AAP 2303: REPRODUCTIVE HEALTH AND MANAGEMENT (70 HOURS)

Pre-requisite(s): AAP 2105: ANIMAL PHYSIOLOGY I, AAP 2106: ANIMAL PHYSIOLOGY II, AAP 2102: GROSS
ANATOMY AND EMBRYOLOGY I, AAP 2103: GROSS ANATOMY AND EMBRYOLOGY II

Course Purpose
The course is intended to equip students with knowledge, skills and attitudes that will enable them understand aetiology
and management of theriogenological conditions in farm animals.

Learning Outcomes
At the end of this course the student will be able to:
1. Conduct male and female examination for breeding purposes
2. Perform artificial insemination and pregnancy diagnosis in animals
3. Describe disorders, diagnosis and management of reproductive disorders
4. Discuss biotechnological procedures used in reproduction

Course Description
Overview of reproductive physiology and anatomy in animals. Mating, fertilization, conception, gestation, pregnancy
diagnosis, parturition. Dystocia and its classification, causes and management. Define infertility and sterility. Causes of
infertility, Non- specific causes of infertility, nutritional, stress and intercurrent conditions, anatomical, physiological
dysfunction, managerial, hereditary causes and non- specific infections. Management of reproductive disorders. Specific
infections – Aetiology, signs, diagnosis, transmission, treatment, prevention and control of reproductive diseases
including but not limited to brucellosis, epivaginitis, campylobacteriosis and trichomoniasis. Control of reproduction:
semen collection and evaluation, synchronisation of oestrus, Artificial Insemination, management of A.I schemes and
embryo transfer technology.

Teaching Methodology
Lecture, group activities, class discussions, Demonstration and illustrations

Instructional Materials
LCD projector, overhead projector, Chalk/white board markers, artificial insemination equipment, appropriate
disinfectants

Course Assessment
Continuous Assessment 30% (Tests-10%; Practical- 15%; Assignments- 5%)
Semester Examination 70%

Course Textbooks
1. Youngquist, RS (1997). Current Therapy in Large Animal Theriogenology. Publisher: W.B. Saunders Company.
ISBN-10: 0721693237
2. Stephen J. Robert (1986). Veterinary Obstetrics and genital diseases. Publisher: David & Charles; 3RD edition.
ISBN-13: 978-9997670922
3. H. Joe Bearden, John W. Fuquay, Scott T. Willard (2003). Applied Animal Reproduction (6th Edition) 6th
Edition. ISBN-13: 978-0131128316; ISBN-10: 0131128310

Course Journals
1. Theriogenology Journal. ISSN: 0093-691X.
2. Journal of Veterinary Research. ISSN 1328-925X
3. American Journal of Veterinary Research. ISSN: 0002-9645

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Reference Textbooks
1. Knut Schmidt-Nielson (1997). Animal physiology adaptation and environment. ISBN-10: 0521570980
2. E.S.E Hefez. (1992). Reproduction in farm animals. 6th Ed. ISBN-10: 0683305778
3. Robert S. Youngquist, Walter Threlfall (2006). Current Therapy in Large Animal Theriogenology. Publisher:
Saunders; 2 Edn. ISBN: 9780721693231

Reference Journals
1. Journal of Reproduction and Fertility. ISSN: 0449-3087
2. Journal of in Vitro Fertilization and Embryo Transfer. ISSN: 0740-7769.
3. Journal of Animal Science. ISSN: 1525-3163

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Physiology of Female Reproduction

Reproductive functions in females consists of two phases;-

1) Estrus cycle - Cyclic changes in female reproduction that prepares animal for mating and conception.
2) Gestation period- duration from fertilization of ova through foetal development in the uterus to
parturition.

Estrus Cycle
Functional anatomy- important structures of female reproductive tract includes;-
a) Ovaries- usually paired, in abdominal cavity.
b) Fallopian tubes (oviduct)- ends in funnel-like fimbriae towards ovaries and connects to the uterus
c) Uterus- site for foetal development (has 2 uterine horns)
d) Cervix- muscular orifice between uterus and vagina
e) External genitalia- Vagina, vulva (labia) and critoris

Female reproductive function starts at puberty- a period when inhibition on hypothalamus is removed (by
unknown factors) and production of hypothalamic Gonadotropic releasing hormone ( GnRH ) starts. Puberty is
attained at age that is species specific e.g. 12 – 18 years in man, 14 -18 months in cattle.
GnRH is released into hypothalamo-hypophysial portal system to anterior pituitary where it causes release into
blood of:-
a) Gonadotropic hormones, FSH and LH which are transported in blood to ovaries to stimulate
b) Production of steroid hormones
i. Estrogen- produced by developing ova and stimulates estrus
ii. Progesterone- Produced by corpus luteum and maintains pregnancy.
c) Circulating ovarian steroids (estrogen and progesterone) levels increases and inhibits GnRH production
by hypothalamus until parturition or another reproductive cycle commences.

Sketch- changes in plasma hormones and control system.

Effects of hormones on Reproductive cycle

1) Gonadotropic hormones
FSH and LH are pituitary glycoprotein hormones that target Primordial germ cells in ovaries.
a) FSH initiates differentiation of ovarian primordial follicles to develop to primary follicles
through meiosis. Half of the chromosomes are shed as a first polar body from primary follicle
that becomes a secondary follicle. A second polar body is shed from secondary follicle whose
nucleus is left with haploid unpaired chromosomes and develops into a mature (graafian) follicle
that contains the ovum ( female sex cell) surrounded by theca cells and a fluid (antrum).
b) Theca cells produce estrogen into the antrum and the hormone diffuses into blood circulation.
Estrogen causes positive feedback production of FSH by the pituitary that causes full maturation
of ova. In the ovary, FSH and estrogen promote formation of LH receptors on the theca cells
surrounding the ova.
c) A sudden drop in estrogen and FSH production follows while pituitary LH production increases
rapidly.
d) LH causes ovulation- degeneration of ovarian and theca cells around mature ova causing release
of mature ovum or ova (in multiparous animals) through ovarian wall into the abdominal cavity
near fimbriae of oviduct.

Development of corpus luteum

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 Rupture of mature ovum causes hemorrhage into the follicular cavity, growth of blood vessels in the cavity
and enlargement of granulosa cells (formed from theca externa cells) lining the cavity. The structure is then
called a corpus haemorrhagicum.

Granulosa cells produce lutein- a yellow substances that fills cavity of corpus luteum; process called
luteinization that forms a corpus luteum. Mature granulose cells in corpus luteum secrete
1) large quantity of Progesterone
2) Small amount of estrogen

Effects of hormones on the uterus

In follicular phase estrogen causes:-
1) Thickenning of inner walls of uterus through proliferation of endometrial epithelia.
2) Development of uterine glands and extensive endometrial blood capillaries.
3) Cornification of vaginal epithelium that prevents vaginal infection or abrasion during coitus.
4) Production of lubricating mucus by vaginal and labial glands.
5) Opening of cervix through relaxation of its muscular wall and liquefaction of mucus plug. This
allows sperms to pass into the uterus.

Estrogen also causes development of secondary sex characterics in female animals e.g.
a) Muscle growth and fat deposition beneath skin – particularly around pelvic region and mammary
glands.
b) Bone growth at puberty and epiphysial closure at maturity.
c) Development of blood vessels in subcutaneous tissue and increased sodium and water retention in
body fluids.

Progesterone
1) Inhibits contractions of uterine muscles (myometrium) for maintenance of pregnancy i.e. quietens the
uterus.
2) Increases deposition of fat in the body.
3) Stimulates uterine glands to secrete nutrients that nourishes developing fetus (uterine milk).
4) Causes development of milk secreting portion of mammary glands (acinar).
5) Inhibits effects of FSH, LH and estrogen on ovary so that estrus cycle does not occur (during luteal
phase or pregnancy).

Signs of estrus

Most animals display behaviour around time of ovulation that shows readiness for mating e.g.
- Restlessness and production of characteristic sounds
- Anorexia (lack of appetite).
- Seeking the male
- Slight drop in milk production (dairy cows).
- Hyperemia (redness) of vulva and production of a thin, clear mucoid secretion by vulval and
vaginal glands.
- Females show readiness to be mounted by males (e.g. standing heat in pigs).

End of cycle
If conception does not occur, the corpus luteum develops and produces progesterone over the luteal phase
which is terminated by degeneration of corpus luteum- luteolysis. Prostaglandins secreted by uterine walls (e.g.
FGF2α) cause luteolysis and a decline in progesterone secretion that removes inhibition on pituitary FSH and LH
production so that a subsequent estrus cycle commences. In humans, menstruation (degeneration of
endometrium observed as bleeding) marks end of cycle.
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Gestation period

Gestation period spans from fertilization to parturition e.g. 270 – 275 days in cattle.

Fertilization

During coitus, semen is deposited at anterior vagina by ejaculation. Flagella beating of sperm tail and
retrograde contraction of vaginal and uterine walls (probably caused by prostaglandins in semen) propel sperms
through vagina, cervix and uterus towards the ovary.

After ovulation, the ovum is shed into abdominal cavity and beating of fallopian villi sweeps ovum together
with peritoneal fluid towards fimbriae of oviduct; fertilization takes place in the oviduct. Only a few sperms
reach the ovum.
In most animals ovulation occurs after first meiotic division of primary oocyte. Second meiotic division takes
place as the sperm penetrates the ovum and a second polar body is shed to complete meiosis so that a haploid
number of chromosomes remain in ovum.

Acrosome reaction- Attachment of a sperm to theca cells around ovum causes release of proteolytic enzymes
(hyaluronidase) from the sperm acrosome that digests theca cells and wall of ovum. The cell walls of sperm
and ovum fuse together and chromosomes of the two gametes align to constitute a common nucleus with
diploid number of chromosomes. The ovum wall become impervious to other sperms and undergoes rapid
mitotic divisions forming a blastomere (revise embryology). The fallopian epithelium secretes nutrients that
nourish the developing embryo.

Implantation
Cillia along epithelium of oviduct moves the blastocyst (follows dev of blastomere) to the uterus where the
blatocyst embeds itself within endometrial tissue- process called implantation- to become an embryo. Later
protective, fluid-filled (amnion and chorion) fetal membranes develop around fetus (stage of embryo after
implantation) and a placenta connects fetus to maternal uterus; through the placenta, the fetus obtains nutrients
from, and excretes metabolic waste products to maternal circulation.

Progesterone and estrogen from corpus luteum cause uterine enlargement to accommodate developing fetus in
early pregnancy. When placenta develops, it starts secreting progesterone and a little estrogen and takes over
production of these hormones by corpus luteum, which degenerates in most animals. In human, placenta also
produces human chorionic gonadotropin (hCG) that prolongs life of corpus luteum (CL) for maintenance of
pregnancy (CL is present throughout gestation in woman).

Towards end of third trimesta, progesterone production drops as that of estrogen increases. Contractions of
myometrium are initiated by estrogen to mark onset of parturition.

Parturition
Expulsion of fetus from uterus at the end of gestation period that is caused by:-
1) Increased production of Estrogen by the placenta that causes myometrial instability i.e. Uterine muscle
starts contracting.
2) Decreased production of progesterone that is necessary for maintenance of pregnancy.
3) Cortisol (stress hormone) is produced by fetal adrenal glands in response to stress to fetus (probably
caused by inadequate space for mature foetus in uterus or inadequate nutrient supply through placenta).
Cortisol initiates parturition in a manner not fully understood.
4) Stretch of uterine muscle by mature fetus initiates myometrial contraction.

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 5) The foetal head is pressed against cervix by uterine contractions and the pressure stimulates
mechanoreceptors in the cervix that send impulses to maternal posterior pituitary gland cause release of
oxytocin hormone into maternal blood.
6) Oxytocin causes powerful myometrial contractions that push fetus further into the cervix and increases
magnitude of cervical pressure receptors i.e. positive feedback that increases frequency and force of
myometrial contractions until fetus is expelled through external female genitalia.
7) Contraction of abdominal muscles enhance parturition process
8) Parturition ends with separation of placenta from the uterine wall (endometrium).

LACTATION

Functional anatomy:

Mammary glands are tuboalveolar and cutaneous in origin arising from two lateral lines in ventral abdomen
during fetal development. In adult, gland are located in inguinal (ruminants and equidae), along entire
abdominal length (canine, pig) or thoracic (primates) region.

Udder in ruminants consists of glands and associated teats which have streak canals-
- 1 in bovine
- 2 in goat, pig, horse
- 10-20 in carnivores and primates.

The mammary tissue consists of secretory parenchyma and connective tissue – stroma.

Bovine udder the most extensively studied and consists of:

1) Four quarters – each a separate functional unit having a teat and a gland.
2) A median suspensory ligament - separating the 2 halves
3) Lateral suspensory ligaments - binding the udder on lateral aspects.
4) Streak canal opening to environment and having folds of mucus membrane- Furstenberg’s Rosette- that
acts as a valve preventing milk leakage to environment.
5) Teat cistern
6) Gland (lactiferous) - cistern into which secretory ducts from gland parenchyma open.
7) Secretory tissue - organized into lobes, lobules and alveoli
8) Contractile smooth Myoepithelial cells - surrounding alveoli, involved in milk ejection process.

Arterial blood supply is through pudic artery, a branch of internal iliac artery while venous drainage occurs
through subcutaneous vein. The udder has extensive lymphatic drainage that anastomose forming cisterni
chyli that drains into venous circulation through the thoracic duct.

Sensory nerves arise from 1 -4 lumber; efferent nerves originate from lumber sympathetic plexus.

GROWTH AND DEVELOPMENT OF MAMMARY GLAND

Mammary gland growth starts at embryo stage along ventral mammary lines. Development of the duct system
(canalization) occurs before that of secretory system and mammary gland is distinct but small in size at birth.

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At Puberty

Rapid mammary gland development occurs after puberty influenced by the cyclic changes of steroid hormones
associated with estrus cycle.

Estrogen stimulates:
1) duct system growth and enlargement
2) fat deposition in glandular stroma that increases mammary gland size.

Hormones that have a general anabolic effect (mainly protein deposition) influence mammary growth e.g.
Growth hormone, thyroxine, insulin, glucocorticoids and prolactin.

Progesterone

Acting synagistically with estrogen stimulates development of lobule-alveolar system through growth of
secretory epithelium in alveoli particularly during pregnancy when progesterone is produced in large quantities
by the corpus luteum and placenta. (human chorionic somatomammotropin has similar effects in man).

INITIATION OF LACTATION

Despite causing mammary tissue growth, Estrogen and Progesterone inhibit secretion of milk by alveolar
epithelial cells.

PROLACTIN

A polypeptide hormone produced by the anterior pituitary stimulates milk synthesis (galactopoiesis) and
secretion (lactogenesis) by alveolar epithelium. During pregnancy prolctin is synthesized and stored in anterior
pituitary gland but its release into the blood is blocked by both estrogen and progesterone.

After parturition, a decline in circulating levels of progesterone and estrogen removes inhibition on prolactin
release into blood thus stimulating milk synthesis and secretion by alveoli.

Role of Hypothalamus

Normally the hypothalamus stimulates production of anterior pituitary hormones but inhibits prolactin synthesis
before puberty. A prolactin inhibitory hormone (probably dopamine) is transported from hypothalmus through
the hypothalmo-hypophysial portal system to cause inhibition which is removed (unexplained mechanism) at
puberty when prolactin production starts.

MILK EJECTION (Let-down)

Mammary alveolar epithelium continually secretes milk into alveolar cavity where milk is held. Ejection of
milk into the ductal system is a neurogenic and hormonal mechanism involving oxytocin- the posterior pituitary
hormone.
1) Stimulation of teat by suckling or milking initiates transmission of sensory impulses to posterior
pituitary and causes oxytocin release into blood and transport to udder
2) Sight of or sound from neonate, sounds and activities associated with milking (milk cans!) also causes
oxytocin release into blood circulation.
3) Oxytocin causes contraction of myoepithelial cells surrounding alveoli and squeezes milk into the
mammary ducts so that milk flows towards the gland (lactiferous) cistern.

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 4) Suckling or milking removes milk from teat and gland cistern by suction allowing more milk to flow
from gland parenchyma.
5) Adrenaline (released by painful milking, panic etc) inhibits contractile effect of oxytocin on the smooth
myoepithelial cells thus inhibits milk let-down.

Male Reproduction

Male reproduction is broadly divided into:-

1) Spermatogenesis- formation of sperms in the testis
2) Male sexual behaviour
3) Control of male reproduction.

Functional anatomy

1) Testis:- Paired ovoid organs encased in scrotal sac below abdomen in most mammals. Scrotal muscles
relax or contract to lower or raise testis relative to abdominal cavity. The movement regulates testicular
temperature at 1 -2 degrees C below body temperature for effective spermatogenesis.
2) Seminiferous tubules:- Numerous tubules forming testicular tissue in which spermatogenesis occurs.
Seminiferous tubules join up to form epididymis; a long tubule in which sperms are stored after
formation.
3) Vas deferens:- Connects epididymis to internal urethra through a short ejaculatory duct.
4) Seminal vesicles and prostate gland- Secrete fluids containing-
a. Nutrients for spermatozoa (mainly fructose and citric acid), prostaglandins and fibrinogen which
are produced by seminal vesicles while
b. Prostate glands produce a thin, milky secretion containing buffers (phosphate ions and citric
acid), calcium, a clotting enzyme and fibrinolysin. Prostatic secretions neutralize acidic
environment in the female reproductive tract after ejaculation while fibrinolysin breaks up
coagulum formed by seminal vesicle’s fibrinogen.
5) Bulbourethral glands- line internal urethral epithelium and secrete a mucoid lubricant.
6) Penis- part of male external genitalia consisting of erectile tissue having sinusoids that fill up with blood
to cause erection. Ruminants have a fibroelastic penis that does not erect.

Spermatogenesis
Sperms are formed in seminiferous tubules. Spermatogenesis starts at basement membrane of seminiferous
tubules where:
A) Primary spermatocytes (spermatogonia) from stem cells near basement membrane undergo mitotic
division to become type B spermatogonia which migrate into intercellular spaces of sertoli cells towards
lumen of seminiferous tubules.
B) Spermatogonia then undergo meiosis forming TWO secondary spermatocytes each having a haploid
number of chromosomes (23 in man).
C) Secondary spermatocytes undergo second meiotic division giving rise to 4 spermatids. One of the
chromosomes in the spermatid is either X or Y that determine sex of offsprings.
D) Spermatids undergo modifications near lumen of seminiferous tubules and become mature sperms that
have
a. A head containing chromatin material and acrosome (contains proteolytic enzymes- mainly
hyaluronidase- necessary for penetration of ovum by sperm in fertilization).
b. Neck
c. Body- contains numerous mitochondria that provide energy for sperm propulsion in female
reproductive tract.

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 d. Tail- a flagellum having an axoneme (skeleton with 11microtubules) whose whiplash motion
propels sperm forwards. Morphological abnormalities of the tail impede forward, progressive
motility of sperms.
When spermatozoa are formed, they are immature and incapable of rapid motility. Maturation occurs in the
epididymis where the gametes attain motility. However, inhibitory substances produced by epididymal
epithelium prevent motility and maintains sperms in a dormant state. Full motility is achieved in female
genitalia after ejaculation.

Hormonal regulation of Male Reproduction.

In the developing fetus, chorionic gonadotropins produced by the placenta stimulates production of
testosterone by germ cells in genital ridge.
Testosterone causes:-
i. Differentiation of germ cells into male organs
ii. Descent of testis into the scrotum (failure to descend called chriptochirdism).
After birth, testosterone production does not occur until puperty. Male reproductive functions commence at
puberty when:-
a) Hypothalamus starts producing Gonadotropin releasing hormones (GnRH) viz. FSH-RH and LH-RH.
The releasing hormones are transported to the anterior pituitary through the hypothalamo hypophysial
portal system and stimulate pituitary cells -called gonadotrophs- to secrete follicle stimulating and
luteinizing hormones; both glycoproteins. The two hormones are transported in blood to the testis
where:-
a. LH binds to intracytoplasmic receptors in Lydig cells (interstitial cells) and, through cAMP
second messenger, causes transcription of DNA into RNA and subsequent translation forming
enzymes that synthesize Testosterone from cholesterol or acetylCoA.
i. Testosterone stimulates spermatogenesis i.e development of seminiferous tubule’s
germinal epithelial cells into spermatids
ii. FSH stimulates sertoli cells to convert testosterone into estrogen which is essential for
sperm maturation (conversion of spermatids into spermatozoa) i.e. called
spermiogenesis. Sertoli cells also provide nutrients and a favourable environment
for spermatogenesis.
b) Testosterone enhances Pituitary production of Growth hormone that causes rapid growth of male
animals after onset of puberty.

Regulation of blood Testosterone levels

Testis produces a group of steroids called androgens that includes testosterone, dihydrotestosterone and
androsteindione. Adrenal glands also produce small quantities of androgens.
In blood testosterone is loosely bound to plasma albumin or firmly bound sex-hormone binding globulin. High
concentration of plasma testosterone inhibits GnRh (gonadotropin releasing hormone) and therefore inhibits LH
and FSH production by anterior pituitary leading to reduced testosterone secretion by testis.

Secondary Sexual Characteristics

Apart from initiating spermatogenesis, testosterone causes development of secondary sexual features in the
male including:
a) Elongation of bones at epiphysis so that males of most species are taller than female counterparts. The
hormone increases bone calcium retention therefore, bone thickness. The pelvic cavity becomes narrow
and long for weight bearing as opposed to pear shape in females. However, testosterone also causes
fusion of epiphysis and terminates growth.
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 b) Thickening of laryngeal mucosa that “breaks the voice”.
c) Growth of facial and body hair
d) Enlargement of penis and testis
e) Growth of skeletal muscles and deposition of protein in body organs
f) Secretion by sebaceous glands that cause acne in humans and production of pheromones in animals.
g) Baldness in men with a genetic predisposition towards the condition.
h) Aggression and sex drive.

Coitus
In males with erectile penis, onset of coitus is marked by penile erection caused by filling of erectile tissue
(corpus cavenosum and corpus spongiosum) with arterial blood and blockage of venous out flow by
ischiocavenosus muscle. Tactile stimulation of genitalia and perineal region enhance erection. Erection is
caused by parasympathetic nerves from spinal cord and psychic influences from limbic (emotional) system in
the brain.

Reflex parasympathetic impulses from lumbosaccral region causes emission- secretion of seminal and prostatic
fluids that mix with spermatozoa flowing towards urethra due to contractions of epididymis. Mixture of fluids
and spermatozoa forms semen.

Presence of semen in anterior urethra causes strong rhythmic contraction of smooth muscles ejaculatory duct
and urethra that expels semen through external erethra- called ejaculation- mediated by sympathetic (pudendal)
nerves. Draining of blood from erectile tissue ends coitus.

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