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likely to subside after initial exposure and to recur only when the
source of infection reappears.
5 Reports of the disease in goats are sparse, therefore the following
generalizations may not be valid. However, S. typhimurium seems to
affect any age goat with a short, fatal course and is highly
contagious. S. dublin may be less contagious and infected goats seem
more apt to recover.
6 Clinical Signs -- The peracute case is found dead without previous
signs and is most frequent in the newlyborn. The acute form has been
reported in 2-4 week old kids with a high morbidity and mortality (32
of 35 animals dying) and in adults over 1 year old. First there is a
profuse, watery, (the fecal consistency may be more like paste or putty
with S. dublin) yellow diarrhea; this is rapidly followed by
depression, rapid dehydration and weakness. Some die in 8-12 hours,
most in 24-48 hours and a few live for a week. The temperature may
reach 106-108 but often returns to normal or subnormal near death.
7 Tissue Changes -- Post mortem findings are often not striking. The
peracute case may have excess fluid in the abdominal (peritoneal) cavity
and heart sac (pericardial space); there may be tiny (petecchial)
hemorrhages in various parts of the body especially around the heart,
the middle small intestine may fill with gas, contain some fluid and
have a thin wall.
8 Acute cases will have mild to moderate inflammation (reddening) of
the inner lining (mucosa), and less frequently hemorrhagic enteritis
will be present. The outer surface of the intestine and linings of the
body cavities (serosa) will likely have petechial hemorrhage. The
messenteric lymph nodes are usually enlarged, wet and when cut have a
soft consistency. In animals that live longer, the liver will appear
enlarged, have rounded edges and often the gall bladder is full. Only
rarely will the intestinal mucosa show varying degrees of erosion or
ulceration. Increased volume of amber joint fluid with or without white
fibrinous clots or casts are not an uncommon finding in the joints of
longer lasting acute cases.
9 Diagnosis -- Signs will mimic colibacillosis, coccidiosis, certain
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parasite infestations and enterotoxemia; tissue changes are also
nonspecific. It is important to conduct a necropsy examination on the
first as well as all animals dying. It is equally important to attempt
isolating the causative organism at least from the intestinal
contents, the messenteric lymph nodes and the liver. A diagnosis of
Salmonellosis is important because it will indicate the need to
concentrate more on prevention than on drug therapy. However most
laboratories will not be able to type the species of Salmonella that
was isolated. It is important that this be done, however, and for this
purpose the isolate can be sent to the National Animal Disease Center
in Ames, Iowa via your regional Federal Veterinarian's Office.
10 Prevention and Treatment -- The few reports of Salmonellosis in
goats have been very discouraging regarding prevention and treatment.
However, the strict management practices employed in well run cow
dairies should always be followed and should help keep Salmonellosis at
a low level.
11 Prevention and fluid therapy will be discussed as a separate
section because it applies to all enteric and many other diseases.
Management practices that prevent or reduce the amount of exposure to
Salmonella sp. is the only real hope of control for an endemic herd.
The following treatment recommendations are made with the reservation
that they are often not successful.
12 Chloramphenicol is a drug that is not cleared for use in goats and
should only be given under veterinary prescription. It is inactivated
by a functioning rumen and should therefore not be given orally to the
kid that has started to eat roughage in any significant quantity.
However, it is often the only drug to which the organism is sensitive.
Trimethoprim-sulfadoxine combinations and nitrofurans have been
successfully used in calves and systemic Salmonellosis will sometimes
respond to ampicillin.
13 Dehydration and acidosis should be combated with oral, intravenous
or subcutaneous administration of fluids, electrolytes and energy as
will be discussed later.
14 Colibacillosis
The bacterium Escherichia coli (E. coli) has several serotypes,
most of which are normal nonpathogenic inhabitants of the
gastro-intestinal tract. There are pathogenic serotypes, however; some
of these are capable of gaining entrance to the body (septicemic form)
through the intestinal wall, others remain in the intestinal tract and
liberate a toxin which is absorbed by the body and causes generalized
disease and diarrhea (enterotoxogenic form). A milder enteric form,
without signs of toxemia but causing diarrhea, is a third and
intermediate form. Colibacillosis is a disease of very young animals
usually 2-10 days old.
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DIARRHEAL DISEASES
15 Clinical Signs -- The septicemic form usually occurs in the first 4
days of life and when there has been no absorption of colostral
antibodies. The animal is depressed, weak, anorectic (won't eat), the
temperature is elevated early but drops below normal when the animal
becomes weak and goes down. Diarrhea is not common. Death usually
occurs in 2 days. Animals surviving for a week may show signs of the
organism localizing in the joints, brain, eyes or lungs. The septicemic
form is the most common form in lambs and is usually peracute. The
same may be true in kids. ++++MISSING DATA++++
16 The most important factor in determining an animal's ability to
survive colibacillosis is the serum immunoglobulin level before the
animal develops the disease. Antibiotic therapy may help animals with
marginal to adequate serum antibody levels but are probably of no value
in helping the agammaglobulinemic (no immunoglobulin in the serum)
animal.
17 Prevention of Colibacillosis and Salmonellosis
Newborn ruminants are born with antibodies against various disease
producing microorganisms (germs). These antibodies are proteins called
immunoglobins. A newborn kid receives all of its protection
(immunoglobulins) against germs as a result of drinking the colostrum
milk produced by its mother. Milk of the very first milking contains
many times more antibodies than does that of the second and later
milkings. Further the intestinal tracts of the newborn can absorb the
antibodies at maximum rate only during the first 12 hours of life;
absorption decreases rapidly from 12 to 36 hours after which time no
more are taken into the blood stream. In addition to these circulating
antibodies there is another type (local antibodies) that attach to the
surface of the intestinal tract, are never taken into the blood stream
and do a certain amount of bacterial neutralization from this
position.
18 Thus, colostrum is the first essential nutrient of the newborn.
Without it, death of the newborn can be assumed. As a rule of thumb,
one ounce of first milking colostrum per pound body weight (of the
kid) should be received by that kid in the first 8-12 hours of life.
Ideally this would be given in small quantities frequently. Removing
the kid from the mother immediately after kidding has two advantages.
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