Enterotoxemia-'Over-eating Disease'

18 September, 2015rodster385Comments (0)

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

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

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.