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COLLECTION: GOAT HANDBOOK
ORIGIN: United States
DATE INCLUDED: June 1992
Extension Goat Handbook
This material was contributed from
collections at the National Agricultural Library.
However, users should direct all inquires about the
contents to authors or originating agencies.
DOCN 000000026
NO C-5
METABOLIC AND NUTRITIONAL DISEASES
D. R. Nelson; U. of Illinois, Urbana
S. B. Guss; Pennsylvania State U., University Park
Nutrition
1 Pregnancy Toxemia Also known as pregnancy disease,
ketosis or twin lamb disease. Pregnancy toxemia is
a metabolic disease of goats and sheep in late pregnancy.
Factors important in the development of the disease
are: (1) Presence of two or more fetuses; (2) Undernourishment
during late pregnancy when the fetuses have the most
rapid growth; (3) Addition of stress such as severe
weather, sudden changes in feed, other disease or
transportation upon the previous factors. The disease
usually appears in the last 30 days of pregnancy and
is more common after the first pregnancy. The does
show signs of ketonemia, ketonuria, acidosis and central
nervous system involvement. The mortality rate is
high in affected animals. Most information available
is the result of studies in sheep.
2 Cause -- As pregnancy progresses,
an increasing demand is on the available blood glucose
supply of the doe or ewe because of fetal development.
The principal source of energy to the fetus is glucose
and utilization by the fetus occurs at the detriment
of the mother. Glucose requirements during late pregnancy
are increased 70-800ver the nonpregnant state since
800f fetal growth occurs during the last 40 days of
pregnancy. Blood sugar levels decrease as pregnancy
progresses (hypoglycemia) from a normal 35-45 mg per
100 ml blood to 20-25 mg per 100 ml blood in late
pregnancy. Pregnancy toxemia may develop when levels
decrease to about 18 mg per 100 ml blood. The severity
of hypoglycemia will be directly affected by undernourishment
of the mother or by increased requirements of the
fetus(es).
3 As the glucose supply diminishes
from increasing fetal demands and decreased glucose
production due to undernourishment, energy requirements
are furnished by other metabolic pathways, i.e. from
free fatty acids and amino acids. Breakdown of the
free fatty acids results in increased production of
ketones, acetoacetate and B-hydroxybutyrate. As hypoglycemia
becomes more severe, the ketone level in the blood
increases (ketonemia) and ketosis occurs.
4 As ketosis increases, the bicarbonate
level in the blood decreases and acidosis may result.
When the bicarbonate level declines sufficiently,
the animal will become comatose. During the later
stages of pregnancy toxemia, water consumption decreases,
urine output is decreased and kidney function is impaired.
The blood sugar level may increase severely (hyperglycemia)
during the late stages of the disease as a result
of the response of the adrenal glands to stress.
5 Circumstances which cause severe
hypoglycemia will usually result in pregnancy toxemia.
Under-nourishment of the doe may not meet the demands
for glucose production. The level of nutrition should
be increasing as pregnancy progresses so that the
doe will be able to provide fetal requirements. The
doe should be gaining weight during pregnancy. As
previously mentioned, multiple fetuses greatly increase
the glucose requirements. A gradual onset of undernourishment,
as would be seen if the feed intake was not increased
during pregnancy, may be tolerated by the doe and
toxemia may not develop. However, if the animal is
starved for several days, pregnancy toxemia may develop
readily. Sudden changes in weather, infections or
transport may result in periods of inappetence and
may trigger pregnancy toxemia. Excessively fat animals
may develop periods of poor appetite under stressful
situations.
6 Clinical Signs -- Clinical signs
are those observed with involvement of the central
nervous system. Initially, the animal tends to separate
from others. There is mild depression. Evidence of
blindness develops, the animal runs into objects,
shows little or no reaction when approached, and wanders
aimlessly. Dullness and depression become progressively
severe. There is reluctance to move. Eventually they
go down in sternal or lateral recumbency and show
little or no response to their environment. The does
become comatose and eventually die.
7 Occasionally, animals may show
a short period or intermittent periods of hypersensitivity.
There may be quivering, twitching of the ears, muzzle
or eyelids or spasms of certain muscles. Incoordination
may be evident. Recumbent animals may have convulsive
paddling movements.
8 Chewing, teeth grinding or vigorous
licking movements may be seen. Mild scouring may be
present. A snuffling respiration due to excessive
nasal secretion may be common. Drooling of saliva
is also seen.
9 Temperature and pulse are within
normal limits. Respiration is usually normal until
the later stages when it may become labored. The appetite
is poor or absent. Ketones may be detected in the
urine.
10 In some herds, 200r more may be
affected. Mortality may reach 80 Some may recover
spontaneously following parturition or abortion.
11 Post Mortem Findings -- The liver
is enlarged and has a pale yellow to orange coloration.
The adrenal glands may be enlarged. The uterus contains
two or more fetuses.
12 Treatment -- Oral administration
of glycerol or propylene glycol or intravenous administration
of glucose may be effective in the early stages of
the disease. Insulin may be used with these treatments
for better utilization of glucose. During the late
stages of the disease, glucose administration may
be ineffective or detrimental because the blood glucose
levels may be very high.
13 During the later stages of the
disease, acidosis and dehydration may be important
factors. Intravenous administration of large volumes
of electrolyte solutions with sodium bicarbonate may
be important. Corticosteroids may not be effective
in the later stages unless given at dosages utilized
to combat endotoxic shock.
14 Cesarean section or other methods
of terminating pregnancy may be effective in some
cases.
15 Prevention -- An adequate nutritional
level throughout the pregnancy will prevent pregnancy
toxemia. Protein and energy levels during the last
30-40 days of pregnancy should meet the doe's maintenance
requirements as well as the growth requirements of
the fetuses. Allowing the animal to become excessively
fat should be avoided.
16 Management during late pregnancy
should be directed at avoiding appetite problems in
the animals. Avoid sudden feed changes, diminish stresses
of severe weather, delay or avoid transportation and
prevent concurrent disease problems.
17 Parturient Hypocalcemia Also known
as milk fever. Parturient hypocalcemia is a metabolic
disease in does following kidding characterized by
poor milk production, poor appetite, lethargy and
low blood calcium levels. A hyperirritability characterized
by tetany may occasionally occur.
18 Cause -- Much research has been
done on hypocalcemia in dairy cows but knowledge is
still incomplete.
19 Following kidding, most does may
have a lowered calcium level in the blood (hypocalcemia).
This is partially due to the drain on available calcium
by the production of colostrum. (Colostrum contains
twice as much calcium as milk). Calcium is supplied
from two sources: 1) dietary; 2) mobilization of calcium
from the bone. Normally, calcium requirements following
kidding are provided primarily from the diet since
mobilization of calcium from the bone does not provide
significant amounts until about 10 days after parturition.
A loss of gastrointestinal function for any reason,
before or at parturition, may cause a severe drop
in the blood calcium level. Signs of hypocalcemia
may develop. Since older animals have more digestive
upsets at parturition, they have more problems with
hypocalcemia.
20 A high level of calcium in the
ration during gestation places almost complete reliance
on the dietary source of calcium. If the prepartum
diet is low in calcium, calcium mobilization from
the bone is instituted to meet the calcium needs.
If a gastrointestinal dysfunction occurs at parturition,
the effects are not severe since part of the calcium
requirements is supplied by mobilization from the
bone.
21 Clinical Signs -- Usually high
producing older does are affected shortly after kidding.
The does show lethargy, poor appetite and poor milk
production. Occasionally, hypocalcemia tetany may
be observed. The doe is hyperirritable and may show
muscle twitching of the lips, eyelids and ears. Trembling
or twitching of other muscles of the body may also
occur. Convulsions may develop.
22 Blood calcium levels may be 5-7
mg per 100 ml blood. The response to calcium therapy
may be diagnostic.
23 Treatment -- Administration of
calcium preparations, intravenously or subcutaneously,
will provide dramatic relief of clinical signs. Lethargic
does may begin eating and become more active and alert
within 12 hours. Tetany usually subsides in 30-60
minutes after treatment.
24 Prevention -- The problem often
involves many does in the milking herd. Usually, there
is excessive calcium in the gestation diet from a
mineral source and/or high quality legume hay. Correction
of the calcium imbalance is necessary. A low calcium
level during late pregnancy will help to control the
problem.
25 Polioencephalomalacia Also known
as cerebrocortical necrosis. Polioencephalomalacia
(PEM) is a disease of ruminant animals characterized
by derangement of the central nervous system due to
necrosis of the cerebral cortex of the brain.
26 Cause -- The cause and development
of the disease have not been entirely elucidated.
Thiamine is produced in the rumen. In PEM, thiaminase,
an enzyme that destroys thiamine, is thought to be
produced by certain bacteria within the rumen and
thiamine deficiency develops. A thiamine - analogue
is also produced within the rumen which may replace
thiamine in important metabolic reactions in the brain.
Necrosis of the brain occurs.
27 Clinical Signs -- Young animals
on high grain diets are affected more often. Older
animals and pastured animals may be occasionally involved.
28 The onset is often sudden with
blindness and disorientation. The head may be elevated.
Excitement may be seen but is usually replaced with
dullness. The animal may go down on its side with
its head thrown back. The legs may be rigidly extended.
Convulsions may occur. If untreated, death usually
occurs within a few days.
29 The appetite is lost and the animal
does not drink. Temperature and respiratory rate are
usually normal but the heart rate may be depressed.
30 Treatment -- Administration of
large doses of thiamine intravenously and/or intramuscularly
early in the disease will usually produce a dramatic
improvement within a few hours. In the later stages
of the disease, the brain necrosis may be too severe
for the animal to recover.
31 Prevention -- Until further elucidation
of the cause and development of the disease, little
can be done to economically prevent the disease. If
a case of PEM is diagnosed in a group of animals,
it is advisable to inject the remaining animals with
thiamine to prevent further cases.
32 Calculosis Also known as urinary
calculi, urolithiasis, kidney/bladder stones or waterbelly.
Calculosis is a metabolic disease of male ruminants
characterized by formation of concretions within the
urinary tract with obstruction to the outflow of urine.
This often results in rupture of the bladder or the
urethra.
33 Cause -- The disease occurs in
animals on a high concentrate diet with a mineral
imbalance resulting in excessive phosphorus intake.
A high phosphorus level develops in the blood and
in the urine. Magnesium and ammonium phosphate precipitate
to form a concretion or calculus. The size may vary
from sand-like particles to as much as 5-10 mm.
34 In the female ruminants, the calculi
are passed easily through the short expandable urethra.
In the male ruminant, the urethra is long and does
not expand easily. The calculus must pass around three
curves in the urethra. In sheep and goats, the urethral
process is a short (2-3 cm) extension of the urethra
beyond the tip of the penis. The diameter of the urethral
process is slightly smaller than the remaining urethra.
Calculi have a tendency to lodge at the lower curve
of the penis or at the urethral process.
35 Once calculi have lodged, the
wall of the urethra is damaged. Urine flow is obstructed
and pressure may build up in the bladder until the
bladder ruptures. If severe damage occurs to the wall
of the urethra, it may rupture and urine may flow
into surrounding tissues.
36 Urinary calculi problems are seen
most frequently during the winter or periods of very
warm weather when water consumption may be reduced.
37 Clinical Signs -- Signs do not
develop until there is partial or complete obstruction
of the urethra. Uneasiness, frequent attempts to urinate
and straining are seen early. Crystal deposits may
collect on the preputial hairs. The animals may refuse
food, isolate from the group and kick at the abdomen.
If the bladder ruptures, the abdomen may enlarge.
If the urethra ruptures, the lower abdominal wall
may become thickened from urine infiltration. If the
bladder or urethra rupture, the animals may show temporary
improvement. However, as time progresses, the animal
becomes depressed and death eventually results.
38 Treatment -- Once clinical signs
develop, damage to the urethra may be severe and while
the animal's life may be saved, its reproductive capabilities
may be lost. Since the calculi may frequently lodge
in the urethral process, this may be easily removed
and may eliminate the obstruction. Removal of the
urethral process has no effect on the reproductive
abilities of the buck.
39 Prevention -- The calcium-phosphorus
ratio should be 1.5-2:1. Often in breeding males,
it is advisable to decrease the grain and increase
the roughage. Adequate clean water should be available.
Prevent freezing of the drinking water in the winter.
40 If calculosis is a herd problem,
feed ammonium chloride 0.5-10r gradually increase
the salt in the diet to 5-10
METABOLIC AND NUTRITIONAL DISEASES
COLLECTION;GOAT HANDBOOK
ORIGIN;United States
DATE_INCLUDED;June 1992
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