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.     

Clostridium botulinum type B toxicosis in a herd of cattle and a group of mules

Clostridium botulinum type B toxicosis was diagnosed as the cause of generalized weakness and death in a group of cows and mules fed from the same batch of rye silage. One severely affected cow was treated and recovered, as did other less severely affected cows. All affected mules died. The remaining cattle in the herd were then vaccinated before continued feeding of the silage.     

Feedtrough dirt as a source of Clostridium botulinum type C intoxication in a group of farm horses

Four horses from the same farm developed clinical signs of botulism during the winter months; three of these horses died. One horse survived an initial attack and recovered over a three-week period, but died during a second attack. The horse that survived took six weeks to recover. Clinical and postmortem examination ruled out other causes of disease. Confirmation of the diagnosis was made by isolation of Clostridium botulinum type C toxin from the dirt in the bottom of an oak feedtrough used by all horses, and from the colonic contents of one of the horses that died. To our knowledge, this is the second case of C. botulinum type C intoxication reported in horses in North America. In both cases, soil and sand near aquatic environments were identified as the source of toxin.     

Association between Key-Gaskell syndrome and infection by Clostridium botulinum type C/D

There is growing evidence that equine dysautonomia is a toxicoinfection with Clostridium botulinum type C. The possibility that feline dysautonomia has the same aetiology was investigated by attempting to detect botulinum type C neurotoxin in the food, faeces and the contents of the ileum of affected cats, and by serology. The toxin was detected directly in four of eight affected cats and after enrichment in seven of them, and in their dried food. No toxin was detected in healthy control cats or in their tinned food. Recent exposure to the organism was assessed by the detection of immunoglobulin A (IgA) in the faeces of healthy control cats and affected cats. The levels of IgA antibodies to the toxin and to surface antigens of C. botulinum type C in the faeces of the affected cats 14 weeks after the outbreak were significantly higher than in the faeces of the control cats.     

Mycoplasmal mastitis in a dairy herd

In October 1985, mycoplasmas were isolated from bulk tank milk samples in a large Florida dairy (greater than 1,400 lactating cows). At that time, measures to isolate and control the spread of infection were instituted. In an initial screening test, Mycoplasma bovis was isolated from 21 of 153 milking string samples (milk from all quarters of 10 cows/string). Composite quarter milk samples from all quarters of every individual lactating cow in the herd were obtained for culture in November 1985 and December 1985. In October, 88 of 1,535 (5.7%) cows were identified as Mycoplasma-positive. An additional 31 Mycoplasma-infected cows were identified in December. The dairy elected to maintain the infected cows in a separate Mycoplasma-positive subherd, which would be milked at the end of each milking session. Seven additional Mycoplasma-positive cows were identified at initiation of lactation. All newly identified infected cows were transferred to the Mycoplasma-positive subherd. After segregation of Mycoplasma-positive cows, bulk tank milk samples obtained routinely from the main herd remained culture negative throughout the study. From February 1986 to October 1986, quarter milk samples were obtained monthly from cows in the Mycoplasma-positive subherd. Any cow that developed clinical mastitis or substantial decrease in milk production was, at the discretion of the herdsman, culled. Of the 126 cows in the subherd, 22 (17.5%) were culled for mastitis, 35 (27.8%) were culled for low production, and 9 (7.1%) were culled for other reasons. Of the remaining 60 cows, 16 (12.7% of the 126 cows) were Mycoplasma-positive on the basis of results from one or more samples obtained after February 1986.(ABSTRACT TRUNCATED AT 250 WORDS)     

Monensin toxicosis in a dairy herd

An acute onset of illness was reported in a lactating dairy herd in Canada in which monensin had been incorporated in error in its ration at almost 10 times the prescribed level. All of the lactating cows became lethargic, were inappetant, developed diarrhea, and had decreased milk production from 28 kg/cow/day, the day before exposure, to 23 kg/cow/day, 3 d later. Within 9 d, all animals recovered from the incident and milk production returned to previous levels.     

Phosphorus deficiency in a dairy herd

Phosphorus deficiency was diagnosed in a 90 cow seasonal supply dairy herd which showed low milk production, ill-thrift, infertility and osteophagia. Serum inorganic phosphorus and pasture phosphorus levels were low, pasture Ca:P ratios high and soil phosphorus levels very low; the soil phosphate retention value was 96%. The deficiency, which had probably existed for several years, was considered to be due to inadequate annual phosphate fertiliser applications on a high phosphate retaining soil. Phosphorus deficiency may have been exacerbated by the application of lime without phosphate several months before the onset of severe clinical disease. The finding of low sodium levels in pasture samples suggested that sodium deficiency may have co-existed and contributed to the clinical picture. Treatment, comprising bone flour dusting of pasture, water trough supplementation and phosphorus-containing injections, appeared to induce ovarian activity in anoestrous cows and suppress osteophagia, though controlled treatment trials were not performed. No improvement was noted in milk production or cow condition. Increased annual super-phosphate and reduced potassium applications were recommended, together with the monitoring of pasture and soil macro elements and serum phosphorus levels. A decision on whether to supplement with sodium would be based on the results of pasture monitoring, since a direct animal test is not currently available. It is suggested that phosphorus deficiency may not be uncommon in dairy herds in some North Island districts; based on the present case, the decline in New Zealand superphosphate quality in the 1970's and recently published data which has shown a high proportion of pasture phosphorus deficient sites in some North Island areas.     

Terbufos poisoning in a dairy herd

This report describes the accidental poisoning of over 200 head of Holstein cattle by the organophosphate, terbufos. The ingestion of an acutely toxic dose (approximately 7.5 mg/kg) of terbufos by 84 heifers resulted in severe respiratory distress as the primary clinical sign and death within 12 hours. There was no response to treatment with atropine sulfate. One hundred and twenty milking cows received a portion of the contaminated feed diluted approximately ten times. These cattle had typical signs of organophosphate poisoning and responded to atropine sulfate. Severely affected cows received pralidoxime chloride and activated carbon 48 h after terbufos ingestion but did not respond to the drugs. Diagnosis of organophosphate poisoning was confirmed by tissue and feed analysis for terbufos and measurement of whole blood cholinesterase activity.