Acute salinomycin toxicosis of pigs

Tags: copper toxicosis, ppm, discolored urine, salinomycin, liver extract, daughter ions, dicoumarol, ion chromatograms, liver tissue, diatomaceous earth, clinical signs, Francis D. Galey Salinomycin, Konstanze H. Plumlee, Journal of Veterinary Diagnostic Investigation, California Veterinary Diagnostic Laboratory System, American Association of Veterinary Laboratory Diagnosticians, Inc., skeletal muscle, Francis D. Galey, Federal Drug Administration, Bill Johnson
Content: Journal of Veterinary Diagnostic Investigation Acute Salinomycin Toxicosis of Pigs Konstanze H. Plumlee, Bill Johnson and Francis D. Galey J VET Diagn Invest 1995 7: 419 DOI: 10.1177/104063879500700327 The online version of this article can be found at: Published by: On behalf of: Official Publication of the American Association of Veterinary Laboratory Diagnosticians, Inc. additional services and information for Journal of Veterinary Diagnostic Investigation can be found at: Email Alerts: Subscriptions: Reprints: Permissions: Citations: >> Version of Record - Jul 1, 1995 What is This? Downloaded from by guest on April 10, 2012
J Vet Diagn Invest 7:419-420 (1995) Acute salinomycin toxicosis of pigs Konstanze H. Plumlee, Bill Johnson, Francis D. Galey
Salinomycin is a monovalent carboxylic ionophore that forms lipid-soluble complexes primarily with potassium ions.6 It was approved as a coccidiostat for chickens by the Federal Drug Administration in 1983.6 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 muscle tremors. Clinical signs included ataxia and voiding of dark red to brown urine. Twenty-four hours before the pigs became ill, the owner fed the pigs from a new load of feed that contained a considerable amount of floor sweepings from a local feedmill that processed mostly poultry feeds. Typically, the owner mixed the feed obtained from the feedmill with some of his own grains and ground alfalfa hay, but this time the owner fed the new load undiluted to both his cattle and his pigs. None of the cattle that ingested the feed became ill. At necropsy, the 3 carcasses were in excellent flesh and well preserved. All 3 had strands of fibrin over the abdominal viscera and between liver lobes. No excess fluid was observed in the abdomens. All 3 sets of lungs failed to collapse, had slightly doughy texture, and exuded light yellow, frothy fluid. The bladders of all 3 pigs contained a dark reddish brown urine. The bladder mucosa was normal. Grossly, no visible lesions were noted in the kidneys, heart, liver, spleen, skeletal muscle, brain, or intestines. Two of the pigs had milk ulceration in the nonglandular portion of the stomach. Histologically, a nephrosis in sections of kidney from all 3 pigs was characterized by medullary tubules containing eosinophilic granular pigmented material along with shrunken degenerative tubular epithelium. No inflammatory Cell Response was present in the kidney. In sections of lung, the alveolar walls, interlobular septa, and the adventitia around arterioles were thickened by a nonstaining edema. The airways and alveoli were free of inflammatory cell infiltrate. No abnormalities were noted microscopically in sections of myocardium, skeletal muscle, liver, brain, or intestines. The feed sample submitted contained 2 visible types. One was a very finely ground mixture and the second was more coarse and in clumps. No mold was visible in either type. The two types of material in the feed sample were separated and submitted individually for ionophore analysis. The feed samples were extracted into methanol : water (9:1), passed
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.6 Clinical signs frequently include myoglobinuria, progressive weakness, and dyspnea.6,8 Concurrent use of the antibiotic tiamulin increases the likelihood of toxicosis, presumably by interfering with the metabolism and excretion of salinomycin.4,5,7 Tiamulin was not being fed to the pigs in this case. A case of salinomycin toxicosis was reported in Ireland, where salinomycin is approved for use as a growth promoter in pigs.3 The approved dose is 60 ppm for pigs up to 4 months old and 20-30 ppm for pigs over 4 months old.3 However, toxicosis occurred in finishing pigs accidently fed 166 ppm of salinomycin in the diet, which did not contain tiamulin.3 Clinical signs of toxicosis did not appear until 5 days after the introduction of contaminated feed to the ration. The pigs developed rear limb trembling, lethargy, reddish-brown urine, and reluctance to stand or move. The discolored urine continued for at least 5 days after the removal of the contaminated feed, and a severe degenerative myopathy was noted in both skeletal and cardiac musculature.3 In the present case, microscopic evidence of a degenerative myopathy was not seen. However, the presence of the pigmented urine suggests a release of myoglobin from skeletal muscles. Several sections of heart were taken, but only 1 representative section of skeletal muscle was taken from each pig; therefore, a degenerative skeletal myopathy could have been missed. However, the pigs in this report died just less than 24 hours after the introduction of the contaminated feed, which may have precluded any morphologic changes visible grossly or with the light microscope. The most striking clinical and postmortem finding was the dark red to reddish brown urine noted in many of the affected pigs. Discolored urine not due to hematuria is rare in pigs. Hemoglobinuria in pigs may be seen with copper toxicosis and Leptospira pomona infection.1,2 Pigmented urine in the absence of a hemolytic crisis suggests the presence of myoglobinuria. Ionophore toxicosis should be considered in those cases of pigmented nephrosis without evidence of a hemolytic crisis.
From the California Veterinary Diagnostic Laboratory System, PO Box 1770, Davis, CA 95617. Received for publication February 3, 1994.
1. Carson TL: 1986, Toxic chemicals, plants, metals, and mycotoxins. In: Diseases of swine, ed. Dunn HW, 6th ed., p. 688. Iowa State University Press, Ames, IA.
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Brief communications
2. Hanson LE, Tripathy DN: 1986, Leptospirosis. In; Diseases of swine, ed. Dunn HW, 6th ed., pp. 593-597. Iowa State University Press, Ames, IA. 3. Kavanagh NT, Sparrow DSH: 1990, Salinomycin toxicity in pigs. Vet Rec 127:507. 4. Miller DJS, O'Connor JJ, Roberts NL: 1986, Tiamulin/salinomycin interactions in pigs. Vet Rec 118:73-75. 5. Morgan JH, Collins P, Aitken IA, Thomas LH: 1991, An ex-
perimental study of the toxic interaction between tiamulin and salinomycin in pigs. Acta Vet Scand Suppl 87:365-367. 6. Novilla MN: 1992, The veterinary importance of the toxic syndrome induced by ionophores. Vet Hum Toxicol 34:66-70. 7. Pott JM: 1990, Salinomycin toxicity in pigs. Vet Rec 127:554. 8. Van Vleet JF, Ferrans VJ: 1984, Ultrastructural alterations in skeletal muscle of pigs with acute monesin myotoxicosis. Am J Pathol 114:461-471.
J Vet Diagn Invest 7:420-422 (1995) Dicoumarol (moldy sweet clover) toxicosis in a group of Holstein calves
Behzad Yamini, Robert H. Poppenga, W. Emmett Braselton, Jr., Lawrence J. Judge
During a 3-week period of mid-fall 1991, 6 of 25 6-monthold Holstein calves developed progressive rear limb stiffness and recumbency and died 4-12 hours after the onset of clinical signs. Affected animals were initially treated by the referring veterinarian with sulfadimethoxinea and vaccinated with a 7-way clostridial bacterin-toxoid.b Necropsy of 3 calves by the referring veterinarian revealed hemorrhage in the thorax and epicardial petechial hemorrhages. There was no previous history of vaccination or Vitamin E/selenium or any other supplementation. The last calf to die was treated with thiamine and injectable vitamin E and selenium and developed swelling at the site of injection. The affected animals were born on the farm in a closed herd and fed grass hay alternating with alfalfa hay. One animal was submitted for diagnostic investigation. At necropsy, the carcass appeared to be in good nutritional state and weighed 123 kg. There was a diffuse subcutaneous hemorrhage and edema throughout the body, including lateral aspects of the larynx and esophagus. There was approximately 1 liter of blood in the abdominal cavity. Diffuse hemorrhages were present on the neck, thigh, stifle, and hock muscle, lung, epicardium, endocardium, perirenal areas, and serosal surface of the colon, uterus, and urinary bladder. Aerobic cultures of lung, liver, and small intestine yielded no significant growth after 48 hours. Bovine viral diarrhea and infectious bovine rhinotracheitis viruses were not detected in the lung, liver, and spleen using a fluorescent antibody test and virus isolation. Clostridium species (C. chauvoei, C. sordelli, C. septicum, C. novyi) were not identified in skeletal muscle using fluorescent antibody testing. Microscopically, the liver contained diffuse, moderate, bridging, centrolobular degeneration and necrosis. Cardiac and skeletal muscles contained multifocal areas of myofiber degeneration and necrosis associated with severe hemor- From the Animal Health Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansin, MI 48824 (Yamini, Poppenga, Braselton), and Animal Health Associates, 2120 E. Remus, Mt. Pleasant, MI 48858 (Judge). Received for publication August 17, 1994.
rhage. Multifocal to diffuse, severe hemorrhage was present in sections of lung, intestine, uterus, kidney, and urinary bladder. A diagnosis of dicoumarol (moldy sweet clover) toxicosis was made based on the clinical history, postmortem findings, and detection of dicoumarol in liver tissue by thinlayer chromatography (TLC).3 Dicoumarol was confirmed and quantified by mass spectrometry/mass spectrometry (MS/ MS).4 Daughter ion spectra of dicoumarol were generated by collision-activated dissociation (CAD) at a collision offset of ­10 V from the 70-eV electron impact (EI) parent ion, M+ = 336, and also from the methane chemical ionization (CI) parent ion, MH+ = 337. Characteristic EI daughter ions of M+ = 336 were m/z 215, 175, 162, and 121 in both reference dicoumarol and liver extract (Fig. 1). Characteristic CI daughter ions of MH+ + 337 were m/z 234 and 163, present in both reference dicoumarol and liver extract (data not shown). Results were confirmed by generation of parent ion scans of selected CAD daughter ions, using both EI and methane CI techniques. The direct insertion probe volatilization profiles of reference dicoumarol, the extract of liver from an affected calf, and extract from a bovine liver control were compared (Fig. 2). At 2:14-2:18 minutes, the reference dicoumarol and the extract from the affected calf both exhibited a peak in the reconstructed total daughter ion chromatogram and in the selected ion chromatogram of daughter ion m/z 215. Only background noise at a signal strength 1-2 orders of magnitude less could be observed in the control liver chromatograms. Dicoumarol was quantified in the liver of the affected calf using the ratio of the peak heights of the m/z 215 ion chromatograms (Fig. 2): liver conc. (ppm) = (P1/Pd)·( 100 ng/50 mg), where P1 is the m/z 215 ion current peak height of the liver extract equivalent to 50 mg liver and Pd is the m/z 215 ion current peak height of 100 ng dicoumarol. The liver of the affected calf contained 2.6 ppm dicoumarol, which is within the range of 1-5 ppm found in liver in other reported cases of dicoumarol toxicity in cattle.2,7 A sample of the suspect hay submitted at a later date contained 18 ppm dicoumarol on a dry weight basis (the sample contained < 10% moisture) by TLC and high-performance liquid chromatography. A
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