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.
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.
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.
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For a baby kid, treat with 5cc CD antitoxin SQ, 5cc oral
penicillin (the long acting) 5cc SQ penicillin, 15cc Pepto
Bismol orally. If the kid is in acute pain, you can give .15cc
of Banamine and this will also prevent damage to the
kidneys and Liver by toxins. Clostridial bacteria growing in the
gut are killed topically by the penicillin, which is the drug of
choice for the species, Pepto is antacid, anti gas, and reduces
pain. Usually give 500mg of thiamin orally also. You must treat
the kid for two days, and allow it to nurse if it wants
to. On day three, give only the penicillin, and CD
antitoxin, and Penicillin SQ, and Calf Pac the kid.
-----From Coni Ross of CR Ranch.-- |
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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.
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.
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.
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.
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.
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.
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.
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.
Tissue
Changes
Type C is associated with acute hemorrhagic inflammation and
necrosis of the mucosa of the omasum and small intestine.
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.
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.
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.
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.
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.
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.
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.
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.
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.
The National Dairy Database (1992
TITLE;ENTEROTOXEMIA
COLLECTION;GOAT HANDBOOK
ORIGIN;United States
DATE_INCLUDED;June 1992
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