Liver Group
Clostridial diseases (black, bacillary, hemoglobinuria, redwater) which
effect the liver. cl. novyi, also known as cl. haemolyticum.
Affecting cattle, sheep, goats, swine and horses.
Information supplied from Schering-Plough
Animal Health Corp. information booklet, Clostridials, (SPAH-BOV-94)
Page 3 of 4
Closdridial Diseases of Livestock (Page
1)
Muscle Group. (Page
2)
Liver Group. (Page 3)
Gastrointestinal Group. (Page
4)
Organism
|
Disease
Name
|
Muscle
|
Liver
|
Gut
|
|
| cl. novyi, Type B |
Black Disease |
|
+
|
|
| cl. novyi, Type D* |
Bacillary |
|
+
|
|
| |
Hemoglobinuria |
|
| Redwater Disease |
|
| * Also known as cl. haemolyticum |
History
Geographical Distribution
Exposure
How Disease is Triggered
Disease Signs and Effects
Protection
Diagnosis
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Page
History
The identity of the two clostridial organisms whose
principal infection site is the liver dates back to the late 1800s and
early 1900sd. Since that time, they have been variously regarded as either
two types of the same clostridial
species (Cl. novyi Type B and Type D), or as two distinct species
(Cl. novyi and CL haemolyticum). The latter view is based primarily
on differences and disease manifestations.
The pathogenic (disease producing) characteristics of these two clostridial
organisms are quite similar, for liver tissue and both are dependent on
some form of liver damage for the activation of latent spores.
This has been confirmed through a series of studies in cattle. When live
spores of Cl. novyi type or type D were inoculated, along with
a tissue debilitant to the liver, 85 to 100% of the rest animals died.
When this same material was inoculated into muscle, deaths from Type D
did not occur at all, and death from Type B did not occur consistently.
These results indicate that although Type B infections in the muscle are
possible, such tissue is not the optimal site for multiplication of these
organisms.
Geographical Distribution
Laboratory and field evidence shows the disease of the liver
group to be widespread.
Early, it was the belief that both type B and type D infections were
threats only in a limited number of areas, and that the diseases occurred
only in poorly drained pastures suspected of being "hot spots"
for soil-borne spores. It is now believed that higher incidence of disease
in these areas is more a function of liver damage created by parasitic
flukes which abound in such areas than the presence or absence of soil-borne
spores.
The improvement of transportation systems (the trucking industry, primarily)
and the expansion of livestock raising and feeding into new areas have
greatly increased the movement of animals from region to region. Realizing
that clostridial spores are spread through excretions, etc., there is
probably no region in the United States where these diseases are not a
threat.
The risk to feedlot and dairy animals has been increased as the result
of liver stress produced by the use of high performance rations. Cl. novyi
diseases in feedlot animals is not a recent finding. Heavy losses were
described over fifty years ago by Records and Vawter among cattle eating
hay cut from infected fields (University of Nevada Technical Bulletin,
1945). These pioneering workers also stated, "Cases have occurred
in feeder cattle originating in regions where the disease was prevalent,
the ranch or feed yards at destination having shown no former evidence
of it." The authors of Diseases of Cattle (Second edition, American
Veterinary Publications, Inc.) stated "… the disease has occurred as long
as one month after arrival at a farm or feed yard at which there has
been no previous evidence of it."
How Exposure Occurs
As with the muscle group, spores which reside within the animal are always
a potential source of infection. Infection occurs when activation conditions
make it impossible for the bacteria to multiply and release destructive
toxins.
Spores of the liver group enter the body through contaminated feed ant
water. They do not usually enter through wounds and scratches as do Cl.
septicum and Cl. sordellii. A reservoir is established in
the intestinal tract from which spores enter the bloodstream for distribution
to the liver and other tissues of the body.
How Disease Is Triggered
Some form of liver damage is required for activation of the spores. As
with organisms of the muscle group, triggering conditions are those that
impede blood circulation, damage or destroy cells, and reduce oxygen availability.
Common sources of liver damage include abscesses, chemicals, fatty changes,
internal parasites, flukes, plant toxins, sawdust liver (telangiectasis)
and bacterial or viral hepatitis.
In he presence of liver damage, latent spores germinate. Potent toxins
are produced which expand the area of tissue damage. Toxins are also absorbed
by the bloodstream through which they reach and damage life-sustaining
organs and systems. A unique effect is the interruption of the oxygen-carrying
capacity of the blood through destruction of red blood cells and the linings
of small blood vessels.
Disease Signs and Effects
These diseases follow a rapid course. The acute stage is usually reached
before outward signs appear. Often animals are found dead before clinical
signs are observed.
If observed, early signs include depression and fever. Animals stand
apart from the herd and are reluctant to move. Many will assume an arched
back posture with neck extended. As the disease progresses, breathing
becomes difficult and blood-tinged froth may appear in the nostrils. In
lingering cases of Type D, the passage of red-color urine (hemoglobinuria)
may occur, but may not be observed.
Protection
The nature of the diseased in the Cl. novyi group makes routine
vaccination essential. As with all clostridial diseases, affected animals
rarely get a second chance; death usually occurs faster than the body
can mount a defensive response. Those being vaccinated for the first time
(primary immunization) should receive two doses three to four weeks apart.
Those vaccinated under three months of age should be revaccinated at weaning
or five to six months of age. Subsequent to this, animals should be revaccinated
every five to six months.
The degree of liver stress resulting from any management program should
be considered. Stock should be revaccinated prior to periods of special
risk of such as pastures infested with snails (the liver fluke intermediate
host) and being placed on a concentrated feeding program.
Diagnosis
As with the clostridial diseases of the muscle group, diagnosis of clinical
disease caused by Cl. novyi Types B or D may not be possible due
to the brevity of clinical illness prior to death. If clinical signs of
infection with Type D persist beyond 24 hours, and if affected animals
are observed frequently enough, a presumptive diagnosis may be made on
the basis of hemoglobinuria which may be observed. In most cases, however,
animals will be found dead.
Postmortem diagnosis of death due to acute cases of CI. Novyi Types
B or D presents a challenge in differentiating between the tow because
of similarities in gross pathology. Lesions of acute toxemia are present,
accompanied by varying degrees of edema and hemoglobin-containing fluid
in body cavities. Carcasses of animals which have died as the result of
Type D infections may exhibit more extensive evidence of hemolysis and
may have red urine in the bladder. These signs, however, may not be found
at all in animals that have died within 24 hours of infection. Anemic
infarcts in the liver may be present as the result of infection due to
either type. Those associated with Type D are generally the more evident.
In any case, careful examination is required to locate such infarcts.
Laboratory assistance is frequently required to confirm the diagnosis.
Such diagnosis requires the isolation and identification of the causative
organism from an area of liver necrosis. The fluorescent antibody (FA)
test, although useful, must be interpreted with caution. This test may
detect CI. Novyi not responsible for, but which has multiplied
following, death of the animal. Further, FA conjugates prepared from CI.
Novyi Type B antisera will cross-react with CI. Novyi Type
D. Thus, final differentiation may necessitate extensive biochemical and/or
toxin identification tests.
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