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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 000000064
NO G-10
ENTEROTOXEMIA
J. L. Ayers; Los Olivos, CA
S. B. Guss; Pennsylvania State U., University Park
Health and Disease Management
1 Enterotoxemia is one of the very important diseases
and in some areas it is the most prevalent disease
of goats. Despite the fact that it is also called
''Overeating Disease'' it is not caused by overeating.
Actually, the cause (etiology) of the disease is the
toxin (poison) produced by the bacterium Clostridium
perfringens type C or type D.
2 The bacteria are normally present
in the soil and the intestinal tract in relatively
small numbers. Under certain conditions the organisms
proliferate (reproduce billions of their own kind)
in the intestine and produce toxin in lethal quantities.
These conditions are those which (1) provide an ideal
environment and food for bacterial proliferation and
(2) slow down the normal movement of material through
the intestinal tract; they are often satisfied by
ingesting large amounts of starch when the intestinal
tract is not accustomed to it. The disease is often
associated with lush fast growing pasture or cereal
crops, heavy grain feeding or access to a lot of milk.
Illnesses which slow down the intestinal tract, may
predispose to the accumulation of dangerous quantities
of the toxin.
3 Most of our knowledge about the
disease comes from sheep. There are some important
differences in purpose and manner of raising (management
systems) that exist between sheep and goats that should
be kept in mind when one reads and applies sheep information
on goats. First, the disease usually occurs in single
(rarely in twins) lambs of a high milk producing ewe;
all the milk is consumed by that lamb. In contrast,
most goat births are twins, triplets or quadruplets
and in the best caprine management systems, the kids
are removed from their mother soon after birth. Thus,
the type of birth is no factor in goats. Second, dairy
kids are seldom fed large amounts of high energy diets
for meat production and therefore do not have the
same opportunity (unless accidentally or by mismanagement)
of exposure to grain. Finally, goats are natural browsers
(eat from bushes and trees with their head reaching
out or up); they do graze but do not consume as much
lush feed (usually in a pasture) as rapidly as sheep.
Summarizing, the well understood predisposing factors
in the sheep disease are not strictly applicable to
goats.
4 The predominant predisposing factors
in goats have to do with sudden exposure to grain
or large increases in quantity of milk consumed without
gradually increasing the amount over several days.
This leads to indigestion with slowing of the intestinal
tract. This probably plays a large role in the disease
in goats by allowing more time for toxin to accumulate
within the intestinal tract.
5 The Type D infection is probably
far more common than Type C. The latter type produces
a toxin called ''Beta Toxin'' which causes intestinal
necrosis and severe intestinal hemorrhage. It occurs
in adult goats.
6 Epsilon toxin is produced by the
Type D bacteria. It produces vascular damage and increases
the permeability (openness) facilitating its own absorption.
In the animals that die with neither signs nor tissue
changes, an extremely large amount of toxin was absorbed
very rapidly. When less toxin is produced, the animal
lives longer and there is more time for clinical signs
and pathological changes to develop.
7 Signs In the Peracute disease course,
a baby kid may be found dead with no signs or lesions.
It may occur after consuming excess feed or after
sudden access to highly palatable feed or after prolonged
hunger and a normal quantity of feed.
8 The Acute course of disease lasts
4-26 hours and usually ends in death. Initially the
temperature may go to 105F with severe abdominal pain
(the kid cries so loudly it is best described as screaming).
Profuse slimy or water diarrhea will occur. Depression,
wobbly gait, recumbancy (lying down on side often
with head down) occur early. Convulsions often occur
intermittently and may be accompanied by continuous
or intermittent opisthotonos (head thrown straight
over back). The animal may slip into a coma before
death or die groaning or even crying. These signs
occur in kids but can occur in adult milking goats
from either Type C or D bacteria.
9 The Subacute disease is more apt
to occur in older kids and adults. They may be ill
for several days or weeks and show anorexia (refusal
to eat) and intermittent severe diarrhea occasionally
with epithelial shreds in the feces. They will occasionally
eat and with time and appropriate treatment, they
will usually recover.
10 The Chronic form is characterized
by intermittent illness lasting several weeks. The
goat (usually an adult) will have a dull, stary look,
loose feces, an irregular appetite and, if a milker,
drop in production.
11 Tissue Changes Type C is associated
with acute hemorrhagic inflammation and necrosis of
the mucosa of the omasum and small intestine.
12 Type D causes mild to moderate
(occasionally severe) inflammation and even hemorrhage
of the small intestinal mucosa. Petechial hemorrhages
may be present anywhere in the body but especially
on the epicardium and endocardium. The pericardial
sac may contain slight excess of yellow fluid. Microscopic
examination of the brain may reveal degeneration of
the vascular endothelium with perivascular and intercellular
edema with foci of necrosis in several subcortical
areas.
13 Diagnosis The diagnosis of ''enterotoxemia''
in goats is probably overdone and is sometimes used
to lump any sudden death or acute intestinal disease.
The peracute and acute signs are helpful but can also
occur with acute salmonellosis or intestinal torsion.
Individual or first cases of salmonellosis would probably
be diagnosed by post mortem bacteriological examination
but if a herd problem exists the history, signs and
lesions would justify a presumptive diagnosis. Intestinal
torsion is an individual and uncommon event and would
rarely be diagnosed ante mortem.
14 Subacute or chronic cases could
resemble coccidiosis, salmonellosis, rumen impaction.
Fecal examination, culture and smears would aid in
diagnosis of the first two and abdominal palpation,
the latter.
15 The petechial hemorrhages, especially
on the epicardium should make one think of enterotoxemia.
However, one should look for at least two other signs
which together give good presumptive evidence of enterotoxemia;
these are, glucosuria and the presence of many short,
plump gram positive rods on an intestinal smear.
16 Ante mortem diagnosis is made
early if one can demonstrate a distinct, though transient,
improvement of signs after the intravenous injection
of 40-100 ml of Type C and D Cl. perfringens antitoxin.
17 Definitive diagnosis, however,
can only be made in the laboratory. Intestinal contents
should be preserved by adding 1 ml of chloroform to
10 ml of contents which have been collected in glass
within 12 hours of death.
18 Prevention and Treatment Vaccination,
with Cl perfringens type C and D toxoid by the following
schedule along with the good feeding practices of
making changes and increases in feed and milk gradually,
has provided excellent prevention of the disease.
Vaccinate unvaccinated adults twice at 4 to 6 weeks
intervals. Vaccinate again during the last month of
each pregnancy in order to ''booster'' her immunity
and provide colostral antibodies for the immediate
protection of the newborn kids. Vaccinate kids at
2-3 weeks of age and 4-6 weeks later.
19 The older literature suggested
that goats produce poor immunity but the results obtained
with the alum precipitated vaccine currently in use
seem to contradict this idea.
20 Treatment is ineffective against
the peracute and acute cases. However, if ante mortem
diagnosis is made one should attempt the use of 50
ml of specific hyperimmune serum intravenously every
4 to 8 hours in the valuable animal. In the subacute
and chronic case, antitoxin along with Tetracycline
orally at the rate of 5-10 mg/lb (11 to 22 mg/kg)
bodyweight will usually effect a cure.
ENTEROTOXEMIA
COLLECTION;GOAT HANDBOOK
ORIGIN;United States
DATE_INCLUDED;June 1992
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