Francis D. Galey

Type C botulism in dairy cattle from feed contaminated with a dead cat

Four hundred twenty-seven of 441 adult Holstein dairy cattle from a 1,200-cow dairy died over a 1-week period during early spring 1998. Affected animals were from 4 late lactation pens, one of which included the bull string. Signs included weakness, recumbency, watery diarrhea, and death. Eighty animals from the 4 pens were dead approximately 8 hours after the first ill cows were noted. Affected cows would collapse on stimulation and extend all 4 limbs with moderate rigidity. Several lacked lingual tonus and had abdominal breathing patterns. The animals had been fed a load of total mixed ration that included a rotten bale of oat hay containing a dead cat. No common toxicants were identified, and pathologic examination revealed no consistent lesions. Testing of tissue from the cat carcass found in the feed sample using mouse protection bioassay identified the presence of type C botulinum toxin. Samples of feed, tissue from affected animals, cat tissue from feed, milk, and serum were also tested using an enzyme-linked immunosorbent assay (ELISA) specific for type C botulinum. Two samples of rumen contents were tested and found to be positive for botulism by ELISA, and 1 of 3 liver samples had a weak positive finding. No botulinum toxin was found in milk or sera using the ELISA.

Diagnosis of Oleander Poisoning in Livestock

Since mid- 1989, 37 cases of oleander poisoning in livestock have been diagnosed at the California Veterinary Diagnostic Laboratory System. The most frequent source for oleander exposure was plant clippings. Sudden death was the most common presenting complaint. Other signs reported included diarrhea, pulmonary edema, tachycardia, cardiac arrhythmias, colic, and lethargy. In the past, a presumptive diagnosis of oleander poisoning could be based only on matching clinical signs with evidence of consumption of oleander. A new 2 dimensional Thin-layer chromatography analysis of ingesta for oleandrin and an awareness of lesions in heart muscle have greatly improved the ability to diagnose oleander toxicosis.

Acute Salinomycin Toxicosis of Pigs

Salinomycin is a monovalent carboxylic ionophore that forms lipid-soluble complexes primarily with potassium ions. It was approved as a coccidiostat for chickens by the Federal Drug Administration in 1983. Overdosage or use in nontarget animal species can result in toxicosis. A case of salinomycin toxicosis in pigs is reported here. Three crossbred pigs and a feed sample were submitted for testing to the California Veterinary Diagnostic Laboratory System. These animals were from a group of 150 pigs that were 11-16 weeks old. A total of 25 pigs from the group died within a 24-hour period, and another 20-30 pigs exhibited abnormal behavior during this time. Some pigs were listless, with elevated rectal temperatures preceding death. Other pigs seemed alert but were reluctant to stand. A few had mild through a charcoal (G-60 charcoal : diatomaceous earth [3: 1]) column for cleanup, and spotted on a silica thin-layer chromatography plate. Ionophores were visualized by this method using a p-anisaldehyde reagent. Neither sample contained detectable levels of monensin or narasin. The fine feed contained 720 ppm of salinomycin, and the coarse feed contained 441 ppm of salinomycin. A diagnosis of salinomycin toxicosis was made based on history, clinical signs, lesions, and excessive levels of this ionophore in the feed made with the floor sweepings. Typically, ionophore toxicosis in pigs results in severe myodegeneration. The lesions are more pronounced in skeletal muscle than in cardiac muscle. Clinical signs frequently include myoglobinuria, progressive weakness, and dysmuscle tremors. Clinical signs included ataxia and voiding pnea. 6,8 Concurrent use of the antibiotic tiamulin increases of dark red to brown urine. Twenty-four hours before the the likelihood of toxicosis, presumably by interfering with pigs became ill, the owner fed the pigs from a new load of the metabolism and excretion of salinomycin. Tiamulin feed that contained a considerable amount of floor sweepings was not being fed to the pigs in this case. from a local feedmill that processed mostly poultry feeds. A case of salinomycin toxicosis was reported in Ireland, Typically, the owner mixed the feed obtained from the feedwhere salinomycin is approved for use as a growth promoter mill with some of his own grains and ground alfalfa hay, but in pigs. The approved dose is 60 ppm for pigs up to 4 months this time the owner fed the new load undiluted to both his old and 20-30 ppm for pigs over 4 months old. However, cattle and his pigs. None of the cattle that ingested the feed toxicosis occurred in finishing pigs accidently fed 166 ppm became ill. of salinomycin in the diet, which did not contain tiamulin. At necropsy, the 3 carcasses were in excellent flesh and Clinical signs of toxicosis did not appear until 5 days after well preserved. All 3 had strands of fibrin over the abdominal the introduction of contaminated feed to the ration. The pigs viscera and between liver lobes. No excess fluid was observed developed rear limb trembling, lethargy, reddish-brown urine, in the abdomens. All 3 sets of lungs failed to collapse, had and reluctance to stand or move. The discolored urine conslightly doughy texture, and exuded light yellow, frothy fluid. tinued for at least 5 days after the removal of the contamiThe bladders of all 3 pigs contained a dark reddish brown nated feed, and a severe degenerative myopathy was noted urine. The bladder mucosa was normal. Grossly, no visible in both skeletal and cardiac musculature. lesions were noted in the kidneys, heart, liver, spleen, skeletal In the present case, microscopic evidence of a degenerative muscle, brain, or intestines. Two of the pigs had milk ulcermyopathy was not seen. However, the presence of the pigation in the nonglandular portion of the stomach. mented urine suggests a release of myoglobin from skeletal Histologically, a nephrosis in sections of kidney from all muscles. Several sections of heart were taken, but only 1 3 pigs was characterized by medullary tubules containing representative section of skeletal muscle was taken from each eosinophilic granular pigmented material along with shrunkpig; therefore, a degenerative skeletal myopathy could have en degenerative tubular epithelium. No inflammatory cell been missed. However, the pigs in this report died just less response was present in the kidney. In sections of lung, the than 24 hours after the introduction of the contaminated alveolar walls, interlobular septa, and the adventitia around feed, which may have precluded any morphologic changes arterioles were thickened by a nonstaining edema. The airvisible grossly or with the light microscope. ways and alveoli were free of inflammatory cell infiltrate. No The most striking clinical and postmortem finding was the abnormalities were noted microscopically in sections of mydark red to reddish brown urine noted in many of the affected ocardium, skeletal muscle, liver, brain, or intestines. pigs. Discolored urine not due to hematuria is rare in pigs. The feed sample submitted contained 2 visible types. One Hemoglobinuria in pigs may be seen with copper toxicosis was a very finely ground mixture and the second was more and Leptospira pomona infection. Pigmented urine in the coarse and in clumps. No mold was visible in either type. absence of a hemolytic crisis suggests the presence of myogloThe two types of material in the feed sample were separated binuria. Ionophore toxicosis should be considered in those and submitted individually for ionophore analysis. The feed cases of pigmented nephrosis without evidence of a hemolytic samples were extracted into methanol : water (9:1), passed crisis. References From the California Veterinary Diagnostic Laboratory System, 1. Carson TL: 1986, Toxic chemicals, plants, metals, and mycoPO Box 1770, Davis, CA 95617. toxins. In: Diseases of swine, ed. Dunn HW, 6th ed., p. 688. Iowa Received for publication February 3, 1994. State University Press, Ames, IA.

The correlation between serum selenium and blood selenium in cattle.

The selenium (Se) concentration of paired blood and serum samples from cattle was determined by 2 methods: 1) atomic absorption spectroscopy using hydride generation (HG-AAS), and 2) inductively coupled argon plasma emission spectroscopy using hydride generation (ICP). Samples from 327 cattle were analyzed by HG-AAS, and samples from 344 cattle were analyzed by ICP. The data were examined by linear regression analysis, and the technique of inverse prediction was utilized to determine prediction intervals for estimating blood Se concentration from known serum Se concentration. The correlation coefficients, by simple linear regression of serum Se on blood Se, were 0.79 (r 2 = 0.62) and 0.88 (r 2 = 0.77) for the HG-AAS data and the ICP data, respectively. For the HG-AAS data, the inverse prediction formula for estimating blood Se when serum Se is known, at the 95% prediction interval, was For the ICP data, the inverse prediction formula for estimating blood Se when serum Se is known, at the 95% prediction interval, was The prediction intervals were quite wide, and the accuracy of estimating blood Se from a known serum Se was not useful for diagnostic purposes. The use of serum Se concentration to assess nutritional status of cattle with respect to Se does not appear to be appropriate.

Normal and toxic zinc concentrations in serum/plasma and liver of psittacines with respect to genus differences

Determination of zinc concentration in serum/plasma and tissue of caged and aviary birds is commonly requested by practitioners because of an increased awareness of zinc toxicity. However, interpretation of zinc levels is often based on normal zinc concentrations established for poultry. Also, it is likely that intergenus differences exist in normal zinc concentrations of pet birds. In an attempt to determine normal and toxic concentration ranges, zinc concentrations in liver (n = 276) and serum/plasma (n = 260) collected from psittacines between 1990 and 1998 were analyzed. Zinc concentrations were determined by inductively coupled argon plasma emission spectroscopy analysis. The results were categorized by genus and, when available, by history. Birds that were diagnosed with zinc toxicosis (on the basis of history, clinical examination, pathology, and laboratory findings) were exempt and not included in establishing normal ranges. The results indicate that important differences occur with respect to genera. For example, cockatoos and Eclectus parrots have higher normal zinc concentrations in serum or plasma than other psittacines. In addition, analysis of all the submitted cases suggests that potentially toxic zinc concentrations in livers of psittacines can be well below the range considered toxic in chickens (>200 ppm).

Systemic granulomatous disease in a horse grazing pasture containing vetch (Vicia sp.)

A lo-year-old quarterhorse gelding was presented to theCalifornia Veterinary Diagnostic Laboratory in early Mayfor euthanasia and necropsy. Presenting clinical signs in-cluded weight loss; severe generalized dermatitis; dependentedema in the limbs, preputial sheath, and ventral abdomen;lymphadenomegaly of superficial and palpable lymph nodes;

Zinc Toxicosis Due to Ingestion of a Penny in a Gray-Headed Chachalaca (Ortalis cinereiceps)

Zinc toxicosis was diagnosed in a gray-headed chachalaca (Ortalis cinereiceps) due to ingestion of a copper-plated zinc penny. Histopathological lesions were most marked in the pancreas. These lesions included apoptosis, zymogen granule depletion, and loss of normal acinar architecture. There was also severe gizzard erosion. Heavy metal analysis revealed abnormal levels of zinc and iron in the liver. Iron pigment in the liver was most concentrated in Kupffer cells. This, along with evidence of erythrophagocytosis in the spleen, suggested that extravascular hemolysis was also associated with zinc toxicosis in this case.

Comparison of Disease in Calves Dosed Orally with Oak or Commercial Tannic Acid

Commercial tannic acid has been used as a substitute for leaves and acorns in studies of oak toxicosis in some species. The toxicity of a commercial tannic acid given orally to calves was determined, and the clinical signs, laboratory findings, and pyrogallol production were compared with those found in calves dosed orally with oak leaves. The oak-fed calves developed the clinical signs and lesions characteristic of renal failure. Proteinuria developed by 48 hours in 1 calf and by 72 hours in the other calf. Both calves developed hematuria on day 4 and glucosuria on day 5. The blood urea nitrogen and creatinine values increased markedly on day 6. Pyrogallol was detected in the serum only at 3 and 6 hours after the calves began ingesting the oak leaves. Pyrogallol was detected in urine from 1 calf until 60 hours and in the other calf until 48 hours after the beginning of oak intake. The 2 calves that were dosed with tannic acid at the same level as found in the leaves fed to the other calves did not develop clinical signs, abnormal laboratory findings, or pyrogallol production. Calves given high levels of tannic acid at doses of 4.4–5.5 g/kg developed methemoglobinemia rather than renal disease. Therefore, commercial tannic acid given orally cannot be used as a substitute for oak in studies of toxicosis in cattle.

Copper Toxicosis in Two Herds of Beef Calves following Injection with Copper Disodium Edetate

herpesviruses isolated from six sheep and four goats by restriction endonuclease analysis and radioimmunoprecipitation. Am J Vet Res 49:781-785. 16. Whetstone C, Miller J, Bortner D, et al.: 1989, Changes in the restriction endonuclease patterns of four modified-live infectious bovine rhinotracheitis virus (IBRV) vaccines after one passage in host animal. Vaccine 7:527-532. 17. Whetstone CA, Miller JM, Bortner DM, et al.: 1989, Changes in the bovine herpesvirus 1 genome during acute infection, after reactivation from latency, and after superinfection in the host animal. Arch Virol 106:261-279. 18. Whetstone CA, Wheeler JG, Reed DE: 1986, Investigation of possible vaccine-induced epizootics of infectious bovine rhinotracheitis, using restriction endonuclease analysis of viral DNA. Am J Vet Res 47:1789-1795. 19. Wyler R, Engles M, Schwyzer M: 1989, Infectious bovine rhinotracheitislvulvovaginitis (BHV-1). In: Herpesvirus diseases of cattle, horses, and pigs, ed. Wittmann G, pp. 1-72. Kluwer Academic Publ., Norwell, MA.

Botulism in the Horse

Botulism should be considered in cases where weakness, paralysis, or intolerance to exercise might be seen in the horse. Dysphagia may also be present, although it is not a consistent finding. Potential sources include carrion in hay, moldy or otherwise rotted vegetation or forage, birds carrying material from animal burial or other similar sites, and contaminated carcasses on-site. Horses, especially foals, may also suffer from toxicoinfectious botulism, a condition where the C. botulinum might colonize and produce toxin within the gastrointestinal tract. Wounds also may harbor the organism and otherwise promote botulism. Diagnosis of botulism is often a clinical diagnosis backed up by elimination of other possible infectious, injurious, or toxic causes of weakness of the horse. Definitive diagnosis and type identification in the laboratory are difficult and usually require a suitable sample of the source material. Treatment often is unrewarding unless a case is identified early and the proper antitoxin is readily available. Prevention involves common sense approaches to feeding and care of the horse and, where possible, judicious use of vaccination in endemic areas.