The authors give an overview of the etiology, pathogenesis and clinical fin
dings of botulism in horses in connection with a clinical case describing t
he disease in a three-year-old, castrated horse.
The animal was taken to the hospital 36 hours after the appearance of the f
irst clinical signs, colic symptoms, swallowing disorder and ataxia.
Main clinical signs in the following included colic symptoms, medium-level
dehydration, slight cyanosis on the mucous membrane of the lips, medium-lev
el mixed-type dyspnoea, tachycardia, atonic tongue, missing intestinal soun
ds and symmetric muscular tremor in the region of the scapula and the shoul
der on both sides. Consciousness was not impaired. In standing position the
horse was staggering in straddle position and during walking the front lim
bs also showed ataxic symptoms. The horse tried to pick up some oat but it
fell out from its mouth and when it tried to drink it couldn't forward the
water to its oral cavity.
During rectal examination a full, atonic urinary bladder was found. With na
sogastric tube we gained 6 liters of stenchy brownish yellow gastric conten
t which had a pH value of 8.
The laboratory examination of the blood revealed increased packed cell-volu
me and decreased white blood cell number. The AST-, lipase- and CK-activiti
es of the plasma increased and the albumin-concentration decreased. We foun
d some protein and bilirubin in the urine.
The state of the patient became worse in spite of immediate intensive thera
py, therefore euthanasia was applied 2 hours after arrival.
The pathological examination found focal encephalomalacia in the white matt
er of the cerebellum, bleedings in the medulla oblongata and severe pulmona
ry edema. The examination of the brain for rabies was negative.
We detected Clostridium Botulinum toxin in the patient's serum with mouse b
io-assay (intraperitoneal injection).