PART 2 SPECIAL MEDICINE • Chapter 29: Metabolic diseases
69. StuderVA et al. J Dairy Sci 1993; 76:2931.
70. Goff JF, Horst RL. Acta Vet Scand Suppl 3003;
98:214.
71. DeFrain JM et al. J Dairy Sci 2004; 87:4195.
72. Ballard C et aI. Anim Feed Sci Technol 2001; 93:55.
73. Mandebvu P et al. Anim Feed Sci Technol 2003;
105:81.
74. HeuerYH et al. J Dairy Sci 2001; 84:1085.
75. Duffield IF, Bagg RN. CanVet J 2000; 41:388.
76. Neilsen N, Ingvartsen KL. Acta Vet Scand Suppl
2003; 98:306.
77. Hutjens MP. Vet Clin North Am Food Anim Pract
1992; 81:525.
78. Clark CE et al. Livestock Prod Sci 2005; 94:199.
79. Neilsen NI et al. J Dairy Sci 2005; 88:2441.
80. Larson T, Nielsen NI. J Dairy Sci 2005; 88:2004.
PREGNA NCY TOXEMIA IN SHEEP
Synopsis
Etiology A mu ltifactorial disorder of
energy metabolism. Negative energy to
i coupled with a short period of food depri­
hypoglycemia and ketonemia (the
accumulation in blood of acetoacetate,
p-hyd roxybutyrate and their decarboxylation
products acetone and isopropanol).
Epidem iology The disease in sheep is
associated with a falling plane of nutrition,
principally in the last month of pregna ncy,
I such as inadequate pasture management
in ewes bearing twins and triplets but can
be induced by other stress at this time.
Clin ical findings Sheep have
encephalopathy with blindness, muscle
tremor, convulsions, metabolic acidosis and
a clin ical course of 2-8 days, usually
terminating fatally un less treated early.
Clinical pathology Hypoglycemia,
ketonemia, ketonuria.
Necropsy findings None specific. Twin
lambs and fatty liver.
Diagnostic confirmation Ketonemia,
ketonuria or elevated ketones in m i lk .
Elevated P-hydroxybutyrate ( B H BA) i n
aqueous h umor of dead sheep.
Treatment Parenteral gl ucose with
corticosteroid and oral glu cose precu rsors
such as propylene glycol, occasionally
i nsulin, or oral g l ucose and electrolyte
therapy. Caesarean section or ind uction of
parturition in sheep. Case fatality high.
Control Correction of energy imbalance.
Flock biochemical monitoring coupled with
condition scoring.
ETIOLOGY
Hypoglycemia and hyperketonemia are
the primmy metabolic disturbances in
pregnancy toxemia. TI1e precipitating cause
is the energy demand of the conceptus in
the latter part of pregnancy but there i s a
great deal of variation between sheep flocks
in incidence of the naturally occurring
disease under conditions which appear to
be conducive to its development. The most
important etiological factor in pregnancy
toxemia is a decline in the plane of
nutrition during the last 4 to 6 weeks of
pregnancy. This is the period when fetal
growth is rapid and the demands for
energy markedly increased, particularly in
ewes that are carrying twins or triplets.
The disease also occurs in goats during
late pregnancy with the same initiating
causes.
The following classification of pregnancy
toxemia is according to cause as the
determination of the management cause
is critical to control and prevention. These
are further described below.
o Primary pregnancy toxemia
o Fat ewe pregnancy toxemia
" Starvation pregnancy toxemia
Secondary pregnancy toxemia
Stress-induced pregnancy toxemia.
EPIDEMI OLOGY
Primary pregnancy toxemia
This is the most common manifestation
and results in most flocks from a combi­
nation of a fall in the plane of nutrition
during the latter half of pregnancy often
vation in conjunction with a management
procedure in late pregnancy such as
crutching, shearing, change of environment,
or drenching. In pastoral sheep, the fall in
the plane of nutrition can result from factors
and improper stocking densities. In pastoral
flocks, the occurrence is more common in
early-lambing flocks where there is no
provision for added feed in years where
there is a long winter. In some outbreaks
the ewes have been moved on to better
pasture during late pregnancy to prevent
the occurrence of ketosis but it occurs
because the ewes are unaccustomed to
the type of feed and do not eat well.
With sheep housed in late pregnancy,
the provision of poor quality hay may
predispose pregnancy toxemia. A change
in fee d type and the feeding of moldy
feed or feed contaminated with manure
can also lead to decreased intake, especially
with goats. Competition for inadequate
trough space can also be important.
Goats exhibit greater dominant/submissive
characteristics than sheep and this can
result in lower food intake in submissive
goats in groups that are hand fed.
In all management systems, failure to
identify and separate ewes bearing twins
and triplets and to feed them separately
from ewes bearing singles and a general
failure to increase the nutritional plane of
pregnant sheep in the last 6 weeks of
pregnancy are predisposing factors.
Fat ewe preg n a n cy to)(emia
This occurs without a stress induction in
ewes that are very well fed and are in an
overfat condition in late pregnancy. Fat
ewes will experience a voluntary fall in
food intake in late pregnancy, due to the
reduction of the rumen volume by the
pressure of intra- abdominal fat and the
developing fetus. This can occur especially
if there is reliance at this time on high
water content feeds such as silage or root
crops. Traditionally, a lack of exercise is
also believed to predispose this type of
pregnancy toxemia. Commonly there is
concurrent hyp ocalcemia.
Starvation preg n a n cy toxe m i a
This occurs i n ewes that are excessively
thin. It is relatively uncommon but occurs
in extensive grazing systems where there
is prolonged drought and no alternative
feed supply and can be seen in any
production system where there is
mismanagement.
Secondary pregnancy toxe m i a
This usually occurs a s a sporadic disease
as the result of the effect of m1 intercurrent
disease such as foot rot or foot abscess,
which affects food intake. Heavy worm
infestation, e.g. with Haemonchus contortus,
would add a similar drain on glucose
metabolism and increase the chances of
development of the disease.
Stress-ind uced pregnancy toxe mia
This is the least common cause of the
disease, one where stress is the initiator.
Examples are the close shepherding or
housing of late-pregnant sheep of breeds
not used to being housed, the transport of
late pregnant sheep and outbreaks that
occur following a period of flock attack by
dogs.
Pregnancy toxemia occurs in ewes in the
last 6 weeks of pregnancy with the peak
incidence in the last 2 weeks of pregnancy.
It occurs primarily in ewes carrying triplet
or twin lambs.
Occurrence
Pregnancy toxemia occurs wherever sheep
are raised but it is primarily a disease of
sheep raised in intensive fanning systems,
either grazing or housed during the
winter. In part, this is because the breeds
of sheep used in intensive farming are more
likely to bear twins or triplets. In contrast,
sheep breeds in extensive grazing systems
commonly bear single lambs and signifi­
cant outbreaks of pregnancy toxemia are
uncommon except where there is drought
or poor pasture management. The attack
rate in a flock varies with the nature and
severity of the nutritional deprivation
and the proportion of the flock at risk. It
can be very high in starvation pregnancy
toxe mia, whereas fat ewe pregnancy
toxemia is generally of sporadic occurrence.
In outbreaks that follow management
procedures or other stressors, clinical
disease is not manifest until 48 h afterwards
and new cases will develop over several
days. Intercurrent disease in late pregnant
ewes, such as foot rot or foot abscess, may
predispose pregnancy toxemia.
The natural incidence in intensively
farmed sheep is approximately 2 % of
pregnant ewes but where there are severe

management deficiencies of the disease, '
the disease may affect the majority of late
pregnant ewes. In a study of sheep diseases
in Canada, 19% of flocks were reported to
have the disease.1 The case fatality is high
unless treatment is initiated early in the
clinical course. Even with eady treatment
case fatality can be high.2,3
Expe ri mental reprod uction
Hypoglycemia and ketosis can be exper­
imentally produced in pregnant sheep by
under-nourishment but the resultant
syndrome has biochemical and clinical dif­
ferences to spontaneously occurring preg­
nancy toxemia. For example, loss of appetite
is an early sign in spontaneous occurring
disease whereas starved experimental
animals, even though hypoglycemic and
ketotic, will eat feed when offered and
there is debate that hypoglycemia is the
primary precipitating cause of the clinical
signs in the naturally occurring disease.3-5
There is a great deal of variation
between sheep in the ease with which the
hypoglycemia and ketosis can be pro­
duced experimentally, and in the variation
in incidence of the naturally occurring
disease in conditions which appear to be
conducive to its development.
It is probable that the difference
between sheep depends upon the meta­
bolic efficiency of the liver
Animal risk factors
Pregnancy
The disease occurs only in ewes in the
last 6 weeks of pregnancy, usually during
the last month, with the peak incidence in
the last 2 weeks of pregnancy. It occurs
primarily in ewes carrying triplet or twin
lambs, although ewes bearing a single,
large lamb may also be affected.
Parity
The disease is uncommon in maiden
ewes because of their low fecundity and
increases in prevalence up to parity three.
B reed
Rreed differences largely reflect differences
in fecundity and differences in manage-
ment sys tems. Thus, the disease is more
common in British lowland breeds and
their crosses than the Merino. British
hill-breeds are traditionally believed more
resistant to the development of pregnancy
toxemia in the face of nutritional depri­
vation of the ewe but resistance is achieved
at the expense of lamb birth weight
and has the penalty of higher neonatal
mortality. There are however differences
in the susceptibility of individual sheep
that appear to be related to differences in
rate s of hepatic gluconeogenesis.6
Economic sign ificance
The economic effect of the disease is
considerable. Without treatment, the
case-fatality rate can approach 100% and
in individual flocks, the disease can reach
a level of incidence sufficient to be classed
as an outbreak . Treated ewes that recover
may have dystocia and die during partur­
ition or develop retained placenta and
metritis. Flocks that experience pregnancy
toxemia also have a significantly higher
than normal mortality in neonatal lambs
and often a severe decrease in wool quality.
Flocks that experience pregnancy toxemia
are predisposed to the subsequent occur­
rence of hypomagnesemia in the lactating
period.
PATHOGEN ESIS
Pregnancy toxemia results from inadequate
energy intake in late pregnancy in ewes
with more than one fetus. Approximately
60% of fetal growth takes place in the last
6 weeks of pregnancy. Ewes that are predis­
posed to the disease have an ineffective
gluconeogenic response to the continued,
preferential demands for glucose by the
growing fetuses resulting in hypoglycemia,
lipid mobilization and the accumulation
of ketone bodies and cortisol. The reason
for this predisposition is not known.
The subsequent disease and metabolic
changes are associated with excessive
lipid mobilization.7-9 Elevated concen­
trations of �-hydroxybutyrate further
suppress endogenous glucose production
and exaggerates the development of
ketosis and the negative feedback of
hyperketonemia on glucose production can
result in a vicious circle.lO,n
The disease manifests with an
encephalopathy, believed to be a hypo­
glycemic encephalopathy resulting from
hypoglycemia in the eady stages of the
disease.12-14 The encephalopathy and the
disease are frequently not reversible
unless treated in the early stages. The
onset of clinical signs is always preceded
by hypoglycemia and hyperketonemia,
although the onset of signs is not related
to minimum blood glucose or maximum
ketone levels and hypoglycemia may not
be the initial precipitating cause of the
'
syndrome.3-5 In affected ewes, there is an
abnormally high level of cortisol in
plasma and it has been suggested that
adrenal steroid diabetes contributes to the
pathogenesis.5
The increase of plasma concentrations
of non-esterified fatty acids results in a
depression of cellular and humoral immune
responses in the experimentally produced
disease15 but the clinical significance of this
to naturally occurring disease is not clear.
Renal dysfunction is also apparent in
the terminal stages of ovine ketosis, and
contributes to the development of clinical
signs and the fatal outcome.
Those ewes which are carrying only
one lamb and have been well fed prior to
Prod uction diseases
a short period of undernutrition may
develop a subacute syndrome both
clinically and biochemically.4,9
CLINICAL FIN DINGS
Ovi n e ketosis
The earliest signs of ovine ketosis are
separation from the group, failure to
come up for feeding in pastoral animals
or standing near the trough with the
group of sheep but not eating, in housed
animals, altered mental state and apparent
blindness, which is manifested by an
alert bearing but a disinclination to move.
The ewe will stand still when approached
by attendants or dogs and will turn and
face them but make no attempt to escape.
It is eaSily captured but more difficult to
restrain than normal sheep. If it is forced
to move, it blunders into objects and
when an obstacle is encountered, presses
against it with its head. Many affected
ewes stand in water troughs all day and
lap the water. Constipation is usual, the
feces are dry and scanty and there is
grinding of the teeth.
In later stages, marked drowsiness
develops and episodes of more severe
nervous signs occur but they may be
infrequent and are easily missed. In these
episodes, tremors of the muscles of the
head cause twitching of the lips, champing
of the jaws and salivation, ar.d these are
accompanied by a cog-wheel type of
clonic contraction of the cervical muscles
causing dorsiflexion or lateral deviation of
the head, followed by circling. The muscle
tremor usually spreads to involve the
whole body and the ewe falls with tonic­
clonic convulsions. The ewe lies quietly
after each convulsion and rises normally
afterwards but is still blind.
In the periods between convulsions
there is marked drowsiness which may
be accompanied by head pressing, the
assumption of abnormal postures includ­
ing unusual positions of the limbs and
elevation of the chin - the 'stargazing'
posture - and incoordination and falling
when attempting to walk. A smell of
ketones may be detectable on the breath
of the ewe.
Affected ewes usually become recum­
bent in 3-4 days and remain in a state of
profound depression or coma for a further
3-4 days, although the clinical course is
shorter in fat ewes with pregnancy toxemia.
Terminally there may be a fetid diarrhea.
Fetal death occurs commonly and is
followed by transient recovery of the ewe,
but the toxemia caused by the decomposing
fetus soon causes a relapse.
Affected ewes commonly have difficulty
in lambing. Recovery may ensue if the
ewe lambs or the lambs are removed by
caesarean section in the early stages of
the disease. In an affected flock, the disease
f
1 670 PART 2 SPECIAL MEDICINE • Chapter 29: Meta bol i c diseases
usually takes the form of a prolonged
outbreak; a few ewes become affected
each day over a period of several weeks.
Recovered ewes may subsequently show
a wool break.
CLINICAL PATHOLOGY
y
Hyp ogl cemia, ketonemia, and ketonuria
are characteristic of the disease. The initial
changes are similar to ketosis in cattle but
the sequel is not. Hypoglycemia can be
used as a diagnostic aid in the early
stages of the disease but is of limited
value later in the course as by the time
that sheep become recumbent, blood
glucose levels may be normal or grossly
elevated. This may be the result of fetal
death which has been shown to remove
the suppressing effect of the fetus on
hepatic neoglucogenesis.6
Ketonemia and ketonuria are constant
and serum �-hydroxybutyrate concen­
trations are in excess of 3000 llmol/L,u
Sheep develop a severe metabolic
acidosis, renal failure with a terminal
uremia, and become dehydrated. Liver
function tests show liver dysfunction. 16
Elevation of plasma cortisol occurs in
pregnancy toxemia and concentrations
above 10 ng/mL are indicative of pregnancy
toxemia,17 but pregnancy toxemia and
clinical hypocalcemia can both cause suffi ­
cient stress to promote such an elevation.
NEC ROPSY F I N D I N G S
Pregnancy toxemia i n ewes is almost
always fatal without treatment intervention.
At necropsy, there is severe fatty degener­
ation of the liver and there is usually
evidence of constipation, but some have
fetid light coloured diarrheic feces. A large
single but more commonly twin or greater
number of fetuses are present. Fetuses
may have died before the ewe and show
autolysis.
Histopathologically there is also a
poorly defined renal lesion and there may
be evi dence of neuronal necrosis.1s The
lambs may be dead and in varying stages
of decomposition. Hepatic glycogen levels
are usually very low. Concentrations of
�-hydroxybutyrate in the aqueous humor
or the CSF >2500 or 500 llmol/L respect­
ively, are supportive of a diagnosis of
pregnancy toxemia.13
Sheep
Pregnancy toxe mia is usually suspected in
late pregnant ewes which show nervous
signs and die within 2-7 days and there
may be a h istory of exertion, stress or
sudden deprivation of food. Hypocalcemia
can occur under similar circumstances but:
1 . The onset is within 12 h of the stress
2. A considerable proportion of the flock
will be affected at the same time
3. The disease is manifest with myasthenia
4. It has a much shorter course of 1 2-24 h
5. Affected animals respond well to
treatment with solutions of calcium salts.
• Listeriosis
• Cerebral abscess
• Acidosis
• Uterine torsion or i m pending abortion
• Rabies.
TR EATMENT
Treatment in sheep
Sheep treated very early in the course of
the disease generally respond favorably,
but response to therapy is poor once
sheep have become recumbent and the N
administration of 50% dextrose at this
time may hasten death. Therapy requires
the correction of fluid, electrolyte, and
acid-base disturbances in addition to
replacement therapy with glucose.
Parenteral therapy
Ideally, individual sheep should be
examined biochemically and the corrective
therapy based accordingly, with fluids,
electrolytes and glucose (dextrose) given
over a prolonged period of time. One rec­
ommendation for glucose therapy is
the administration of 5-7 g of glucose
N 6-8 times a day in conjunction with
20-40 units of zinc protamine insulin
given 1M every other day for 3 days .7 In
many sheep-raising areas, intensive labora­
tory monitoring and therapy is not pOSSible
because of access, expense, or the number
of sheep involved in an outbreak. In the
absence of biochemical monitoring, therapy
with glucose should be accompanied
by the N injection of isotonic sodium
bicarbonate or lactated Ringer's solution
and the administration of further fluids by
a stomach tube.
Standard doses of corticosteroids
have little therapeutic effect in sheep
and therefore treatment with these drugs
is not recommended although they are
commonly used. Very large doses are
effective in ewes still able to stand but the
success probably rests in the removal
of the glucose drain by the induction of
premature parturition. Treatment with
recombinant bovine somatotrophin
(0.15 mg/kg body weight) in conjunction
with dextrose and electrolytes may result
in a shorter duration of treatment, improve
ewe survival and result in a greater
viability of lambs born4,19,2o but reported
results are not impressive.
Oral therapy
Traditionally, propylene glycol
glycerine (110 g/d) given by mouth is used
to support parenteral glucose therapy. Less
intensive therapy includes the use of
propylene glycol or glycerine alone which
has given excellent results for some
workers but poor results for others.
Success is reported with the oral
drenching, every 4-8 h, of 160 mL of a
solution containing 45 g glucose, 8 .5 g
sodium chloride, 6 . 1 7 g glycine and
electrolytes, which is available commercially
as a concentrated oral rehydration solution
for calves with diarrhea.21 This th erapy
i s now commonly used in the UK. 22
Drenching of non-pregnant sheep with
this solution is followed by higher blood
concentrations of glucose than those
achieved follOwing drenching with glycerol
or propylene glycol. Reported recovery rates
in pregnancy toxemia are 90% in early
cases and 55% i n advanced cases. 21
Vasopressin has been used to induce
closure of the esophageal groove in con­
junction with the oral administration of
glucose. Treatment with insulin in addition
to treatment with oral glucose precursors
and electrolytes showed a Significantly
higher survival rate (87%) compared with
treatment with oral glucose precursors
and electrolytes alone.3
C aesarean
Caesarean section can be used as an
alternate to replacement therapy. Provided
ewes are in the early stages of the disease,
removal of the lambs by cesarean section
is probably the therapy that has the greatest
success rate. The demand for glucose by
the lambs is immediately removed and
both the ewe and the lambs have a high
chance of survival providing the caesarean
section is conducted before there is
irreversible brain damage in the ewe and
providing the lambs are close to term. If
the ewe is in the recumbent stage then
her chance of survival is low. Cesarian
section can still offer the chance for
survival of the lambs but also less viable at
this stage and may be dead. Ultrasound to
determine if the lambs are alive, aids in
the decision for caesarean section.
Induction of parturition is a further
option but should only be used if the ewe
is in the early stage of the disease as lambs
will be delivered no earlier than 36 h after
therapy, and often later. If the ewe is
judged unlikely to survive this period,
caesarean section is a better option. Induc­
tion with corticosteroids has been effecte d
with dexamethasone 21 -isonicotinate or
the sodium phosphate form at a dose rate
of 16-25 mg per ewe but dexamethasone
trimethylacetate appears to be ineffective.
Lambs will be born 48-72 h after injection.
Induction of parturition in normal sheep
is reported with 10 mg of betameth ason e
or 2.5 mg of flumethasone23 but there are
or
no reports of their efficacy in sheep with
pregnancy toxemia.
CONTROL
When clinical cases occur, the rest of the
flock should be examined daily for any
evidence of ketosis and affected anim als

trea ted immediately with propylene
glyc ol or glycerol or oral glucose/glycine/
electrolyte solutions. Supplementary feed­
ing of the flock should be commenced
immediately, with particular attention
given to an increase in carbohydrate
intake. Cereal grain starting at 0.5 Ib/head
per day and increasing to 2 lb/head per
day (0.25-1 kg/head per day) for large
frame breeds is recommended.
Prev ent ion
Ensure that the plane of nutrition is rising
in the second half of pregnancy, even if it
means restricting the diet in the early
stage s . Ewes that are in condition score
2.5-3.0 on a 1.0-5 . 0 scale at 90 days of
gestation and are in an ideal situation to
respo nd to increased feeding in the latter
part of gestation.22,24 If necessary, ewes with
higher condition scores at the end of the
first month of pregnancy can be fed to
lose 0.5 condition score durin g the period
to the third month of pregnancy without
any significant effect on the ewe or lamb
size or viability. Many small farm sheep
producers have sheep in too high a condi­
tion score early in pregnancy.
The last 2 months are particularly
important in the prevention of pregnancy
toxemia as 70 % of the lamb's birth
weight is gained during the last 6 weeks
of pregnancy. During this period, the
provision of cereal grain or a concentrate
containing 10% protein at the rate of
0.25 kg/d, increasing to 1 kg/d in the last
2 weeks, has provided good protection.
During this period, the ewe should gain
an increase of body weight of 10% for
ewes with single lambs and 18% in ewes
carryin g twins. For the flock this represents
a flo ck body condition score that maintains
or gains to 3.0-3.5 during this period.
Higher body condition scores can result in
higher birth weight of lambs but other than
in stud flocks these are not economic and
the standard commercial flock runs the
risk of fat ewe pregnancy toxemia with
higher targeted body condition scores.
At the beginning of the fourth month
of pregnancy, the flock can be conditioned
scored and divided into three groups; those
with acceptable condition scores, those
with sub-optimal condition scores, and
those that are fat and the groups fed
accordingly. Response should be evaluated
by condition scoring at 2 weekly intervals
through the fourth and fifth month of
pregnancy. Maiden ewes should be fed as
a separate group in order to provide for
the requirement for growth in addition to
the requirement for pregnancy. Attention
should also be given to broken-mouthed
eWes to ensure that they are maintaining
an adequate body condition.
There are managemental difficulties in
any nutritional program for sheep because
of the way they are husbanded. Ideally,
sheep should be divided into a number of
sub-flocks and fed depending on whether
there are one, two or three, or no fetuses
present. Ultrasound offers a method for
this selection.
When feeding sheep, account needs
to be taken of those ewes (and does) who
are timid and for this, or other reasons,
slow feeders. If supplementary feeding
is practiced in a confined space, with
insufficient trough space for all the flock
to eat at one time, and if the feed fed is
in small amounts and highly edible, a .
proportion of ewes will get little or no feed.
Before embarking on a nutritional
support program, it is advisable to estimate
cost effectiveness. In sheep breeds with
low twinning rates that are well managed,
it is often more profitable to do nothing
and to let the disease occur in the very
occasional sheep and treat it accordingly.
Sudden changes in type of feed should
be avoided and extra feed provided during
bad weather. Shelter sheds should be
available, and in purely pastoral areas,
lambing should not be planned before the
pasture is well grown . A high incidence is
often encountered in small, well-fed flocks
where the ewes get insufficient exercise.
In such circumstances the ewes should
be walked 30 min daily and, if pasture is
available, only concentrate should be fed
I so that they will be encouraged to forage
for themselves.
Flock monitoring for latent pregnancy
toxemia during the last 6 weeks of preg­
nancy can be conducted using serum
�- hydroxybutyrate as an indicator with
concentrations of 800 !lmollL indicating
adequate energy intake, 800-1600 Ilmol/L
inadequate energy intake and levels
greater than 1600 Ilmol/L indicating severe
undernourishment. Pooled samples have
been used to reduce the cost of analysis.9
Serum glucose and �- hydroxybutyrate
concentrations have been found to vary
significantly be tween flocks within the
normal range.
REVIEW LITERATURE
Marteniuk JW, Herdt TH Pregnancy toxemia and
ketosis of ewes and does. Vet Clin North Am Food
Anim Pract 1988; 4:307-315.
Andrews A. Pregnancy toxaemia in the ewe. In
Practice 1997; 19:306-311.
Rook JS, HerdtTH Metabolic disorders of ruminants.Vet
Clin North Am Food Anim Pract 2000; 16:293-317.
REF ERENCES
1. Dohoo IR et al. Can J Comp Med 1985; 49:239.
2. Scott P. In Fractice 1995; 17:266.
3. Henze P et al. J Vet Med A 1998; 45:255.
4. Andrews AH et al. Small Rum Res 1996; 23:191.
5. Sigurdsson H. Acta Vet Scand 1988; 29:407.
6. Wastney ME et al. Aust J BioI Sci 1983; 36:271.
7. Martenuik JV et al.Vet Clin North Am Food Anim
Pract 1988; 4:307.
8. Rook JS, Herdt TH.Vet Clin North Am Food Anim
Pract 2000; 16:293.
'1
I
Production diseases 1 67 1
9. Van Saun RJ. J Am Vet Med Assoc 2000; 217:1536.
10. Schlumbohm C, Harmeyer J. J Dairy Sci 2004;
87:350.
11. Schlumbohm C, Harmeyer J. J Dairy Sci 2003;
86:1953.
12. Jeffrey M, Higgins R JVet Rec 1992; 301.
13. Scott PR et al. BrVet J 1995; 151:587-589.
14. Sargison ND et al. BrVet J 1994; 150:271.
15. Lacetera N et al. Am JVet Res 2002; 63:958.
16. West HJ. Br J Nutr 1996; 75:593.
17. Ford EJR BrVet J 1990; 146:539.
18. Jeffrey M, Higgins RJ.Vet Rec 1992; 301.
19. Scott PR et al.Vet J 1998; 155:197.
20. Andrews AH, Wilkinson J. Large Anim Pract
1998; 19:31.
21. Burwell JF et al.Vet Rec 1986; 118:208.
22. Andrews A. In Practice 1997; 19:306.
23. Ingoldby L, Jackson P In Practice 2001; 23:228.
24. Russel A. In Pract 1985; 7:123.
FADY LIVER IN CADLE (FAT COW
SYNDROME, HEPATIC LIPIDOSIS,
PREGNANCY TOXEMIA IN
C ADLE)
Fatty liver or hepatic lipidosis is a major
metabolic disease of dairy cows in early
lactation and is associated with decreased
health status and reproductive perfonnance.
Etiology Mobilization of excessive body
fat to liver during periods of negative
energy balance at time of part u rition o r in
early lactation of dairy cows and late
pregnancy of beef cows.
Epidemiology High-producing dairy cows
overfed during dry period may develop fatty
liver syndrome just before or after calving
precipitated by any factor or disease which
interferes with feed intake. Occurs in well­
conditioned beef cattle in late pregnancy
when energy intake suddenly decreased.
Moderate and subclinical degrees of fatty
infiltration may adversely affect reproductive
performance of dairy cows.
Signs Ina ppetence to anorexia, ruminal
atony, lethargic, inactive, ketonuria, fat
body condition, weakness and recumbency
if worsens. Recover if conti n u e to eat and
a ppetite i m p roves.
Clinical pathology Increase in serum
hepatic enzyme levels, increase in ketone
bodies; increased fat in liver bi opsy.
Necropsy findings Fatty infi ltration of
liver.
Diagnostic confirmation Liver biopsy.
D ifferential diagnosis l ist
• Left-sided displacement of abomasum
• Right-sided displacement of abomasum
• Milk fever
• Parturition syndrome
• Abomasal i m paction
• Vagus indigestion
• Peritonitis.
Treatment Fluid and electrolyte therapy
including glucose IV. Propylene glycol
orally. Provision of palatable feed.
Control Avoid overfeeding d u ring late
lactation and dry period. Avoid situations
which reduce feed intake at time of
parturition.