result from glucocorticoid treatment until the last
month of gestation.
• During the final month of gestation, glucocorticoids act at the fetoplacental unit to increase the
production of oestradiol and PGF2α, resulting in induced parturition.
• A combination of PG and glucocorticoids will induce abortion from 150 days of gestation.
ESTROGENS
• During the first 2 to 3 days after ovulation, administration of estrogens alters oviductal
transport of the bovine embryo and terminates pregnancy.
• After corpus luteum formation, estrogens cause luteolysis by inducing the endogenous PGF2α
luteolytic cascade from the endometrium.
• The endometrium must be intact for estrogens to induce abortion.
• Estrogen is an exogenous luteolysin with unknown effects on the feto-placental unit; therefore,
abortion can be induced reliably at up to 150 days of gestation.
• Administration of 30mg estradiol valerate, alone or in combination with dexamethasone in
cows between 200 and 220 days of gestation has not been shown to decrease serum
progesterone or result in abortion.
• Treatment with estradiol or its synthetic derivatives results in prolonged estrus behaviour,
vulvar swelling, mucopurulent discharge, and relaxation of parts of the posterior reproductive
tract.
• The function of the utero-tubal junction as a sphincter may be impaired, possibly allowing
ascending infection and salpingitis.
• Time to return to fertile oestrus after estrogen treatment may be longer than after
prostaglandin treatment.
OXYTOCIN
• Treatment of cows with oxytocin from days 2 to 7 after oestrus with 100 to 200 IU of oxytocin
prevents pregnancy, probably by preventing normal luteal development.
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TERMINATION OF NORMAL PREGNANCY UP TO 150 DAYS
Prostaglandins
• During first 5 months of pregnancy, treatment of choice is PGF2α or an analogue.

• Until 5 to 7 days after ovulation, cows do not respond. Later stages majority of cows respond by
returning to fertile oestrus within 3-5 days of treatment. Cows not in oestrus within 5 days
should be retreated.
• PGF2α or an analogue
o PGF2α : 25 mg IM
o Cloprostenol: 500 µg IM
o Fenprostalene: 1 mg SC
Oxytocin
• First few days after ovulation may prevent the establishment of pregnancy.
Intrauterine infusion of irritating solutions
• Between days 5 and 10 after ovulation, prevents the establishment of pregnancy and may
cause luteolysis and early return to oestrus.
• Later than 11 days after ovulation occasionally lengthens the oestrous cycle.
• Up to 90 days of gestation, causes embryonic death necessitating manual evacuation of uterine
contents.
• Suitable solutions
o Aqueous iodine 0.5%
o Tetracycline 2 Gm in saline.
Oestrogens
• Administration within 72 h of ovulation impedes oviductal transit of embryos.

• Up to 5 months of gestation, administration of an oestradiol ester, such as oestradiol valerate,
results in abortion within 7 days. Occasional abortions occur up to 14 days after treatment.
• Oestradiol should be administered every 4 days until abortion.
o Diethylstilesterol: 40-80 mg IM
o Oestradiol ester: 4-8 mg IM
Manual techniques
Manual enucleation of the CL
• By transrectal manipulation manual enucleation of CL removes progesterone support for

pregnancy and results in abortion at up to 150 days. Conceptus will be aborted in 2-5 days late
or resorbed.
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• Procedure
o Per rectum grasp the prominent CL
o Express between the index finger and thumb
o Drop the CL in to the abdominal cavity
o Arrest bleeding by manual compression for 3-5 minutes
• Limitations
o Induce adhesions of the ovary and ovarian bursa and,
o Occasionally, severe hemorrhage, sometimes fatal.
Manual rupture of the amniotic vesicle
• By transrectal manipulation it is possible to manually rupture once the vesicle can be palpated
at 30 to 35 days of gestation.
• After 60 days and up to 120 days of gestation, when the amniotic vesicle can no longer be
isolated within the fluid-filled chorioallantois, it may be possible to terminate pregnancy by
manual decapitation of the fetus.
• The mean time to abortion is 25 days, but abortion may occur up to 8 weeks after treatment.
TERMINATION OF NORMAL PREGNANCY AFTER 150 DAYS
• In feedlot heifers, unwanted pregnancy leads to financial loss due to

o Reduced feed conversion
o Lower carcass prices, and
o Periparturient diseases including dystocia.
• Heifers should be examined on arrival at the feedlot to select appropriate candidates.
• Between 5 and 8 months of gestation, a combination of PGF2α and dexamethasone is necessary
to remove both luteal and extraovarian sources of progesterone.
• All pregnant feedlot heifers are routinely treated with the combination of PGF2α and
dexamethasone (Preferred combination to all other treatments), regardless of their stage of
gestation.
o Inj.PGF2α : 25 mg IM
o Inj. Dexamethasone: 25 mg IM
• Abortion will occur reliably, with a mean time to abortion of 5 days.
• Abortion may be preceded or accompanied by oestrus behavior for duration of 9-12 h.
Approximately 95% effective, although repeat treatments occasionally are necessary.
• Progestin-containing growth promotants should not be used until after abortion has been
induced, as it may interfere with treatment.
• All heifers should be examined after treatment. Those still pregnant usually will respond to a
second treatment.
• In the final month of pregnancy, either dexamethasone or prostaglandin alone induces
premature parturition within 2-3 days.
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SEQUELAE
• Approximately 80% incidence of retained fetal membranes after the fourth month of gestation.
Majority of cases expel the placenta within 7 days without treatment.
• Fetal mummification develops in 2-4% of pregnant feedlot heifers treated with a combination
of PGF2α and dexamethasone.
• In some cows, metritis or pyometra will develop after induced abortion; however, acute toxic
metritis is an unusual sequelae.
IN HYDRALLANTOIS AND HYDRAMNIOS
• Pregnancy can be terminated within 48 h in cows with simultaneous administration of PGF2α

and dexamethasone, using doses recommended for normal pregnancy.
• Supportive treatment is necessary to compensate fluid loss.
• Parturition usually is abnormal.
• C-section may be an alternative to induced parturition.
IN FETAL MUMMIFICATION
PGF2α or an analogue
• Therapeutic agent of choice.

• Excellent prognosis for return to fertility within 1-3 months.
• Expulsion of the fetus usually occurs within 24-72 h.
• Retreatment of cows with mummified fetuses still present at reexamination occasionally is
necessary.
Oestrogens
• Luteolytic doses of estrogen also results in expulsion of mummified fetuses.

• Repeated treatments may be necessary at 48 h intervals.
• After treatment, the mummified fetus may become lodged in the vagina, requiring lubrication
and manual removal.
IN FETAL MACERATION
• Response to treatment with PGF2α or oestrogen is unrewarding.

• Macerated bones may be removed at surgery or through a partially dilated cervix, before or
after administration of PGF2α or oestradiol however, endometrial damage carries a poor
prognosis for return to fertility.
• In treating fetal maceration and mummification, glucocorticoids are ineffective because an
intact feto-placental unit is necessary for their mode of action.
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INTRODUCTION
• Elective induction of abortion or parturition is easily accomplished in goats.

• In does, throughout gestation a functional corpus luteum (CL), the source of progesterone, is
essential for maintenance of pregnancy.
• The placenta produces little or no progesterone.
• Anything that interferes with proper function of the CL during gestation will result in
termination of pregnancy.
PHYSIOLOGY OF PREGNANCY MAINTENANCE
• Events that lead to normal parturition require functional maturation of the fetal adrenal cortex.
• Parturition is triggered by activation of the fetal pituitary-adrenal axis. Adrenocorticotropic
hormone (ACTH) is released by the fetal pituitary, which stimulates release of corticosteroids by
the fetal adrenal glands.
• An increase in fetal corticosteroids stimulates placental estrogen biosynthesis, which in turn
stimulates the synthesis and release of PGF2 alpha from the placenta and endometrium.
• The cascade continues and PGF2 alpha causes luteolysis, which results in a decrease in
progesterone.
• An increase in estrogen and decrease in progesterone stimulates myometrial activity, which is
further enhanced by the effects of PGF2 alpha, causing a direct effect on the myometrium and
stimulating oxytocin release.
• By mimicking some of these events, abortion or parturition can be artificially induced.
INDICATIONS
• Mismated does that may be too young or small for breeding, may be held in reserve for
breeding at some future date, or scheduled to be bred by AI or to a different buck.
• Injury or disease that may compromise the life of the doe or the completion of pregnancy.
• Most commonly used agent to achieve termination of pregnancy in goats is PGF2 alpha or its
analogs, but corticosteroids and estrogens have also been employed.
• In cases of mismating, the doe should not be treated until 5-7 days after breeding, at the
earliest, to allow the CL to mature and become receptive to the effects of PGF2 alpha. If the
gestational age is 30 days or greater, PGF2 alpha will terminate pregnancy but the subsequent
oestrus may be anovulatory, followed by a shortened interoestrus interval.
• If abortion is induced late in the breeding season, does may not exhibit oestrus or cycle again
until the next breeding season. Daily doses of cortisol acetate, 100 mg IM before day 112 and
after day 136 results in delivery at normal term, but given on days 113 - 120 results in abortion
by day 125.
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• Administration of methylprednisolone acetate prior to day 84 caused no early termination of
pregnancy, but doses of 240-270 mg IM given on day 111 or day 125 resulted in abortion in 6
days.
• Administration of oestradiol benzoate 12 mg IM at 126-138 days of gestation resulted in live,
non-viable fetuses in 58-87 h.
• Doses as low as 1.25 mg PGF2 alpha have been shown effective for luteolysis, as has 0.0385
mg/kg.
• In elective termination of pregnancy in mares, many methods may be employed. However, care
should be exercised to select a procedure that is safe and effective and that minimizes damage
to the mare’s reproductive tract and future breeding health.
• When terminating pregnancy, consider the following factors
o Stage of gestation
o Presence of endometrial cups
o Expected time of return to estrus
o Presence of twin fetuses, and
o Physical condition of the mare.
• In every case of elective abortion, the mare should be re-examined at an appropriate time after
the procedure to ensure that pregnancy has been effectively terminated.
INDICATIONS
• Elective termination of pregnancy is performed for several reasons

o Mismating
o Change in ownership
o Age or health of dam
o Abnormal gestation, and
o Twin pregnancy.
INDUCED ABORTION BEFORE FUNCTIONAL ENDOMETRIAL CUPS (DAYS 0—33)
• It would be safe and successful, if pregnancy termination is attempted earlier,

• No method has been shown to reliably terminate pregnancy before day 5 after ovulation.
Days 5-6 after ovulation, elective abortion is easily accomplished by luteolysis of fully functional
corpus luteum (CL).
• Prostaglandin F2α (PGF2α) or a PGF2α analogue can be administered as an intramuscular

injection.
• Dinoprost tromethamine and Cloprostenol commonly are used.
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• Both have similar efficacy.
• Common side effects of sweating and mild colic are avoided with the administration of
Cloprostenol.
Before maternal recognition of pregnancy (Approximately by days 12—14)
• A single injection of either 10mg of Dinoprost or 500µg of Cloprostenol cause lysis of the CL and
effectively terminate pregrancy.
After pregnancy recognition
• Two or more consecutive injections may be necessary to lyse diestrual, or secondary, corpora
lutea.
• Mares can be expected to return to estrus within 3 to 5 days.
After day 6
• Intrauterine infusion or lavage performed also terminates pregnancy.

• Abortion is likely caused by embryotoxic effects or release of endogenous PGF2α, as a result of
cervical and uterine manipulations.
• Sterile saline (2-3 L divided into 500-1000 ml aliquots) is the preferred solution for uterine
lavage because it is relatively nonirritating.
• Infusions of Lugol’s solution, dilute povidone-iodine, or nitrofurazone have been used
successfully. These antiseptic solutions are potentially irritating to the genital tract and should
be used with care.
• Chlorhexidine solution should not be used for intrauterine infusion.
• Any technique that necessitates invasion of the cervix can result in bacterial contamination and
endometritis.
Between days 16 and 25 after ovulation
• Manual crushing of the conceptus can be performed easily.

• More difficult and less efficacious after day 25.
Between days 20 and 45
• Transvaginal ultrasound-guided pregnancy reduction has been successful in terminating

pregnancies.
• Ovariectomy, although not a practical technique, consistently results in abortion during this
period.
INDUCED ABORTION WHILE ENDOMETRIAL CUPS ARE FUNCTIONAL (DAYS 34-120)
• During days 34-120 of gestation, mares may not return to normal estrous cycles after
pregnancy termination.
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• Multiple doses of PGF2α or an analogue have been shown to effectively terminate pregnancy in
several studies.
• Mares injected once or twice daily aborts 3 to 5 days after treatment.
Prior to chorioallantoic attachment to the endometrium (at approximately 80 days of gestation) :
• Intrauterine infusion or lavage it is more successful to induce abortion.
After attachment
• Manual invasion of the cervix

• Rupture of the chorioallantois, and
• Manual extraction of the fetus and membranes are more expeditious.
• Following manual abortion, a sterile saline lavage aids in removal of any remaining fetal
membranes, blood clots, or fibrin tags.
After day 34
• Manual crushing of the conceptus is technically difficult because of the size of the vesicle and
the position of the uterus in some mares.
Between days 40 and 65
• Transvaginal ultrasound-guided allantocentesis, with aspiration of allantoic fluid, successfully

terminates pregnancy
INDUCED ABORTION AFTER FOUR MONTHS OF GESTATION
• After the first trimester of pregnancy, elective termination may be complicated by dystocia,
retained placenta, and trauma to the genital tract.
• Various techniques are available, but there appears to be no consensus on which technique is
the most efficacious.
• Multiple injections of PGF2α have resulted in abortions in mares between 100 and 245 days of
gestation.
• Abortion induced using PGF2α in two mares at 150 days gestation; abortion occurred 37 h after
treatment in one mare and after 61 h after treatment in the other.
Termination of late pregnancies
• Manual disruption of the fetal membranes and removal of the fetus is a more reliable
technique.
• Easily accomplished if cervical dilation is enhanced by methods other than manual distention.
• Oestrogen treatment (6-10mg oestradiol) 24 h prior to induction of abortion results in success.
• Cervical dilation can also be achieved using intracervical application of PGF2α.
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• Oxytocin treatment (especially following oestradiol therapy) may hasten the expulsion of the
fetus and fetal membranes.
• Infusions of large volumes of saline have been recommended by many authors to aid
myometrial contractions and expulsion of the fetal membranes.
• Transabdominal ultrasound-guided fetal cardiac puncture, followed by injection of potassium
chloride, has been successful in reducing twin pregnancies in midgestation and could be used
for single pregnancy termination.
• Intra-allantoic injection of dexamethasone (administered transcervically) induced abortion
within 3 days in treated mares.
• In contrast to other species, systemic dexamethasone (dose of 10-80mg administered
parenterally for 4 consecutive days) does not appear to cause abortion in mares.
MEDICAL TERMINATION OF PREGNANCY DURING PRE-OSSIFICATION PERIOD IN CANINE
DURING PRE-OSSIFICATION PERIOD IN CANINE

( Days 20-22 through 40 -42 after LH peak )
Drugs Dose Route Frequency
PGF2 alpha 0.1-0.25 mg/kg SC BID for 4-6 days
Cloprostenol 1.0-2.5 µg/kg SC Once a day for 5 days
Cabergoline Plus 5 µg/kg Oral Once a day for 5 days
Cloprostenol 1 µg/kg SC Once in 48 h
Bromocriptine Plus 30 µg/kg Oral TID
Cloprostenol 1 µg/kg SC On days 28 and 32 after LH peak
Bromocriptine PlusPGF2 alpha 10 µg/kg Oral TID
100 µg/kg SC TID
Aglepristone 10 mg/kg SC Once a day for 2 days
Source: T.W Fossum (2007)
MEDICAL TERMINATION OF PREGNANCY DURING PREATTACHMENT PERIOD IN CANINE
DURING PRE-ATTACHMENT PERIOD IN CANINE

(Fertilization to days 20-22 after LH peak)
Drugs Dose Route Frequency
Aglepristone 10 mg/kg SC Once a day for 2 days
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Oestradiol 10 µg/kg (max SC Divided in to 2-3 injections / once in 48 h. Begin
Benzoate 1 µg) 2-4 days after mating
Cloprostenol 1.0-2.5 µg/kg SC BID to QID for 5 days begining of day 5 of diestrus
Natural PGF2 10-250 µg/kg SC BID to QID, days 5-11 of diestrus

alpha
Source: T.W.Fossum (2007)
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MODULE-10: BASIC AND IMMEDIATE CAUSES - FORMS OF DYSTOCIA
DEFINITIONS
• Eutocia refers to safe, easy, natural, or physiological parturition.

• Dystocia (Greek terminology) refers to difficulty in birth. When the first or usually the second
stages of parturition gets markedly extended, it becomes difficult or impossible for the dam to
deliver without artificial interference.
CLASSIFICATION OF CAUSES FOR DYSTOCIA
• The causes of dystocia may be classified into

o Basic, and
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o Immediate causes.
• A better understanding of the basic causes will help to prevent the occurrence of dystocia.
BASIC CAUSES OF DYSTOCIA
• It may be divided into the following categories:

o Hereditary
o Nutritional and management
o Infectious, and
o Traumatic
• Many cases of dystocia may have two or more basic causes.
HEREDITARY CAUSES
This may be divided into as those that have produced defects in the dam which predispose to dystocia
or those hidden or recessive genes which may produce a defective fetus.
• Persistence of the median wall of the mullerian duct with a large band inside or caudal to the
external os of the cervix.
• Twining in cattle commonly result in dystocia.
• The hidden and recessive genes produce a variety of pathological conditions affecting the
foetus or foetal membranes.
o Dropsy of foetus
o Hydro amnion - achondroplastic calves results from in breeding.
o Acroteriasis congenitia, hydrocephalus.
o Foetal anasarca
o Autosomal recessive gene causing prolonged gestation.
o Muscle contracture monsters are usually produced by general functional ankylosis with
an abnormal development of muscle and tendons causing an immobility and extreme
rigidity of affected lambs.
NUTRITION AND MANAGEMENT CAUSES
The nutrition of a pregnant animal and its management at parturition may be the basic causes of
dystocia.
• Improper nutrition of the growing heifers was the most important factor in retarding body and
pelvic growth.
• Dystocia may arise due to
o Small pelvis
o Under developed juvenile genital tract, and
o Lack of strength to expel the foetus.
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• Breeding a poorly grown, underfed female that may be old enough to breed, but the body
growth has been greatly retarded due to poor nutrition, parasitisms or diseases. It has been
suggested that dairy heifers may be bred by size or weight rather than by age.
• High feeding levels may favour dystocia
o By excessive deposition of fat in the pelvic region predisposing to difficult parturition,
especially in heifer.
o Favour the development of a larger fetus (especially high feeding during the last third of
pregnancy).
• The balance between fetal size and pelvic or genital tract diameter is thus upset and dystocia is
favoured.
• Malformation of the pelvis such as pelvic rickets due to improper mineral balance or lack of
vitamin-D is seen in humans.
• Close confinement of pregnant animals without exercise, are prone to
o Torsion of uterus, and
o Uterine inertia.
• Exercise increases
o Body tone
o Strength and resistance, resulting in stronger labour contractions.
• During parturition all animals should be watched closely, if possible, so that prompt aid may be
given if parturition is not normal.
• This aid may prevent
o Secondary uterine inertia
o Death of the foetus
o Rupture of the uterine or birth canal
o Septic metritis
o Retained placenta, and
o Obturator nerve paralysis.
INFECTIOUS CAUSES
• Any infection or disease affecting the pregnant uterus and its contents may cause dystocia.
• In infection of the uterus, the uterine wall may lose its tone or ability to contract a condition
resulting in complete dilation of the cervix and uterine inertia.
• To help control infections that predispose to uterine disease and foetal death, both the sire and
dam should be free of infection at the time of service.
• All known infectious diseases such as brucellosis, leptospirosis, vibriosis, salmonellosis, viral and
other septic diseases should be controlled according to our best knowledge at the present time.
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TRAUMATIC CAUSES
• The traumatic causes for dystocia are not common.

• Ventral hernia and rupture of the prepubic tendon late in gestation may occur from traumatic
causes. These injuries render the abdominal wall incapable of strong contractions resulting in
inability to force the foetus through the birth canal.
• A fracture of the pelvis with secondary deformity and exostosis is seen most commonly in small
animal, which may result in a stenosis of the birth passage resulting in severe dystocia.
• The basic causes of dystocia are multiple, but by properly applying our knowledge, its incidence
may be kept at a minimum.
IMMEDIATE CAUSES OF DYSTOCIA
• Dystocia is regarded as being either maternal or fetal in origin.

• Practically dystocia should be considered in relation to defects in the three components of birth
process:
o Expulsive forces (Expulsive defect)
o Adequacy of the birth canal (Constriction), and
o Size and disposition of fetus.
COMMON FORMS OF DYSTOCIA IN COW
• Both relative and absolute fetal oversizes are common, especially in the Friesian.
• Disproportion due to emphysema is frequently encountered, an outcome rather than a primary
cause.
• Local or general edema of fetus is a rare cause of oversize seen in Ayrshire.
• Monsters are relatively high; generally distorted and celosomian types: Schistosomus reflexus
and Perosomus elumbis are common.
• Abnormal longitudinal presentation is uncommon.
• Anatomical arrangement of the uterine cornua and absence of a distinct uterine body do not
favour transverse presentation.
• Postural irregularities of the head and limbs are common, usually carpal flexion, lateral
deviation of the head and breech presentation.
• Simultaneous presentation of twins is well recognized cause of dystocia.
• In pluriparous cows, uterine inertia is often associated with hypocalcemia.
• Uterine torsion has highest incidence.
• Incomplete dilatation of cervix is occasionally seen.
COMMON FORMS OF DYSTOCIA IN MARE
• More serious dystocias are of maternal origin (5%), and mainly uterine torsions.
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• Abnormal presentation, position and posture of fetus: Most common single cause is lateral
deviation of head.
• Feto-maternal disproportion and uterine inertia are rare.
• Transverse presentation of foal across the uterine body (either dorso -transverse or
ventrotransverse) is well known.
• Transverse disposition in which the extremities of the fetus occupy the uterine horns is
notorious and peculiar.
• An obliquely vertical or dog sitting position is well known and peculiar.
• Failure of fetus to rotate into the dorsal position and its consequent engagement at the
maternal pelvis in the ventral or lateral position is often encountered. May be complicated by
laceration of the dorsal wall of the vagina and even rectum and anus.
• All forms of postural abnormality
o Lateral and downward deviation of the head and neck.
o May be further complicated by rotation of the cervical joints
o Limbs are frequently presented abnormally. Either one, several or all of the joints of the
limbs may be flexed.
o Irregularities classified according to their clinical significance
Carpal flexion
Shoulder flexion
Hock flexion, and
Hip flexion. Bilateral hip flexion is known as Breech presentation.
o Exceptional anterior presentation postural abnormality-displacement of one or both
extended forelimbs above the fetal neck (Foot-nape posture).
• Gross fetal abnormalities are rare.
• Developmental anomalies such as wry neck (fixed lateral deviation) and hydrocephalus
occasionally observed. Wry neck is likely to occur with transverse bicornual pregnancy.
COMMON FORMS OF DYSTOCIA IN EWE
• Feto-pelvic disproportion is most common.

• If pelvic size of the dam is a major factor in the disproportion it is likely to have repeated
dystocia.
• In certain breeds and flocks the incidence of dystocia due to malposition exceeds that due to
feto-pelvic disproportion. More common in pluripara than in primipara and is more frequent
with twins than with still births.
• Among maldisposition: shoulder flexion commonest followed by carpal flexion, breech
presentation, lateral deviation of head and transverse presentation.
• Twining does not significantly increase overall dystocia.
• Posterior presentation markedly predisposes to difficult births.
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COMMON FORMS OF DYSTOCIA IN SOW
• Maternal forms being almost twice as common as fetal forms.

• Incidence of fetal dystocia increases when the litter is small, for in these the size of the
individual tends to be large and obstruction may result.
• Irregularities of limb posture and even uncomplicated posterior presentation often cause
dystocia when the litter is small whereas had the litter been large and its individuals small,
these irregularities would not have interfered with normal expulsion.
• Monstrosities are common, generally of double type. But schistosomus, perosomus and
hydrocephalus also occur.
COMMON FORMS OF DYSTOCIA IN BITCH
• Two principal causes of dystocia are:

o Primary uterine inertia
o Feto-pelvic disproportion
• Dachshund and Aberdeen terrier prone to uterine inertia
• Corgi shows extreme variation in the size of its puppies; absolute and relative oversize may
occur.
• Brachycephalic breeds together with Sealyham and Scottish terrier are prone to obstructive
dystocia due to fetuses having comparatively large heads and the dams having narrow pelvis.
• Absolute fetal oversize is commonly encountered in bitches gravid with only one or two young;
it may also result from pathologic fetus.
• Primigravid bitch of small breed often has trouble from relative fetal oversize with her first
puppy but provided timely assistance is forthcoming she usually expels the remainder normally.
If assistance is delayed the outcome becomes serious.
• Irregularities of limb posture are of little importance provided puppy is normal size.
• Many puppies are born with their fore or hind limbs flexed, if fetuses relatively large cause
dystocia.
• Not infrequently in a bitch attempting to expel a fetus with forelimbs retained partially succeed.
Head is born, but the thorax with limbs becomes obstructed in the maternal pelvic inlet.
Similarly puppy may have hind parts born while its distended thorax is obstructed.
• Irregularities of head posture are common; vertex (Butt) presentation and lateral deviation of
the head frequently encountered. Interesting feature of later abnormality, often involves last
puppy.
• Fetal hydrocephalous and anasarca occasionally seen.
• Other forms of monster are rare.
• Abnormalities of position are common in both anterior and posterior presentation.
• Failure of fetus to rotate prior to presentation results in its engaging in the pelvic inlet in the
ventral or lateral position.
• Transverse presentation is rare. When it occurs, the bitch is generally gravid with a single fetus
only and gestation is of bicornual type and generally accompanied by uterine inertia.
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GENERAL HANDLING OF DYSTOCIA
APPROACH TO AN OBSTETRICAL CASE
• Each case of dystocia is a clinical problem, which may be solved if a correct procedure is
followed.
• A correct diagnosis is the basis of sound obstetric practice.
CASE HISTORY
• Before proceeding to examine the animal, a brief history of the case should, whenever possible,
be obtained.
• Much of it will be the outcome of questioning the owner or attendant, but many points will also
be elicited from personal observation of the animal.
o Has full term arrived or is delivery premature?
o Is the animal a primigravida or multigravida?
o What is her previous breeding history?
o What has been the general management during pregnancy?
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o When did straining begin?
o What was its nature – slight and intermittent or frequent and forceful?
o Has straining ceased?
o Has water bag appeared and, if so, when was it first seen?
o Has there been any escape of fluid?
o Have any parts of the fetus appeared at the vulva?
o Has an examination been made and has assistance been attempted?
o If so, what was its nature?
o Is the animal still taking food?
• By consideration of the answers to these and similar questions, it is possible to form a fairly
accurate idea of the case to be dealt with.
• The greatest attention should be paid to the duration of labour.
• The onset of vigorous and frequent straining, together with the appearance of the amnion, the
expulsion of the fetal fluids, or the appearance of a fetal extremity, indicates the onset of the
second stage of labour, and parturition.
PREDICTION OF EXPECTED DATE OF DELIVERY
Question
• Has full term arrived or is delivery premature?
To have an answer to this question, if you have

the date of service, then the expected date of
delivery can be obtained from the gestation
calculator. This gestation calculator is easy to use
and serve as a ready reckoner.
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Directions
• First set the bold arrow to the date of service, and then
• Read the expected date of delivery directly for each animal.
o For eg., If the date of service is 10-02-2008, then the expected date of delivery (± 5 days)
will be as follows:
Species Date of service Expected date of delivery (± 5 days)
Cow 10-02-2008 16-11-2008
Buffalo 10-02-2008 12-12-2008
Mare 10-02-2008 12-01-2009
Cat 10-02-2008 11-04-2008
Bitch 10-02-2008 15-04-2008
Sow 10-02-2008 02-06-2008
Ewe 10-02-2008 07-07-2008
GENEARAL EXAMINATION OF THE DAM
• Animal’s physical and general condition should be noted.

• If recumbent, is she merely resting or is she exhausted or suffering from metabolic disease?
• Body temperature and pulse rate should be noted and the significance of abnormalities
considered.
• Particular attention should be paid to the vulva.
• Parts of a fetus may be protruding and it may be possible to assess the nature of the dystocia
from these.
• Are exposed fetal parts moist or dry? Such evidence serves not only as a guide to the duration
of the condition, but also to the effort that will be necessary to correct it.
• Should parts of the amnion protrude, what is their condition?
• Are they moist and glistening and is fluid caught up in their folds?
• If so, their exposure is recent and the case is an early one.
• If however, the membranes are dry and dark in colour, it may be taken that the case is
protracted.
• May be nothing protrudes from the vulva, in which case particular attention should be paid to
the nature of the discharge.
• Fresh blood, especially if profuse, generally indicates recent injury to the birth canal.
• A dark brown fetid discharge indicates a grossly delayed case.
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• Where it is clear from the evidence already obtained that the fetus is dead and the uterus
grossly infected, the desirability of inducing epidural anaesthesia before proceeding to a vaginal
examination should be considered.
DETAILED EXAMINATION OF THE DAM
• Animal should be effectively restrained for the safety of both the veterinarian, any assistants
and the animal concerned, in a clean environment.
• In the case of cow, buffalo and goat it is easier if they remain standing.
• Supply of clean hot water with soap or surgical scrub should be available and an instrument
trolley to place the instruments.
• With an assistant holding the tail to one side, the external genitalia and surrounding parts are
thoroughly washed from one bucket.
• Administer epidural anesthesia.
• The operator should wash his hands and arms from another bucket and after wearing a clean
disposable plastic sleeve, proceeds to make a vaginal examination.
• The introduction of the hand through the vulval labiae almost invariably provokes defecation
and it becomes necessary to wash the vulva and the operator’s arms again.
• If on examination of the vagina is found to be empty, attention should be directed to the cervix.
• Is it completely effaced? If it is not, is it partially dilated and is still occupied by some sticky
mucus?
• If so, then it may be concluded that the first stage of labour has not completed and the second
stage of labour has not yet begun, and the animal should be given more time.
• May be the case is one of uterine torsion. Does the vagina end abruptly at the pelvic brim and is
the mucosa drawn into tight, spirally arranged folds?
• In the event of the vagina being occupied by amnion only, the nature of the fetal parts
presented at the pelvic inlet must be ascertained.
• Can a fetal tail and anus be identified?
• If so, it is highly probable that the case is one of breech presentation.
• Is it the flexed neck which is being palpated?
• Can the mane be detected?
• A search on one or other side may reveal the ears and occiput, the case being one of lateral
deviation of the head.
• But what of the fore limbs?
• Can the flexed carpi be felt beneath the neck or is there complete retention of the fore limbs in
addition to the head abnormality?
• The protrusion of the allantochorion into the vagina and from the vulva - “red bag” - indicates
placental separation.
• In majority of cases, some part of the fetus occupies the vagina – the head, a limb or limbs.
• Recognition of the head is not difficult; the mouth and tongue, the orbits and the ears are
generally obvious.
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• In the case of a limb, the first requirement is to ascertain whether it is a fore or hind limb.
• If the plantar aspect of the digit is downward, it is highly probable that it is a fore limb;
converse is equally true.
• Proof is obtained by noting the direction of flexion of the limb joints.
• If the joint immediately above the fetlock flexes in the same direction as he latter, the limb is a
fore one, and the converse holds true.
• If two limbs are present, it must be established that they are both fore or hind, and if they are
from the same fetus.
• Not infrequently, it is necessary to repel the fetus in the uterus to ascertain the nature and
direction of displaced parts.
• The assessment of the viability of the presented fetus is necessary at an early stage in the
examination because this influence the options for treatment. This can be done by attempting
to elicit reflexes such as corneal/palpebral, suckling, anal if they are in posterior presentation,
and limb withdrawal.
• If the fetus is dead, then it may be important to be able to estimate the time interval since
death.
• When there is fetal emphysema and detachment of hair, then the fetus has been dead for at
least 24-48 h
• If after the fetus has been removed there is no emphysema and the cornea is cloudy and grey,
then the fetus has been dead for 6-12 h.
OBSTETRICAL INSTRUMENTS
• The best obstetrical instrument available should be used.

• Poor or makeshift instrument is not conducive to good surgical procedures.
• The instruments should be clean and sterile.
• During obstetrical operations surgical procedures of cleanliness should be followed in so far as
this is possible.
• If possible a table should be provided and covered with a sterile sheet upon which the
obstetrical instruments may be placed or kept in a bucket of water with an antiseptic solution
during the operation.
INSTRUMENTS FOR TRACTION
• Obstetrical chains.
• Long obstetrical hook.
• Snares.
• Forceps.
INTRUMENTS FOR FETOTOMY
• A heavy scalpel or Bard parker knife.
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• Fetatomes.
• Wire saws.
INSTRUMENTS FOR REPULSION AND ROTATION
• Kuhn’s crutch.
• Cammerer’s torsion fork.
OBSTETRICAL ANAESTHESIA
• To achieve safe, expeditious and humane delivery in some of the more severe types of dystocia
the induction of local anaesthesia in the dam is essential.
o Epidural anaesthesia
o Infiltration analgesia.
EPIDURAL ANAESTHESIA IN CATTLE
• Ideal for obstetric purposes.

• It is a form of multiple spinal nerve blocks in which, by means of a single injection of local
anesthetic solution into the epidural space, the coccygeal and posterior sacral nerves are
affected, thus producing anaesthesia of the anus, perineum, vulva and vagina.
• Painless birth is possible with an additional advantage by abolishing pelvic sensation, reflex
abdominal contraction (straining) is prevented.
• Intravaginal manipulations are facilitated, retropulsion is made easier, fetal fluid supplements
are retained and defaecation is suspended.
• Animal stands more quietly and if recumbent initially, often gets up when relieved of painful
pelvic sensations; makes the obstetrician’s task easier and cleaner.
• Useful whenever straining is troublesome, as in prolapse of the uterus, vagina, rectum or
bladder.
• Also indicated for episiotomy and for suturing the vulva or perineum.
• The method is free from risk provided it is made with due regard to asepsis.
• It does not affect uterine contractions; the main force of labour is not antagonized and the third
stage of labour, as well as uterine involution is not affected.
EPIDURAL SITE
• Between the last sacral vertebrae and first coccygeal vertebrae (Sacro-coccygeal space) or
between first and second coccygeal vertebrae (Inter coccygeal space).
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Diagramatic representation In live animal
LOCATION
• The site for insertion of the needle is determined by elevating and lowering the tail and feeling
where the vertebral joints are located by the depression and movement between the
vertebrae.
• The joint between the first and second coccygeal vertebrae is most moveable in the cow.
• In proceeding caudally the first vertebrae joint in which movement can usually be felt is
between the last sacral and first coccygeal vertebrae.
TECHNIQUE OF EPIDURAL ANAESTHESIA
• Properly shave and disinfect the site.

• Insert the needle between the last sacral and first coccygeal vertebrae or between the first and
second coccygeal vertebrae.
• Insert the needle, which is 18 gauge and 5 cm long, at a 10 degree angle caudally from the
perpendicular.
• The veterinarian should be careful to insert the needle directly on the midline.
• In the cow and buffalo the needle is inserted downwards to about 2-4 cm deep until it strikes
the floor of the epidural space, it is then slightly withdrawn.
• If the needle is inserted carefully one can then feel the point of the needle “pop” through the
thick connective tissue sheath covering the nerve.
• Confirmation that the needle is correctly placed is obtained by attaching to it the syringe and
making a trial injection; if there is no resistance to injection, the needle point is in the epidural
space.
• Alternatively, the hub of the needle can be filled with anaesthetic solution. As the needle is
advanced in to the epidural space, the anaesthetic solution will be sucked in as a result of the
slight negative pressure which exists there.
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• Within 2 minutes of the injection the tail becomes limp, but it takes a slightly longer time
interval (10-20 minutes) before the perineum is desensitized and the straining reflex is
completely abolished.
• A dose rate of 1 ml /100 kg of 2% lidocaine or lignocaine hydrochloride injected at a rate of 1 ml
per second will produce obstetric anaesthesia lasting about 30-150 minutes.
• Heifers and small cows and buffaloes may require a volume 5 ml and large cows and buffaloes
7-10 ml.
• The addition to the local anaesthetic of 2% of adrenaline prolongs the period of anaesthesia.
EPIDURAL ANAESTHESIA IN GOAT
• The injection can be made into the sacro-coccygeal or the first coccygeal interspace with a 3.5
cm, 20 gauge needle using 2% lignocaine hydrochloride with adrenaline at a dose rate of 1 ml
/50 kg body weight.
• A mixture of 1.75 ml of 2% lignocaine hydrochloride and 0.25 ml of 0.25% xylazine is injected
into the epidural space at a dose rate of 1ml/50kg, the duration of effect can be as long as 36 h,
and this can be extended by repeated doses.
INFILTRATION ANALGESIA
• May be used for all forms of laparotomy including the flank, ventrolateral and ventral midline
approach.
MATERIALS REQUIRED
• Scissors
• 15 gauge short needles
• 15 cm long 18 gauge hypodermic needles
• 10 ml hypodermic syringes
• 2% lignocaine hydrochloride solution
• Swabs and disinfectants.
TECHNIQUE OF LOCAL INFILTRATION
• Infiltration of the actual incision line with analgesic should be avoided whenever possible as this
hinders wound healing.
• Infiltration of 2% lignocaine solution about the incision line is more widely used.
• This method may be applied in the form of the so-called inverted L block for cesarean
operations in the flank region and can be modified to suit the ventrolateral or ventral midline
approach.
• The operating site is clipped and surgically prepared.
• The skin is punctured at points a and b with the short 15 G needle.
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• A long needle is then inserted through the punctured hole a and the line a-c infiltrated, first
subcutaneously and then intramuscularly with a total of 20-30 ml of analgesic solution.
• The needle is then redirected, preferably without withdrawing it completely, and the line a-d
infiltrated in a similar way.
• The needle is then withdrawn and inserted through the puncture hole b to infiltrate lines b-d
and b-c.
Fig.1: Technique of local Infiltration analgesia in cow
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MODULE-11: OBSTETRICAL OPERATIONS
ASSESSMENT OF FETAL VIABILITY
• The assessment of the viability of the presented fetus is necessary at an early stage in the
examination because this influence the options for treatment.
• Assessment can be done by attempting to elicit reflexes such as corneal/palpebral, suckling,
anal if they are in posterior presentation, and limb withdrawal.
• If the fetus is dead, then it may be important to be able to estimate the time interval since
death.
• When there is fetal emphysema and detachment of hair, then the fetus has been dead for at
least 24-48 h
• If after the fetus has been removed there is no emphysema and the cornea is cloudy and grey,
then the fetus has been dead for 6-12 h.
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MUTATION
• Mutation refers to procedures such as

o Repulsion
o Rotation
o Version, and
o Adjustment or extension of the extremities carried out on the fetus thereby restoring it
to a normal presentation, position and posture.
o In monotoccus animals, normal delivery will occur only if the fetus is presented in
anterior or posterior longitudinal presentation (P1), dorso-sacral position (P2) and with
the head, neck and limbs extended posture (P3).
o In polytoccus animals, due to small and flexible limbs, normal delivery can occur even
though the limbs are retained alongside of or beneath the body.
REPULSION (Retropulsion)
• Repulsion refers to the act of pushing the fetus from the vaginal passage into the uterine cavity,
in order to create space and thereby rectify the defects of presentation, position and posture.
POINTS OF REPULSION
• In anterior presentation: Arm or instrument is placed between the shoulder and chest or across
the chest beneath the neck of the fetus.
• In posterior presentation: Arm or instrument is placed in the perineal region over the ischial
arch.
PROCEDURE
• Epidural anesthesia is indicated to prevent abdominal straining.

• Since it has no effect on myometrial contractions, spasmolytics such as clenbuterol may be
used.
• Essential to have the animal standing or in recumbent animals with its rear quarter elevated.
Repulsion is difficult or impossible in recumbent animals resting on its sternum.
• Repulsion is effected by pressure with the operator’s arm or with the use of crutch repeller. If
an obstetrical instrument is used, the operator should guard the instrument from slipping and
causing injury to the birth canal. If it slips, it should be immediately withdrawn.
• Repelling force should be exerted in the intervals between bouts of straining.
• In protracted cases of dystocia, excessive repulsion may be dangerous.
• In neglected dystocia or fetal emphysema cases, repulsive forces should be carefully controlled.
ROTATION
• Rotation refers to the act of turning the fetus on its long axis to restore the fetus in to a dorso-
sacral position. More often required in mares than in cows.
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PROCEDURE
• Easily effected on the responsive live fetus by applying digital pressure on the eyeballs,
protected by the lids; evokes a convulsive reaction and slight rotational force then completes
the manoeuvre.
• If digital pressure fails to correct the defect or in case of a dead fetus, intrauterine liquid
replacement is essential.
• After thorough lubrication, rotational force can be exerted on the crossed extended limbs
either by hand or instruments such as cammerer’s torsion fork or Kuhn’s crutch.
VERSION
Version refers to the act of rotation of the fetus on its transverse axis into an anterior or posterior
presentation.
• Version is usually limited to 90 °

• Transverse presentation is corrected to either anterior or posterior longitudinal presentation by
repulsion of either the cranial or caudal portion of the fetus, and exerting traction to the other
end.
• Converting transverse presentation into posterior longitudinal presentation is preferred, as this
prevents the complications of corrections of abnormal presentation or posture.
EXTENSION AND ADJUSTMENT OF EXTREMITIES
• Extension and adjustment of extremities refers to the process of correction of abnormal

postures usually due to flexion of one or more of the extremities leading to dystocia.
• To effect a prompt, easy correction of a flexed extremity, it is essential to follow three basic
mechanical principles
o Repulsion of the proximal portion of the extremity such as the shoulder or chest in
anterior presentation and on the buttocks, stifle, or tarsus.
o Lateral rotation of the middle portion of the extremity, carpus, tarsus, or neck, and
o Traction on the distal portion of the extremity such as the pastern, lower jaw or, until
these distal structures can be reached, the structures between the body and the distal
portions of the extremity.
DEFINITION
• Forced extraction refers to the delivery of the fetus which is in normal presentation, position
and posture through the birth canal of the dam with the aid of external force or traction.
INDICATIONS
• Uterine inertia
• Following epidural anesthesia and mutation operation.
• Fetus is relatively too large to be expelled through the birth canal without assistance.
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• In primipara with a small birth canal.
• In cases where birth canal compressed by tumors or fat or other pathological conditions.
• In posterior presentation of the fetus to hasten delivery and prevent the death of the fetus.
• To save time or in order to avoid fetotomy or cesarean section.
• In case of emphysematous fetuses after thorough lubrication of the birth canal and fetus.
• As an aid in fetotomy operations.
RESTRAINT
• Epidural anesthesia is recommended, but not always necessary.
MATERIALS AND ASSISTANCE
• Nylon snares
• Obstetrical chains
• Long blunt obstetrical hook
• Calf puller
• Obstetrical lubricants
• Soft and flexible rubber tube
• Inj. 2% Lignocaine, and
• One to three assistants.
POINTS OF TRACTION
In anterior presentation
• Applied to pasterns or above the knee or elbow.

• Around the lower jaw. Around the neck in dead fetus.
• Loop around the poll, under the ears and through the mouth.
• Inner canthus of the orbit.
In posterior presentation
• Applied to pasterns or above the hocks.

• In dead fetus, on top of the fetal croup and turned ventrally to engage the posterior border of
the ischium or sacrosciatic ligament.
TRACTION FORCE
• Vary greatly with the species of animal and the condition causing the dystocia.
• Even though simple and quick it is potentially dangerous to the fetus and to the dam.
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• In old or young primiparous mares, to dilate the birth canal and vulva gradually, traction force is
applied with obstetrical chains by one or two men.
• Care should be exercised to avoid lacerating the vulva or the perineal region. In normal
circumstances the force of 2 to 3 or more men apparently causes no harm and may be
indicated. With the help of fetal extractor one can exert great force in the proper manner, if
necessary.
• Traction should be synchronous and as far as possible, with the dams explusive efforts.
• Apply traction in a direction initially parallel to the dam’s posterior spine and then, as soon as
the fetal head and shoulders (in anterior presentation) and fetal pelvis (in posterior
presentation) has been delivered, in an increasingly ventral manner.
CONTRAINDICATIONS
• Exercise great care in cases of abnormal presentation, position or postures.

• Excessively large or defective fetus.
• Birth canal is obviously small.
• In secondary uterine inertia
• Cervical stenosis or failure to dilate.
• Obturator nerve paralysis.
• Severely lacerated birth canal.
• In the multiparous animals (sow, dog, and cat) should not be used when one is short of time or
patience as it may require a number of hours of intermittent work to complete the delivery of
all the fetuses.
FETOTOMY
• Fetotomy refers to those operations performed on the fetus for the purpose of reducing its size
by either its division or removal of certain of its parts. In most cases these operations are
performed within the uterus of the dam.
INTRODUCTION
• In veterinary obstetrical practice, fetotomy has its own significance and relevance and should
not be considered as a substitute for cesarean section.
• Both techniques are important in veterinary practice, the choice of method in individual cases
being influenced by the circumstances.
• In a case of dystocia, where the fetus is dead, the decision should be made entirely based on
the life of the dam.
TYPES OF FETOTOMY
• Fetotomy can be performed in 2 ways

o Subcutaneous or intra fetal method
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o Percutaneous or extra fetal method.
• The methods can be combined or modified according to need.
ADVANTAGES OF FETOTOMY
• Rapid reduction in the size of the fetus facilitates safe delivery per vaginum.
• Subjecting the dam to major abdominal surgery is avoided.
• The dam is spared inhumane treatment and possible trauma associated with application of
excessive force to extractive devices (fetal extractor).
• Post fetotomy care is generally minimal.
• Recovery time is shorter.
• The general condition of the dam tends to remain more stable after c - section.
• The monetary return is equal to that from cesarean section.
DISADVANTAGES OF FETOTOMY
• More time consuming than cesarean.

• Exhausting to the obstetrician.
• Operator may have the risk of injury from the instrument or from sharp projections of fetal
bone.
• Risk of causing injury to the dam.
• Most of the unsatisfactory results of fetotomy are attributable to the operator's lack of
experience, to poorly designed instruments, to improper fetotomy technique, and to the use of
fetotomy only as a last resort.
INSTRUMENTS AND ASSISTANCE
Fetotomy instruments
• A large number of instruments have been designed for use in fetotomy, some are practical,
others quite inadequate and unsafe.
• Recommended instruments are
o Fetatome
o Wire saw handles
o Fetatome threader
o Krey hook
o Obstetrical chains
o Saw wire introducer
o Williams long cutting hook,
o Long cutting chisels (Williams-slight concave flat bed, Guards-V-shaped head and Ames-
resembling a nasal septum chisel) and
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o Fetotomy knife.
Assistance
• Although fetotomy can be performed with the help of only one assistant, two assistants are
desirable.
Instruction in the use of instruments
• Assistants must be thoroughly instructed in the use of the instrument and in the sawing
technique.
• A little time spent in instruction before the operation may save the obstetrician much time
during the actual fetotomy.
Lubrication
• Proper lubrication is often the key to success.
The dam and fetotomy
• If at all possible, the cow should be in the standing position throughout the operation.
COMPLETE FETOTOMY IN ANTERIOR PRESENTATION
Perfection in fetotomy depends upon four factors
• Technical knowledge
• Adequate training and experience
• Correctly designed instruments
• Proper lubrication.
Complete fetotomy in anterior presentation involves the following
• Amputation of the head

• Percutaneous amputation of the forelimb
• Transverse division of the fetal trunk
• Longitudinal division of hind quarters
AMPUTATION OF THE HEAD
• The fetatome is threaded and held exterior to the vulva.

• A loosely formed loop of saw wire is carried into the genital opening, positioned over the fetal
head immediately behind the ears and around the neck.
• While very slight tension is maintained on the saw wire, the fetatome is introduced into the
genital tract and positioned so that the head of the fetatome is placed either between the
mandibles or posterior to ramus of the mandible.
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PERCUTANEOUS AMPUTATION OF THE FORE LIMB
• The obstetrical (OB) chain is fixed to the pastern or metacarpus of the limb to be amputated.
• The fully threaded fetatome is held exterior to the vulva.
• The free end of the OB chain is passed from above, through the loop of the saw wire.
• The loop of saw wire is fixed in the interdigital cleft.
• The fetatome (with the head protected by the obstetrician’s hand) is introduced into the genital
canal and guided along the lateral surface of the fetal limb until it rests mid way on the scapula.
• The attached chain is anchored to the fixation plate.
• The loop of the saw wire is loosened from the interdigital cleft and guided anteriorly so that its
ventral portion rests between the fetal elbow joint and chest, the dorsal portion resting medial
to the humero-scapular joint.
• The OB chain is disengaged and the fetatome is introduced deeper in to the uterus until the
head of the instrument is dorso caudal to the cartilaginous fetal scapula.
• Simultaneously, strong tension is applied to the limb, producing maximum extension of all
joints.
• The chain is then anchored under tension to the fixation plate and the limb is amputated.
Forelimb amputation
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TRANSVERSE DIVISION OF THE FETAL TRUNK
Anterior portion of the chest
• The krey hook may be affixed before the fetatome and wire are positioned.
• With the fetatome fully threaded and the loop of saw wire held exteriorly the instrument is
introduced and passed anteriorly along the dorso lateral fetal surface until the head of the
fetatome rests in the area of the cartilaginous attachment of the scapula.
• While the fetatome is held in position, the wire loop is guided around the cervical stump and
worked caudally around the fetus until it rests more or less at right angles to the head of the
fetatome.
• The ventral portion of the loop is positioned midway on the sternum.
• If it has not been affixed previously the krey hook is affixed to the exposed thoracic vertebrae.
• At this time, the OB chain is detached and tension is applied. The fetatome is positioned just
caudal to the cartilaginous attachment of the scapula.
• The OB chain is then fixed to the fixation plate of the fetatome.
• The head of the fetatome is covered by the hand, with strong medial pressure being applied.
• The fetal chest is divided.
Posterior portion of the chest
• The procedure for positioning the fetatome and saw wire loop is exactly the same as described
for the anterior portion of the chest.
• The head of the fetatome should be positioned so that it rests on the dorso-lateral fetal surface
just posterior to the last rib, the wire surrounding the fetal trunk at right angles, to the head of
the fetatome.
• If the severed chest is of such diameter that it cannot be extracted without difficulty, the hand
is introduced in to the thoracic lumen to perforate the diaphragm in a dorsal location.
• The fetatome is partially unthreaded (wire remains threaded through one tube only) and the
free end of the wire is attached to an introducer, with attached saw wire is passed in to the
thoracic lumen through the rent in the diaphragm and is directed dorsally.
• The introducer is retrieved over the dorsal thoracic wall brought to the exterior and the
fetatome fully threaded.
• The fetatome is passed into the genital canal until it rests against and is almost lateral to the cut
surface of the thoracic vertebrae.
• The ribs are divided at their vertebral attachment.
• The severed rib wall (with attached sternum) is repelled and the chest (now greatly reduced in
diameter) is extracted.
LONGITUDINAL DIVISION OF THE HIND QUARTERS
• The krey hook is affixed to the bony lumbar vertebrae.

• The fetatome is partially threaded (one tube only).
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• The free end of the wire at the head of the instrument is attached to an introducer, passed
dorsally over the fetus and drawn out ventrally between the hind limbs.
• In its final position, the wire passes between the tail and the tuber ischium.
• The fetatome is threaded and positioned so that the head rests just cranial to the tuber coxa.
• This positioning of the fetatome is preferred where the head of the fetatome is positioned
against the cut surface of the lumbar vertebrae.
COMPLETE FETOTOMY IN POSTERIOR PRESENTATION
• Complete fetotomy in posterior presentation involves the following

o Percutaneous amputation of posterior limb
o Transverse division of fetal trunk (Lumbar area)
o Transverse division of fetal trunk (Scapular area)
o Diagonal - Longitudinal division of the fore part
o Percutaneous amputation of both fore limbs
PERCUTANEOUS AMPUTATION OF POSTERIOR LIMB
• The OB chain snare is affixed to pastern or lower metatarsus of the limb to be amputated.
• While the fully threaded fetatome is held exterior to the vulva, the free end of the OB chain is
passed from above, through the wire saw loop.
• The loop of wire is affixed in the interdigital cleft.
• The fetatome is introduced and passed cranially on the lateral surface of the limb until the head
of the instrument rests in the region of the trochanter major.
• The OB chain is anchored to the fetatome.
• The wire loop is then disengaged, guided around the limb and worked cranially until the ventral
portion is medial to the stifle joint and the dorsal portion is fixed between the tuber ischium
and the tail head.
• The chain is disengaged and traction is applied, forcing the limb in to complete extension.
• The fetatome is introduced deeper until the head of the instrument is positioned dorso-cranial
to the trochanter major.
TRANSVERSE DIVISION OF FETAL TRUNK (Lumbar Area)
Following amputation of one rear limb
• The fetatome and wire are positioned, using the techniques described for amputation of the
rear limb.
• The head of the fetatome is positioned dorso-laterally in the lumbar region, preferably just
caudal to the last fetal rib.
• The wire is positioned so that it surrounds the fetal trunk at right angles to the fetatome.
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Following amputation of both rear limbs
• The krey hook may be affixed before or after the fetatome and saw wire has been positioned.
• Using procedures described for anterior presentation, the fetatome is positioned so that its
head is just caudal to the last fetal rib.
• The wire loop is guided cranially around the trunk until it is positioned at right angles to the
head of the fetatome.
• The chain of the krey hook is anchored under tension to the fixation plate of the fetatome.
TRANSVERSE DIVISION OF FETAL TRUNK (Scapular area)
• The fully threaded fetatome is positioned just caudal to the scapular attachment.
• The wire is guided around the scapular area and the ventral portion is mid way on the sternum.
• When necessary, the diameter of the chest is reduced by severing the ribs as close as possible
to their attachment to the thoracic vertebrae.
• The diaphragm is perforated; the saw wire is passed through the rent and retrieved dorsally.
• The head of the fully threaded fetatome is held against the ribs, slightly lateral to the body of
the vertebrae.
DIAGONAL - LONGITUDINAL DIVISION OF THE FORE PART
• The krey hook is affixed slightly lateral to the body of the exposed vertebrae.
• Only one tube of the fetatome is threaded.
• With the aid of the introducer, the free end of the wire is passed dorsally over the fetus and
directed ventrally between the neck and one forelimb.
• The introducer with attached wire is then retrieved ventrally and withdrawn diagonally so that
it passes medial to the elbow joint of the opposite limb.
• After the fetal forepart has been divided, the largest portion is extracted with the aid of the
attached krey hook.
• The remaining portion is then easy to remove.
PERCUTANEOUS AMPUTATION OF BOTH FORE LIMBS
• The scapular attachments of each limb are separated from the chest by blunt dissection. The
separation should be sufficient to provide adequate space for placing the head of the fetatome.
• The fetatome is threaded through one tube only and an introducer is attached to the free end
of the wire.
• The introducer is passed dorsally between the neck and the fore limb and retrieved ventrally,
the wire passing between the elbow joint and chest.
• After retrieval of the introducer, the fetatome is fully threaded.
• The head of the fetatome is positioned within the space created between the scapula and
thorax and the limb is amputated.
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• The same procedure is repeated for amputation of the opposite fore limb.
MODIFIED PERCUTANEOUS FETOTMY
Fig.1 Wire saw attached to cotton rope Fig.2 Wire saw positioned around the fetus
Procedure for bisection of pelvis by modified percutaneous fetotomy
• Both free ends of the wire saw (2 feet) were attached by applying a knot with a separate cotton
rope, each measuring 2 feet length (Fig.1).
• One free end of the snare was taken inside by hand and the wire saw was carried by the snare
over the top of fetal pelvis and then down behind the ishcial arch.
• By passing the hand under the fetus and fetal pelvis, the free end of the snare attached to wire
saw was drawn out through vulva and leaving the wire saw between the hind leg of the fetus.
• After making a loop for holding, the free ends of snare (lower and upper) were directed in
opposite manner while performing fetotomy operation (Fig.2) so that wire saw gets fully
opposed or placed over the dorsal and ventral aspect of the fetus, preventing and/or reducing
the risk of damage to the dam's endometrium.
Reference
• S.Balasubramanian, S.Jeyakumar, K.Krishnakumar and S.R.Pattabiraman (2003). Modified

percutaneous fetotomy technique in a cow - A case report. Indian Vet. J. July, 80: 685-686.
GUIDELINES FOR FETOTOMY IN MALPOSTURES AND MALPRESENTATIONS
Fetal malposture/ Part(s) to be amputated

malpresentation
Carpal flexion posture Amputation of head or one or both the forelimbs

below the knee
Shoulder flexion posture Amputation of head or one or both the forelimbs
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Lateral deviation of head Amputation of one forelimb opposite to the side of
head deviation or head and neck
Hock flexion posture Amputation of hindlimbs(s) below the hock or

amputation of the hindlimb
Hip flexion posture Amputation of one or both the hindlimbs
Hip-lock condition Lumbar division and bisection of pelvis
Dog sitting posture Amputation of either head and forelimbs or lumbar

division
Ventral transverse Amputation of approachable part or bisection of

presentation fetus at lumbar region
Dorsal transverse Bisect in middle of fetal trunk.

presentation
Source: Brar et al (2004)
GUIDELINES FOR COMPLETE FETOTOMY
Cut Fetal part to be amputated Position of fetatome Position of wire saw loop
head
In Anterior presentation
First Head Posterior border of Caudal to ears around the

mandible neck
Second Forelimb Dorso-caudal to In between point of

cartilaginous part of elbow and chest
scapula
Third Other limb Dorso-caudal to In between point of

cartilaginous part of elbow and chest
scapula
Fourth Transverse division of fetal trunk at Point of scapular Middle of sternum

anterior portion of chest attachment
Fifth Transverse division of fetal trunk at Posterior to last fetal At right angle to fetatome
posterior portion of chest (at rib head around abdomen
lumbar region)
Sixth Longitudinal division of hind Just cranial to tuber In between tail and tuber
quarters (Pelvic bisection) caxarum ischium
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In Posterior presentation
First Hind limb Near trochanter major Between tuber ischium

and tail head
Second Other hind limb Near trochanter major Between tuber ischium
and tail head
Third Transverse division of fetal trunk Just caudal to last fetal At right angle to fetatome
(lumbar region) rib head around fetal
abdomen
Fourth Transverse division of fetal trunk Posterior to At right angle to fetotome

(scapular region) cartilaginous part of head around fetal chest
scapula
Fifth Diagonal longitudinal division of Posterior to scapular Neck and forelimb on one
the fore part attachment side and medial to
opposite limb
Sixth Amputation of both limbs Space between scapula Between elbow joint and
and thorax chest
Source: Bierschwal and deBois (1972).
DEFINITION
• Caesarean operation (C-section) refers to the surgical procedure whereby the fetus is removed
through an abdominal and uterine incision.
INTRODUCTION
• In cattle, C- section is a routine obstetrical procedure.

• Maternal and fetal survival rates are high and are less exhausting, speedier and safer than
fetotomy.
• Optimum success depends on prompt decision.
INDICATIONS
• Feto-maternal disproportion
• Incomplete dilatation of the cervix
• Irreducible uterine torsion
• Fetal monsters
• Faulty fetal disposition (presentation, position or posture)
• Fetal emphysema.
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RESTRAINT
Depending on the surgeon’s preference, condition of the animal and available facilities, it can be
performed with the dam
• In standing
• In sternal
• In lateral, or
• In dorsal recumbency.
Surgery in standing animal
• Animal should be restrained.

• Avoid sedation as it can cause recumbency during surgery and may be detrimental to fetal
survival.
• If necessary, administer inj. xylazine 0.05-0.1 mg/kg intramuscular or a reduced dose
intravenously.
Surgery in recumbent animal
• Cast the animal after administration of Inj. xylazine 0.2 mg/kg intramuscular or using a rope.
• Place the animal in right lateral or semi-sternal recumbency with the body slightly tilted to the
right.
• Some prefer the left hind leg to be extended caudally and fixed by a rope.
Surgery in a recumbent buffalo
• For successful surgery, one assistant to restrain the cow and one to deliver the calf are
required.
• Prior to surgery discuss with the team about the modality.
• Carefully choose a clean location with suitable floor surface, lighting and facilities for restraint.
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ANAESTHESIA
• Choice varies between surgeons and the selected surgical site.
For flank incisions
Paravertebral anaesthesia
• Paravertebral anaesthesia of the nerves associated with the transverse processes of T13, L1, L2
and L3 is indicated. Injection of 2-3% lignocaine with adrenaline, 12-14 ml to block the ventral
nerve branches, 6—8 ml for the dorsal branches.
o Signs of successful anaesthesia - warm, hyperaemic and flaccid flank with no response
to pain when tested with an 18 gauge x 1.5 inch needle.
o Advantages
Entire flank musculature is desensitized and flaccid, which facilitates exploration
of the abdomen during surgery and closure of the wound.
The flank incision can also be extended readily if necessary during surgery.
o Disadvantages
Technique is more difficult to perform than other methods.
Animal may become unsteady after surgery due to loss of lumbar muscle tone
and paresis of the ipsilateral hindlimb.
Vasodilatation in the muscle layers causes a greater degree of haemorrhage that
requires careful haemostasis.
A local anaesthetic line block or inverted-L block
• Administer inj. 2% lignocaine with adrenaline at several sites using an 18 gauge x 1.5 inch
needle.
• Number of sites is dependent on the length of the proposed incision.
• At each point, 5 ml of local anaesthetic is injected subcutaneously in each direction of the
incision line, and a further 10 ml into the musculature.
• Technique is quick and reliable, and requires minimal training.
• However, the parietal peritoneum may not be effectively anaesthetized; causing reaction by
the animals when it is incised.
Epidural anaesthesia
• Using inj. lignocaine can provide adequate anaesthesia of the flank, although such anaesthesia
also tends to cause recumbency, which may be prolonged in cattle.
PRE-OPERATIVE PREPARATION
• Pre-operative antibiotics are strongly recommended. Commonly, inj. procaine penicillin and
dihydrostreptomycin, 10 mg/kg each of an antibiotic mixture is administered intramuscularly.
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• Tocolytic agents, β-adrenergic agonist, clenbuterol hydrochloride (30 g) administered by
intramuscular or slow intravenous injection facilitates exteriorization of the uterus during
surgery and counters the effect of xylazine on the uterus.
• A caudal epidural injection may be administered to reduce straining.
Surgical field
• A wide surgical field should be prepared.

• Initially, dirt and dust should be brushed from the flank
and back of the animal before the operative field is
clipped or shaved.
• In the case of a flank incision, the entire flank should be
clipped from the transverse processes dorsally to the
milk vein ventrally and from the caudal ribs to the hind
leg, level with the tuber coxae.
• The skin should be prepared using a surgical scrub
(7.5% povidone iodine or 4% chlorhexidene gluconate
solution) followed by surgical spirit.
• Sterile drapes should be applied.
• Operators should wear protective surgical scrub suits, even in the field situation.
• Consideration should be given to wearing sterile surgical gowns and surgical gloves.
• Prior to surgery, carefully test the adequacy of anesthesia, as the muscle and peritoneum may
remain sensitive despite skin desensitization.
• In standing animal, left flank incision is most common and appropriate, since the rumen
prevents exposure of the intestines, easy to correct uterine torsion and wound dehiscence is
more manageable.
OPTIONS FOR INCISION
• A vertical skin incision is made in the middle of the left flank starting 10 cm ventral to the
transverse processes and extending approximately 30-40 cm long, or
• A slightly oblique incision from caudo-dorsal to cranio-ventral, about 30° from vertical can be
used, starting 10 cm from the tuber coxae, or
• Ventrolateral incision - an oblique incision, starting from the flank fold dorsal to the attachment
of the udder, is continued cranially, parallel to the ventral border of the ribs. The advantage of
this approach is that it gives good exposure of the uterus, even when it is friable, and it
minimizes the risk of uterine contents contaminating the abdominal cavity.
• A midline or paramedian incision is not commonly used in the field because general anaesthesia
or heavy sedation is required and respiratory function of the dam is compromised.
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SURGICAL APPROACH
Left lower abdominal approach
• An oblique skin incision (Fig.1) is made followed by incision of the muscle layers (cutaneous,
external abdominal oblique, internal abdominal oblique and the transverse abdominal muscles)
using a scalpel (Fig.2).
• Usually minimal haemorrhage occurs from the muscle layers. If large vessels get involved, apply
haemostats and if required it should be ligated. While incising the peritoneum care should be
excercised not to puncture the rumen which is beneath the peritoneum.
• Gently pass the hand into the abdominal cavity and indentify the presentation of the fetus
inside the uterus. Grasp and apply traction to a distal extremity of the fetus, usually the hind leg
to exteriorize the uterus.
Fig.1: Skin incision Fig.2: Muscle incision Fig.3: Uterine incision
• The incision on the uterus (Fig.3) is made over the calf’s leg from toe to hock along the greater
curvature and parallel to the longitudinal muscle layers of the myometrium.
• Care should be taken to avoid incising the fetus as it is presented just beneath the uterine wall,
especially in case of reduced fetal fluids. At the same time, avoid incising cotyledons, which can
lead to profuse haemorrhage. This can be largely overcome by palpating the uterine wall before
incsion is made. In certain instances, where the uterus cannot be completely exteriorized often
because the uterus has become friable and liable to damage by further handling, incision can be
made using a Roberts’ embryotomy knife within the abdominal cavity.
• Manually rupture the allantochorion and amnion, grasp the fetal fetlocks (Fig.4), exteriorize
and pass to an assistant. Initially, in the case of forelegs, both the legs and the head should be
exteriorised. It is important to hold the uterine ends while the calf is extracted by assistants.
Immediately following delivery of a live calf it should be attended to by an assistant. The
obstetrician should examine the uterus, initially for the presence of another fetus, any
lacerations or rupture of the uterine wall.
• Subsequently, remove the fetal membranes (Fig.5) if they are easily separable. Otherwise,
leave in situ and trim the protruding membranes so that it is not incorporated in the suture line
of the uterine incision.
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Fig.4: Grasping of fetal fetlocks Fig.5: Removal of fetal membranes
UTERINE SUTURE PATTERNS
• A variety of continuous inversion suture patterns have been used to create a water-tight seal by
apposing serosal surfaces and to prevent minimum of subsequent adhesions and uterine
scarring.
• Utrecht method, a modified Cushing pattern, is started using a buried knot and then a
continuous interlocking, inverting pattern.
o Advantage
Minimal adhesion formation following surgery.
A single layer is usually sufficient, and this pattern is particularly efficient if the
uterine wall is flaccid during repair of the wound.
• In Lembert suture pattern, the needle passes at right angles to the incision.
• In Cushing suture pattern, needle passes parallel to the incision.
• Exercise care not to include the fetal membranes during uterine repair.
• A non-absorbable suture should be used for repair of all muscle layers of the incision because
postoperative wound dehiscence has severe implications, including herniation.
CLOSURE OF UTERINE AND ABDOMINAL INCISIONS
• Exteriorize both uterine horns before the genital tract begins to involute and inspect the edges
of the uterine incision for haemorrhage, particularly from the cotyledonary vessels.
• The uterus is supported by an assistant and the incision is sutured using 6-8 Metric catgut or
polyglactin.
• Suturing should start at the cervical end of the uterine incision because if the uterus starts to
involute the cervix retracts into the abdomen before the ovarian extremity.
• Uterine surface should be cleaned with sterile gauze to remove blood clots and other debris
and returned to its correct location within the abdomen, ensuring that there is no torsion of the
genital tract.
• To hasten uterine involution, administer inj. Oxytocin (20-40 i.u.) intramuscularly.
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• The administration of water-soluble antibiotic, such as crystalline penicillin, within the
abdominal cavity is recommended.
Uterine suturing Closure of uterine incision
• Close the peritoneal cavity quickly to reduce the chance of bacterial contamination.
• The abdominal flank incision should be repaired in three layers:
o peritoneum and transverse abdominal muscle,
o internal oblique muscle, and
o external oblique muscle.
• A continuous suture pattern is used, starting at the ventral commissure of the incision for the
first layer.
• Care is taken to appose the peritoneum and transverse abdominal muscle to avoid leakage of
air from the abdominal cavity into the muscle layers following surgery.
Closure of abdominal incision
• Sutures should be placed approximately 1 cm apart using 6-8 Metric catgut.

• To reduce potential dead space between the muscle layers of the flank, deeper bites with the
suture can be made periodically into the deeper muscle layers.
• Antibiotics may be infused between each muscle layer; approximately 250 mg/ml each of
procaine penicillin G and dihydrostreptomycin as a mixture is commonly used.
• The skin incision is repaired using 5-7 metric sheathed multifilament nylon in a Ford interlocking
pattern.
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• A single simple suture may be included at the dorsal and ventral aspects of the wound to allow
drainage and or flushing in the case of wound infection.
• Alternative suture patterns include a horizontal mattress or cruciate suture.
Skin suture
PROGNOSIS DEPENDS ON SEVERAL FACTORS
• Skill and speed of the surgeon

• Duration of dystocia
• Availability of skilled assistance
• Surgical environment
• Concurrent disease
• Presence of a live calf.
POST-OPERATIVE CARE OF CALF
• Immediately following surgery, clean the calf free of mucus and dress the navel with antiseptic.
• Feed the calf with 2-3 litres of colostrum using an oesophageal feeding tube, if necessary.
• Allow the dam promptly to the calf to form a maternal bond.
POST-OPERATIVE CARE OF DAM
• Clean the surgical wound.

• Examine the teats and udder.
• Stimulate uterine involution by administration of Inj. Oxytocin (20-40 i.u.) intramuscularly.
• In dairy cows, to prevent hypocalcaemia and facilitate uterine involution, administer Inj.
calcium borogluconate intravenously.
• In severe dystocia, uterine torsion or uterine infection prior to surgery, a non-steroidal anti-
inflammatory agent should be considered.
• In case of surgical shock, intravenous fluid therapy, preferably 2-3 litres of hypertonic (7.2 %)
sodium chloride.
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• Administer antibiotic for an appropriate period, usually 3-5 days, or until the fetal membranes
are expelled.
• Re-examine the dam 24-48 h after surgery and record the
o rectal temperature,
o general condition,
o appetite, and
o fecal consistency.
• Usually following surgery, the feces are often dry and the cow mildly constipated.
• Pyrexia, depression, inappetance and diarrhoea may indicate peritonitis.
• If in case of retained fetal membranes, give appropriate treatment.
• Remove skin sutures 3 weeks after surgery.
• Perform genital examination to rule out endometritis.
• Delay AI until >60 days postpartum.
SUCCESS RATES AND COMPLICATIONS OF C-SECTION
• Fetal survival following C-section partially depends on the indication for surgery.
• Maternal survival rates following C-section are high.
• The usual complications that follow C-section are
o Subcutaneous emphysema
o Metritis and retained fetal membranes
o Peritonitis
o Wound dehiscence
o Nerve paralysis
o Fractures, and
o Postpartum haemorrhage.
POST-OPERATIVE FERTILITY
• Post-operative productivity implies not only the maintenance of bodily condition and an
acceptable level of lactation, but also the ability to conceive again and sustain a developing
fetus to term.
• Reduced fertility may occur as a consequence of increased incidence of retained fetal
membranes and endometritis, uterine adhesions that hinder involution and adhesions that
affect the ovary or uterine tube, and reduced endometrial tissue competence.
• Increased frequency of abortions during subsequent pregnancies, possibly as a result of scar
tissue formation within the uterine wall limiting expansion of the uterus and or nutrition of the
fetus.
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MODULE-12: DIAGNOSIS AND TREATMENT OF DYSTOCIA
TERMINOLOGY
Presentation [P1]
• The relation of the spinal axis of the fetus to that of the dam
• The portion of the fetus that is approaching of entering the pelvic cavity.
• Presentations are either longitudinal or transverse
o Anterior/ Posterior longitudinal
o Dorsal/ Ventral transverse
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Position [P2]
• The position includes the dorsum of the fetus in longitudinal presentation, or the head in
transverse presentation, to the quadrants of the maternal pelvis.
• The quadrants are the sacrum, the right ilium, the left ilium and the pubis.
Posture [P3]
• The posture signifies the relation of the extremities of the fetus or head, neck and limbs to the
body of the fetus
• The normal presentation in uniparous animals is the anterior longitudinal presentation, dorso-
sacral position with the head resting on the metacarpal bones and knees of the extended fore
legs.
• Birth can also take place without assistance, if the fetus is in the posterior longitudinal
presentation, dorso- sacral position.
DYSTOCIA IN ANTERIOR PRESENTATION
• Deviations of head and neck are common types of abnormal posture in anterior presentation
causing dystocia in all species.
• In swine, because the neck is so short this type of dystocia is very rare.
LATERAL DEVIATION OF THE HEAD
• The head may be displaced to either side and this constitutes one of the commonest types of
dystocia.
Diagnosis
• In cow, this condition is easily made by finding the two fore limbs in the birth canal but not the
head. By passing the hand and arm along side the fetal body as possible and then carrying it
around the body, the head and neck are found and the direction of the deviation determined.
• In mare, this may be more difficult because the head is usually out of reach of the hand. By
locating the withers, mane and trachea of fetus these may be followed to the left or right.
Correction
• If the bovine fetus is alive, the deviation may be corrected with least amount of difficult. This is
performed under epidural anesthesia with the animal standing. If the animal is down, it should
be placed in lateral recumbency with rear parts higher, the with the fetal head in the upper
flank of the dam above the fetal body. In mare, protracted cases of head displacement with
greater loss of fetal fluid, fluid substitute renders the calf mare buoyant.
• The fetus is repelled by pressing forwards at the base of its neck. The hand is then quickly
transferred to the muzzle of the calf, which is firmly grasped and brought in line with the birth
canal. In a more in accessible case the muzzle may be reached after preliminary traction on the
commissure of the mouth. The incisor teeth should be guarded to prevent laceration of the
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uterus. A head snare and fore limb snares are now affixed and traction synchronously applied
with the cows expulsive effects, leads to delivery.
• If mutation fails because the fetus is emphysematous or because the uterine wall is contracted
tightly around the fetus, fetotomy and amputation of the head and neck is indicated.
WRY - NECK
• Is seen in equine but rarely in bovine foetuses.

• It usually occurs in transverse bicornual pregnancy in the mare in which movement of the fetal
head and neck is restricted during most of the gestation period.
• The cervical vertebrae are curved and the articulations and atrophied muscles produce a
sharply bent "muscle contracture" condition of the neck that cannot be strengthened.
• Correction is impossible and decapitation is required.
DOWNWARD DEVIATION OF THE HEAD
• Downward deviation of the head between the fore limbs is occasionally seen in all species
except swine.
• In mild cases, only the nose of the fetus is caught on the brim of the pelvis with the fore head
entering the pelvic inlet, vertex presentation.
• In severe flexing of head and neck, the ears and the poll of the head are presented, poll
posture.
• In more severe cases, the neck extends between the fore limbs and the head is against the fetal
sternum or abdomen, nape presentation.
• In this type of nape presentation, the fore limbs do not come together and that in the mare the
mane of the fetus may be felt between the legs.
Correction
• Repelling the fetus and grasping the muzzle of the foetus and raising it into the pelvic cavity
usually correct vertex posture and poll presentation.
• Neglected cases may require epidural anesthesia and fetal fluid supplement.
• During the correction of nape after the fetus is repelled, a forelimb may be flexed along side the
body. This gives room for the head to be rotated laterally and then brought upward and
forward over the pelvic brim.
• The leg is then extended and the fetus removed by traction. In very difficult case it may be
advantageous to replace both forelimbs into the uterus.
• Casting the cow and placing her in dorsal recumbency greatly facilitate extension of fetal head.
• When manipulative delivery fails fetotomy may be done.
DEVIATIONS OF THE FORELIMBS
• These are relatively common cause of dystocia in uniparous animals.

• They are rarely seen in multiparous animals because their forelimbs are short and flexible.
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Carpal flexion
• One or both limbs may be affected. In unilateral cases, the flexed carpus is engaged at the
pelvic inlet and the other foot may be visible at the vulva.
Correction
• Requires retropulsion of the fetal head and the retained foot is then grasped and as the carpus
is pushed upwards the foot is carried outwards, forwards and extended alongside the other
limb.
• More difficult case requires a snare attached to the retained fetlock to help extend the limb.
Shoulder flexion
• This type of dystocia may be unilateral or bilateral.

• The diagnosis of bilateral retention is usually obvious by observing that the head is partly or
completely born, but there is no sign of feet.
Correction
• Retropulsion is necessary and if the head is much swollen, the calf being dead, the head should
be amputated outside the vulva.
• Following repulsion, the calf forearm is grasped and the defect is easily converted into carpal
flexion and then relieved.
DYSTOCIA IN POSTERIOR PRESENTATION
• This is relatively more common than dystocia in anterior presentation.

• Posterior presentation is considered pathological in all except the multiparous animals.
• The frequency of physiological birth in posterior presentation in mare and cow is quite low.
• The fetal mortality in posterior presentation is high.
HOCK FLEXION
• This condition is usually bilateral.

• They are caused by failure of the hind limbs to extend into the pelvic cavity or by the foot or
fetlock catching on the birth canal or pelvic brim; causing the hind limbs to become flexed.
• It may be diagnosed by palpation of the perineal region and tail.
Correction
• The fetus is first repelled by pressing forward in its perineum and the hand then grasps the fetal
foot.
• As the foot is drawn back through, the hock is firmly flexed and retropulsion maintained as far
as possible, eventually with the digit in the cupped hand the foot is lifted over the pelvic brim
and the limb extended in the vagina.
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Alternate method
• Supplement manual extension by traction on a snare fixed to the retained foot on the pastern
and the snare is placed between the digits, so that when traction is applied to it the fetlock and
pasterns joints are flexed.
• The flexed hock is grasped and repelled forward, while the foot is drawn caudally and extended
through the birth canal.
• In occasional case, where it is impossible to extend the hock, simple embryotomy may be
performed. Achilles tendon may be severed so as to make maximum possible flexion or the
limb may be amputated below the point of hock by means of wire saw.
HIP FLEXION
LATERAL VIEW OF A BREECH PRESENTATION IN BOVINE FETUS
The rear limbs are completely extended

beneath the fetus. Usually both hind legs are
retained (Breech) in the uterus than
unilateral retention.
Diagnosis
• On vaginal examination, the buttocks and tail are in the pelvic cavity and occasionally the tip of
the tail is hanging from the vulva.
• In many cases, no part of the limb can be reached until the fetal buttocks are repelled cranially
out of the pelvic inlet.
Correction
• The aim of the treatment is to convert the condition into one of the hock flexion posture.
• The manipulative procedure is to repel the calf perineum forwards and upwards with a view to
bring the retained limbs within reach, by grasping the cranial aspect of the tibia with the hand
or pass a cord around the tibia and pull the fetal leg back into hock flexion posture.
• Now the hock flexion can be relieved as described previously.
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• B - By replusion on the buttocks and traction on the tibia the leg is drawn in to a hock flexed
posture.
• C, D and E - Caudal and lateral views show how by upward repulsion and lateral rotation on the
hock and medial and caudal traction on the fetlock and pastern, the leg is extended into the
pelvis.
INTRODUCTION
Feto-pelvic disproportion
• Includes relative and absolute fetal over size, small maternal pelvis and narrow birth canal.
• This can be regarded as one syndrome in which both fetal and maternal factors interplay.
• This is type of dystocia is caused by a disparity in size between the fetus and maternal pelvis
when the cervix is fully dilated and vagina and vulva are relaxed.
INCIDENCE
• In dairy cattle it ranges to about 30%.

• Incidence is higher in primiparous and in heifers less than 2 years old.
• Dystocia due to feto-pelvic disproportion is frequently observed in bitch.
• The incidence of this type of dystocia is higher in cross breeding lamb for meat purpose.
ETIOLOGY AND PATHOGENESIS
Birth weight of calf
• Most important single factor associated with feto pelvic disproportion. Birth weight is affected
by the nutritional status of dam during late pregnancy and autosomal recessive gene.
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Sex of the calf
• Male calves are heavier and larger at birth and are more frequently associated with dystocia.
Breed
• Mating a bull of a large breed to a heifer of a smaller breed leads to dytocia.
Absolute fetal oversize
• Dystocia may occur as a result of fetal giantism, excessive volume of parts of the fetus excessive
volume of fetal fluids, and multiple births in uniparous animals.
• The area and shape of the dam’s pelvic inlet and volume of the pelvic cavity constitute another
group of important factors associated with feto pelvic disproportion.
• The pelvic in let undergoes the least change in size during parturition when compared to other
parts of maternal birth canal. The size of the maternal pelvis also varies with the age of the
dam. Heifers on a low plane of nutrition will have a sub optimal body weight and growth rate.
Obesity often leads to fat deposits narrowing the pelvic canal.
Following changes may take place when the fetus becomes impacted in the vagina
• Compression of the umbilical cord may cause interruption of fetal blood supply and death
within 4 minutes.
• Presence of tightly impacted fetus in the vagina also causes continuous stimulation of nerve
receptor areas and excessive reflex straining.
• This may cause in coordinated uterine contractions culminating in myometrial spasm and
straining finally ceases.
• Decomposition of fetus commences soon after the death.
CLINICAL SIGNS AND DIAGNOSIS
• Strong and continuous but unproductive straining may be observed initially.

• When fetal head cannot pass through the pelvic inlet, little straining may be observed.
• Extremity of one or two limbs protrudes from the vulva.
• On vaginal examination
o The passage is found to be dry, and
o It is difficult or impossible to pass the hand alongside the fetal parts
o Both the vulva and vagina are relaxed
o The cervix is fully dilated while the foetus lies anterior to the pelvic inlet
o The calf is in normal P1, P2 and P3
o Traction fails to bring the fetus into the pelvic cavity
o Abnormal enlargement of parts of the fetus may be found.
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TREATMENT
• Replacement of intra uterine liquid and lubrication of birth canal.

• Traction is applied after administration of spasmolytic drugs.
• Traction is done by effort of three persons.
• P1 - Parity factor of 0.95 for heifersP2 - Correction factor for posterior presentation of 1.05.
o E - Correction factor for breeds 1.05.
o T.R. of 2.5 or more indicates that successful traction can be applied.
o T.R. of less than 2.5 requires cesarean section.
• When delivery cannot be achieved by traction within 10 or 15 minutes one of the following
methods should be employed.
o A caesarean operation is done if traction is unsuccessful. It is preferable to choose this
method if the calf is alive.
o Fetotmy is the only feasible method when calf is dead.
PREVENTION
• In dystocia due to feto-pelvic disproportion, it is important to consider the preventive aspects

o Dam selected for breeding should be of adequate size.
o Select cow with good pelvic conformation. The pelvis should slope cranio-caudally with
wide pin bones.
o Sire selection.
o Ensure that cows or not overfed and hence become over fat
INTRODUCTION
Dystocia due to twins
• In cattle, twin gestation often results in dystocia, whereas in mares most cases of twin
conception are followed by early death of one or both of the conceptuses.
• About 2% of equine gestations start as normal twin fetal development, but mummification or
abortion frequently occurs so that less than 1% reaches term.
• In sheep, it is unclear whether twin gestation predisposes to dystocia, due to maldisposition
and the added risk of simultaneous presentation dystocia are balanced by smaller fetuses and a
reduction in feto-pelvic disproportion.
TWIN DYSTOCIA TYPES
• Both fetuses present simultaneously and become impacted in the maternal pelvis.
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• One fetus only is presented but cannot be born because of defective posture, position or
presentation; posture is often most at fault, the lack of extension of limbs or head being due to
insufficient uterine space.
• In uterine inertia, defective uterine contractions are caused, either by overstretching of the
uterus by the excessive fetal load, or by premature birth. When inertia is present, birth of the
first or second fetus does not proceed although presentation is normal.
TREATMENT
• Manipulative correction and delivery is possible due to smaller size of twin fetuses; for the
same reason natural or obstetric delivery may be possible despite defective posture.
o The first essential is diagnosis.
o It is very important, in obstetric practice involving dystocia, that the presenting fetal
appendage is identified. If this is made a rule the obstetrician will not blunder into
applying traction simultaneously to two fetuses.
o Twins should not be mistaken for a schistosome, double monster or ventro-transverse
presentation of a single fetus.
o Where a twin is presented with an abnormality of posture, it is treated as if it were a
single fetus; in such cases the presence of twins is not known; but may be suspected on
account of small fetal size and the history of the dam; until the uterus is searched after
delivery and another fetus found.
o Association of uterine inertia with twins may be known only after delivery of the first
fetus.
o Little attention has been given by veterinary surgeons to the relationship between the
type of dystocia and the disposition of the twins within the uterus. Simultaneous
presentation would seem probable when a twin from each horn approached the pelvic
inlet; abnormality of posture and inertia would be more likely when both fetuses
occupied the same horn.
o If twins are present and retropulsion is required to correct the posture of the closely
presented fetus or of the less advanced fetus to allow delivery of the first twin, it should
be performed very carefully.
o In both cattle and sheep, if case of twin pregnancy there is greater chance of causing
uterine rupture. Spontaneous rupture can occur when both fetuses are in the same
horn.
o Breech presentations are common.
o Simultaneous presentation of twins is treated in logical sequence.
o The polarity of the fetuses is determined, the more advanced fetus recognized and its
presenting extremity appropriately snared.
o Any defect of presentation, position or posture must be diagnosed and treated.
o Correction may be greatly facilitated by means of epidural anaesthesia. Then, with
continuing retropulsion on the less advanced fetus, the nearer one is brought into the
pelvis and delivered by simple traction. The other fetus, which may be presented in the
opposite direction, is then appropriately manipulated.
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o The delivery of ovine twins is more easily achieved if an assistant holds the ewe by its
hindlegs in an inclined supine position. When the ewe is delivered of twins the uterus
should always be examined for a third fetus.
o In cases of gross delay and corrective manipulation is impossible fetotomy of the
presenting fetus may be required. Severe pelvic impaction of dead fetuses may be more
readily relieved by a caesarean operation. The afterbirth of bovine twins is likely to be
retained.
INTRODUCTION
Dystocia due to monsters
• In dairy cattle, most often cause dystocia.

• Common conditions include:
o Schistosoma reflexus,
o Ankylosed calves including
Perosomus elumbis
Double monsters
Dropsical fetuses, including anasarcous and hydrocephalic calves, and
anchondroplastic monsters.
• In sheep, same occur but to a lesser extent.
• In mares, with the notable exception of wryneck, monstrosities are uncommon.
• In pigs, hydrocephalus, double monsters and perosomus elumbis occur occasionally. With the
exception of anasarcous fetuses, gross malformation is often associated with ankylosis of joints
and muscular atrophy; consequently many monsters weigh less than normal calves. This
coupled with the fact that they are sometimes associated with abortion or premature birth
means that a monster may be sufficiently small to be passed spontaneously.
• However, the grossly irregular development, including bending or twisting of the vertebral
column and ankylosis or duplication of limbs, means that a wider than normal fetal diameter
presents at the pelvic inlet and that severe dystocia results.
PRINCIPLES OF DELIVERY OF MONSTERS
• Recognition of the exact disposition of the fetal extremities, and an estimate of fetal size, may
be very difficult.
• The obstetrician must then consider whether careful traction with due regard to lubrication and
protection of the birth canal from irregularly disposed appendages is likely to succeed.
• Prior to the attempt at vaginal delivery, the diameter of anasarcous, ascitic and hydrocephalic
fetuses may be reduced by appropriate multiple or single incisions with a fetotomy knife.
• If moderate traction does not soon succeed, fetotomy or a caesarean operation must be
employed. In view of the worthless nature of monstrosities, fetotomy should be first
considered, and in all cases where sufficient reduction of the fetal diameter may be achieved by
simple section(s), fetotomy should be practised. Thus, for ankylosed fetuses, including wryneck
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and perosomus elumbis, for cases of anterior duplication and for schistosomes presented
viscerally, fetotomy is indicated. The most suitable instrument will be the wire-saw fetotome.
• The hydrocephalic whose head is too rigid to be reduced by cranial puncture must have the
dome sawn off by means of a fetotomy wire. Where it is obvious, because of excessive fetal size
as in anasarca and extensive duplication or because of very irregular presentation, that several
fetotomy sections will be required, the veterinary surgeon should resort to the caesarean
operation. This will be less arduous for the operator and, in general, better for the immediate
health and the future breeding potential of the cow.
• Occasionally, monstrosities present baffling problems to the obstetrician. This happens when
the presenting part of the fetus is normal and the distal extremity is grossly malformed; birth
proceeds normally until the malformed portion engages the pelvic inlet. The cause is not
apparent and may be impossible to ascertain.
• Examples are provided by perosomus elumbis where the front half of the calf negotiates the
birth canal but the ankylosed and distorted hindlimbs become impacted; a hydrocephalic fetus
in posterior presentation; and cases of anterior duplication presented posteriorly. In these
instances, heavy but unsuccessful traction has usually been applied before the arrival of the
veterinary surgeon. This history, together with the normal appearance of the presenting
portion, should make the veterinary surgeon suspicious that an abnormality is present in the
distal portion.
• A caesarean operation provides the easiest solution.
OBSTETRICAL MANAGEMENT OF SCHISTOSOMUS REFLEXUS
• This most familiar bovine monstrosity requires special consideration.

• The weight of the monster calf is usually around 22 kg.
• It may occur in other ruminants and swine, and may be presented viscerally or by its
extremities.
• It is not uncommon for a fetus in visceral presentation to be naturally born. With this type of
dystocia, fetal viscera may be seen protruding from the vulva; if not they are soon located by
vaginal exploration. The viscera may be mistaken for those of the mother and uterine rupture
may be suspected, but it should not be difficult by careful examination to dispose of this
suspicion, the absence of a uterine tear and the continuity of the viscera with the fetus being
soon established. The viscera must be torn away from the fetus whose rigid vertebral
angulation may then be felt at the pelvic brim.
• The fetal diameter is now compared with that of the birth canal; where it seems favourable to
birth, Krey’s hooks are fastened to the presenting fetus.
• Reasonable traction, with adequate lubrication, is now applied, the veterinary surgeon paying
particular regard to the possibility of damage by bony fetal prominences to the birth canal. In
this way, the expulsive efforts of the cow are gently aided, and smooth delivery may be
achieved.
• Where, after a short period of such traction, it is obvious that safe vaginal delivery is not
possible; the fetus should be bisected by means of the wire-saw fetotome.
• One arm of the instrument is loaded and the protruding wire is carried in on an introducer and
passed around the spinal flexure of the fetus. Passing the introducer around the fetus may be a
tedious task; when accomplished, the other arm of the fetotome is loaded and the head of the
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instrument is passed into the vagina until it abuts on the fetus. The fetal vertebral column is
then sawn through, and the smaller fetal segment withdrawn by means of Krey’s hooks. Should
difficulty arise over withdrawal of the remaining portion, it too may need to be divided
perpendicularly to the first section, again using the wire-saw. When a schistosome presents by
its extremities three or four legs, with or without the head the excessive fetal diameter,
together with the ankylosis of joints, is likely to prevent natural or manipulative delivery per
vaginam, and unless the fetus is very small in relation to the maternal pelvis as might occur in a
schistosome twin to a normal calf time should not be wasted on an attempt at vaginal delivery.
Fetotomy or a caesarean operation will be required. In general, it is far easier to deal with such
a presentation by the latter method since the fetotomy required will take a long time,
Exceptions may be met in the case of small fetuses where the removal of a head or single limb
will make birth possible.
• When performing the caesarean operation for the removal of a schistosome, the veterinary
surgeon should always consider the advantage of fetotomy from the laparotomy site; in this
way the requisite length of the uterine incision may be kept within reasonable bounds and the
risk of uterine rupture during extraction minimized.
• After successful removal of a schistosome, the uterus should always be searched for injury and
to ensure the absence of a second fetus.
UTERINE TORSION: CLINICAL SIGNS AND DIAGNOSIS
• Torsion's are either to the right side (clockwise) or to the left side (counter clock wise).
Symptoms
Symptoms of uterine torsion of the cow occurring at the time of parturition and resulting in dystocia
are mild.
• Uneasy
• Restless
• May show colic by kicking the abdomen
• Tenesmus or abdominal straining characteristic of the second stage of labor is either absent or
mild.
In the severe cases of torsion
• Increasing restlessness, but more probably all parturient behaviour will cease, and
• Unless the animal has been closely observed, there may be no knowledge that parturition has
begun.
Degree of torsion
• Varies considerably 90 ° , 180° , 270° and 360°.

• In torsion of greater than 180° the birth canal is usually tightly closed, so that the cervix and the
fetus are not palpate per vaginum.
• If the torsion exceeds 270° it is difficult or impossible to pass the hand through the twisted
portion of the vagina.
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• The symptoms of torsions may be completely lacking if torsion is of a mild degree 45° to 90°.
• When the torsion is 180° or more definite signs of
o Abdominal pain
o Anorexia
o Constipation
o Restlessness or colicky symptoms.
• Uterine torsion in ewe is characterized by a stiff, stilted gait and a stretched, "Sawhorse"
attitude resembling signs of peritonitis and intussusception or volvulus.
On Rectal examination
• In right uterine torsion

o The right broad ligament is pulled strongly downward and the left broad ligament is
pulled tightly across over the top of the cervix, the body of the uterus.
• In left uterine torsion
o The direction of the two broad ligaments is reversed.
o The middle uterine arteries on both sides are tightly stretched.
o The fetus is often difficult to palpate but the position of the fetus may help to indicate
the degree of torsion.
o A dorso-pubic position of the fetus usually occurs when the torsion is 180 ° .
On vaginal examination
• The vaginal walls are spirally twisted and stenosis of the vagina is present.
• Starting from the dorsum of the vagina if the folds spiral in counter clockwise direction it is left
side uterine torsion.
• If the fold spiral in a clockwise direction, it is right side uterine torsion.
UTERINE TORSION: TREATMENT APPROACHES
• Various methods have been described for relieving uterine torsion in bovines (Sloss and Dufty.,
1980).
• The choice of method depends on the:
o Degree of torsion
o Stage of gestation, and
o Condition of the dam, fetus and the uterus.
Different correction methods
• Manual detorsion per vaginum

• Manual detorsion per vaginum in combination with external pressure on the abdomen
• Stimulation of vigorous fetal movements
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• Abdominal ballotment
• Suspension of the cows body
• Detorsion by simple rotation
o Objective
o Technique
o Clinical evaluation
• Schaffer’s method (Modified rolling technique)
o Objective
o Technique
• Intra abdominal manipulation/Flank laparotomy
• Cesarean section
• Medical termination
INTRODUCTION
Incomplete Cervical Dilatation (ICD)
• In the cow, goat and ewe: Occasional

• In other domestic animal: Rare
• In mature and old cow: More frequently seen than in heifers.
• In cow, goat and ewe, the cervix is more muscular, fibrous and tightly closed during pregnancy
than in majority of domestic animal and may cause a severe dystocia if not properly relaxed or
dilated.
RING-WOMB
• Incomplete dilation of the cervix of the ewe is descriptively named "Ring womb".
• The condition is suspected when, after protracted restlessness, the ewe does not progress to
the second stage of labour.
• Manual exploration of the birth canal reveals that the cervix is in the form of a tight, unyielding
ring which will admit only one or two fingers.
• Usually the intact allantochorion can be felt beyond the cervix, but occasionally this membrane
has ruptured and a portion of it may have passed into the vagina.
• This latter observation distinguishes the condition from a protracted first stage.
• Sometimes there is fetid vaginal discharge and necrotic fetal membrane in the vagina in the
presence of non-dilated cervix.
DEGREES OF INCOMPLETE CERVICAL DILATATION (ICD)
• For better and clear understanding of the condition, Incomplete Cervical Dilation (ICD) is
clinically subdivided into four degrees
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ICD DEGREES DESCRIPTION
FIRST DEGREE • Cervix seems to be fully dilated but when the fetal head, limbs
and even the chest have entered or are brought in to the
cervical canal further progress is hindered by a tight, cuff-like
constriction which can be felt on vaginal examination.
SECOND DEGREE • There is more noticeable narrowing of the cervical canal so that
onlythe fetal head or limbs can be brought through it.
• Since delivery is arrested, the cervix moves with the fetus when
traction is continued.
THIRD DEGREE • The operator's hand can be passed through the cervix with
difficulty and one fetal limb may be brought into the vagina.
FOURTH DEGREE • Permits insertion of only one to three fingers into the cervical
canal.
• No fetal part with the exception of the tail or a strand of fetal
membranes can pass through.
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INCOMPLETE CERVICAL DILATATION (ICD): ETIOLOGY AND PATHOGENESIS
• ICD may be brought about by inadequate preparation with hormones, estrogen, PGF2α ,
oxytocin and relaxin. This frequently happens during premature birth or abortions before
estrogens and relaxin have reached optimal levels. Premature birth or abortions due to disease
of the cervix and uterus, that renders cervix and uterine muscles in capable of responding
normally to the hormonal stimulus.
• Faulty stimulation by the autonomic nervous system, which sets myometrial tone at an
incorrect level, can also interfere with passive or active dilation of the cervix.
• Excessive dominance by the sympathetic system causes abnormality low myometrial tone, -
passive dilation of cervix will occur, but the active phase does not follow or is incomplete due to
uterine contractions being either weak or absent.
• Parasympathetic dominance causes an abnormally high myometrial tone, causing
incoordinated myometrial contractions causing in complete cervical relaxation of may even
cause occlusion.
• Cervix may fail to dilate when myometrial contractility is lowered as in primary uterine inertia.
• Hypocalcaemia can also cause ICD.
• The cervix may fail to dilate be cause of severe fibrous, induration or sclerosis of cervix. This is
often observed in older cows. The cervical induration may be caused by trauma inflicted at
previous parturition.
• Secondary uterine inertia with cervical involution also result in incomplete dilatation.
• ICD is an accompaniment of uterine torsion.
• Ischema of cervical region may also be responsible for delayed or in complete dilation of cervix
during and following correction of uterine torsion.
• ICD may be the result of cervical fibrosis caused by trauma inflicted at previous parturition of by
unskilled passage of a cervical catheter.
• Secondary uterine inertia with cervical invocation also results in incomplete dilation of cervix.
• ICD is an accompaniment of uterine torsion.
INCOMPLETE CERVICAL DILATATION (ICD): CLINICAL SIGNS AND DIAGNOSIS
• History of a prolonged first stage with no progression to the second stage.

• Clinical examination per vaginum
o Cervix is only partially dilated and is in sufficient to allow the passage of the calf
extremities.
o Fetal membranes may be protruding.
• Neglected cases of dystocia are characterized by a dead, usually emphysematous fetus,
ruptured membranes, loss of fluids and dry birth canal.
• This condition of incomplete cervical dilation should be differentiated from (In completion of
first stage of labour) early stages of first stage of labour.
• Important to differentiate ICD from early stages of physiologically normal parturition.
o Difficult in the absence of accurate breeding records
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o When the animals are not inspected at appropriate intervals, or
o Signs of approaching parturition are not correctly interpreted.
• Diagnosis obviously correct when
o ICD is associated with ruptured membranes
o Presence of a dead fetus with some degree of decomposition, or
o Sometime by presence of a putrid serosanguineous uterine discharge.
o In those cases where the fetus is live, the membranes have not ruptured, it is likely that
expulsion stage has not yet commenced, and a re-examination after a period of time is
done to check the progress of cervical dilation.
INCOMPLETE CERVICAL DILATATION (ICD): TREATMENT
• The handling of incomplete cervical dilatation (ICD) cases will depend on the
o Cause, and
o Conditions of the fetus, uterine contents and uterus.
• Stimulation of uterine contractions with oxytocin or an oxytocin like drug is recommended for
weak myometrial contractions when these have caused incomplete dilation of cervix.
• When cervical constriction is caused by fibrosis
o Cervicotomy may be attempted.
Not recommended in valuable breeding animals.
Ropes are attached to the fetal limbs and head.
Traction is applied to the fetus so that the cervix is stretched and brought
posterioly.
Using scissors, several incisions, about 1cm deep are made in the cervix over the
tightly engaged fetal parts.
This technique may increase the cervical lumen so that the fetus can be
delivered.
The incisions need not be sutured unless severe haemorrhage develops.
Permanent fibrosis or deformity of the cervix may results.
• Intravenous infusion of a 20% calcium borogluconate should be given if parturient paresis due
to hypocalcaemia is suspected.
• C-Section is performed.
• Dinoprostone Gel, Cerviprime Gel, – PGE2 can be tried.
INTRODUCTION
• The expulsive force of labour comprises the contractions of the uterine and abdominal muscles.
Because the abdominal muscles do not come into play until the uterine muscles has lifted the
conceptus into the pelvic inlet it is logical to consider first the expulsive deficiencies that may
occur in the myometrium. These are known as
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o Primary uterine inertia, and
o Secondary uterine inertia.
DEFINITION
• Primary uterine inertia implies an original deficiency in the contractile potential of the
myometrium.
• It is less common than secondary uterine inertia and is seen most often in the dog and sow,
occasionally in cow but rarely in other species.
• Incidence in cattle is more as age advance.
PRIMARY UTERINE INERTIA: ETIOLOGY
• Intrinsic muscular weakness of myometrium - Idiopathic.

• Over stretching of the myometrium due to excessively large fetus (eg) hydrallantois, fetal
ascites.
• Toxic degeneration in bacterial infections.
• Fatty infiltration of the myometrium.
• Senility - rare.
• Chemical environment of the uterus:
o Ratio between progesterone and estrogen concentration.
o Lack of oxytocin: The hormonal causes may be inherited.
o Lack of calcium: The transmission of inherited neuro-hormonal stimuli depend on the
presence of calcium.
o Metabolic disorder (eg) ketosis, hypomagnesemia.
• Late abortion, premature birth and twin birth in cattle.
• An innate nervous disposition as well as environmental disturbances - These interfere with the
hypothalamic regulation of oxytocin secretion.
• Rupture of uterus or twisting of the uterus causes cessation of myometrial activity.
• Lack of exercise.
PRIMARY UTERINE INERTIA: CLINICAL SIGNS AND DIAGNOSIS
o History
o Examination of the birth canal and presenting fetus
• The animals with primary uterine inertia are obviously parturient and in the first stages of
labour as denoted by mammary changes, ligamentous relaxation and discharge of mucous from
the vulva.
• The animal may be standing or lying down and exhibits little or no labour activity.
• There is no sign of progression of labour.
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• The animals shows no distress and the second stage of labor does not occur for 6 to 36 h or
more.
• In cases of hypocalcaemia, the cow may be depressed and recumbent with a characteristic
lateral bend in the neck or the head turned into the flank.
• In multiparous species after an adequate beginning of second stage labour, all further activity
has ceased.
Vaginal examination
• The cervix is relaxed and dilatable beyond which fetus with its membranes can be felt.
• In some cases the cervix fails to dilate normally.
• There is usually no abnormality in presentation, position or posture of the fetus.
Prognosis
• Good in most cases that are diagnosed early.
PRIMARY UTERINE INERTIA: TREATMENT
• In large uniparous species

o Treatment is generally simple.
o By vaginal manipulation the membranes are ruptured, and the fetus delivered by gentle
traction.
o If cervix is dilated and obstructive dystocia is not present, oxytocin at 20-100 IU large
animals and 10-20 units for small animals may be given to stimulate uterine contraction.
Oxytocin injection in saline by i/v drip over a period my help.
o Administration of 20% calcium boroglucmate i/v 500 cc in large animal and 10 cc in
small animal - Repeat the treatment after 1 - 2 h if no progression is made.
• In multiparous animals
o Calcium solutions and oxytocin are the drugs of choice in cases of uterine inertia.
o Oxytocin has a direct action on the rate of calcium influx into the myometrial cell, which
is essential for myometrial contraction.
o Many do not respond to oxytocin alone but require prior administration of a calcium
solution. Therefore, some 10 minutes before the administration of oxytocin, 10%
calcium gluconate, 0.5-1.5 ml/kg BW should be given by slow i.v. infusion (1 ml/min)
with careful monitoring of the heart rate.
o The dose of oxytocin in bitch is between 1-10 IU maximum/dog. It can be repeated 2 or
3 times at 20-30 min. intervals.
o Oxytocin administered early in second stage of labour is advantageous.
o In late stages, it may cause contraction of cervix and thus interfere with expulsion of a
puppy or fetal membranes and by promoting placental separation of unborn fetuses,
their survival may be jeopardized.
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• Hypoglycemia may be another cause of secondary inertia and may be observed as sole cause of
the problem or associated with hypocalcemia. In such cases, a dilute (10-20%) glucose solution
can be added to the infusion or given i.v. in doses of 5-20 ml.
• If no satisfying responses are observed surgery is certainly recommended.
• In case of nervous animals, sedative like morphine may be administered to calm the animal
0.25 mg/kg.
• If inertia extends into the third stage of parturition and beyond leads to retained fetal
membranes, metritis, pyometra and delayed involution of the uterus.
• Immediately after removal of fetus, parental antibiotic therapy may help prevent septic metritis
and other complication.
DEFINITION
• This usually follows a prolonged dystocia and is characterized by exhaustion of the uterine
muscles.
• It is essentially a result of, rather than a cause of dystocia.
o This condition is seen in all species of animals and is more common in large animals.
o Secondary uterine inertia is frequently followed by retention of fetal membranes and
retarded uterine involution.
SECONDARY UTERINE INERTIA: CLINICAL SIGNS AND DIAGNOSIS
Clinical Signs
• After an intial period of strong but unproductive labor all expulsive efforts by the dam cease.
• Irregular bouts of straining may resume when intra uterine pressure rises because of
developing fetal emphysema.
Diagnosis
• Based on the history of prolonged dystocia, in multipara on the birth of one or two fetuses with
cessation of labour.
• Intrauterine examination reveals the nature of the condition causing dystocia, usually an
abnormal P1, P2 and P3.
Prognosis
• In secondary uterine inertia, prognosis is more guarded than in primary uterine inertia because
the fetuses may be weak, dead or emphysematous.
Sequelae
• Retained Placenta
• Metritis.
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SECONDARY UTERINE INERTIA: TREATMENT
• The condition causing the original dystocia should be corrected by mutation and the fetus then
removed by moderate, careful traction.
• Lubrication of the fetus and birth canal is usually necessary.
• Excessive traction should be avoided since rupture of the uterus may occur.
• Fetotomy or cesarean section.
ETIOLOGY
• Usually seen in very old animals.

• Hydrops of fetal membranes causing over stretching beyond the capacity of their natural
elasticity.
• Tears in muscles in case of ventral hernia.
• Rupture of prepubic tendon.
• Painful conditions of the abdomen, diaphragam or chest: Traumatic reticulitis/Pericarditis.
FAILURE OF ABDOMINAL EXPULSIVE FORCE: CLINICAL SIGNS AND DIAGNOSIS
Clinical signs
• Birth fails to occur.

• Vaginal examination reveals dilated cervix.
• P1, P2, and P3 are normal.
• In ventral hernia, the fetus may be just palpable beyond the reach.
Diagnosis
• Based on clinical signs and vaginal examination.
FAILURE OF ABDOMINAL EXPULSIVE FORCE: TREATMENT
• Delivery by traction.
• The fetus may be raised by assistant’s lifting the abdominal floor.
• Delivery done by patient lying down.
• In traumatic conditions – Elective surgery may be performed.
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MODULE-13: INJURIES AND DISEASES IN RELATION TO PARTURITION
INTRODUCTION
• During postpartum, trauma, lacerations, or rupture of the genital organs may occur and results
in hemorrhage or bleeding into the uterus or birth canal.
o In the cow or ewe, bleeding may be due to an incised or torn caruncle or caruncular
stalk.
o In the mare, it may be as a result of incised or lacerated endometrium, or from
premature removal of the fetal membranes or placenta.
o In the bitch, a hemorrhagic discharge from the vulva may due to an invagination of a
portion of one horn not visible externally.
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OCCURRENCE
May occur
• At the time of parturition

• During a cesarean section or fetotomy, or
• May take place later due to improper or too early removal of a retained placenta in any
uniparous animal.
• Severe intrauterine hemorrhage in rare cases occurring from several hours to a day or so after
calving and dropping of the placenta, that resulted in a massive blood clot filling the gravid horn
of the uterus.
• Rarely death may occur.
• Slight bleeding may be observed, from the ruptured end of the umbilical cord or from slight
lacerations of the uterus, cervix, vagina, or vulva.
In severe lacerations or rupture
• Particularly of the cervix, vagina, and in rare instances, the vulva, hemorrhage may be profuse
due to a rupture of a large vessel.
• Blood may flow in a stream from the vulva as soon as the fetus is removed.
• Most of these lacerations and injuries follow forced extraction.
• Intraperitoneal or intrapelvic hemorrhage may occur and if severe enough produce acute
symptoms of anemia and rarely death, especially in the mare.
• Ordinarily seen in cases of
o Dystocia
o Rupture of the uterus and uterine vessels before, during, or after correction of torsion
of the uterus
o In prolapse of the uterus, and
o In trauma especially in fetotomy operations or forced extraction in young heifers.
• These hemorrhagic conditions would be greatly aggravated in cattle fed sweet clover.
• In the treatment or handling of these conditions the usual surgical procedures to control the
hemorrhage and supportive treatment are indicated.
• If slight bleeding occurs from the genital tract at parturition:
o Not serious, and
o Require no treatment.
• If profuse hemorrhage occurrs from a uterine laceration:
o Prompt contraction of uterus should be promoted by means of injection of 20-50 IU of
oxytocin intravenously.
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o Injecting 500 cc of calcium borogluconate intravenously may also aid in hastening the
clotting of blood, and thus control the hemorrhage.
o If bleeding occurs from a large blood vessel through a laceration in the vaginal wall, the
vessel may be clamped using forceps. This should be left in place for 24 - 48 h or the
vessel should be ligated.
• In severe intrauterine hemorrhage
o The clot should be left for 24 h and then may be broken down manually the next 2 or 3
days until entirely removed.
o If the clot is unnoticed for several weeks or months, the uterus would probably break it
down and absorb it.
o Injections of estrogens as in cases of mummification of the fetus may aid the expulsion
and absorption of the clotted blood.
• Intra pelvic or perivaginal bleeding may cause a stenosis of the vagina during or after forced
extraction or fetotomy by neither it nor the intrauterine hemorrhage is usually fatal.
In Mares
o In 12 to 21 years old mares, rupture of the uterine vessels and sudden death due to
hemorrhagic shock may occur before, during or after an apparently normal gestation
and parturition. The middle uterine artery was most commonly involved but the iliac or
utero-ovarian arteries occasionally were affected. Most fatal hemorrhages occur intra-
peritonealy due to rupture of the large vessels in the broad ligament caused by
degenerative changes in the vessel wall, especially in horses, or by torsion of the uterus
or prolapsed of the uterus.
o Definite symptoms of severe hemorrhage may be observed. Indicated by weakness,
depression, very rapid pulse and respiration rates, and pale mucous membranes.
o If the operator promptly enters the peritoneal cavity through the abdominal wall in the
flank region or through the uterine wall in prolapse, he may be able to control bleeding
by ligating the ruptured vessels. The prognosis is very poor in these cases as severe
hemorrhage, shock and death may occur in rapid succession.
o Early signs: colic, sweating, pain, rapid pulse rate and moderate anemia may occur due
to rupture of a uterine vessel with relatively slow loss of blood between the two layers
of the broad ligament causing a large haematoma. If this ruptures intra peritoneally
then severe acute signs of shock, rapid weak pulse, anemia, prostration, prostration and
death follow.
o If hemorrhage is severe enough to cause clinical symptoms, blood transfusions of 2000
to 8000 cc or more in large animals, saline injections, gelatin or other types of solutions
designed to maintain blood pressure should be given, and repeated as often necessary.
Excessive fluids should be avoided.
o The mare should be sedated with a large dose of a tranquilizer and closely confined.
• In lacerations or ruptures of the genital tract preventive treatments to control infection should
be used, such as the administration of sulfonamides, antibiotics, or local mild antiseptics.
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• Thrombosis of the large uterine arteries and veins is occasionally observed. Thrombi are seen
most often in the veins following prolapsed of the uterus or uterine torsion when circulation
has been restricted.
• Occasionally an aneurism of the middle uterine artery may be palpated on rectal examination
after parturition in the cow, or a haematoma in the broad ligament of the mare.
• Adhesions between the genital tract and ovaries and other pelvic and abdominal organs and
tissues may occur following postpartum hemorrhage.
DEFINITION
• In the bitch, during the post parturient period it is normal to have a serosanguineous vaginal
discharge for up to 3-6 weeks. Sub-involution of placental sites (SIPS) is suspected if a
sanguineous vaginal discharge persists for longer than 6 weeks.
• SIPS almost exclusively affects the young primiparous animal.
CLINICAL SIGNS
• Vaginal discharge beyond 6 weeks without any complication.

• Bitches usually do not show any symptoms of illness.
• Vulva may be slightly enlarged and flaccid.
• Vaginal mucosa normal.
DIAGNOSIS
• Rarely, abdominal palpation reveals single or multiple discrete, firm, spheroid enlargements
spaced along the length of the uterus.
• These palpable structures are large eosinophilic masses protruding in to the uterine lumen from
the endometrium.
• These lesions are raw and ooze blood, accounting for the vaginal discharge.
• They represent a failure of slough these eosinophilic masses of collagen, which is part of the
normal involution healing process of the endometrium, accounting for the descriptive name
"Subinvolution of placental sites".
• Vaginal cytology may reveal syncytial trophoblast-like cells, which aids in confirmatory
diagnosis.
Syncytial trophoblast-like cell Group of cells
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TREATMENT
• Bitches with persistent small amount of hemorrhagic vaginal discharge postpartum usually do
not require any treatment.
• Some recommend use of antibiotics; helpful only if infection is present.
• Curettage via hysterotomy.
• Prostaglandins (natural) 0.25 mg/kg, once daily for 4-5 days may be tried.
• Inj. of oxytocin following whelping has been suggested to aid in preventing SIPS.
• In rare cases of profound permanent bleeding or uterine infection, ovariohysterectomy is
indicated.
• Prolonged post partum vaginal bleeding should be differentiated from

o Metritis
o Vaginitis
o Coagulopathies
o Proestrus
o Trauma
o Neoplasia, and
o Cystitis
LACERATIONS AND CONTUSIONS OF THE BIRTH CANAL
• It is mandatory for the obstetrician to carefully examine the birth canal of the animal,
immediately after attending to a dystocia for evidence of any contusions and lacerations.
In uniparous animals
• Following forced extraction and fetotomy procedures to relieve a dystocia, it is common to

have some minor lacerations and trauma, especially to the vulva and cervix. Vagina being freely
dilatable it is less often injured.
o Minor lacerations are of little importance
o Usually heal promptly without treatment.
o Severe lacerations of the cervix in cattle seldom result in rupture; some recommend
immediate suturing through the vagina to prevent the healed cervix from gaping or
being ectopic, and to prevent the formation of excessive connective tissue in the cervix.
o Mild lacerations of the endometrium heal promptly.
o Healing may be aided by hastening involution process by administration of Inj. pituitrin
or oxytocin and estrogens.
o Vaginal lacerations usually occur near the vulva-vaginal border.
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o Lacerations of the vulva are usually mild when parturition is physiological. Occasionally
the mare, especially if sutured by the Caslick operation, will tear the vulva in a normal
parturition.
In the mare and cow
• Vulvar lacerations are quite common

• Usually occur when strong traction is applied too rapidly to permit normal dilation of the vulva.
• Mild lacerations need not be sutured.
• Deep lacerations or episiotomy incisions should be promptly sutured with deep vertical
mattress nylon or catgut sutures after parturition to prevent gaping and scarring of the vulva
and thereby predisposing to vulvitis and vaginitis.
• Administer parenteral antibiotics.
• In mares and cows with relaxed, flaccid, tipped or horizontal vulvas, the dorsal half or two-
thirds of the commissure should be sutured using Caslick or vulva-suturing technique.
• Lacerations, if not sutured
o Infection usually sets in the traumatized or devitalized tissue or if metritis and retention
of the fetal membranes are present.
Symptoms in infected lacerations of the vulva
• Pain
• Swelling, and
• Persistent straining or “wind sucking” conditions
Recommended treatment
• Parenteral antibiotics
• Local treatment of lacerations by suturing early, or
• Application of protective mild antibiotic dressings.
• In mare, administer Inj. Tetanus antitoxin.
HEMATOMAS
• Occasional in all animals.

• Most common in the mare and sow.
• May be confused with or mistaken for tumors or prolapse of the vagina or bladder.
• On vaginal examination hematomas involving the vaginal wall could be detected.
• Rarely may protrude between the vulvar lips.
• Hematomas of the vulva can clearly be observed.
• Usually get absorbed within 1 to 3 weeks, if left undisturbed.
• Some may spontaneously rupture through the mucous membrane.
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• Surgically it can be treated by incising, removing the clot and carefully suturing to control
further bleeding and to obliterate the area that contained the large blood clot. Do not perform
this operation until after 3-4 days postpartum.
• In early cases, ice packs or cold water spray might be indicated.
CONTUSIONS
• Results in swelling and edema.

• Occur most frequently due to trauma during fetotomy operations or from external injuries.
• Occasionally a blow or a kick in the region of the clitoris will result in marked edema of the
clitoris and vulva.
• In most cases these swellings subside fairly promptly
• Do not confuse with edema from the udder that may extend upward and involve the vulva.
In case of severe oedema
• Cold and hot applications

• Massage, and
• In certain cases, small punctures or incisions through the mucous membrane may release the
fluid or reduce the swelling of the vulva.
INTRODUCTION
• Generally, handling of the fetus or instruments used in fetotomy procedures during dystocia
may often lead to
o Intra-pelvic hematomas
o Hemorrhages
o Obturator nerve paralysis or
o Gluteal nerve paralysis by injury to those nerves at parturition.
GLUTEAL NERVE PARALYSIS
• Rare
• Observed only in the mare those apparently give birth without difficulty.
• Contusions due to a bony prominence on the fetus pressing on the gluteal nerve as it passes
over the bony portion of the lumbo-sacral articulation or ileum.
• May be a bilateral or unilateral injury.
Symptoms
• Some difficulty in rising and may require assistance in rising if the injury is bilateral.
• Gait: Characterized by a definite lameness and weakness of the affected limb. After a few days
to a week, a marked atrophy of the gluteal muscles on the affected side.
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• After a few weeks, the lameness or paralysis of the limb becomes less observable. Complete
recovery may take 6 to 18 months.
Prognosis: Favorable
Treatment
• Good nursing
• Mare should be in a large, well-bedded box stall with good footing.
• In some cases slings or assistance in rising may be necessary for several days or a week.
• Do not allow the affected mares to struggle or exert themselves in rising.
• External applications, massage, or other treatments are of no value.
OBTURATOR NERVE PARALYSIS
• Occur in the mare or cow but is most common in the latter.

• More common in heifers than in cows.
• Before relieving dystocia due to hip lock in the anterior presentation, first rule out obturator
paralysis.
• Before carrying out the obstetrical operation, carefully examine and if detected inform the
owner to avoid the blame for the injury later.
• May affect one or both rear limbs.
• Dystocia due to a hip lock condition in a recumbent cow, the underneath leg and nerve is the
one most commonly and severely affected.
• Contusion is due to the bony tuberosities of the fetal hips, especially the greater trochanters,
rubbing on the obturator nerve as the nerve either passes over the bony prominence of the
lumbo-sacral articulation, or much more commonly as it passes down the shaft of the ilium
before it enters the obturator foramen.
• In heifers, it is common in protracted dystocia due to hip lock condition.
• When strong forced extraction has to be applied manually or with the fetal extractor to draw a
large fetus through the pelvis, obturator paralysis seldom occurs.
Symptoms
• Paralysis of the medial, or adductor, muscles of the thigh, namely, the obturator externus,
pectineus, adductor, and gracilis.
• If unilateral
o Cow can stand on the unaffected limb and as it walks the affected limb is moved stiffly
forward and is abducted so the foot is placed on the ground 6 to 10 inches lateral from
the normal position.
o Cow is unsteady and is likely to slip and fall.
• If bilateral
o Both limbs are stiffly extended and abducted
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o Cow usually is unable to rise.
o If assisted to its feet and the hind limbs held together, the animal can stand but when it
takes a step the limb is abducted and it falls to the ground.
Prognosis
• If paralysis is severe and bilateral: Guarded

• If mild and the animal can walk, even though with difficulty: Good.
• In most cases the condition improves rapidly and in 2 to 7 days the animal is able to walk quite
well.
• Some may take longer for recovery, even up to 4 to & weeks.
• In rare cases the damage to the obturator nerve may be severe and permanent. The chances
for recovery after 2 to 3 weeks are poor, and slaughter may be recommended.
Treatment
• Good nursing
• Tying the animal’s feet together in order to prevent excessive abduction and possible
complications of a dislocated hip or fractured pelvis.
• Use of straps such as hame straps around the pasterns tied with a 14- to 20-inch length of rope
or chain aids in preventing abduction of the limbs and helps the animal to rise.
• Some veterinarians strap or tie the hocks together but it is difficult to fasten straps or ropes
above the hocks tightly enough so that they do not slide down and yet loosely enough to allow
movement of the gastrocnemius tendon.
• Use of slings in the mare and occasionally in the cow may be of value in assisting the animal to
rise to its feet and supporting it for a short period.
• Keep in a well- bedded large box stall or pen, preferably with a dirt floor.
• Under such conditions, dairy cattle should be milked by rolling the cow first to one side and
then to the other.
PERONEAL NERVE PARALYSIS
• Observed in cattle confined in stanchions with their rear parts over the edge of the gutter.
• Occurs most often in cows with dystocia and milk fever that struggle to rise.
• Due to injury or trauma to the peroneal nerve as it passes over the dorsolateral condyle of the
tibia and fibula.
Symptoms
• Injury to the peroneal or fibular nerve results in

• Anesthesia of the cranial surface of the fetlock and metatarsus, and
• Paralysis of the muscles that extend the digit and flex the hock, namely the long and lateral
digital extensors, the peroneus tertius and the anterior tibial muscles. Knuckling of the fetlock
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• Dropping of the hock
• Difficulty in rising, standing and walking.
• Peroneal paralysis should be differentiated from rupture of the gastrocnemius muscle and
posterior paresis due to lesions in the spinal cord.
Treatment
• Good nursing care

• Close confinement.
• A rigid supporting bandage to the lower leg may prevent knuckling of the fetlock.
RUPTURE OF GASTROCNEMIUS MUSCLE
• Apparently secondary to Zenker’s degeneration of the muscle.

• Usually follows considerable struggling or efforts to rise during dystocia or milk fever.
• In cows confined for long periods with very limited exercise, Zenker’s degeneration may be due
to excessive muscular activity.
• Seen more often in selenium deficiency.
Diagnosis
• By the inability to support weight on the affected leg

• Flaccid gastrocnemius tendon, and
• Swelling due to edema and hemorrhage in the region of the gastrocnemius muscle.
Treatment
• Mild cases that can stand may recover in several weeks if they are confined and possibly a
support such as a metal brace or Thomas splint provided.
• In most advanced cases slaughter is indicated.
• Possible prophylactic injections of selenium may be indicated in selenium deficient areas.
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RUPTURE OF UTERUS / VAGINA / PERINEUM - PROLAPSE OF ABDOMINAL / PELVIC VISCERA
INTRODUCTION
• In normal presentation, forced extraction of a bovine fetus may cause

o Rupture of the uterus, cervix, or vagina by forcing these structures against a sharp bony
prominence occasionally found on the cranial portion of the pubic symphysis.
o Transverse rupture of the uterus may be caused by retraction or contraction rings of the
uterine wall.
o Rupture of the cervix, if the cervix is poorly dilated.
o Rupture of the vagina may occur, if perivaginal fat is pushed caudally as the fetus is
forcibly drawn toward the vulva. In this latter instance the vaginal wall near the hymenal
ring or vestibular-vaginal border ruptures to allow the escape of the fat.
o A similar tear or rupture of the vagina occasionally results in a prolapse of the bladder.
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• In prolonged dystocia, the uterus and vagina should be carefully examined prior to any
obstetrical operation to be certain that a rupture of the uterus, cervix, or vagina is not present.
• Rupture produced by the operating veterinarian even if due to his fatigue is extremely
embarrassing and should be avoided if possible.
• After attending to a case of dystocia, carefully examine the uterus and birth canal for the
presence of a rupture of the uterus so that it may be treated promptly or in hopeless cases
slaughter may be advised.
ETIOLOGY
• May occur in any species and may be due to

o Prolonged dystocia with fetal emphysema
o Torsion of the uterus, in which transverse rupture may occur in prolonged cases
o Improper manipulations and traction on the fetus
o Fatigue of the operator, or to an accident in fetotomy operations in large animals or to
forceps removal of a fetus in dogs; to protruding bones of the fetus after fetotomy
o Inexpert manipulations of the fetus by laymen.
• Hence, prior to any obstetrical operation, carefully examine the uterus and vagina to rule out
rupture of the uterus, cervix, or vagina. If the veterinarian becomes fatigue and as a result
creates a rupture, it would be embarassing and therefore should be avoided if possible.
In Bovine
• Forced extraction of a fetus in a normal presentation may cause rupture of the uterus, cervix, or
vagina by forcing these structures against a sharp bony prominence occasionally found on the
cranial portion of the pubic symphysis
• Transverse rupture of the uterus may be caused by retraction or contraction rings of the
uterine wall
• Rupture of the cervix if the cervix is poorly dilated
• Rupture of the vagina may occur if perivaginal fat is pushed caudally as the fetus is forcibly
drawn toward the vulva. In this latter instance the vaginal wall near the hymenal ring or
vestibularvaginal border ruptures to allow the escape of the fat. A similar tear or rupture of the
vagina occasionally results in a prolapse of the bladder.
• Forced extraction with the fetus in abnormal posture or position or in torsion of the uterus may
cause a portion of the uterine or vaginal wall to be caught by a deviated extremity and folded
upon it to produce a rupture.
• A dry, emphysematous fetus and a swollen, dry birth canal are conducive to rupture of the
vaginal, cervical, or uterine walls when strong traction or repulsion is applied.
• Administration of oxytocin or pituitrin to dogs or other animals with dystocia and/or uterine
torsion may cause uterine rupture.
• In a few cases spontaneous uterine rupture may occur due to unknown causes.
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In mare
• After each dystocia the veterinarian should carefully examine the uterus and birth canal for the
presence of a rupture of the uterus in order that it may be treated promptly or in hopeless
cases the cow may be slaughtered and some value thereby salvaged.
• Common in rotated bicornual pregnancy if traction is applied.
SYMPTOMS
• Symptoms of rupture of genital tract vary

o With the animal and the portion of the genital tract involved
o Size of the rupture
o The character of the rupture
o Whether regular or irregular, horizontal or vertical
o The nature of the uterine contents
o The amount of uterine contents that have escaped into the abdominal cavity, and
o Whether or not intestines or bladder have prolapsed through the rent in the wall of the
genital tract.
• In a mare unless the uterine rupture is small and absence of infection in the uterus, a fatal
peritonitis usually develops rapidly.
• In the cow or other domestic animal rupture of the uterus due to an emphysematous fetus
rapidly produces a fatal peritonitis.
• A similar termination can be expected in a uterine rupture in any animal in which the uterine
contents are severely infected.
• In rare cases in cattle, a rupture of the uterus may occur which releases a live or recently dead
fetus into the abdominal cavity.
• Occasionally in the cow, symptoms may be slight, but usually
o Anorexia
o Lack of ruminations and rumen contractions
o Restlessness
o Rapid pulse and respiration rates, and
o Cold extremities.
o Body temperature is usually normal or subnormal but may occasionally be elevated.
• If infected fetuses and material are released into the abdominal cavity
o Acute, severe septicemia symptoms develop rapidly.
o Shock, prostration, and death usually occur in 1 to 2 days.
o In less severe cases, peritonitis is less marked and the animal may survive with the fetus
becoming walled off, or death may occur in 3 to 7 days.
o The fetus may be removed through a laparotomy incision and the uterus sutured.
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PROGNOSIS
• If there is retained placenta, septic metritis, an atonic uterine wall, or prolapsed intestines :
POOR.
• In cow, sheep and sow with most severe cases of uterine rupture: POOR and slaughter is
usually advised if the animal is in an otherwise satisfactory condition.
• Even if recovery takes place, the future breeding life of that animal is very questionable, as
chronic perimetritis and peritonitis are the probable results.
• In the dog uterine rupture is usually characterized by
o Anorexia
o Depression
o Weakness
o In the early stages an elevated and in late stages a depressed body temperature, rapid
pulse and respirations; cold extremities; constipation, or fetid diarrhea; pale mucous
membranes especially if there is internal hemorrhage or shock.
o Prostration and death in 1 to 3 days.
• In the dog laparotomy and hysterectomy, if performed early, together with flushing of the
abdominal cavity with warm saline solution and antibiotics, and treatment to prevent shock and
infection, occasionally results in recovery of the bitch.
• In all species except the mare extrauterine fetuses may be walled off or encapsulated.
• Never fluids be introduced into the ruptured uteri nor should manipulations of retained
placentas take place. Allow the placenta to drop from the uterus without assistance.
APPROACH TO UTERINE RUPTURE
• Vaginal delivery is attempted when the fetus is easily accessible. If , after a reasonable effort,
this cannot be done and uterine rupture is suspected a laparotomy is performed.
• When the fetus is partly displaced into the abdomen and the uterus tightly contracted, and tear
must be enlarged to permit delivery. Repair of the uterine defect is completed after
debridement of its edges. Exteriorization of the partly involuted uterus for repair may be
difficult spasmolytic drugs are of limited help.
• Oxytocin is recommended to restore myometrial tone after the completion of surgery. Basically
the procedure is similar to a cesarean operation.
• If vaginal delivery is successful, the uterine tear can be repaired per vaginum as per the
following procedure.
o The anterior end of the laceration is located and both lips of it grasped with one hand in
an attempt to approximate the edges.
o The needle (No. 2, curved), with approximately 1 m of catgut (No.2) attached, is
introduced with the other hand.
o The needle is inserted through both lips of the laceration just beyond the fingers which
hold the edges.
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o The suture is then tied and carried on as an inverted, continuous blanket suture until the
posterior end of the laceration is reached. A knot is then tied and excess catgut
removed.
• Parenteral, intrauterine, and intra peritoneal treatment with broad spectrum antibiotic or
chemotherapeutic parparations is essential.
• Supportive electrolyte therapy to combat shock is recommended during the operation and
corticosteroids during convalescence.
RUPTURE OF THE VAGINA
• Not serious
• Simple ruptures of the vagina especially of the lateral or dorsal wall need not be sutured unless
the operator desires to do so.
• In most cases there is no need to suture small ruptures even on the floor of the vagina, but
some veterinarians prefer to do so in order to prevent a possible perivaginal abscess if a
retained placenta or metritis develops.
• In rare cases these perivaginal abscesses, which may also occur secondary to an infected
perivaginal hematoma, become large and finally after 2 to 6 weeks or more break out between
the vulvar lips and the tuber ischii.
• Mild wounds of the vagina heal rapidly.
• Recto-vaginal fistulas due to rupture of the dorsal wall of the vagina and ventral wall of the
rectum are occasionally observed, especially in mares in which parturition is violent.
• In chronic cases, Some feces and a mucopurulent discharge are expelled from the vulva.
• Due to straining, rupture of the uterus may be followed by prolapse of the intestines into the
uterus or birth canal or through the vulva.
• If rupture of the vagina or cervix extends into the peritoneal cavity it may also result in prolapse
of the intestines.
Prognosis
• Much better unless the rupture extends into the peritoneal cavity.
Treatment
• In fresh cases
o Should be sutured immediately
o Exercise care that the rectal wall is tightly sutured in a transverse manner. Suturing of
the vaginal wall is not as essential.
• In delayed cases
o After 24 - 48 h of occurrence, it usually is impossible to correct at that time and one
must wait until the edema, swelling, granulation tissue, and wound edges have
completely healed before surgical intervention is undertaken to correct the fistula.
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RUPTURE OF THE PERINEUM AND VULVA
• Observed chiefly in the mare.

• Occasionally observed in cattle and possibly sheep when excessive traction is applied to rapidly
remove the fetus. Thus the vulva and perineal region may rupture before it has time to dilate
gradually.
• Rarely observed in dairy heifers; hemorrhage may be severe and in some cases fatal.
In Mare
• In anterior presentation, forelegs and even the nose or in the dorso-pubic position, the long
limbs of the fetus:
• May be pushed dorsally into the vaginal roof and rectal floor
• This sacculated portion, due to the violence of parturition, is forced into the dilated anus.
• Vagina and rectal floor rupture
• The feet protrude from the anus, and
• As the fetus is expelled the vulva and anus are torn longitudinally.
• In rare cases the vulva and vestibule remain intact and the fetus is expelled through the
ruptured rectum, anus and perineal tissues.
• Presence of the ruptured perineum or “gill flirter” condition cause the rectum and vestibule to
become a continuous cavity or “cloaca”.
Prognosis
• For the life of the patient is good, if hemorrhage or shock is not immediately fatal.
• If the condition is not corrected, the future breeding life of the animal is poor.
• Very rarely “gill-flirter” mares may concieve. Prognosis for this operation is usually guarded.
Treatment
• Advisable to correct and suture the rupture immediately

• Exercise care to suture the rectal wall and anal sphincter.
• If the operation is not performed immediately, postpone about 6 weeks until the swelling and
granulation tissue has subsides and the wound completely heals.
• If surgery is not performed, the feces drop into the vagina, the vulva and vaginal mucous
membranes are irritated, and the animal sucks air, pneumovagina, and there is a profuse
discharge of mucus and feces that soil the rear parts. This condition is seldom observed in the
cow but mild vulvo-anal lacerations and ruptures are seen especially in beef heifers and rarely
in ewes.
• In cattle, proper use of episiotomy incisions would prevent this condition.
• Technique of Aanes : A two-phase operation is recommended for the surgical repair of third
degree perineal lacerations and rectal vaginal fistulas.
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o First operation: Produces a firm shelf of tissue between the rectum and vagina by
suturing the scarified tissues between the rectum and vagina and the vaginal mucus
membrane but not placing sutures through the rectal mucosa.
o Second operation: Performed in about 2 weeks that closes and reforms the perineal
area, the anus and vulva.
RUPTURE OF THE PELVIC AND ABDOMINAL ORGANS
• Rupture of the pelvic and abdominal organs other than the genital tract have rarely been
described in the cow and mare.
• Reports are available on
o Rupture of the rectum in cows.
o Four cases where the free end of the caecum ruptured through the rectal wall. In all
these cases the fetus was in posterior presentation.
o Rupture of the intestine of cattle.
o Rupture of the cecum and ventral colon during parturition in the mare.
o Death always occurred in mares after rupture of the gut and usually occurred in cattle. A
few cows operated on immediately after the rupture survived.
o Rupture of the bladder may occur occasionally.
o In very rare instances rupture of the diaphragm in a mare may result from violent
straining.
PROLAPSE OF THE INTESTINES
• At the time of parturition, a rupture or laceration in the uterus, cervix, or cranial portion of the
vagina leads to prolapse of intestines and may only enter the uterus or may pass into the vagina
and out the vulva.
Differentials
Should be differentiated from
• A Schistosomus reflexus or
• A ruptured umbilical hernia of the fetus.
Prognosis
• Invariably poor
• Dystocia causing the rupture usually is severe, contamination and infection of the intestines
and abdominal cavity is probable, and it is difficult to control the intestines to prevent their
injury during removal of the fetus.
Treatment
• Slaughter is usually recommended.
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• If infection or trauma to the intestines is minimal, replacing the intestines, suturing the rupture
and removing the fetus might be possible.
• Uterine rupture may be closed pervaginum, or better through the laparotomy incision after a
cesarean operation.
• If the intestine is traumatized or severely contaminated resection of a portion of it after a
laparotomy may be necessary.
• Perforating lacerations or ruptures of the cervix and anterior vagina are sutured through the
birth canal.
• Aftercare consists of carefully suturing the rupture, and administering local and parenteral
antibiotic treatment to control peritonitis, as recommended for the handling of uterine rupture.
PROLAPSE OF THE RECTUM
• Occasionally occur in any animal in dystocia due to persistent violent straining and a relaxed
anal sphincter.
• At parturition: Slight eversion of the rectum is common.
• Severe prolapse: Rare.
In mare
• Prolapse of 2-3 feet of rectum is usually fatal since rupture of the rectum or small colon often
occurs secondarily.
• Prolapse of the rectum should be controlled by holding the rectum in place forcibly with a
towel over the anus until the fetus is expelled or withdrawn.
In other species
• Neither as serious nor as extensive.

• It should be prevented if possible or replaced promptly before or after the fetus is removed.
• A purse-string suture of heavy nylon material around the anus is often indicated after
replacement.
• If unnoticed until trauma and edema are present
o Perform surgery including either the reeling operation or amputation, and
o To replace and maintain it in position, retaining sutures may be necessary.
PROLAPSE OF THE BLADDER
• Occur in all species.

• Most commonly in the larger domestic animals before or after parturition. Usually takes place
through a rupture or tear in the floor of the vagina and the bladder is noticed hanging from the
vulvar orifice after parturition.
• Due to the sharp bend in the urethra the prolapsed organ fills with urine.
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Differentials
• Eversion of the bladder through the urethra

• Vaginal or vulvar tumors
• Cysts
• A mass of fat protruding through a rupture in the floor of the vagina
• Vaginal or vulvar hematomas.
Treatment
• If the bladder is distended with urine it may be replaced and the urine forced out or it may be
drained with a needle before replacing.
• The external surface of the bladder should be carefully cleaned, dusted with a sulfonamide or
with an antibiotic solution, and the organ replaced.
• The rupture in the vaginal floor permitting the prolapse should be sutured.
EVERSION OF THE BLADDER
• Observed mainly in the mare, in which the urethra is large and parturition violent. Rarely
observed in the other animals such as the cow or sow.
• Eversion of the bladder may occur before or during parturition.
• It seldom if ever obstructs the passage of the fetus but occasionally the everted bladder and
urethra may be severely traumatized when the fetus passes through the vestibule.
Symptoms
• Eversion of the bladder is easily recognized, as this organ is attached to the area of the ventral
floor of the vulva where the urethra orifice is normally located.
• The everted bladder is pear-shaped.
• The openings of the two ureters drip urine and the mucous lining of the bladder may be noted
and felt.
• If the everted bladder is small it may not become exposed through the vulvar lips until the
animal lies down.
• In rare instances in the mare intestines may prolapse into the everted bladder and prevent
reduction.
Treatment
• Bladder should be thoroughly cleansed.

• If a tear or rupture is present it should be sutured or if a portion is damaged severely that
portion might be removed and the edges of the incision sutured. Administer epidural
anesthesia
• Use both hands to compress the bladder and force it back through the urethra. Massage the
bladder and press through the vagina floor until it is in its proper position.
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Postoperative care
• Irrigate the bladder with saline solution and antibiotics

• Administer antibiotics parenterally so that the urine will contain a high concentration of the
antibiotic for a number of days.
• Seldom necessary to place a stitch in the external urinary meatus to prevent another eversion
once the fetus has been removed and labor has ceased.
PROLAPSE OF PERIVAGINAL FAT
• Observed in fat dairy heifers or beef cattle.

• Occur through a small rupture of the caudal portion of the vagina during forced extraction of
the fetus especially.
• Fat should be differentiated from prolapse or eversion of the bladder, as they are likely to
resemble those structures.
Diagnosis
• On vaginal examination, quite small vaginal rupture may be found at the base of the prolapsed
mass of fat.
Prognosis
• Good as a perivaginal abscess seldom develops.
Treatment
• Fat may be cut off with a knife or scissors, as there will be little bleeding.
• Vaginal rupture may be sutured or left to heal without suturing.
• Sulfonamide powder or antibiotics are customarily placed in the wound before suturing.
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MODULE-14: UTERINE PROLAPSE IN CATTLE / GOAT / BITCH
DEFINITION OF TOTAL UTERINE PROLAPSE
• When the gravid horn following the expulsion of the fetus gets everted along with the non
gravid horn and protrudes through the vulva it is referred to as postparturient total uterine
prolapse.
o Uterine prolapse is a common complication encountered in the cow, buffalo, sheep and
goats during the third stage of labour.
o It is generally referred to as casting of wethers or casting of the calf bed.
o Most often it occurs immediately after parturition, occasionally up to several hours
thereafter and in rare instances it may occur 48-72 h after parturition.
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INCIDENCE
• In cow, there is high occurrence of prolapse compared to other domestic animals.

• In bovine, it is observed in 0.5 % of all assisted dystocia cases. However, the condition occurs
mostly in unassisted deliveries.
• Observed in 0.3-0.5% of all parturitions.
• Incidence in goats recorded at Madras Veterinary College Hospital during 1985-1990
constitutes 4.6% of the post partum complications (Rajasekaran et al., 1993).
• Occurs in all age groups, but more in pluriparous and debilitated animals.
ETIOLOGY
• Not clear, but it occurs during third stage of labour shortly after delivery of the calf.
Predisposing factors
• Long and relaxed mesometrial attachments and lack of suspension of anterior portion of the
gravid horn allows excessive mobility in longitudinal direction.
• Violent or strong tenesmus.
• Relaxed, atonic and flaccid uterus.
• Retention of placenta at the ovarian pole of the gravid horn in cows and non gravid horn in
mares.
• Excessive relaxation of the pelvic and perineal regions.
• Dairy cows that calve after long confinement in stables with their rear quarter sloping
downwards and hanging over the gutter.
• In the relief of dystocia, use of great force in forced traction of fetus predisposes to tenesmus.
• in dystocia, when the uterus is contracted tightly around the dry fetus, forced extraction is
likely to result in prolapse.
• Most common in pluriparous cows.
• In poorly grown, thin debilitated dairy heifers.
• In milk fever, atonic uterus may prolapse due to increased abdominal pressure to labour.
• Low plane of nutrition.
PATHOGENESIS
• During the process of fetal expulsion or immediately after delivery, an intussusception which
begins at the ovarian end of the gravid horn gradually progresses posterior leading to the
eversion of the mass.
• When abdominal straining begins, the mass suddenly gets prolapsed through the vulva.
• The gravitational force accelerates the intussusception and eversion in recumbent or standing
animals with the hind quarters in an inclined plane.
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• Subsequently, the stretching of the myometrium and uterine ligament leads to abdominal
discomfort.
• Further the prolapse is accelerated due to straining as a result of the stimulation of receptor
areas by the everted mass.
CLINICAL SIGNS IN TOTAL UTERINE PROLAPSE
• Animal will be usually recumbent (Fig.1a) or standing (Fig.1b), with the prolapsed uterus
hanging up to the level of the hocks.
Fig 1: Total uterine prolapse
a) In recumbent cow b) In standing buffalo
• Retention of the placenta may also accompany (Fig.2).
Fig.2: Prolapse with placental retention in

cow
• The fetal membranes and/or mucous membrane of the uterus are exposed.
• Except in fresh cases, the prolapsed mass would usually be covered by dung, dirt, or blood
clots.
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• If the uterine prolapse exists for 4–6 h or longer, it will usually be enlarged and edematous
• In the cow, the gravid horn prolapses or everts sufficiently so that the cervix is usually seen at
the vulva.
• Because of the strong intercornual ligaments, the non-gravid horn is held inside the peritoneal
surfaces of the prolapsed gravid horn and does not evert.
• An oval or slit like orifice observed near the vulva on the ventral or lateral side of the prolapsed
gravid horn is the opening of the non-gravid horn.
• In the doe, uterine prolapse (Fig.3) is similar to that observed in the cow.
Fig.3: In goat
PROGNOSIS
• Varies greatly.
• In most cases, Prognosis for the life: GOOD, If observed early
o prompt veterinary aid,
o cow able to stand and
o no severe injury of the uterus
• Future breeding: GOOD or POOR depending upon the severity of the uterine lesions, the
promptness of treatment and the rate of involution.
• Prognosis is more GUARDED, If
o uterus grossly contaminated, or
o dried due to exposure to sun, or
o if lacerations are present
• Future breeding life: QUESTIONABLE - due to possibility of a septic metritis, perimetritis or
peritonitis.
• It is surprising how much trauma, irritation, and contamination the uterus can withstand.
• After replacement of uterus this infection is overcome, the traumatic lesions heal, and the
animal recovers.
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• Prognosis: POOR to HOPELESS
o if animal is prostrate.
o unable to rise and
o conditions complicated by shock, internal hemorrhage, or incarceration of the
intestines.
• If hypocalcemia or obturator paralysis is present, the prognosis is based on the severity of these
conditions.
• In cattle, prognosis: poor, although some may survive
o uterus badly damaged or diseased,
o replacement cannot be considered and
o amputation of uterus is only recourse
• In ewe, prognosis for prolapse of uterus is similar to that of cow
• Amputation of uterus should seldom if ever be attempted since it is indicated only when the
uterus is severely traumatized and lacerated – Prognosis is extremely GRAVE.
GENERAL CONSIDERATION IN TREATMENT
• Instruct the farmer to keep the uterus of the animal moist and clean by either wrapping in a
wet towel or sheet or place in a plastic bag until replaced.
• Until arrival of the veterinarian, the uterus in a standing animal should be raised and kept
supported in level with the vulva.
• In recumbent animals, uterus should be supported and prevented from hanging. By doing so,
edema formation in the uterus and possibly rupture of the uterine vessels can be prevented.
• Prompt and easy replacement is facilitated by proper restraint of the animal.
• Epidural anaesthesia should be administered in sufficient dose to provide good anaesthesia and
at the same time keep the animal standing. In some recumbent animals that refuse to stand
may rise up after administration of epidural anaesthesia. Further, it controls and prevents
defecation during the process of reduction and repositioning of the uterus.
• In bovines, for certain types of obstetrical maneuvering it is advisable to have the animal
standing and preferably with elevated rear quarters.
METHODS TO ELEVATE REAR QUARTER OF THE ANIMAL
• An inclined platform is the most practical method to elevate the rear quarters of the cow.
• In recumbent animals, in order to elevate the hindquarters the following are employed:
o Sandbags
o Straw stuffed bags, and
o Inclined ramps
• These improvised conventional methods have many disadvantages.
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• Hence a device suitable to elevate the rear quarters of bovine and to provide adequate space
for obstetrician to work comfortably and effectively was fabricated by Pattabiraman and
Balasubramanian (1999).
PORTABLE BOVINE REAR QUARTER ELEVATOR DEVICE
• This device was designed by Pattabiraman and Balasubramanian (1999), and has been
successfully employed in certain obstetrical cases presented at the Large Animal Obstetrics unit
of Madras Veterinary College Teaching Hospital, Tamilnadu Veterinary and Animal Sciences
University, Chennai.
Fig.1: Portable bovine rear quarter Specifications

elevator device
• The device has two portions, one fixed and the other
movable on a lever - hinge system. The fixed portion
has a rectangular frame work (100 x 85 cms) only with
an inclination (20°). The lower end rests on the
ground while the raised end (40 cms) rests on two
sturdy rubber wheels. The movable top portion has a
wooden plank with non-slippery grooved aluminium
sheet fixed on a sturdy metal frame (Fig.1).
Fig.2: A cow on the rear quarter • On one side of this top portion is attached with the
elevator device lower end of the fixed framework by hinges.
• The other side towards the elevated side is movable
and can be raised or lowered by thread system.
• The linear rod fixed to the thread system can be easily
worked by rotating a handle.
• Metallic rings are provided on either side of the metal
frame to secure the animal with thick cotton tapes or
ropes.
• A handle is provided at the lower end so that the
device can be easily lifted and moved over the wheels
a) Side view to any desired place.
• The lower end of the device can be easily pushed
underneath the hindquarters of the recumbent
animal.
• By rotating the handle the movable part of the device
can be elevated along with the animal to any desired
heigh (Fig.2).
b) Rear view
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ADVANTAGES
• It is very useful in
o Reducing total uterine prolapse
o Repulsion of fetus in dystocia, and
o During intrauterine liquid replacer therapy.
• There is no stress to the animal due to the inclined posture.
• The device provides comfortable and effective working space for the obstetrician and can be
used with advantage in veterinary instituitions.
HANDLING OF TOTAL UTERINE PROLAPSE IN BOVINE
• Carefully prepare the prolapsed uterus for replacement.

• During the replacement process, hold the uterus in level with the ischial arch or vulva (Fig. 1) so
as to relieve the pressure on the broad ligament and uterine veins and to restore normal
circulation in the prolapsed uterus. Further edema of the uterine wall is prevented which leads
to absorption and disappearance of the edema already present.
Fig 1. Uterus held in level with ischial

arch using a prolapse tray
• The position of the uterus facilitates the bladder and intestines to return to their original sites.
• Animal is more comfortable in this position and the possible rupture of vessels in the broad
ligament is greatly reduced.
• Uterus can be supported in a towel or sheet held by an assistant on either side of the rear
quarters of the animal, or on a wooden or metal tray.
• If placental attachment is present, it should be gently separated.
• Placenta may be left undisturbed, if removal is difficult without severe trauma and hemorrhage.
After complete reduction and repositioning of the uterus, the case should be treated in the
same manner as severe retained placenta in an animal not affected with prolapse of the uterus.
• Uterus should be cleansed thoroughly with a warm physiological saline solution or with water
(Fig 2) and small amount of mild antiseptic.
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Fig 2. Cleaning of uterus with warm
physiological saline
• The adjacent vulva and perineal region should be washed and cleansed including the folds and
creases in the skin.
• If laceration, tear, or perforation is present in the uterus, it should be carefully sutured.
• In case of severe uterine hemorrhage, the vessel should be ligated.
• If the prolapse of the uterus has been present for sometime and edema is severe, the massage
or washing the uterus and the holding of the uterus level with the vulva may not be sufficient to
readily reduce its size so that it can be replaced.
• Vigorous massage of the uterus with the palm of the hand, with the fingers extended but held
tightly together, may be accomplished by wrapping a towel or piece of sheeting tightly around
the uterus and applying pressure through the towel without the danger or possibility of forcing
a finger through the uterine wall or edematous mucosa.
• Palpate the bladder before replacing the uterus, if distended, catheterize (Fig 3 and 4) so that it
does not interfere with the replacement process.
Fig 3. Locating the urethra and Fig 4. Relieving of urine

inserting of urinary catheter
PROCEDURE FOR REPLACING PROLAPSED UTERUS
• Hold the uterus above the level of the floor of the pelvis.
• Pull apart the vulval lips, and first the ventral portion and then the dorsum of the prolapsed
portion of the uterus should be replaced, starting at the cervical end of the uterus nearest to
the vulva.
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• Pressure should be exerted with the palm of the hand, with the fingers (Fig 5) extended but
held tightly together, to avoid perforating the uterus.
Fig 5. Pressure exerted using palm

and fingers
• Finally the ovarian pole of the uterus is pushed by the fist through the vulva, vagina and cervix,
into the uterine cavity.
• If the cervical rings are contracted, pull them gently backward (Fig 6) with one hand and work
the uterus through with the other.
Fig 6. Holding of cervical rim
• The ovarian pole is pushed through the vagina, cervix and uterus with the clenched fist and arm
by a piston like or shaking motion on various parts of its perimeter until the horn is completely
straightened out and no invagination is present.
• Exercise care not to tear or remove the caruncle and thus cause bleeding.
• If it is difficult to achieve complete reduction and repositioning of the ovarian pole, then in such
cases introduce of 9–14 litres of warm water or physiological saline in to the uterine cavity
(Fig.7).
• This stimulates uterine contractions and will help to clear out the uterine debris.
• It is important to remember that this fluid should be siphoned out after correction.
• If the uterus is sutured, douching should not be done after replacement.
• After proper and complete replacement of the uterus (Fig.8), administer 30–50 IU of oxytocin
intramuscularly or intravenously.
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Fig 7. Infusion of warm saline Fig 8. Complete replacement of
in to uterus prolapsed uterus in a buffalo
Redrawn from Sloss and Dufty (1980)
• Even if the animal shows no clinical signs of hypocalcemia, calcium borogluconate therapy
should be given, together with parenteral antibiotics to control uterine infection after
replacement.
• Temporary suturing of the vulva with an umbilical tape in to the vulval hair line for 1-3 days.
FIELD APPROACH TO CORRECT UTERINE PROLAPSE
• In cow, the replacement of total uterine prolapse (Fig.1) places considerable stress on the
animal. Severe straining which occurs during replacement can be controlled to some extent by
the administration of epidural anesthesia. Unless the prolapse is of very recent origin, it
becomes swollen, hardened and friable, making the reduction more difficult. The method
outlined below has been the standard practice for atleast 30 years and found to be very
successful.
Technique
• Roll the animal over in to lateral recumbency.

• If placental attachment is observed, gently detach it.
• Two wide belts (Fig.2), such as those used in a foot paring crush, are used to loop over the hock
joints (Fig.3) and tighten proximal to the joint.
• Two belts, linked by a short rope are attached to a fore end lifting tractor and raised until the
vulva of the cow is about one meter from the ground level (Fig.4).
• Wash the prolapsed mass with luke warm water (Fig.5).
• Gently raise the mass above the level of the vulva (Fig.6).
• With minimal help and guidance replace the mass. Ensure that there is no rotation of the uterus
and thus no uterine torsion (Fig.7).
• Once returned to the inside of the cow, ensure complete repositioning of the uterus through
the cervix (Fig.8).
• Apply vulval tape retention sutures after replacement (Fig.9).
• After replacing the uterus, lower the cow to the ground, so that the cow regains her feet
(Fig.10).
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Stepwise Procedure
1 2 3
4 5 6
7 8 9
10
Source: A. Whites (2007) UK Vet (12) 1: 1-3
355
Advantages
• Quick, easy and essentially a practical method

• No evidence of damage to the muscular skeletal system as a result of the hoist.
• Involved only 6 minutes of suspension, and the whole procedure from approaching the case to
the cow standing up with uterus replaced, took 25 minutes.
• Above all, the physical effort required of the veterinarian is minimal.
TOTAL UTERINE PROLAPSE IN BUFFALO
Before correction After correction
CERVICOTOMY AND TRACHEOLORRAPHY
• This method was developed by Asokan et al. (1993).

• Effective in delayed cases of irreducible uterine prolapse in buffaloes.
• It can be carried out under epidural anaesthesia with very much reduced stress and trauma to
the animals even under field conditions.
Procedure
• Stretch and pull the cervix posterior by applying traction to the cervical rim using a cotton tape
(Fig.a).
• A single incision of 5-7 cm length is made on the dorso lateral aspect of the cervix
(Cervicotomy)involving only the circular muscles (Fig.b).
• Wash the prolapsed mass with mild antiseptic solution.
• Lubricate the prolapsed mass with an emollient and gently reduce and reposition the uterus.
• Retract the cervical rim and expose through the vulva (Fig.c) and suture the incision made on
the cervix (Tracheolorraphy) using chromic catgut No.2 adopting continuous suture pattern.
Reduce, reposition and finally apply vulval tape retention sutures (Fig.d)
• If the prolapsed mass has been properly reduced and repositioned, recurrence is rare.
• In uncomplicated cases, the cervix closes within 24 h and prevents recurrence.
• Placement of pessaries may result in straining and hence are not recommended.
• To control uterine infections, parenteral antibiotics are indicated.
356
Fig. a Fig. b Fig. c Fig. d
Reference:
• S.A.Asokan, S.Balasubramanian and S.R.Pattabiraman (1993). Cervicotomy and Tracheolorraphy

- A new method to treat irreducible uterine prolapse in buffaloes. Indian Vet. J. 70: 355-356.
UNUSUAL COMPLICATION
• Cecilia et al., (2001) have reported an unusual development of necrosis and gangrene of the
skin and superficial tissues from the vulva up to the umbilical region involving the perineum,
escutcheon (Fig.1) and the udder as a complication of post partum uterine prolapse in a she
buffalo.
• In the udder also only the skin was involved (Fig.2) as a result of which the milk was normal
from the secretory cells.
Fig.1: Necrosis and Fig.2: Raw wound in

gangrene the teat
TREATMENT OF TOTAL UTERINE PROLAPSE IN GOAT
• Replacement of the prolapsed uterus in goat is similar to the procedure adopted in bovines.
• Due to the difference in the placental physical relationship to the caruncles it is difficult to
detach.
• In fastly adherent cases, forceful detachment can damage the uterus.
• Preferable to leave them attached and replace along with the uterus.
• Failure to detach will not affect the prognosis.
• In easily separable cases, gently detach the placenta from the maternal caruncles.
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Elevating the hind quarters of
the animal by an assistant aids
in easy replacement of the
prolapsed uterus.
In Standing Position
• Clean the uterus thoroughly with a warm physiological saline or water with a small amount of
mild antiseptic.
• Carefully wash and clean the adjacent vulva and perineal region including the folds and creases
in the skin.
• Elevate the rear quarter
• After through lubrication the uterine mass is gently reduced and repositioned.
In Recumbent Position
• Sequential procedure of handling uterine prolapse.
TOTAL UTERINE REDUCTION STEP -1 STEP-2 STEP - 3

PROLAPSE
STEP - 4 AFTER REDUCTION REPOSITIONING AFTER REPOSITIONING
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UTERINE PROLAPSE IN BITCH - DEFINITION
Uterine prolapse (Synonym: Uterine eversion) is an eversion and protrusion of a portion of the uterus
through the cervix into the vagina during or near parturition.
• Uterine prolapse is rare.

• Similar to estrus associated vaginal prolapse/hyperplasia.
• Uterine prolapse is associated with parturition, usually prolonged labour and involves the entire
vaginal circumference.
• For uterine prolapse to occur, cervix must be dilated.
PATHOPHYSIOLOGY
• One or both the uterine horns gets prolapsed and may be located in the cranial vagina or gets
everted through the vulval lips.
• Prolapsed mass resembles that of a "Doughnut"
• Due to venous congestion, trauma and debris the mass is discoloured.
• Tearing of broad ligament and uterine artery hemorrhage may occur.
• Hypovolaemic shock may result due to hemorrhage, unless it is swiftly arrested.
DIAGNOSIS
Diagnosis of uterine prolapse is based on
• Clinical presentation
o Signalment
Condition is rare
May occur near or at parturition
No recognized age predisposition
More common in cats than in dogs.
o History
Associated with excessive straining during parturition
Mucosal mass is generally noticed from the vulva
Vague signs of abdominal distress and tenesmus
If ovarian or uterine vessels rupture, there may be signs of hemorrhagic shock.
Other signs include
Restlessness
Abnormal posture
Pain
359
Perineal bulging
Licking, and
Dysuria.
• Physical examination findings
o By digital examination of the vagina or visual observation
o Perineal bulging may occur
o Everted mucosa may protrude through the vulva or be digitally palpated in the vagina
o In vaginal prolapse, inserting a probe or finger along the protruding mass will reveal
fornix
o Dog may be stable or may show signs of hemorrhagic shock
Pale mucous membrane
Tachycardia, and
Weak pulse.
• Diagnostic imaging
o Gravid uterus or postpartum uterus may be identified by radiograph or ultrasound
o Vaginoscopy may be used to confirm.
• Laboratory findings
o Specific laboratory findings are not seen
o In case of uterine artery rupture, anemia may be present.
• Uterine prolapse should be differentiated from

o Vaginal prolapse/Hyperplasia
o Vaginal tumour
o Uterine torsion
MEDICAL MANAGEMENT
• Rarely successful
• Treat shock with fluids with or without corticosteroids
• Correct acid-base and electrolyte imbalances
• Lavage the the prolapsed mass with warm saline
• Reduce edema by gentle massage
• Reduce swelling using hypertonic dextrose solution lavage
• Lubricate the mass with water soluble gel
• Manually replace the mass using external pressure and flushing sterile fluid under pressure in
to the uterine horn
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• To prevent recurrence after replacement, administer inj. oxytocin 5-10 IU (This will aid in
uterine involution and, together will help in closure of cervix).
SURGICAL TREATMENT
• Goal
o Replace the prolapsed mass and prevent infection
• Treatment options
o Manual reduction
o Manual reduction with immediate ovariohysterectomy (OHE)
o Reduction during celiotomy, and
o Amputation (Note: The urethra should be catheterized during uterine amputation to
prevent traumatizing it or the urethral papilla).
• OHE should be performed if the tissue is devitalized, irreducible, or vessels in the broad
ligament have ruptured.
• Laparotomy may be necessary to facilitate manual reduction by placing cranial traction on the
broad ligament or uterus.
• Vaginopexy may be performed during cesarean, celiotomy, or when the patient is stable.
• In dogs under shock, surgery should be performed as soon as they are stabilized.
• Shock should be treated with fluids (with or without corticostroids), and acid-base and
electrolyte imbalances corrected.
• If prolapse is contaminated or traumatized, as a prophylactic measure antibiotics should be
administered.
• Hair should be clipped from the abdomen and perineum.
• Prepare the area for aseptic surgery.
• Prolapsed tissue should be assessed for viability, and if the tissues appears healthy, lavage the
mass with hypertonic dextrose sloution to reduce the swelling and replace after application of
water soluble gel.
ANAESTHESIA
• General anaesthesia is recommended.
Selected Anaesthetic protocols for Debiliated/Shock patients
Premedication and • Hydromorphone (0.02-0.2 mg/kg; IV or IM) plus Diazepam (0.2

Induction mg/kg IV).
• Give incremental doses.
• Intubate if possible.
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• If necessary, give etomidate (0.5-1.5 mg/kg IV).
• Alternatively, if no vomition, mask induction can be used or give
thiopental or propofol at reduced doses.
Maintenance • Isoflurane or Sevoflurane
Epidural Anaesthesia
• Epidural anaesthesia may facilitate reduction of prolapse and minimize the post-operative
straining.
Drug Dose Onset of action (in min) Duration of action (in hour)
Lidocaine 2 %* 1 ml/3.4-4.5 kg 10.0 1.0-1.5
Bupivacaine 0.25% or 0.5 %* 1 ml/4.5 kg 20.0-30.0 4.5-6.0
Morphine (preservative free) 0.1 mg/kg 23.0 20.0
Buprenorphine 0.005 mg/kg 30.0 12.0-18.0
* Aviod head down position after epidural
SURGICAL TECHNIQUE
Surgical Anatomy (Click for information)
• Surgical anatomy of the female reproductive tract is discussed in Lesson 12 under pyometra in
bitches.
Positioning
• Manual reduction may be accomplished with the dog in ventral, dorsal, or lateral recumbency.
• A perineal position is recommended for episiotomy and dorsal recumbency for celiotomy.
Surgical Technique
• Reduce acute prolapses manually.

• Lavage the protruding tissue with warm saline or water and diluted antiseptic.
• Hypertonic agents may help reduce edema and facilitate reduction.
• Gently compress the mass to reduce edema while attempting to reduce prolapse.
• If necessary, perform an episiotomy to assist reduction.
• Insert a urethral catheter.
• Place horizontal mattress sutures between the vulvar lips to maintain reduction and prevention
of recurrence.
362
• If necessary, perform celiotomy to facilitate reduction by cranial uterine traction, ensure proper
alignment of the uterine horns, and assess integrity of the vasculature.
POST-OPERATIVE CARE
• Treat shock, dehydration and bloosd loss.

• If necessary administer analgesics.
• Urethral obstruction may arise due to swelling and pain, hence monitor urination.
• Place urinary catheter, if dysuria or anuria is anticipated.
• Continue antibiotics if uterus appeared moderately to severely traumatized and
ovariohysterectomy was not performed.
• Complications include
o Hemorrhage
o Shock
o Dehydration
o Infection
o Necrosis
o Urethral obstruction
o Recurrence, and
o Death.
PROGNOSIS
• Spontaneous regression will not occur in complete uterine prolapse

• Successful manual reduction may often lead to survival, but infertility and dystocia may occur
with subsequent breeding
• Prognosis is excellent following ovariohysterectomy, provided shock and hemmorhage are
taken care of.
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MODULE-15: RETAINED FETAL MEMBRANES (RFM)
INTRODUCTION
• Retention of Fetal Membranes (RFM) is one of the most common post partum disorders
encountered in cattle and less common in other domestic species.
• This condition is considered pathologic and has been associated with
o An increased incidence of metritis
o Reduced subsequent fertility
o Increased mastitis incidence, and
o Increased culling.
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DEFINITION
• In strict sense, parturiton is completed only after expulsion of the fetal membranes, which
normally gets detached and expelled within 12 h following the delivery of the fetus. When the
dehiscence is prolonged beyond 12 h, delay in expulsion occurs. Fetal membranes when not
expelled within 24 h, are considered as retained.
INCIDENCE
• Placental retention tends to increase with parity, and there is an individual tendency to
recurrent retention.
• Incidence is very high with twins and late abortions (but not with early abortions in which the
whole conceptus is easily expelled).
• Genetically high-yielding dairy cows and cows on high nutritive planes at parturition are more
prone to placental retention.
ETIOLOGY
• When the normal processes of dehiscence and expulsion fails, RFM occurs.
• Three main factors involved in the separation and expulsion of the fetal membranes are:
o Maturation of the placenta.
o Exsanguination of the fetal side of the placenta when the umbilicus ruptures, which
causes collapse and shrinkage of the trophectodermal villi and their physical separation
from the maternal crypts.
o Uterine contractions, which aid the exsanguination of the fetal side of the placenta and
cause physical separation of the placenta by distorting the shape of the placentomes
(thereby causing ‘unbuttoning’ of the cotyledon from the caruncle), expulsion of the
dependent and detached parts of the fetal membranes can then occur.
MYRIAD OF PROBABLE CAUSES
• Retained Fetal Membranes have been associated with the following myriad of causes
o Selenium or Vit A deficiency
o Excessive weight gain during dry period
o Increased age
o Heat stress
o High milk production
o Late winter, early spring calving
o Premature calving - short gestation
o Uterine atony
o Milk Fever
o Stillbirths
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o Twins
o Dystocia
o Abortions
o Hydrops.
o Brucellosis
o Induced parturition
o Fetotomy
o Caesarean section
EXPLICIT CAUSES
Group-I Group-II
Interference with normal loosening process between Uterine inertia

maternal caruncle and fetal cotyledon.
• Immature placentomes • Uterine distension

• Edema of chorionic villi • Uterine fatigue associated
• Prolonged gestation with dystocia
• Metabolic disorders –
• Hyperemia of placentomes
Postpartum hypocalcemia
• Necrosis
• Inflammation
NEW CONCEPT FOR CAUSE OF RFM
• Weight loss/gain during the dry period has been hypothesized as a risk factor for RFM.
• Changes in energy balance are felt to influence the degree of hypertrophication and
interdigitation of the microvilli of cotyledons with the crypts of the caruncles.
• Actual separation of the placenta starts well before the actual calving event.
CLINICAL FEATURES
• Symptoms are obvious, a portion of the fetal membranes hang from the vulva (Fig.1 a, b and c)
12 h or more following abortion, normal parturition or dystocia.
• Occasionally membranes do not hang from the vulva but are entirely within the vagina or
uterus.
• If fetal membranes are not expelled within 36 h or so are likely to retain it for 7-10 days.
• Myometrial contractions largely cease from 36 h after expulsion of fetus, so, if the membranes
have not been expelled by this time, freeing of the fetal villi from the maternal crypts
eventually occurs as a result of autolysis and bacterial putrefaction. This process starts within
24 h of calving but takes several days to complete.
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Retention of Fetal Membranes
a. In cow b. In buffalo c. In goat
• Natural sloughing of the maternal caruncles also contributes to the subsequent dehiscence of
the membranes, such that eventual expulsion of the membranes depends upon uterine
involution.
Duration of retention depends on
o Extent of the areas of attachment of the fetal membranes

o Rate of uterine involution
o Amount of uterine exudates, and
o Proportion of the afterbirth which had already passed through the cervix when
retention began.
• The toxic products of putrefaction accumulate within the uterus causing a fetid odour which
pervades the atmosphere and, more importantly, taints the milk, and makes it unacceptable for
human consumption.
• Delayed involution of the uterus and a variable degree of metritis commonly accompany
retention.
• In cows with RFM which have calved spontaneously after a normal length of gestation there are
subtle changes in health. Whereas, if retention occurs following extensive assisted delivery in
dystocia, a severe metritis and toxaemia can supervene within 2 or 3 days which, if untreated,
can be fatal.
• If RFM is accompanied by metritis, the symptoms depend upon the severity of the uterine
disease.
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GROSSS OBSERVATIONS OF PLACENTA
Normal Placenta
• Cotyledons appear grey to brown, occasionally

dark red in colour.
• Intercotyledonary are thin and free of gross
lesions.
Normal Cotyledon
• Villi of the cotyledons appear uniform in size with

tapering ends with smooth surface.
Abnormal Placrenta
• Retained placenta from aborted animals show

congested reddish brown cotyledons.
• Intercotyledonary portion is thick and covered with
fibrinous strands and serosanguineous exudate.
Abnormal Cotyledon
• Villi thick and appear in clumps.

• Presence of necrotic areas free of villi and contain
inflamatory exudate.
GENERAL CONSIDERATIONS OF RFM TREATMENT
• Stillbirths, obstetrical procedures and RFM can impair the cow's defense mechanisms. Normal
phagocytosis is decreased and intrauterine infusions or chemical curettage may be necessary to
decrease bacterial colonies in the uterus.
• An inflamed uterus is friable. Therefore, any physical manipulation can tear the uterus and
produce adhesions or a systemic illness (Septicemia).
368
• Cattle owners are concerned with the cost of treatment and any added labor for intensive care.
The economics must be justified for the use of the animal.
• Does the owner have the facilities to treat the cow? Is individual attention possible?
• Evaluate the history of the cow
o What are the uterine contents?
o What about the size of the uterus?
o Whether the membranes were retained?
o What was the calving date, was it a dystocia?
o What was the physical condition of the cow?
• A decision for rational treatment is based upon how well the animal and its reproductive tract
will respond to the drug(s) selected.
• There are different types of medications available
o An infusion requires a specific volume to dilute the character and quantity of uterine
fluid. Thick, purulent exudates are less likely to be responsive to a small amount of
antibiotics deposited intrauterine.
o The endometrium is a sensitive lining that will overreact to irritating compounds such as
Lugol's solution.
o A bolus can be placed through the cervix but the question is left unanswered if or when
the bolus dissolves?
o A gelatin capsule filled with tetracycline powder retards normal involution by being
acidic and causing tissue necrosis.
INSTRUCTIONS TO THE FARMER
The veterinarian should properly inform the farmer the following points to avoid complications
• Tying extra weight to the hanging portion of the membranes should be strictly avoided, as it
might cause tearing.
• The placental membranes should be kept moist. To do this
o Add tablespoon salt for every pint of water to be roughly isotonic.
o Pure water will irritate the endometrium.
• The placenta should be kept lubricated with the use nitrofurazone and petroleum jelly.
MANUAL REMOVAL OF RFM IN CATTLE
• Manual removal procedure has been in practice for years.

• It is advisable to excercise caution, if there is an existing metritis or a friable uterine wall. In
such cases, the cow can become septic or toxic.
• Whether manual removal has an adverse effect on future fertility is still under debate.
• RFM will lead to constant straining. Hence postponing treatment will only increase the chances
for complications.
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• The approach would be to try to separate the RFM without causing damage to any caruncles. If
the membranes are not easily separable, it is advisable to push the placenta back in and
redistend with warm saline.
PROCEDURE FOR MANUAL REMOVAL OF RFM [Roberts,1986 and Arthur and Bee,1996]
• A clean, manual examination of the uterus should be done.

• The operator should wear rubber coveralls or an apron and boots, a rubber glove and long
sleeve on one arm and a surgical glove on the other to protect him from brucellosis or an
infection of the arm or hand. Disposable plastic gloves and sleeves of good quality are more
sanitary and practical than rubber gloves and sleeves.
• Epidural anesthesia may be used to prevent frequent defecation or straining.
• The cow’s tail should be held out of the way by an assistant or tied with a tail rope over the
back to one of its fore legs.
• The perineal region of the cow should be carefully cleaned and washed with soap, water, and
mild antiseptic, and kept clean during the operation.
• Insert the left hand in to the uterus and squeeze the fetal cotyledon from the base of the
maternal caruncle. Twist the free part of the fetal membranes together in to a ‘rope’ with the
right hand. Apply a continuous steady traction and rotational force to withdraw the
membranes.
• If much fluid is present in the uterus it should be siphoned off by a sterile soft rubber horse
catheter or stomach tube held in the fist to keep the fetal membranes from plugging the end of
the tube. The siphon may be started by filling the rubber tube with water and holding it pinched
off as it is introduced.
• Manual removal should be done gently and quickly within 5 to 20 minutes, in a clean manner,
and with as few withdrawals and reintroductions of the arm as possible.
CONTRAINDICATIONS FOR MANUAL REMOVAL OF RFM
• Elevated body temperature above 103° F

• In severe necrotic vaginitis and vulvitis
• Septic metritis
• Acute mastitis
• Traumatic gastritis
CURRENT RECOMMENDATIONS
• Cows should not be examined until 96 h after calving and that removal should be gentle.
• It should be limited to the withdrawal of the membranes from the genital tract after they have
become spontaneously detached from the caruncles.
• In many animals, spontaneous detachment may have occurred within 96 h, it is acceptable to
leave the placental membranes for 10 or even 15 days before removal, if this length of time
was needed for their detachment (Roberts, 1986).
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ANTIBIOTICS
• One antibiotic of choice is tetracycline @ 2-6 gm intrauterine.

• Treatment should begin 12 h postpartum and continue daily until total expulsion of the
membranes.
• Systemic penicillin can be given for possible septicemia.
ECBOLIC AGENTS
• To physically cause the caruncle and cotyledon to separate, Oxytocin and Prostaglandin F2α
injections are used within 72 h of parturition.
Oxytocin
• Oxytocin injections (20-40 IU) are continued for 3 days after calving to contract an estrogen
primed uterus.
• It should be given as IM injections in small doses and often.
• High doses exaggerate uterine contractions, may force premature closure of the caruncles, and
favours retention.
Prostaglandin F2α (PGF2α)
• After 3 days, 25 mg of PGF2α injections must be administered IM.

• It can be administered once or twice a day. PGF2α are used because there is no withholding
time for milk.
• Multiple injections stimulate myometrial contractions and luteolysis for a return to oestrus.
ADMINISTRATION OF COLLAGENASE
• An injection of collagenase into the umbilical artery duplicates the cow's response to release
the cotyledons from the caruncles or 200,000units/litre with 500 mg of calcium chloride is
infused into one or both the uterine horns between 24-36 h post partum.
ACUPUNCTURE THERAPY
• By dilating the cervix, and increasing the coordination of uterine contractions, acupuncture can
help to expel the placenta and lochia.
• Strong electro acupuncture (EAP) stimulation at Urinary Bladder (BL) BL31, BL32, BL33 and BL34
for 15-30 minutes will cause the cervix to dilate sufficiently for manual removal of placenta and
placement of intrauterine antibiotics.
• Points for uterus and cervix include Yanchi and Baihui. Associated points - Weiken and Spleen
(SP) SP06.
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PREVENTIVE APPROACH
• Supplementation of anionic salts to the diet. RFM is thought to be influenced by electrolyte

concentrations.
• Uncomplicated cases of RFM require no treatment.
RETAINED FETAL MEMBRANE IN MARE - INTRODUCTION
• Retention of fetal membranes (RFM) is potentially more serious affection than the same in
cattle.
• RFM should be treated as an emergency.
• The average time taken for the fetal membranes to be expelled is about 1 h, and should not
exceed 2 h, although there is debate amongst equine clinicians about the latter.
INCIDENCE AND ETIOLOGY
• One of the most common peripartum problems, with an incidence of 2% to 10%.

• After dystocia much higher, probably due to either uterine trauma or uterine inertia.
• In equine dystocias treated at the Ghent Veterinary School, the incidence was 28% after
fetotomy, and 50% after caesarean operations; in the latter, the likelihood of retention was
doubled if the foal was alive at the beginning of the operation compared with, if it was dead
(Vandeplassche et al., 1972).
• These authors emphasize:
o The branching nature of the numerous chorionic microvilli that interdigitate strongly
with the corresponding labyrinth of endometrial crypts.
o The microvilli are better developed in the uterine horns than in the body, and are
considerably more branched, as well as bigger, in the non-pregnant than in the pregnant
horn.
o This latter property of the villi, coupled with the more marked folding of the
allantochorion and endometrium as well as the slower involution of the non-pregnant
horn, all combine to provide an explanation of the higher incidence of retention in the
non-pregnant horn.
o Retention of placental pieces could arise from other areas, so thoroughly examine the
fetal membranes to determine which portion has been retained.
o The precise cause of retained placenta remains unclear.
o The most likely is uterine inertia due to hormonal imbalance. Oxytocin has an important
role in postpartum uterine contractions, and low levels of this hormone in the
circulation may result in abnormal myometrial activity. This in turn leads to placental
retention.
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CLINICAL SIGNS
• Most obvious sign is presence of a variable portion of tissue protruding from the vulva; less
commonly nothing is visible.
• Either this means that no parts of the fetal membranes have been expelled or, more likely,
portions remain attached.
COMPLICATIONS OF RFM
• Complications include acute metritis, septicaemia, laminitis and even death.

• With prompt and effective treatment these sequelae can be avoided.
• In many cases, uterine involution is delayed even if these more serious complications do not
develop.
TREATMENT OF RFM
• Initially, the protruding membranes should be tied in a knot to prevent them touching the
hocks.
• As uterine contractility plays an important role in the dehiscence of the fetal membranes,
administration of oxytocin is recommended as a first and most successful method of treatment
in up to 90% of cases.
• It is a good rule not to wait longer than 6 h after delivery of the foal; the time interval should be
shorter in heavy breeds. This method of treatment avoids manipulation within the uterus, with
the risk of introducing microorganisms.
• Oxytocin can be given via the intramuscular route (20-40 IU), which can be repeated after 1 h if
the membranes have not been expelled. Alternatively, use slow intravenous infusion of 50 IU
oxytocin in 1 litre of physiologic saline over 1 h. Symptoms of colic often follow injections of
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oxytocin and commonly precede natural expulsion so that pain relieving drugs and sedation
may be required.
• Attempt gentle removal only in cases where treatment is unsuccessful and the membranes are
almost detached but retained within the uterus. Removal of placenta should be carried out with
scrupulous regard to asepsis, and no undue force should be applied, for even moderate traction
on the afterbirth may cause the uterus to become inverted and prolapsed.
• In most cases of retention, some separation of the allantochorion has occurred and
consequently a variable amount of the afterbirth hangs down from the vulva.
MANUAL REMOVAL OF RFM IN MARE
• The mare is effectively restrained and measures should be taken to protect the operator from
being kicked.
• The tail is bandaged and held to one side by the attendant while the obstetrician thoroughly
washes the perineum and rear of the mare.
• With the hand and arm protected by a clean plastic sleeve, the extruded mass, or failing that
the freed part lying within the vagina, is grasped and twisted into a rope (Fig).
• The gloved hand anointed with lubricant is gently introduced along the ‘rope’ to the area of
circumferential attachment in the uterus.
• As the ‘rope’ is gently pulled and twisted, the tips of the fingers are pressed between the
endometrium and the chorion.
• The villi are easily detached, and as the allantochorion is gradually freed it is taken up by further
twisting of the detached mass.
• The allantochorionic membrane is gently separated from the endometrium by moving one of
the hands between them.
• The tightest attachment is usually at the tip of the horn.
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• The process of separation usually goes quite smoothly, and the complete sac of allantochorion
can be gradually detached from the pregnant horn.
• There is a tendency for attachment to be firmer in the non- pregnant horn, and occasionally
retention is confined to this horn.
• If it is found impossible to detach the apical portions of the allantochorionic sac without tearing
the membranes it is better to desist and to try again in 4-6 h, by which time a successful
outcome will be likely.
• Unwanted side-effects of this manual removal may be serious haemorrhage, invagination of
one of the horns and a higher chance of retention of microvilli in the endometrium.
• Vandeplassche and his colleagues (1971 and 1972) refer particularly to the residue of microvilli
that is present in the endometrium even after a normal expulsion of the afterbirth and is vastly
increased when manual removal is effected in a case of retention.
o During a difficult manual removal only the central branches of the chorionic villi are
removed while practically all the microvilli are broken off and retained; rupture of
endometrial and subendometrial capillaries may also occur.
o The consequences of difficult removal are increased puerperal exudate, containing
much tissue debris; endometritis and laminitis; uterine spasm and delayed involution of
the uterus. It is for these reasons they prefer to treat severe equine retention by means
of intravenous drip administration of oxytocin rather than by persistence with manual
removal.
OTHER METHODS
• A method described in the literature, and which may be successful under some circumstances
o Introduce about 10 litres of warm sterile saline inside the chorioallantoic membrane.
o Stretching of the uterine wall stimulates uterine contractions, via endogenous oxytocin
release, and may assist in the separation of the microvilli from their endometrial crypts.
This treatment should be used in combination with exogenous oxytocin administration.
o After removal, it is always important to examine the membranes for completeness
confirming that all the allantochorion has been removed.
o If necessary, the uterus should be flushed and siphoned to remove any fluid exudate
remaining in the uterus by using a stomach tube and funnel.
• Aftercare includes (depending on the severity of the case) regular general clinical examination,
particularly the uterus (for involution and contents) and, if indicated, flushing and siphoning the
uterus once or twice daily for a few days in combination with further injections of oxvtocin.
• The rationale for uterine lavage is to remove both debris and bacteria from the uterus. Warm,
sterile physiologic saline should be used in 2-4 litre flushes (until the recovered fluid is clear).
• Vandeplassche and colleagues (1972) deprecate the use of any antiseptic solution to rinse the
uterus after the expulsion of the afterbirth, because this depresses phagocytosis.
• Special attention is paid for signs of laminitis, and non-steroidal anti-inflammatory drugs are
given when laminitis is a suspected complication.
• Tetanus antitoxin is recommended and, if indicated, treatment with antibiotics.
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• If there is a risk of the mare developing a toxic metritis, mare should be treated with systemic
and intrauterine antibiotics.
• The dominant infective organism is often Streptococcus zooepidemicus initially, but infection
with Gram-negative bacteria such as Escherischia coli frequently develops. The antibiotics
chosen should have broad-spectrum activity and should be effective against endotoxin-
producing organisms.
• Cyclo-oxygenase inhibitors such as flunixin meglumine should be given to either treat or
minimize the risk of development of endotoxaemia.
• Provided treatment is begun at the correct time and no secondary complications develop, the
prognosis for a case of retained placenta is good.
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MODULE-16: PUERPERAL / SEPTIC METRITIS
ETIOLOGY
• Occurs within a few days to 2 to 8 weeks or more postpartum.

• Usually follows an abnormal first or second stage of labour, especially when there has been a
severe dystocia.
• Also associated with uterine inertia, twin births, RFM, prolonged traction and damage to the
vulva and/or birth canal.
• Bacteria colonise the non-involuted uterus, producing toxins which are absorbed and cause
severe symptoms.
• Many species of bacteria can be recovered. The most important are A. pyogenes, group C
streptococci, haemolytic staphylococci, coliforms, and Gram-negative anaerobes, particularly
Bacteroides spp. In rare cases, clostridia are present which rapidly produce disease that is
serious and often fatal.
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SYMPTOMS
• Local and general symptoms

• Toxaemia, septicaemia and pyaemia.
• Temperature may be elevated to 40—41°C, but is more often subnormal.
• Rapid pulse rate (in the region of 100/minute)
• Respirations may be sufficiently frequent to suggest a respiratory disease.
• Anorexic and dehydrated
• Often have toxaemia-induced diarrhoea and exhibit signs of shock.
• Infection may extend through the uterine wall into the peritoneum, causing a localised or
generalised peritonitis.
• Uterus contains a large volume of toxic, fetid, reddish, serous exudate, containing pieces of
degenerating fetal membranes
• Exudate is discharged from the vagina by frequent expulsive straining efforts.
• Vaginal and uterine exploration of an affected case causes acute discomfort and is
accompanied and followed by the most severe and persistence of expulsive efforts.
• Cotyledons are swollen and the fetal membranes often remain firmly attached.
• Vulva and vagina are swollen and deeply congested.
• Primary pneumonia
• Traumatic reticulitis and pericarditis,
• Milk fever, and
• Acute mastitis.
TREATMENT
• Good nursing care and vigorous medication.

• The cow should first be kept warm and made as comfortable as possible by transferring it to a
well-bedded and warm loose-box.
• By gentle external traction, attempt to remove the fetal membranes, but avoid performing per
vaginum examination. Rough attempts at removal of the fetal membranes or even careful
exploration of the vagina and uterus can cause severe damage and predispose to the
absorption of toxins and entry of bacteria.
• If straining persists, caudal epidural anaesthesia can be used; local anaesthetic alone gives
transient relief for 1-2 h and sometimes it will ‘break the cycle’ and stop the straining.
• Inj. xylazine, either alone or in combination, the duration of effect can be prolonged.
• If it is within 2-3 days of parturition, 50 i.u. of oxytocin by intravenous injection may cause
contraction of the uterus and expulsion of fluid and debris.
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• If the exudate is very thick, an enzyme like streptococcic dornase or pancreatic trypsin may be
used to thin it and thus make it easier to siphon out.
• Systemic administration of broad-spectrum antibiotics and supportive therapy.
• Choice of antibiotic and the route of its administration have been the subject of much debate.
• Intrauterine antibiotics are unlikely to eliminate the infection - nitrofurazone, neomycin and
some sulphonamides, may be detrimental to the endometriuin.
• Intrauterine infusions of dilute iodine are considered to be more harmful than helpful.
• Intrauterine infusions of tetracyclines may be effective against mild cases of endometritis, but
they do not penetrate far enough into the uterine wall to be effective against full-thickness
metritis.
• Systemic broad- spectrum antimicrobials, fluid therapy and nonsteroidal anti-inflammatory
drugs are widely recommended.
• Use of oestrogens is contra- indicated in cases of acute puerperal metritis, as they increase the
blood flow to the uterus and, thereby, increase the absorption of bacterial toxins.
• When temperature returns to normal and the cow shows some signs of improvement, uterine
lavage with several litres of warm (49°C) sterile saline and drainage may be beneficial.
• Parenteral and intrauterine antibiotics should be administered daily.
TREATMENT RESPONSE
• Resumption of appetite.
• Cessation of diarrhea, and
• Presence of a less fetid and thick vaginal discharge.
• Recovered cases inevitably show a mucopurulent discharge or leucorrhoea, due to chronic
endometritis.
PROGNOSIS FOR SUBSEQUENT FERTILITY
• Guarded, due to lesions such as

o Ovarobursal adhesions
o Uterine adhesions, and
o Occluded uterine tubes.
• Other complications of metritis include
o Pneumonia
o Polyarthritis.
SEPTIC METRITIS
• In all species, usually observed within 1 to 10 days after parturition with or without retention of
the fetal membranes and are characterized by a fetid, red, watery uterine fluid that is very toxic
and depressing to the animal.
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ETIOLOGY
• Similar to that of retention of the fetal membranes.

• Usually is associated with a uterine atony or inertia.
• More pathogenic types of organisms are present in the uterus and they or their toxins are
absorbed into the circulation, producing severe general symptoms associated with septicemia,
toxemia, and pyemia.
• Most common organisms: coliform organisms, Coryn. pyogenes, hemolytic staphylococci, Ps.
aeruginosa, proteus, hemolytic streptococci, and in rare cases clostridia.
• Usually follows emphysema of the fetus, severe torsion of the uterus with the presence of a
dead and possibly emphvsematous fetus, and other conditions associated with a uterine inertia
such as dropsy of the fetal membranes, fetal anasarca, fetal giantism, twinning, and peritonitis
due to traumatic gastritis.
• In many cases it may follow rough, improper removal of a retained placenta.
• May follow a prolonged dystocia especially if a difficult fetotomy operation has been
performed.
• May follow a prolapsed uterus associated with trauma and infection of the endometrium.
• Occasionally it may result by extension from a necrotic vaginitis.
• May occur in all species through the introduction of infection by unsanitary practices during the
relief of dystocia or removal of a retained placenta.
• In dogs and swine it may occur from neglect at the time of parturition or trauma to the uterus
with forceps, or accidentally allowing one or more placentas or fetuses to remain in the uterus
and macerate.
SYMPTOMS
• Similar in all species of animals.

• Retention of the fetal membranes is frequently observed
• In cow, placentomes are usually greatly swollen and the fetal cotyledons firmly attached to the
maternal caruncles.
• In the mare, a piece of the placenta, often a portion from the nongravid horn is retained and
found in the body or nongravid horn of the uterus.
• Anorexia and dullness.
In cow
• Rapid pulse of 80-120 per minute, and usually weak

• Early phase - temperature may be elevated
• In advanced cases - temperature may be either normal or subnormal. The latter condition
usually occurs shortly before death of the animal. The cow is less apt to show a prolonged
elevation of body temperature than are the other animals
• Shivering and cold extremities
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• Rapid and shallow respirations
• Sunken eyes
• Rough hair coat, and
• Rapid loss of weight.
• In severe cases:
o Marked atony of the digestive tract
o Feces may be hard and firm or may be black, oily, fetid, and liquid in character especially
in the cow
o A marked drop in milk flow or agalactia occurs in all species and the newborn will exhibit
signs of malnutrition or starvation.
SYMPTOMS IN SOWS
• The agalactia often persists and the pigs must be reared as orphans
• There is usually a reddish, watery, fetid discharge from the vulva
• The genital passage is likely to be swollen and inflamed
• Straining may be present or absent before the examination but during or after the examination
it is generally present
• Rectal examinations should usually be confined to cows with no evidence of rectal irritation or
enteritis
• In some cows having septic metritis without a retained placenta the cervix may be quite
contracted
• Vaginal examination
o Normal vagina and clear, or only slightly cloudy, vaginal mucus
o Uterine contents may be toxic and fetid, and occasionally toxic enough to cause death.
o Uterus is atonic or flaccid, walls are usually thin and in some cases.
• Peritonitis due to extension of the infection through the uterine wall with symptoms of
abdominal tenderness or soreness, abdominal distension. Slight to moderate tympany of the
rumen due to atony of the digestive tract, an arched back, stiff, slow gait, and tense abdominal
muscles. Cow may exhibit a characteristic expiratory grunt
• Perimetritis or peritoneal involvement with the uterine infection may occur naturally or be
produced by heroic or too vigorous treatment of a severely infected and inflamed uterus
• Rectal examination on these cases in cows may reveal early fibrin deposition and adhesions
present between the uterus aid the adjacent abdominal viscera. If found, the operator should
terminate the examination at once
• Arthritic symptoms, with swelling and stiffness of the joints, particularly the hock, fetlock and
knee joints, may occur especially in the cow and sow
• Acute laminitis may also be present making the animal reluctant to rise and stand - weak,
staggering, or prostrate and show symptoms of paresis and inability to rise – cold extremities-
easily be confused with milk fever
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• A mild to strong reaction to the Ross test for the presence of ketones may develop on testing
the urine of cattle with septic metritis. This may be due to ketosis as a complication of the
disease but more often it is caused by the severe anorexia
• In early stages, blood count - marked shift to the left, together with a. great drop in the total
white blood cell level. During the recovery stage the white blood cell count shifts to the right,
with a leukocytosis developing
• Occasionally secondary complications of pneumonia, and laminitis in the mare, cow, sow and
ewe, and in all species pyemia with arthritis, liver, brain, or lung abscesses or endocarditis or
myocarditis may develop especially if the condition is prolonged
• Rough removal of the placenta, or lacerations of the endometrium encountered in prolapse of
the uterus may allow organisms to localize in the uterine wall and cause an abscess.
• Traumatic gastritis.
• Gastroenteritis hemorrhagic septicemia.
• Pneumonia.
• Parturient paresis.
• Laminitis and mastitis which may cause paraplegia, reluctance or inability to stand and illness at
parturition.
PROGNOSIS
• Course usually lasts from 2 to 6 days, with recovery or death occurring within that time.
• In the cow a prolonged course may extend over a period of from 1 to 2 weeks.
• In early cases before severe uterine damage, peritonitis: Guarded to poor.
• Failure to respond to treatment, persistent straining or complications such as mastitis and
pneumonia: Grave.
• In severe cases as well as in cases of perimetritis, ovaritis or abscesses of the uterine wall:
Future breeding life poor.
TREATMENT
• Should be conservative.
• Massage and douching of the uterus, attempts to remove the retained fetal membranes should
seldom if ever be performed in cases of septic metritis, or the animal’s condition may become
critical.
• Septicemia and toxemia should be overcome before manipulative procedures are used.
• In early cases pituitrin, 3 to 5 ml. in large animals or 1 to 3 ml. in small animals may be of some
value in producing tonus in the atonic uterus. Usually if the condition is severe hormones are of
questionable value.
• If the uterus is filled with a large amount of fetid fluid this should be gently siphoned off.
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• In the mare and dog, if a portion of the placenta is lying in the uterus it should be removed in as
gentle a manner as possible.
• Intrauterine administration of 1-3 gm. of the broad- range tetracycline Derivatives (Aureomycin
or Terramycin or furacin) in a solution or in a readily soluble form may be of great value.
• Antibiotics (Procaine penicillin, 3000-6000 units per pound of body weight daily and
streptomycin, 5 gm/1000 pounds twice daily, intramuscularly; Terramycin, or tetracycline
intravenously; or in large animals except the horse, intramuscularly, at a rate of 1-3 mg per
pound of body weight, daily) and sulfonamide therapy (Sulfamethazine or sulfamerazine in daily
doses of 1-1.5 grains per pound of body weight may be given intravenously, intraperitoneally,
or orally) are indicated parenterally. In valuable cows antibiotics and sulfonamides may be
combined.
• Other supportive therapy such as saline and glucose solutions and blood may be administered
daily.
• Calcium gluconate seems of value especially in the early cases and may increase the tone of the
uterus, but large doses given too rapidly to toxic cattle may cause death.
• Pyribenzamine or other antihistamines may he of value.
• Forced feeding may be helpful.
• Good nursing in a suitable stall or other equally comfortable environment is essential.
• If possible the large animal should he on green pasture each day or provided with fresh-cut
green feed and with whole oats or other coarse feeds to tempt and encourage it to eat.
• If straining is present epidural anesthesia should be used to control it until the cause of the
condition is determined and corrected.
SYMPTOMS SUGGESTIVE OF TREATMENT RESPONSE
• A drop in pulse rate

• An increase in appetite
• An improvement in the tone of the uterine wall
• A change in the exudate from a watery to a mucoid consistency
• Treatment should be continued until the animal has safely recovered and septic symptoms
have subsided. This should take place before actively treating the uterus and removing the
retained fetal membranes in the cow. It may be advisable to let the afterbirth drop away
• In the mare, septic metritis is likely to cause laminitis, or “colt” founder. The application of ice
packs to the feet is indicated as preventive therapy in septic metritis
• Laminitis may also follow metritis in the cow, ewe, and sow but is usually less severe and may
be unnoticed until months later when deformity of the hooves becomes evident.
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INFECTIONS OF CERVIX - VAGINA – VULVA
CERVICITIS - DEFINITION
• Cervicitis is referred to as an inflammation of the cervix.

• The cervix appears more resistant to infections than either the uterus or the vagina.
• In cow, commonly observed and associated with metritis.
• The internal portions of the cervix appear rather resistant to the introduction of miscellaneous
infections.
• Most cases of cervicitis originate at the time of or following parturition and often are associated
with a metritis.
ETIOLOGY
• Frequently follows abnormal parturitions such as

• Abortions
• Premature birth
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• Dystocia, especially where forced extraction or fetotomy caused cervical lacerations or trauma,
retained placenta, and postpartum metritis.
• Cervicitis especially of the external os of the cervix may follow injuries to the vulva and vagina
allowing “windsucking” and vaginal contamination.
• Vaginal infections whether viral or bacterial usually produce a cervicitis, especially of the
external os of the cervix.
• Due to trauma or puncture of the cervix by a catheter or insemination pipette.
• C. pyogenes are probably more pathogenic than others such as streptococci.
• Coitus can introduce infections that might cause some involvement of the external os of the
cervix as well as the cranial portions of the vagina.
• In older cows, prolapse of the external transverse cervical rings or cervical ectropion is often
chronically thickened and fibrosed and circulation to the epithelium may be poor, permitting
the establishment of infections.
• Severe purulent vaginitis or vaginitis associated with pneumovagina due to a lacerated or
stretched vulva, atrophy of the perineal body and vulvar lips and horizontal tipping of the vulva
may cause a severe cervicitis especially if urine and feces are present in the vagina.
• A poorly developed short cervix with very small transverse rings may readily permit an
endometritis to develop and a cervicitis may also be present.
SYMPTOMS AND DIAGNOSIS
By vaginal examination using a speculum and light
• External os of cervix is usually edematous and swollen.

• External folds are often prolapsed
• Cervical mucosa is a cherry-red to dark-purple color, and
• Mucopurulent exudate may be seen in and on the cervix.
By rectal examination
• Infected cervix may be large and thick or may be normal in size.

• Hypertrophy of the cervix does not necessarily mean that cervicitis is present. Cervicitis does
not occur commonly in the greatly hypertrophied cervices noted especially in Brahman, Zebu
and Santa Gertrudis cattle.
• Occasionally in severe chronic cervicitis the cervix may be very thick and sclerotic. Severity of
the cervicitis will vary depending on the cause and length of time it has existed.
• It may be difficult to differentiate between cervicitis and metritis. If a metritis is present
cervicitis is also invariably present.
• Vigorous manipulation of the cervix will produce a severe hyperemia and congestion of the
mucus membrane that should not be confused with infectious cervicitis.
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INFLUENCE ON FERTILITY
• Even in severe forms of cervicitis, conception may occur.

• In postparturient cows, 40% revealed presence of a wide variety of bacteria, including
streptococci and staphylococci in the cervical mucus. No evidence of that these organisms had
any effect on fertility. Cervicitis rather seldom cause sterility.
• Since cervicitis and endometritis are closely associated and the former usually can be observed
clinically, cervicitis may often be erroneously blamed for infertility.
• Occasionally if pregnancy does occur even though a cervicitis is present the gestation may be
insecure, with the possibility that abortion, retained placenta, and other uterine pathology may
develop.
• Cervical stenosis may occur due to severe cervical inflammation, or an enlarged cervical ring
may extend into the cervical canal, making a sharp bend in the lumen so that passage of a
catheter is difficult or impossible. These cows frequently conceive promptly when bred
naturally or when semen is deposited artificially in the cervix.
• Rarely, a severe sclerotic, fibrosed, indurated cervix may result in cervical stenosis at the time
of calving causing dystocia.
PROGNOSIS
• In most cases, it is good.

• Spontaneous recovery occurs.
• If metritis or severe vaginitis is present, recovery does not occur.
• Cervical infection usually is overcome by natural defense mechanism.
• In severe cases, takes longer period for recovery
• Cervical stenosis or sclerosis does not respond to treatment, but if pregnancy occurs, it may
lead to dystocia at the time of parturition.
TREATMENT
• If associated with metritis or vaginitis, treat the entire reproductive tract.

• Spontaneous recovery does occur.
• Give warm or hot mild antiseptic vaginal douche every 3-4 days.
• Douching of the cervix and uterus may be useful.
• Administration of parenteral antibiotics
• If cervicitis is secondary to vaginitis and pneumovagina, apply vulvar retention sutures.
• In occasional cases following a dystocia a necrotic cervicitis or a severely lacerated cervix may
be amputated. This may be done readily with large serrated scissors. After the prolapsed rings
have been amputated the vaginal mucosa may be sutured to the cervical mucosa to help
control hemorrhage and promote rapid healing hut this is not necessary.
• Epidural anesthesia is not required as there are no sensory nerves in the cervix.
• Trachelorrhaphy is the suturing of cervical lacerations after calving.
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• Partial traehelectomy is the amputation of a portion of cervix. This operation is probably not
necessary since cervical infections of the external os seldom prevent conception and the
internal portion of the cervix provides a firm seal even though the external os may be ectropic
and inflamed. Usually within 3 to 4 weeks after amputation of the prolapsed cervical rings
healing has occurred and breeding can take place. Regular oestrus periods have as definite a
healing effect on cervicitis as they have on endometritis.
• In severe cases, sexual rest is indicated for two or more oestrus periods. Stilbestrol injection or
topical application (20 to 40 mg, i/m) may have some value if it is repeated every 10 days or so.
• Manual or instrumental dilation of an atretic or stenosed cervical canal usually leads to rupture
before a significant dilation occurs.
• Cervicitis may be prevented by avoiding trauma to the cervix whenever possible.
VAGINITIS - DEFINITION
• Vaginitis refers to the inflammation of the vagina.
SYMPTOMS
• Mucopurulent, yellow-grey pus is usually discharged from the vulva at irregular intervals
• Matting of the hair of the vulva, tail and buttocks.
Vaginal examination
• Exudate is observed on the floor of the vagina

• Vaginal walls are congested, edematous, and inflamed.
• In more severe the inflammation - more red and inflamed.
• In some cases ulceration of the mucosa, lacerations and secondary diptheritic or necrotic
lesions occur especially around the vestibulo-vaginal border and in the vestibule and vulva.
• In severe cases: tenesmus, irritation, and pain probably due to the concurrent vestibulitis and
vulvitis.
• If the vulva is stretched, damaged, torn, or deformed, results in pneumovagina - the vagina may
then contain fecal material, urine, and air as well as mucopurulent exudate.
• Failure of conception, particularly in older cows in the large breeds.
• In uncomplicated mild vaginitis: conception not affected.
• Vaginitis associated with cervicitis and endometritis leads to infertility
• In pneumovagina in old cows or Indian cattle with a large heavy cervix pulling the vagina
forward and downward, an accumulation of material in the vagina, often associated with an
atonic uterus hanging low in the abdominal cavity, may cause some infectious material to pass
through the infected and relaxed cervix and thereby cause an endometritis.
• Often in older cows with the characteristically deformed perineum, the vulvar lips may be
parted with the fingers and air will rush into the vagina.
• If metritis or cervicitis is present some of the vaginal discharge may actually come from those
sites and the vagina is involved secondarily.
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• Necrotic vaginitis, as described previously following a difficult parturition, may also follow the
accidental use of caustic agents as a douche. In rare cases secondary stenosis and even atresia
of the vagina may follow a severe vaginitis.
ETIOLOGY
• Observed in cows as a primary or secondary condition.

• Often associated with metritis and cervicitis.
• May occur following trauma, lacerations and bacterial, viral or protozoal infections produced or
introduced at the time of service, abortion, dystocia, fetotomy, retained placenta, prolapse of
the vagina, and postpartum metritis.
• Severe stretching or laceration of the vulva especially of the perineal body, and in older cows
sinking of the anus and tipping of the vulva into a horizontal position, with an atrophy of the
vulvar lips often results in pneumovagina and severe contamination of the vagina by feces,
urine, air, and miscellaneous debris and infection that often cannot be readily expelled because
the uterus and cervix have pulled the anterior portion of the vagina forward and downward into
the abdominal cavity.
• May occur following coitus but this is usually a mild and transient condition.
• In rare instances vaginitis may be due to treatment of the vagina with irritant preparations,
introduction of infection on instruments, or examination of the vagina in a dirty, unsanitary
manner.
• Most vaginitis is due to non-specific infections such as staphylococci, streptococci, coliform
organisms, C. pyogenes, and others.
• Specific infections such as IBR-IPV, “epivag”, and possibly other viral infections, trichomoniasis,
vibriosis and granular venereal disease may also lead to vaginitis.
• Occasionally, necrotic vaginitis and severe vaginal lacerations following calving, dystocia, and
fetotomy may result in vaginitis.
PROGNOSIS
• In simple vaginitis: Good and most cases will respond spontaneously even without treatment
unless pneumovagina is present or unless a severe chronic cervicitis or metritis is also present.
• In severe stenosis or atresia of the vagina: Poor.
• In vaginitis due infectious agent: Local antibodies are usually produced that aid in the
elimination of infections such as V. fetus, Tr. fetus and IBR-IPV.
TREATMENT
• Mild aqueous douches of 200 ppm chlorine solution, antiseptic aromatic soap solutions, dilute
potassium permanganate solutions, 1:1000 to 1:3000 acriflavine solutions, 200 ppm quaternary
ammonium compound solutions, sodium bicarbonate solutions, solutions of chlorhexidine, and
saline solutions.
• Irritating douches are unnecessary and should be avoided.
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• Usually 2 – 4 litres of a solution are used and introduced either by means of a catheter and
funnel, an enema bag and tube, or by holding the extended hand palm upwards in the vestibule
pinching down the cow’s back, and pouring the solution over the palm of the hand into the
vagina.
• Vaginal flushing may be repeated several times to wash out mucopurulent material.
• Retreating may be helpful at daily or at 3- to 4-day intervals.
• Infusion of sulfonamides or antibiotics such as: penicillin, streptomycin, neomycin, furacin,
tetracyclines or others in an ointment form or in oil-and-water emulsions.
• If a cervicitis or metritis is present these should be treated also.
In cases of pneumovagina the vagina is usually douched thoroughly, an antibiotic solution or
preparation is placed in the uterus, cervix, and vagina.
• In mares, Caslick operation may be performed under epidural or local anesthesia. The vulvar
opening after this operation is small and service by artificial insemination usually is necessary.
The last week or two of gestation the vulva should be incised along the original suture line so
that no tearing of the vulva will occur at parturition. The vulva needs to be resutured after
calving.
NECROTIC VAGINITIS/VULVITIS - DEFINITION
• Pressure necrosis of the vaginal and vulvar mucous membranes.
Occurrence
• In dairy and beef heifers having a narrow small birth.

• Occasionally in cows, especially young cows or those of the smaller breeds.
PATHOGENESIS
• In the process of parturition, fetus may have been expelled without artificial interference after
a difficult, prolonged parturition or sometimes aided by traction often result in trauma,
laceration, excessive pressure, and abrasion of the vulvar and vaginal walls.
• Vaginal and vulval mucosa may be further irritated by the presence of a retained placenta, a
metritis, or a torn or ruptured perineum permitting infection to gain entry.
• In heifers, following the removal of an emphysematous fetus by traction or after a prolonged
fetotomy results in pressure necrosis of the vulvar and vaginal mucous membranes.
• In rare cases may be due to douching with too irritating or strong an antiseptic.
• Occasionally a severe necrophorus infection of the vagina may occur.
CLINICAL SIGNS
• Usually observed 1-4 days after parturition and depending on the severity of the lesions last for
1-2 weeks or more.
• Arched back
• Elevated tail
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• Anorexia, and
• Rapid loss of weight.
• Exhibit no straining or straining that is intermittent and mild and only observed at the time of
urination or defecation, or nearly continuous straining with air being sucked into the vagina and
forcibly expelled.
• Vulva and vagina may be very swollen, due to a perivulvar and perivaginal phlegmon.
• A fetid, reddish, watery fluid is present in the vulva.
• Pulse rate is usually elevated.
• Body temperature may be moderately elevated.
• Parting of the vulvar lips reveals a necrotic, diptheritic inflammation of the vulva and vagina,
usually most severe at the vulvo-vaginal border.
• Necrotic portion of the mucous membranes sloughs, and the exposed submucosal tissues
granulate and eventually heal with a cicatrix.
Necrotic vaginitis in cow Necrotic vaginitis with abscess in cow
Follow an excessively forceful delivery. Vaginal necrosis followed by abscess.

Severe bruisings, with or without Abscess pointing and trying to rupture
lacerations, leads to lack of blood through the skin. Skin is very thin and
supply and subsequent necrosis. avascular at the apex.
Source: Drost Project
In acute case
• Passage of the hand through the inflamed vulva and vagina of the cow is likely to cause
bleeding.
• Very painful to the animal, and
• Because of the swollen dry tissues is usually difficult to perform.
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• Straining is probably due to the vestibular and vulvar inflammation and irritation and possibly
the accompanying vaginal swelling or phlegmon, since there are many sensory nerves in the
vulva and vestibule but few if any in the vagina.
• Irrespective of the handling approach, some develop a marked stenosis or even atresia of the
vagina resulting in a distention of the cranial portion of the vagina due to pus or mucus.
In advanced chronic cases
• Even the cervix and the uterus may be distended with 2-3 gallons of a mucopurulent material if
infection persists, or of mucus alone if no infection is present.
DIAGNOSIS AND DIFFERENTIALS
Diagnosis
• Based on the history of the case and clinical signs.
Differential diagnosis
• Straining due to vulvitis, vestibulitis and vaginitis should be differentiated from

o That caused by dystocia
o An undiagnosed retained fetus, rabies, or other conditions which might cause straining.
PROGNOSIS
• In mild cases treated early: fair to good.

• In severe and neglected cases: guarded.
• If necrosis is extensive, straining constant, and the animal is extremely debilitated, death may
result.
• In cases of severe vaginal atresia: future breeding life is usually terminated.
Following healing
• Breeding may be advised if the stenosis is not severe.

• At the time of parturition it may be necessary to dilate this stenotic portion of the vagina.
• In many cases, however, due to the relaxation of the vaginal wall and surrounding tissues, mild
stenoses disappear at the time of parturition.
• If the stenosis is severe and breeding is desired this might be accomplished by artificial
insemination and cesarean section at the time of parturition.
• Most severe cases of stenosis of the vagina are slaughtered.
TREATMENT
• Should be gentle and conservative.
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• Oily bland antiseptics such as 4 to 6 ounces of bismuth formic iodide in oil, together with the
broad range antibiotics, may be introduced in a gentle manner into the cranial portion of the
vagina 2-3 times a day. As this infusion is expelled it coats the inflamed mucous membranes.
• If swelling, phlegmon, elevation of the temperature, and rapid pulse rate are present,
parenteral administration of antibiotics and/or oral or intravenous administration of
sulfonamides are indicated daily for 4-6 days or until recovery is evident.
• Injections of small doses of estrogens, 15-25 mg. of stilbestrol every second or third day may
stimulate healing of the vaginal mucous membrane.
• If in the cow, retained fetal membranes are hanging through the vulva they should be removed
if this can be done easily and without injury to the vulva and vagina. In most cases the placenta
is fastened securely and must be allowed to remain and drop away later. If the membranes are
heavy and hang nearly to the floor they should be cut off at the hocks so the added weight does
not aggravate the vulvitis and induce straining.
• If straining is present, the use of one of the longer-lasting epidural anesthetics such as xylocaine
or lidocaine to which a small amount of adrenaline solution has been added to retard its rate of
absorption, or Cobefrin is of value and may be given twice daily or more often if necessary.
• Pudendal block will also anesthetize the vulva but it is neither practical nor as easily performed
as is the administration of epidural anesthesia.
• Administration of tranquilizers is helpful in controlling pain and tenesmus. Elevation of the rear
parts may be helpful.
• In mild cases of vulvitis and vaginitis with straining, some local anesthetic ointments containing
butesin picrate or benzocaine have been used but difficulty has occurred in applying these to a
moist mucous membrane and their effect is questionable.
• If tenesmus is severe and accompanied by marked sucking and blowing of air into and out of
the vagina, the dorsal two-thirds to three-quarters of the vulva should be tightly sutured after
administration of epidural anesthesia. This prevents ballooning of the vagina with air and
precludes the accompanying irritation and straining. This approach with other supportive
treatments described usually promptly controls the straining. The sutures holding the vulvar lips
together may be removed in 4-7 days.
• In rare cases it may be indicated to insufflate the abdominal cavity with air to prevent
tenesmus. This increased pressure in the abdominal cavity results in increased pressure in the
pleural cavity and relaxation of the abdominal musculature to ease respiration.
• Control of severe straining is essential to prevent rapid loss of weight, weakness, early
exhaustion, and even death.
• Repeated treating and dilating of a necrotic vagina is not indicated, in as much as this
procedure prolongs recovery time, increases the inflammatory reaction in the vagina, and
produces additional scar tissue.
CATARRHAL VAGINITIS AND VULVITIS
• Occurs following or with retained placenta, puerperal metritis, or injuries to the vulva causing
pneumovagina; generally characterized by a persistent mucopurulent discharge from the vulva.
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Treatment
• Dilute, warm vaginal douches, using 200 ppm chlorine, dilute potassium permanganate, dilute
Lysol or other soapy aromatic antiseptics, or saline or sodium bicarbonate are indicated. These
may be repeated at 1- to 3-day intervals. In cows, injections of oestrogens, 10 to 30 mgm of
stilbestrol or 1 to 3 mgm of oestradiol, may be helpful.
• If the vulva is torn it should be sutured, to prevent pneumovagina.
• If puerperal metritis is present the vaginitis may persist in a mild form until the discharge of
uterine exudate ceases.
• In some cases when only a vaginitis is present 1-3 weeks after parturition, some oily antibiotics
or antibiotics in ointment form may be placed in the vagina to aid in overcoming the infection.
Prognosis: Good.
MILK FEVER - POSTPARTUM PARAPLEGIA
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INTRODUCTION
Milk fever, the clinical manifestation of parturient hypocalcemia, is a metabolic disease of considerable
importance for dairy cow welfare and economy.
• The peri-parturient or transition period of 4 weeks before and 4 weeks after calving is
characterized by greatly increased risk of disease.
• The period is dominated by a series of adaptations to the demands of lactation, a process
described as homeorhetic (Bauman and Currie., 1980).
• Homeorhetic processes are the long term physiological adaptations to changes in state, such as
from non-lactating to lactating or non-ruminant to ruminant, and involve an orchestrated series
of changes in metabolism that allow an animal to adapt to the challenges of the altered state.
• An acute disturbance in calcium metabolism with hypocalcemia occurring just before, during, or
most often within 72 h after parturition.
INCIDENCE AND ETIOLOGY
• Affects usually 4 years or older cow

• Parturient paresis is observed in all dairy breeds but most commonly in Jerseys.
• Recurrent attacks of milk fever may occur at subsequent parturitions.
• Considered as an adaptation disease
• Predisposing factors include age and both yield and persistency of production
• Parathyroid glands and the production of parathyroid hormone is normal and not a factor
• In dry cow, a high total dietary calcium intake together with a high Ca:P ratio may stimulate
calcitonin release from the parafollicular cells of the thyroid gland, thus inhibiting bone
resorption by parathormone. Thus at the beginning of lactation when there is an increased
demand for calcium, the cow is forced into a hypocalcemic state and parturient paresis ensues
• Injecting large amounts of calcium intravenously produced a hypercalcemia lasting for several
hours in cows with milk fever or in normal parturient cows. This hypercalcemia suppressed
parathormone secretion and stimulated the secretion of calcitonin, a substance that lowers
blood calcium concentration by inhibiting bone resorption. These effects tend to retard the
normal adaptation of the cow toward the loss of calcium at the onset of parturition and
lactation and result in a high incidence of relapse of milk fever cases.
SIGNIFICANCE OF BLOOD CALCIUM LEVELS
• Blood serum calcium level drops from a normal of 8 to 12 mg per 100 ml to 3-7 mg with
symptoms of parturient paresis becoming progressively more pronounced as the calcium level
drops.
• Hypocalcemic paresis is due to a depression of neuromuscular transmission of motor stimuli.
• Hypocalcemia with calcium levels below 8 mg per 100 ml of serum may last for 11-32 h in
parturient cows without paresis developing.
• Paralysis was usually associated with calcium levels below 5 mg per 100 ml serum.
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SYMPTOMS
• Anorexia
• Cold extremities
• Lowering of the body temperature
• Stiff gait
• Staggering
• Incoordination
• Inability to rise
• An S-curve in the neck
• Failure of the pupil to contract on stimulation by light
• Suppression of urination and defecation
• Constipation
• Slight tympany of the rumen
• Cessation of parturition, if it develops during that period, and
• Coma, and finally death usually occurring in 6 to 24 h if treatment is not instituted.
DIAGNOSIS
• Based on clinical signs

• A practical field test for determining the blood serum calcium levels based on the amount of
EDTA is needed to prevent the coagulation of blood.
TREATMENT
• Administration of 750 to 1500 ml (depending on the size of the cow) of 20% calcium gluconate,
one half of the amount injected intravenously and one half subcutaneously.
• For 2-3 days, remove only a small amount of milk from the udder. Complete emptying of the
udder should be avoided if possible during this period.
• Udder insufflation to raise the plasma calcium concentration by reducing milk secretion and
transferring calcium in the udder back into the circulation.
• Use of irradiated ergosterol or large amounts of vitamin D to prevent the occurrence or prevent
relapses of the disease is questionable.
PROGNOSIS
• Spontaneous recovery is rare.

• With proper care and prompt handling: Prognosis is good
• In uncomplicated cases that do not injure themselves in attempting to rise: mortality should be
less than 2 to 3%.
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CONTROL MEASURES
• Several milk fever control principles and control factors have been described in the literature
within the last 50 years. Currently, for a variety of reasons only four of these are widely used on
commercial dairy farms.
Oral drenching around calving with a supplement of easily absorbed calcium
• Administration of 3-4 doses (30-40 g of calcium per dose as bolus, a gel, a paste or a liquid)
distributed evenly during the period from 12-24 h before calving to 24 h after calving.
• Prevent significant proportion of relapses when given as a 1or 2 dose supplement to
intravenous calcium therapy.
• Drawbacks
o Single cow handling
o Risk of aspiration pneumonia
o Products based on calcium chloride and calcium formate may cause irritation to the
gastrointestinal mucosa and uncompensated systemic acidosis.
The feeding of acidifying rations by anionic salt supplementation during the last weeks of pregnancy
• The principle of cation-anion to work, a surplus of absorbable anions must be fed for at least 10
days prepartum to prevent the cow from being alkalinized
• A dietary cation-anion difference (DCAD) of -100meq/kg [calculated as (Na+ K) – (Cl+S)] has
been recommended.
• Disadvantage
o Low palatability of the anionic salts most commonly used.
Feeding of low calcium rations during the last weeks of pregnancy
• Low calcium principle is highly effective, approaching 100% in preventing milk fever, provided
dietary calcium intake is kept below 20g/d, and exposure period for at least the last 2 weeks
before calving.
• Using commonly available feeds, a calcium level of < 20g/d is difficult to obtain
• A possible solution to this may be addition of a calcium binder to the feed.
Prepartum administration of Vitamin D, vitamin D metabolites and analogues
• Controversial
• Efficacy varies greatly
• Timing of treatment is important
• Injection given 2-8 days before calving has been considered optimal. If the cow fails to calve
after the 8 th day, another injection may be given and repeated every 8 days until calving.
• Disadvantages
o Dose required is very close to toxic dose causing clinical symptoms including
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marked anorexia
loss of body weight
dyspnoea
tachycardia
recumbency
torticollis, and
severe cardiovascular calcifications.
o Risk of hypocalcemia and clinical signs of milk fever 10-14 days postpartum.
LESS SPECIFIC CONTROL MEASURES
• Other possible but less specific control measures for the prevention of milk fever include
management practices such as
o Dietary magnesium level control peripartum
o Body condition control
o Controlling dietary carbohydrate intake peripartum
o Shortening of the dry period
o Prepartum milking
o Reduced milking in early lactation.
WHAT IS A DOWNER COW SYNDROME?
• “Downer” cow syndrome is referred to an animal that fails to rise after dystocia or that goes
down and is unable to rise late in gestation or soon after parturition without any apparent
reason prior to development of the sequelae of recumbency.
• When a specific diagnosis is made, the term downer should not be used.
• This condition by itself is not a disease, but it is a complication.
INTRODUCTION
• Most of these cases occur for the most part, around calving and an early recovery is often
imperative and a prompt accurate diagnosis is desirable from the standpoint of the animal’s
future production and even life.
• When a cow becomes alert and gains control of fore quarters following calcium therapy but
remains recumbent due to inability to use the hind quarters, it is referred to as “Creeper Cow”.
• Downer cow syndrome is a common, challenging and perplexing diagnostic problem for the
veterinarian.
RISK FACTORS
• Peak lactation yield of high producers

• Complications due to delayed or incomplete treatment of various diseases after parturition
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• Poor housing conditions
• Excess body weight
• Septic conditions
• Malnutrition.
CHECK LIST OF ETIOLOGICAL FACTORS

Metabolic and/or • Parturient paresis, hypocalcemia, milk fever
Nutritional Disturbances • Tetany, hypocalcemia and/or hypomagnesemia including
grass and transport tetany
• Ketosis, usually postparturient
• Debility, cachexia, or weakness—due to starvation, senility,
acute or chronic wasting diseases including internal or
external parasitisms and Johne’s disease
• Zenker’s degeneration of muscle—due to a lack of
selenium, vitamin E, and the presence of other factors
including poor quality hay and muscle stress following a
lack of exercise or following vigorous attempts to rise in
cows with milk fever, nerve paralyses, or cows that are cast.
Traumatic and/or Physical • Paralyses- injuries to the obturator, peroneal, gluteal,

Injuries: femoral and brachial nerves or compression of spinal cord.
Lymphosarcoma and abscesses may produce spinal
Often occur during attempts compression
to rise especially where the
• Dislocation of the hip or sacroiliac joints
footing is slippery or in cows
affected with milk fever. • Fractures of the leg, pelvis, spine, and skull
• “Cast” often associated with myositis, Zenker’s
degeneration, tendinitis, arthritis, muscle asthenia and
ischemia, phlebitis and thrombosis, and contusions
• Rupture of the gastrocnemius muscle, usually secondary to
Zenker’s degeneration
• Exhaustion from attempts to rise or exertion from dystocia
may produce a circulatory crisis, low blood pressure and
myocarditis, may be related to a lack of exercise
• Hemorrhage, anemia, or shock as in rupture of the uterine
or pelvic blood vessels in torsion or prolapse of the uterus,
laceration of the genital tract, transportation in advanced
pregnancy, abomasal or duodenal ulcers, coccidiosis,
anaplasmosis, leptospirosis and postparturient
hemoglobinuria.
Infectious Diseases or • Septic metritis, with or without a retained placenta or a

Inflammatory Processes vulvar discharge
398
• Septic mastitis
• Peritonitis, or pericarditis,’ secondary to traumatic gastritis,
uterine rupture or abomasal ulcers with perforation
• Acute laminitis
• Septic arthritis—knee, hocks, and coffin joint
• Miscellaneous diseases—severe pyelonephritis, shipping
fever, blackleg, anthrax, necrobacillosis, rabies, listeriosis,
meningitis, and brain or cord abscess.
CHECK LIST OF FACTORS AND POSSIBILITIES IN DIAGNOSIS
Digestive • Enteritis, severe diarrhea secondary to an intestinal stasis

Disturbances, associated with hypocalcemia, winterdysentery, salmonellosis,
Diarrheas, Toxemias virus diarrhea, etc
and Poisonings
• Toxic indigestion due to overeating on fruit, grain, or forage
• Toxic indigestion of advanced pregnancy occurring in stabled
dairy cows late in the winter confinement period and
characterized by partial to complete anorexia, dullness,
progressive emaciation and increased pulse rate. Normal activity
of the gastro-intestinal tract appears impaired possibly due to
large gravid uterus
• Poisonings--- plant, chemical, etc.
Miscellaneous • Hydrallantois
Causes • Lymphocytoma especially involving the spinal cord, heart, and
abomasum
• “Malingerer”
• Spastic syndrome (“stretches”)
• Severe albuminuria and uremia secondary to nephritis (rare).
Source: S.J.Robert's (1971).
399
EXAMINATION OF RECUMBENT CATTLE
• A complete painstaking physical examination of each system of the animal should be

performed, despite the fact that the animal can’t “cooperate” and stand for the examination.
• In cases where traumatic and physical injuries are present, use of hip slings may aid in arriving
at a diagnosis.
o History
o Observation
o General examination
o Special examination
o Laboratory examination
400
History
• The following questions should be asked to owner

o Was the calving difficult?
o Had it got up since calving?
o Had treatments been given by the farmer?
o When the recumbency started?
o Before / during/soon after calving?
o How long had it been recumbent?
o Had position changed since recumbent?
o How long had it been in current position?
o Whether the floor is slippery?
• Other particulars like proceeding symptom, early disease, frequency of paresis and mineral
feeding 6-8 weeks prior to calving also should be checked.
Observation of recumbent cattle
• General appearance
• Position of the head, neck limbs, and tail in relation to body.
• Angles of limb joints
• Swelling / injuries
• Unusual movement
• State of feet
• Surroundings.
General examination
• General state of health

• Mental status
• Respiration
• Pulse
• Temperature
• Udder/reproductive and circulation system CNS
• Rectal and Vaginal examinations.
Special examination
• Locomotor system
• Foot
• Nervous system
401
Laboratory examination
• Dung examination
• Urine analysis
• Hemogram
• Blood chemistry.
• Cows with infectious diseases may have an elevated body temperature and pulse rate. The
latter is also elevated in digestive disturbances.
• Cows with hypocalcaemia usually respond to intravenous calcium therapy or udder inflation
although some response to calcium therapy may be observed in digestive disturbances.
• In cases of peritonitis, an expiratory grunt is often exhibited.
• One or more of the following symptoms would be sufficient reason for questioning the
diagnosis of parturient paresis in a cow:
o A pulse rate of 90 or more/minute
o Rapid respirations or respirations accompanied by an expiratory grunt
o Diarrheaa
o Attitude that is bright and alert,
o A nearly normal appetite
o A body temperature of 102° F. or higher,
o A hot swollen udder
o Retained placenta
o Persistent tenesmus, and
o Failure of expected response to adequate calcium therapy.
BASED ON CLINICAL SIGNS
Characteristics Downer Cow Creeper Cow
Mental status Depressed Alert
When stranger approaches No response Tries to get up
Temperature 100 °F/Less 100 - 101 °F
Head restraint No resistance Resistance
Nose muzzle Dry Moist
Head posture Drooping Hindleg- fetlock erect
402
Ears Drooping Partly erect
Eyelids Not tensed open Snapping shut
Eye Vacant look Bright look
Pupil Dilated Not marked
Pupillary light reflex Slight/Sluggish Photophobia- Pupil constricts to a mere slit
Gluteal palpation Resistance, not fluid like No tone, fluid like
Abdominal muscle No loss of tone Loss of tone
Fetlock while rising No attempt to rise Pronounced flexure
Dung Stasis No stasis
Response to injection Negative Objects
BASED ON PRESENTING SIGNS
• Possible cause and prognosis can be made by observing the clinical signs and attitude changes
in recumbent cattle.
Recumbent Cattle
Position, it's probable cause and prognosis
Position Cause Prognosis
Creeper to Crawler Hypocalcaemia Good

Attempts arc made to rise with the Hypomagnesaemia
hind quarters being lifted from the Hypophosphatemia
ground Peroneal paralysis
Frog legged cow Hypocalcaemia Mainly

The hind limbs are partially flexed Obturator nerve paralysis good
and displaced distally Tibial nerve damage
Adductor muscle damage
Hindlimbs rigidly extended rostrally Often upper limb problems (eg) Hip Hopeless
so they are in contact with the dislocation, Hip joint Trauma, Rupture of
elbows of the front legs. If the legs ligament, muscular degeneration, sciatic
placed in normal position often they nerve damage, and damage to upper side
return to stance. Rest on one side
If moved on to other side then If due to muscle flaccidity then upper side Poor
returns to original position is normal
403
Sciatic nerve damage, peroneal paralysis, Depends
and pressure syndrome on nursing
Legs extended behind the animal Pubic damage, nerve damage, and muscle Usually
damage poor
Attitude changes and prognosis
Attitude Positive Cases Prognosis
Lateral recumbency with head back Chronic metabolic problems Hopeless
Brain conditions or damage
Mainly brain Condition or damage
Hvperaesthesia, Some show tetany Mainly brain Condition or damage Poor

or lateral recumbency
Non-alert Brain damage Poor
Hypomagnesaemia
Source
B.Nagarajan (2001). Care and Management of Downer cow/ Recumbent cattle. In Training Manual on
"Advances in the Diagnosis and Treatment of Diseases of Ruminants. Centre for Advanced Studies in
Clinical Medicine and Therapeutics, Madras Veterinary College, TANUVAS, Chennai-7.
404
MODULE-17: ANIMAL BIRTH CONTROL
DEFINITION
• Neuter refers to ovariohysterectomy (OHE), the surgical removal of the ovaries and uterus.
INDICATIONS FOR OVARIOHYSTERECTOMY (OHE)
Most common reasons to perform OHE in dogs are
• To prevent estrus, and

• Unwanted offspring.
Other reasons for OHE include
• Prevention of mammary tumors or congenital anomalies
405
• Prevention and treatment of pyometra
• Metritis
• Neoplasia (i.e. ovarian, uterine, or vaginal)
• Cysts
• Trauma
• Uterine torsion
• Uterine prolapse
• Subinvolution of placental sites (SIPS)
• Vaginal prolapse and Vaginal hyperplasia
• Control of some endocrine abnormalities (i.e., diabetes and epilepsy), and
• Dermatoses (eg., generalized demodex).
ANESTHETIC CONSIDERATIONS FOR ELECTIVE SURGERIES OF THE REPRODUCTIVE TRACT
• General anesthesia is recommended

• Careful pre-operative screening
• In apparently healthy animals, complications may arise due to
o Uncorrected hydration
o Electrolyte or acid-base balance
• Since the viscera is exposed during abdominal surgery, the water evaporation rates are
increased
• To replace this loss, fluid administration should be increased
• Hypothermia occurs due to body heat loss as a result of vasodilation and exposed viscera
• Excercise care to maintain body temperature during surgery and rewarm the patient post
operatively.
TECHNICAL VARIATIONS
• Many technical variations of OHE have been described, which includes

o Flank approach
o Laparoscopic approach, and the use of stapling equipment
o Ultrasonic scalpel
o Vessel sealing devices
o Transfixation ligatures, or
o Miller’s Knots.
• Only one technique is described here.
406
SURGICAL PROCEDURE
Surgical procedure
• Clip and surgically prepare the ventral abdomen from xiphoid to the pubis
• Identify the umbilicus and visually divide the caudal abdomen into three.
• In dogs
o Make the incision just caudal to the umbilicus in the cranial third of the caudal abdomen
o More caudal incisions make it difficult to exteriorize ovaries.
• In deep-chested dogs or in those with an enlarged uterus
o Extend the incision cranially or caudally to allow exteriorization of the tract without
excessive traction.
• In prepubertal puppies
o Making the incision in the middle third of the caudal abdomen facilitates uterine body
ligation.
• In cats
o The body of the uterus is more caudal and difficult to exteriorize; therefore make the
incision in the middle third of the caudal abdomen.
• Make a 4-8 cm incision through skin and subcutaneous tissue to expose the linea alba.
• Grasp the linea alba or ventral rectus sheath, tent it outward and make a stab incision into the
abdominal cavity.
• Extend the linea incision cranial and caudal to the stab with Mayo scissors.
• Elevate the left abdominal wall by grasping the linea or external rectus sheath with thumb
forceps.
• Slide the ovariectomy hook (e.g., Cavault or Snook) with the hook against the abdominal wall, 2
to 3 cm caudal to the kidney (Fig.A). Turn the hook medially to ensnare the uterine horn, broad
ligament or round ligament and gently elevate it from the abdomen. Anatomically confirm the
identification of the uterine horn by following it to either the uterine bifurcation or ovary. If the
uterine horn cannot be located with the hook, retroflex the bladder through the incision and
locate the uterine body and horns between the colon and bladder.
• With caudal and medial traction on the uterine horn, identify the suspensory ligament by
palpation as the taut fibrous band at the proximal edge of the ovarian, pedicle (Fig.B).
• Stretch or break the suspensory ligament near the kidney without tearing the ovarian vessels,
to allow exteriorization of the ovary. To achieve this, use the index finger to apply cauda-lateral
traction on the suspensory ligament while maintaining caudo-medial traction on the uterine
horn (Fig.C).
• Make a hole in the broad ligament caudal to the ovarian pedicle. Place one or two Rochester-
Cormalt forceps across the ovarian pedicle proximal (deep) to the ovary and one across the
proper ligament of the ovary (Fig.D).
• The proximal (deep) clamp serves as a groove for the ligature, the middle clamp holds the
pedicle for ligation, and the distal clamp prevents backflow of blood after transection. When
407
using two clamps, the ovarian pedicle clamp serves both to hold the pedicle and to make a
groove for the ligature.
• Place a figure eight ligature proximal to (below) the ovarian pedicle clamps (Fig.E).
• Choose an absorbable suture material for ligatures (i.e., 2-0 or 3-0 chromic catgut,
polydioxanone, polyglyconate, poliglecaprone 25, or polyglactin 910).
• Begin by directing the blunt end of the needle through the middle of the pedicle, loop the
suture around one side of the pedicle, then redirect the needle through the original hole from
the same direction and loop the ligature around the other half of the pedicle. Securely tie the
ligature.
• Remove one clamp or “flash” a single clamp while tightening the ligature to allow pedicle
compression.
• Place a second circumferential ligature proximal to (below) the first to control hemorrhage that
may occur from puncturing a vessel as the needle is passed through the pedicle.
• Some surgeons prefer to place the circumferential ligature or Miller’s knot before the
transfixing ligature to eliminate hemorrhage, if a vessel is punctured during transfixation.
• Place a mosquito hemostat on the suspensory ligament near the ovary (Fig.F). Transect the
ovarian pedicle between the Carmalt and ovary.
• Open the ovarian bursa and examine the ovary to be certain that it has been removed in its
entirety.
• Remove the Carmalt from the ovarian pedicle and observe for hemorrhage.
• Replace the Carmalt and religate the pedicle if hemorrhage is noted.
• Trace the uterine horn to the uterine body. Grasp the other uterine horn and follow it to the
opposite ovary. Place clamps and ligatures as just described. Make a window in the broad
ligament adjacent to the uterine body and uterine artery and vein. Place a Carmalt across the
broad ligament on each side and transect (Fig.G). Apply a ligature around the broad ligament if
the patient in estrus or pregnant or if the broad ligament is heavily infiltrated with vessels or
fat. Apply cranial traction on the uterus and ligate the uterine body cranial to the cervix.
• Place a figure-eight suture through the body using the point of the needle and encircling the
uterine vessels on each side. Place a circumferential ligature nearer the cervix. (Fig.H). Place a
Carmalt across the uterine body cranial to the ligatures. Grasp the uterine wall with forceps or
mosquito hemostats cranial to the ligatures. Transect the uterine body and observe for
hemorrhage. Religate if hemorrhage is observed.
• Some surgeons place one to three Carmalts across the uterine body before ligation.
• In cats, clamps may cut rather than crush a friable or engorged uterus and cause transection
before ligature placement. An alternative to ligatures is to use an ultrasonic scalpel, vascular
sealer or staples.
• Replace the uterine stump into the abdomen before releasing the hemostats or forceps.
• Close the abdominal wall in three layers (fascia/linea alba, subcutaneous tissue and skin).
408
STEP-WISE DIAGRAMATIC REPRESENTATION OF OVARIOHYSTERECTOMY (OHE) PROCEDURE
Steps (A-D) Description

Elevate the abdominal wall with thumb forceps and
slide the ovariectomy hook against the abdominal
wall, 2-3 cm caudal to the kidney.
Exteriorize the uterine horn with the hook and

identify the suspensory ligament at the cranial edge
of the ovarian pedicle.
Stretch or tear the suspensory ligament to allow

exteriorization of the ovary using the index finger to
apply caudo-lateral traction on the suspensory
ligament while maintaining caudo-medial traction on
the uterine horn.
Place two Carmalt forceps across the ovarian pedicle

proximal to the ovary and one across the proper
ligament (or place three forceps proximal to the
ovary). Remove the most proximal clamp and place a
figure-8 ligature at this site.
409
STEP-WISE DIAGRAMATIC REPRESENTATION OF OVARIOHYSTERECTOMY (OHE) PROCEDURE
STEPS (E-H) DESCRIPTION

Direct the blunt end of the needle through the
middle of the pedicle (1 to 2), loop the suture
around one side of the pedicle (3 to 4), then
redirect the needle through the original hole
from the same direction (5 to 6), and loop the
ligature around the other half of the pedicle (7
to 8). Securely tie the ligature (1and 8).
Place a circumferential ligature proximal to

the first ligature, then place a hemostat on the
suspensory ligament near the ovary. Transect
the ovarian pedicle distal to the clamp across
the ovarian pedicle.
Separate the broad ligament from the uterine

horn. Clamp and ligate the broad ligament
(dashed line) if it appears vascular.
To ligate the uterus, place a figure-8 suture

through the uterine body near the cervix.
Place a second circumferential ligature closer
to the cervix, place a carmalt forceps distal to
the ligatures, and transect between the
carmalt forceps and ligatures. Inspect the
uterine stump for hemorrhage (use a
mosquito hemostat attached to the uterine
wall to prevent retraction of the uterus in to
the abdomen).
Source: Fossum TW (2002)
410
TECHNIQUE OF AUSTIN et al (2003)
• Position the dog in dorsal recumbency.

• Place an observation port at the umbilicus, and place two operating ports in the inguinal folds,
on each side of the midline.
• Use Babcock forceps in the left operating port to retract the intestines medially, and grasp the
ligament of the right ovary with forceps placed through the right operating port and lift so that
traction is placed on the suspensory ligament.
• Transect this ligament, the broad ligament of the uterus, and the ovarian vascular pedicle after
first applying coagulation via electrocautery or a suture.
• Continue the transection to the uterus, and transect the uterus and uterine arteries from left to
right.
• Cut the uterus and seal it 1 cm proximal to the cervix, then coagulate and cut the right uterine
artery.
• Lift the left uterine horn so that it can be visualized all the way to the ovary.
• Coagulate the ligament and pedicles, and transect them in reverse order as carried out on the
right side.
• Once the uterus and ovaries are cut from all attachments, enlarge the left operating port as
necessary to allow the uterus and ovaries to be withdrawn through this incision.
• Observe the ovarian pedicles and uterine stump for several minutes, and if no excess bleeding
is seen, remove the trochars and close the incisions.
Reference
• Austin B, Lanz OI, Hamilton SM et al., (2003). Laparoscopic ovariohysterectomy in nine dogs. J.
Am. Anim. Hosp. Assoc. 39:391.
MODIFIED TECHNIQUE OF DEVITT et al (2005)
• Rotate the dog to the right and left as necessary to make retraction of intestines and exposure
of the ovary easier.
• Grasp the left ovary and bring it to the body wall.
• Using a transabdominal illumination and direct laparoscopic observation, direct a
transabdominal suspension suture with a larger taper needle percutaneously through the ovary
and out of the abdominal wall.
• Tie this suture, thus maintaining exposure of the vasculature of the ovary.
• If necessary, use several sutures on one ovary.
• Next, progressively cauterize the ligament and vasculature using bipolar grasping forceps.
• Transect both the ovaries.
• Enlarge a caudal operating port, and exteriorize both uterine horns and the body of the uterus.
• Transect the body of the uterus and uterine arteries, and replace the uterine stump in to the
abdomen.
411
• Close the incisons.
Reference
• Devitt DM, Cox RE, Hailey JJ (2005). Duration, complications, stress, and pain of open
ovariohysterectomy versus a simple method of laparoscopic - assisted ovariohysterectomy in
dogs. J. Am. Vet. Med. Assoc. 227: 921.
INTRODUCTION
• A perfect contraceptive should have nearly 100 per cent efficacy with no risk to the patient that
is widely acceptable and available at a reasonable cost.
• The cheapest and most effective contraceptive is physical confinement to prevent breeding.
IMMUNOLOGICAL METHODS
• Antibodies to luteinizing hormone (LH) to prevent LH from reaching the target organs has
worked for varying periods of time with unpredictable results.
• Antibodies to gonadotropin releasing hormone (GnRH) are promising but not commercially
available to the practitioners.
• Immunization with preparations of porcine zona pellucida prevents sperm from binding to the
ova or masks sperm binding sites and prevents conception.
• Immunologic methods are temporary and require a booster program to have long term effects.
INTRAVAGINAL AND INTRAUTERINE AGENTS
• Anatomical location of the cervix in the bitch makes it impossible to cannulate per vagina, thus
placement of an intrauterine device (IUD) would require laparotomy adding the cost and risk of
major surgery. Hence IUD’s are not feasible in bitches.
• Intravaginal devices were available at one time but were discontinued as a proper fitting device
to a wide range of sizes of dogs was not possible, cost, foreign body vaginitis made it
objectionable with poor acceptance with many of the owners.
PHARMACEUTICAL AGENTS
Progestagens
• The commonly used agents are progesterone, hydroxy-progesterone acetate, medroxy-

progesterone acetate and megestrol acetate.
o Side effects of chronic progesterone administration is cystic endometrial hyperplasia
with or without infection, positively correlated with mammary neoplasia and may be
diabetogenic.
Megestrol acetate
• It is a potent orally active progestagen that is used for prevention of estrus and postponement
of estrus prior to proestrus.
412
o For prevention of estrus megestrol is administered at a dose rate of 2.2 mg/kg daily for
8 days during the first 3 days after observing sanguineous discharge and vulvar swelling.
o For postponement of an anticipated estrus megestrol is administered at a dose rate of
0.55 mg/kg daily for 32 days beginning at least a week prior to the onset of proestrus
based on the patient history.
o Vaginal cytological examination is often useful in timing the therapy.
o Temporary side effects include increased appetite, decreased activity, weight gain, and
may rarely induce lactation.
Androgens
Testosterone
• It is used to prevent estrus in working dogs especially in racing greyhounds.

• Oral and parental routes have been used.
• Bitches administered with 25 mg of testosterone orally at weekly intervals prevented estrus for
5 years.
o Side effects include clitoral hypertrophy and vaginitis.
o Silicone implants containing testosterone effectively prevented estrus for 840 days.
Mibolerone
• It is an androgenic, anabolic anti-gonadotropic steroid that does not possess progestational or

estrogenic activity.
o Dosages ranged from 30 mcg/day to 180 mcg/day for dogs weighing from 1 to 12 kg and
more than 45 kg, respectively and were treated for periods up to 1300 days.
o Observable side effects are clitoral hypertrophy, vaginitis, deepening of voice, increased
lacrymation and seborrhic dermatitis.
413

Eterinary Bstetrics: - Dr. S.Balasubramanian

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VGO-421

MODULE-1: DEVELOPMENT OF FETUS - FETAL MEMBRANES - PLACENTA

The characteristic changes during this phase are:

• True implantation is a phenomenon observed in rodents and humans.

Binucleate Giant Cells (BNGCs)

• Attachment is characterized by the appearance of binucleate giant cells (characterized as being

• BNGCs constitute around 20 per cent of the fetal placenta.

• Implantation or attachment does not occur until days 24-40.

MATERNAL RECOGNITION OF PREGNANCY (MRP)

Two Interdependent System

Non pregnant PGF2 alpha is released in an endocrine

Pregnant Secretion is however, in an exocrine

Species Day of MRP Day of definite Attachment

EARLY EMBRYONIC DEVELOPMENT

PRE-ATTACHMENT DEVELOPMENT OF EMBRYO

• Following fertilization, embryo must undergo certain developments before it is capable of

DEVELOPMENT OF EXTRAEMBRYONIC MEMBRANES

• Following hatching, the conceptus undergoes massive growth.

SCHEMATIC REPRESENTATION OF EXTRAEMBRYONIC MEMBRANES DEVELOPMENT

Source: Redrawn from Patten (1964). Foundations of embryology, McGrawHill.

FORMATION AND DIFFERENTIATION OF GERM LAYERS

DEVELOPMENT OF FETAL MEMBRANES

The fetal or extra embryonic membranes serve as

• Protection of the embryo

The fetal membranes consists of

• Primitive yolk sac

Source: S.Balasubramanian, TANUVAS, Personal Collection

• Clear, colourless and mucoid in nature.

Amounts present toward the end of gestation

Species Amount (in ml)

Cow 2000 – 8000

Mare 3000 – 7000

Goat 400 – 1200

Ewe 350 – 750

Dog and Cat 8 - 30

• Most noticeable during 3-7 month of gestation.

Source: S.Balasubramanian, TANUVAS, Personal Collection

Source: S.Balasubramanian, TANUVAS, Personal Collection

• Clear, watery and amber in colour.

• Towards end of gestation the volume of allantoic fluid varies.

Sheep and goat 500–1500

The cow, horse, sheep, goat and pig

Source: S.Balasubramanian, TANUVAS, Personal Collection

• Hydrallantois is a condition wherein occasionally excessive amounts of allantoic fluid 40–160

BOVINE FETAL MEMBRANES WITH FETUS IN SITU

• The chorioallantoic placentation is characteristic of all farm animals.

Bovine fetal membranes

A ~ 60 day fetus showing the allantoic and amniotic cavities

Source: S.Balasubramanian, TANUVAS, Personal Collection

NON-REJECTION OF PLACENTA IN PREGNANT ANIMALS

It is divided in to 4 general types based on their shape as:

Deciduate or conjoined or placenta vera

• Seen in swine, horses and ruminants.

CLASSIFICATION BASED ON THE TISSUES OR STRUCTURES THAT INTERVENE

Epitheliochorial type (Horse, Pig, Cow and Sheep)

Endotheliochorial (Dog and Cat)

Haemochorial (Man and Rodents)

Source: Redrawn from S.J.Roberts (1971).

BASED ON SITES OF CHORIONIC ATTACHMENT

Source: O.J.Ginther (1992)

• The cotyledonary placenta is characteristic of the ruminants; instead of being uniformly

Species Classification of Chorioallantoic Placentas