Konstanze H. Plumlee

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.

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.

Nicotiana Glauca Toxicosis of Cattle

rent veterinary therapy 7: small animal pratice, ed. Kirk RW, pp. 141-144. WB Saunders Co., Philadelphia, PA. 8. Miller S, Bauk TJ: 1992, Lead toxicosis in a group of cats. J Vet Diagn Invest 4:362-363. 9. Morgan RV, Moore FM, Pearce LK, Rossi T: 1991, Clinical and laboratory findings in small companion animals with lead poisoning: 347 cases (1977-1986). J Am Vet Med Assoc 199: 93-97. 10. Mount ME: 1989, Toxicology. In: Textbook of veterinary internal medicine, ed. Ettinger SJ, pp. 469-470. WB Saunders Co., Philadelphia, PA. 11. Prasse KW, Mahaffey EA: 1987, The hematopoietic system. In: Diseases of the cat: medicine and surgery, ed. Holzworth J, p. 764. WB Saunders Co., Philadelphia, PA. 12. Prescott CW: 1993, Clinical findings in dogs and cats with lead poisoning. Aust Vet J 60:270-271. 13. Puls R: 1988, Lead-cat tissue levels. In: Mineral levels in animal health: diagnostic data, ed. Puls R, p. 117. Sherpa International, Clearbrook, BC, Canada. 14. Reid FM, Oehme GW: 1989, Toxicoses. In: The cat-diseases and clinical management, ed. Sherding RG, p. 206. Churchill Livingstone, New York, NY. 15. Turner AJ, Fairbum AJ: 1979, Lead poisoning in the cat. Aust Vet Pract 9:205-207. 16. Watson ADJ: 1981, Lead poisoning in a cat. J Small Anim Pract 22:85-89. 17. Zook BC, Carpenter JL, Leeds EB: 1969, Lead poisoning in dogs. J Am Vet Med Assoc 155:1329-1342.

Effect of time and storage temperature on cholinesterase activity in blood from normal and organophosphorus insecticide-treated horses

Delays between time of sampling and time of testing are common; therefore, the length of time that blood can be stored at various temperatures was evaluated for effects on cholinesterase activity. Six horses were treated with 16 g of trichlorfon per os, 6 horses were treated with 15 g of dichlorvos per os, and 10 horses were untreated controls. The cholinesterase activity in whole blood from each horse was measured using an adaptation of the Ellman calorimetric method. The blood from each horse was then divided into 3 groups and stored at 5 C (refrigerated), 20 C (room temperature), or 38 C (incubated). Subsequent cholinesterase activities were measured daily and then at weekly intervals. The cholinesterase activities did not significantly increase or decrease (P > 0.05) in the blood from the untreated horses until after 1 week for any of the 3 temperature groups. The cholinesterase activities did not significantly increase or decrease (P > 0.05) in the stored blood from the trichlorfon-treated horses for 4 weeks in all 3 temperature groups. The cholinesterase activities significantly increased (P < 0.05) in the stored blood from the dichlorvos-treated horses after 1 week when the blood was refrigerated and by 24 hours when the blood was stored at room temperature or incubated. Therefore, blood from normal or organophosphate-treated horses can be used for cholinesterase evaluation for up to 1 week when stored at 5 C.

Japanese Pieris Toxicosis of Goats

and laboratory findings in small companion animals with lead 6. Watson ADY: 1981, Lead poisoning in a cat. J Small Anim poisoning: 347 cases (1977-1986). Am Vet Med Assoc 199:93Pract 22:85-89. 97. 7. Zook BC, McCowell BS, Gilmore CE: 1970, Basophilic stippling 5. Scott HM: 1963, Lead poisoning in small animals. Vet Rec 75: of erythrocytes in dogs with special reference to lead poisoning. 830-832. Am Vet Med Assoc 157:2092-2099.

Total Cholinesterase Activity in Discrete Brain Regions and Retina of Normal Horses

2,3,5,7 Cholinesterase activity < 50% of normal has been associated with significant exposure to an anticholinesterase agent. Cholinesterase activity <25% of normal is considered indicative of severe poisoning. 5 Previous studies have demonstrated that cholinesterase activity differs among regions of the central nervous system. Miniature swine have twice the cholinesterase activity in the cerebellum as in the cerebral cortex. 6 The acetylcholinesterase activity in the cerebral cortex is about two-thirds lower than that in the cerebellum of guinea pigs but is about the same in both regions for the rat and monkey. 1 In rabbits, the retina has lower acetylcholinesterase activity than do regions of the brain. The cerebellum, occipital lobe, and parietal lobe have similar activities, which are between those for the retina and those for the temporal lobe. The frontal lobe has acetylcholinesterase activity up to twice that of other regions of the brain. 4 Previous work 2,3,8 measuring cholinesterase activity was performed using homogenates of entire brains. However, when submitting samples from large animals such as horses and cows, it is common practice for the referring veterinarian to only submit part of the brain. Because cerebral tissue appears similar regardless of the area sampled, the diagnostician often does not know which part of the brain is being tested. Therefore, the cholinesterase activity of the sample could possibly differ from the normals established using whole brain even if the animal has not been exposed to an anticholinesterase agent. The purpose of this study was to measure the total cho

Effect of Capillary Tube Sealants on Lead Content of Avian Blood

Intestinal smooth muscle hyperplasia has been recorded in response to an inflammatory process. Thus, the close spatial and temporal relationship noted between the thickening of the muscle layer and the inflammatory response observed in the mucosa and submucosa of the small intestine in rats experimentally infected with Trichinella spiralis larvae would demonstrate the powerful mitogenic action of the local inflammatory process on the underlying intestinal smooth muscle. In this study, an increase in the number (hyperplasia) and size (hypertrophy) of smooth muscle cells was recorded. In this goat, small intestine smooth muscle hyperplasia, mainly affecting the inner circular layer, appeared to be associated with natural infection by parasite forms of S chistosoma spp. This hyperplasia of the smooth muscle probably derived not from direct parasite action but from host response consisting of a cellular inflammatory reaction in the intestinal mucosa. The localized inflammation of the affected stretch of intestine, together with the capacity for stimulating smooth muscle cell division already indicated, probably led to an intrinsic increase in workload. This workload could have been aggravated by the stenosis caused by fibrosis of the serosa resulting from parasite migration. ,9 Also, nervous mechanisms controlling intestinal contraction may be altered until the innervation of new cells is reestablished. During this period, changes might take place in intestinal motility. ,1 1 In mammals, most reported cases of naturally occurring hypertrophy and/or hyperplasia of the smooth muscle are located in a specific segment of the intestinal tract, most frequently the ileum. 5,9,1 4 Hypertrophy affecting the whole length of the small intestine is much less common and has been reported only in horses; its etiology is unknown. In this goat, hyperplasia was observed in the jejunum and was closely associated with the presence in adjacent mesenteric fat of nodules of fibrous connective tissue containing degenerating parasite structures. A similar spatial association was found following the experimental inoculation of Trichinella spiralis larvae in rats. Although the mechanisms that may lead to hyperplasia and/or hypertrophy of the intestinal smooth muscle are numerous and often poorly understood, changes observed in this goat suggest that hyperplasia secondary to inflammation of the mucosa and submucosa as the initial event in the thickening of the intestinal wall.