eprint_2_6604_114

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Bacillary hemoglobinuria is an acute, infectious, toxemic and highly fatal
clostridial disease of primarily cattle and less commonly sheep and swine caused
by Clostridium haemolyticum. It is transmitted by ingestion and inhalation.
Disease is commonly associated with fasiolosis. It is rare in calves less than 1
year old and cattle with poor body condition.
It causes severe hepatic necrosis and local thrombosis.
Clinical Symptoms
Affected animals are depressed, arched back, grunt when walking, fever (4041oC), red dark urine, jaundice, and anemic. Other clinical signs include
abdominal pain, dyspnoea, dysentery, and haemoglobinuria and oedema of the
brisket.
Diagnosis
Exclusion of other diseases such as babesiosis, leptospirosis, postparturient
haemoglobinuria and haemolytic anaemia caused by poisonous plants.
Treatment and Prevention
Management
Non-drug treatment
• Blood transfusions, parenteral fluid, and electrolytes may help to control
hemolytic anaemia and the dehydration. see Appendix 2.
• Antitoxin 500-1000 ml per adult animal
Drug treatment
• Procaine penicillin G, 22,000 IU/kg, IM or SC q 24 h for 3 to 5 days or
Benzathine penicillin or similar repository preparations, q 48-72 h. For S/E, C/I,
D/F, D/I, W/P see page 14.
or
• Tetracycline10 mg/kg IV or IM q 24 h. For S/E, C/I, D/F, D/I, see page 14
Prophylaxis
• Vaccination.
Note: Early treatment should be given; bulls should not be allowed to mate within
3 weeks to avoid liver rupture.
Blackleg
Black leg is an acute, febrile disease of cattle and sheep caused by Clostridium
chauvoei characterized by emphysematous swelling of the heavy muscles and
severe toxemia. Cattle between six months to two years old are mainly affected
though at any age and condition may be affected. Black leg is common in
Ethiopia during dry periods of the year.
Clinical Symptoms
Depression, anorexia, rumen stasis, high fever (41-42oC) and tachycardia are
most common; marked lameness with pronounced muscle swelling of the upper
part of the affected leg with crepitation may follow. At necropsy affected tissues
are filled with rancid serosanguineous fluid and gas pockets, which crepitate
when squeezed and the muscle appear dry.
Diagnosis
The clinical signs and postmortem findings are indicative; the epidemiology and
bacterial isolation are confirmatory.
Treatment and Prevention
Management
Non-drug treatment
• Drainage and slashing of affected tissue to allow oxygen into the tissue plus
supportive treatment with parenteral fluids, analgesics, etc.
Drug treatment
• Procaine penicillin G, 22,000 IU/kg, IM or SC q 24 h for 3 to 5 days or
Benzathine penicillin or similar repository preparations, q 48-72 h. For S/E, C/I,
D/F, D/I, see page 14
plus
• Local antibiotic treatment eg.Oxytetracyline spray 5% at the site of the wound is
helpful.
Prevention
• Vaccination with C. chauvoei bacterin.
Botulism
This rapidly fatal motor paralysis is caused by ingestion of preformed toxin of
Clostridium botulinum from decaying carcasses or vegetable materials such as
decaying grass, hay, grain, or spoiled silage. Ingestion of botulism toxin from
decaying tortoise carcasses has been reported in Bale zone, southern Ethiopia.
Clinical symptoms
Decreased tongue tone that protrudes out and problems associated with
deglutition and prehension of food, followed by progressive muscular weakness
until animals become recumbent in a parturient paresis-like posture, ataxia and
stumbling gait affecting the hind legs are commonly observed.
Diagnosis
Commonly, the diagnosis is made by eliminating other causes of motor paralysis
and look for potential sources of toxin.
Treatment and Prevention
Management
Drug treatment
• Ruminal lavage, followed by 50-80 ml lactic acid in 5-10 L of water per stomach
tube in adult cattle
• Polyvalent anti-C and anti-D antisera (if available)
Control
• Correction of dietry deficiencies and proper disposal of carcass. Removal of
decaying grass or spoiled silage from cattle feed is indicated.
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