耕牛胜红蓟中毒

2000年2月初,福建省某地3家农户的耕牛相继发生饲料中毒死亡,调查结果认为,时值春节,单用花生藤喂牛,而花生藤里面都混有大量的胜红蓟,其含量高达5%～10%,由此推断胜红蓟中毒的可能性极大.为此,我们对死牛进行了解剖和细菌学培养,观察其组织学变化和细菌学变化;在此基础上,又进行了人工饲喂胜红蓟的重复实验,证实了胜红蓟是造成耕牛死亡的直接因素.     

Accidental monensin sodium intoxication of feedlot cattle

Of 1,994 yearling and 2-year-old cattle in a winter feeding program, 117 died within 42 days of being fed toxic amounts of monensin sodium in a liquid protein supplement. Death losses commenced on the third day after ingestion of a toxic amount in the feed. Clinical signs in cattle that died in less than 9 days included anorexia, pica, diarrhea, depression, mild hindlimb ataxia, and dyspnea. Gross necropsy findings in cattle dying in the acute phase of the illness included hydrothorax, ascites, and pulmonary edema, as well as petechial hemorrhages, edema, and yellow streaking in skeletal and cardiac muscle. Cattle dying after 9 days had gray streaks in heart and skeletal muscle, generalized ventral edema, enlarged, firm, bluish discolored liver, and enlarged heart. Microscopic changes in cattle dying in the acute phase (less than 9 days) consisted of pulmonary edema, congestion, and hemorrhage. Cardiac and skeletal muscle had localized areas of edema, hemorrhage, and coagulative necrosis. In cattle dying after 9 days of illness, the changes included lymphocytic infiltration, sarcolemmal nuclear proliferation, and fibrosis in skeletal and cardiac muscle. Lungs contained increased alveolar macrophages and a few neutrophils. Centrilobular necrosis and mild fibrosis were found in the liver. Changes varied somewhat according to the area of heart or skeletal muscle that was affected. Active muscles, eg, those in the heart ventricles and diaphragm, were altered most severely. Intoxication appeared to be a result of sedimentation of monensin in the molasses carrier to give remarkable concentrations of the substance at the bottom of the holding tank.     

Acute cattle intoxication from Nerium oleander pods

Seven outbreaks of acute intoxication from oleander (Nerium oleander) in cattle were reported in Northeast of Brazil. A total of 92 cattle were poisoned by oleander in 7 different herds; 57 animals died (67% of affected cattle). All cases reported here occurred during dry season. Two of the outbreaks resulted from offering oleander triturated and mixed with fodder. In the other cases, accidental ingestion of residual parts of oleander derived from pruning or cutting plants on grazing land were responsible. Clinical signs were diverse; the most common were locomotion disturbances, diarrhoea, depression and sudden death. Postmortem findings varied from no significant lesions to widespread haemorrhage. The presence of oleander leaves in the rumen was noted in all cases. The lack of information about the toxicity of oleanders was the main cause for the accident, which prompt us to stimulate wide divulgation of the common toxic plants.     

Retinal and optic nerve degeneration in cattle after accidental acrylamide intoxication

A herd of cattle was accidentally exposed to monomeric acrylamide and N-methylolacrylamide. Seven cattle underwent repeated examinations during 6–8 months after exposure. Abnormal pupillary light reflexes (PLR) were observed in one cow. Ophthalmoscopic examination showed progressive retinal degeneration and degenerative changes in the optic nerve heads in this cow. Light and electron microscopic examination revealed pathological changes in the retinae and optic nerves consistent with chronic stages of acrylamide toxicity. Ophthalmic examination and light microscopy did not reveal abnormalities in the retinae or optic nerves in either the rest of the cattle from the herd or in offspring of exposed cattle.     

Uniformity of response of identical twin cattle to sporidesmin intoxication

Sixteen pairs of identical twin dairy calves were reared together and at one year of age subjected to a test of uniformity of response to sporidesmin intoxication. The response was measured by scoring livers for toxic injury and by measuring serum gamma-glutamyltransferase at weekly intervals after dosing. Within pair variance in serum gamma-glutamyltransferase was greatest at two and six weeks after sporidesmin dosing when enzyme levels were rising and falling. Within twin variance and the interclass correlation coefficients were least and greatest respectively at five weeks after dosing. At five weeks the GGT correlation coefficient was 0.89 and for liver injury score 0.76. High consistency among twins of a pair, compared with differences among pairs indicates a high relative efficiency in using identical twins rather than singles for experimental work (approximately x 5). It is also consistent with a high heritability of resistance to sporidesmin intoxication in dairy cattle.     

The prophylactic effect of corn supplementation on experimental nitrate intoxication in cattle

Sodium nitrate was administered through rumen cannulae to produce NO-3 intoxication in four cows (382 to 445 kg body wt) fed prairie grass hay and a protein-mineral supplement. The cows were fed 0, 1.6 or 3.2 kg of dry rolled corn daily for 10 d prior to sodium nitrate administration. Sodium nitrate administration was followed by a marked increase in intraruminal NO-2 and NH3 and blood NO-2 and methemoglobin. Six of eight cows fed 0 and 1.6 kg of corn were given methylene blue to treat severe methemoglobinemia, while none of the cows fed 3.2 kg corn required such therapy. Feeding of 3.2 kg of corn protected against nitrate poisoning by reducing intraruminal nitrite and blood methemoglobin (P less than .05).     

Presumptive diagnosis of Clostridium botulinum type D intoxication in a herd of feedlot cattle

Fifty-two feedlot cattle exhibited clinical signs suggestive of botulism. Clostridium botulinum type D organisms were recovered from ruminal fluid of 4 of the 5 affected animals tested and were isolated from bakery waste fed to the cattle. Clostridium botulinum type D has not been reported previously in Canadian cattle.     

Water deprivation-sodium chloride intoxication in a group of feeder lambs

Six of a group of 100 feeder lambs that had been deprived of sodium chloride, then more recently deprived of water, developed water deprivation-sodium chloride intoxication soon after water and a mineral supplement containing sodium chloride were reintroduced. The clinical signs included somnolence, intense thirst, and generalized muscle fasciculations. Serum chemical analyses revealed profound hypernatremia and hyperchloremia. Two mildly affected lambs recovered with partial water restriction and 2 severely affected lambs died despite medication to reduce cerebral edema. Postmortem examination of the 2 treated lambs and the 2 lambs found dead revealed microscopic evidence of cerebral edema and cerebrocorticonecrosis.     

Atrazine intoxication in cattle,confirmed by gas chromatography–mass spectrometry

Ten of 40 cows died within 48 h of gaining access to a barn in which various chemicals were stored. Some of the surviving cows exhibited drooling, muscle tremors, and agitation. Postmortem examinations of 2 cows were performed in the field, and revealed nonspecific, moderate-to-severe pulmonary congestion. Liver and rumen contents, each from a different cow, were analyzed using a qualitative, multi-residue GC-MS method validated for the detection of pesticides and other chemical analytes. Using this method, extracts from the liver and rumen content samples were compared to atrazine (neat standard) and matrix-matched, control samples fortified with atrazine. GC-MS analysis detected atrazine at 215 m/z (NIST match >97%) with a retention time of ~13 min in liver and rumen content samples from our case. Detection of atrazine in the samples from the cows in this herd, combined with the clinical history, indicate that atrazine toxicity was the likely cause of clinical signs and death observed in this herd.