Accidental salinomycin intoxication in calves.

Twenty-four 10- to 16-week-old calves in a dairy herd in Birjand, Iran, inadvertently received an excessive dose of salinomycin mixed with barley grain. There was 58% mortality within 10 d. The calves had high serum AST, LDH, and CK activities; histopathologic lesions in myocardium, liver, and kidneys; and clinical signs associated with acute and congestive heart failure.

Ionophore use and toxicosis in cattle.

Ionophores comprise a rapidly expanding class of antibiotics produced by filamentous branching bacteria of the order Actinomycetales. The use of ionophores as coccidiostats and growth promotants has resulted in the occurrence of toxicoses in target and nontarget species. Clinical and pathologic effects of ionophore poisoning are caused by bioactivity and damage to excitable tissues such as cardiac muscle, skeletal muscle, smooth muscle, and the nervous system. Ionophore toxicoses are often related to errors in feed mixing, so the practitioner should give primary importance to the removal of suspect feeds and testing to confirm excessive exposure.

Accidental poisoning of 17 dogs with lasalocid.

Over a period of 10 days, 17 dogs became weak and developed neurological deficits of different degrees of severity. About 12 hours before these clinical signs appeared they had all eaten a particular brand of commercial dog food from a recently opened bag. They were all quadriparetic and hyporeflexic, and some of them also showed additional systemic or neurological signs, including dyspnoea, a high body temperature, tongue laxity, hyperaesthesia and anisochoria. Serum biochemical abnormalities included high activities of creatine kinase, lactate dehydrogenase and aspartate aminotransferase. Analysis of the suspect food revealed high concentrations of the ionophore lasalocid. Fifteen of the dogs were given supportive treatment at home and two were hospitalised. Five of the dogs died, but the others improved gradually and had fully recovered by one to four days after the appearance of the clinical signs.

Salinomycin poisoning in point-of-lay turkeys.

Salinomycin poisoning occurred in a flock of 700 point-of-lay turkeys; 400 birds died over 7 days as a result of consuming feed contaminated with 50 ppm salinomycin. No gross lesions were detected. Histologic evidence of a myopathy was most readily detected in leg muscles of turkeys 5 to 7 d after ingesting salinomycin. Feeding trials were undertaken and individual susceptibility to the drug was found to vary greatly. In affected birds the plasma concentrations of creatine kinase (CK) and aspartate aminotransferase (AST) were found to be in the range of 500,000 to 2,500,000 IU/l and 9000 to 25,000 IU/l, respectively. The marked increase in the plasma activities of these enzymes preceded histological evidence of segmental muscle necrosis.

Monensin toxicity in preruminant dairy heifers.

Four-to six-week-old calves from a seasonal dairy herd in North Western Tasmania were presented for veterinary attention due to the occurrence of sudden deaths. Necropsy examination of one of the calves revealed several small pale foci of 1 cm diameter on the epicardium. Mortalities were found to be caused by monensin that was added to the milk diet as part of a vitamin/mineral commercial premix that also controlled coccidiosis. No cases of monensin toxicity in preruminant calves have been previously documented, although there have been numerous reports in older cattle and other species.

[Poisoning due to ionophore anticoccidial drugs in poultry]. / Intoxicatie door ionofore anticoccidia bij pluimvee.

Ionophore polyether antibiotics are used as anticoccidial drugs in poultry. However, these pharmaceutical agents are also being increasingly used as growth-promoting substances in stock and pig farming. Overdosage of ionophore anticoccidial drugs may cause typical symptoms of poisoning, viz. paralysis and an increased proportion of rejects. In addition to providing a method for detecting a high dosage in the feed, histological examination and determination of the creatine phosphokinase level of the serum are found to be of importance. The ionophore anticoccidial drugs used and their incompatibility with therapeutical agents are reviewed in tabular form. Seven cases of poisoning in broilers, laying hens, breeding birds and turkeys in the province of Gelderland are also reported.

[Monensin/sulfachlorpyrazine poisoning in turkeys]. / Monensin/sulfachloorpyrazine intoxicatie bij kalkoenen.

Symptoms of paralysis were observed in seven-week-old turkeys on a farm following administration of sulphachlorpyrazine for coccidiosis. Paralysis was particularly common in the females which were separated from the male birds. Of monensin 122 ppm were found to be present in the feed, whereas the amount stated on the label was 100 ppm. When a new batch was substituted for this feed, the symptoms abated. As the result of a possible interaction of monensin and sulphachlorpyrazine, mortality was 1.7 per cent in the male and 11.2 per cent in the female birds.

[Epidemic of nutritional polyneuropathy in the cat. Final report of the investigational team]. / Epidemie van alimentaire polyneuropathie bij de kat. Eindverslag onderzoeksteam.

In June 1996 companion animal practitioners received a report prepared by the Faculty Investigative Team on the outbreak of polyneuropathy among cats, and at the end of August a 'definitive' bulletin was circulated by Spillers Petfoods. The coccidiostatic drug salinomycin, which was present in the vitamin premix supplied by a third party, was considered the cause of the neuropathy. The investigative team is of the opinion that all veterinary practitioners in the Netherlands should receive a conclusive report about the epidemic because of the unique nature of the epidemic, which despite its sudden outbreak could be well documented, and because aspects of the affair merit the attention of veterinary practitioners.

The veterinary importance of the toxic syndrome induced by ionophores.

Monensin, lasalocid, salinomycin, narasin and maduramicin are carboxylic ionophores intended for use as anticoccidial drugs for poultry and as growth promotants for ruminants. Generally, ionophores have been found safe and effective in the target animals receiving recommended dosage levels. However, toxic syndromes can result from overdosage and misuse situations. More information and reports of adverse reactions are available for monensin than the other ionophores because of monensin's longstanding and widespread use in the poultry and livestock industries. Care must be exercised in the diagnosis of ionophore toxicoses since clinical signs and lesions are not pathognomic. However, a feed-related problem characterized clinically by anorexia, diarrhea, dyspnea, ataxia, depression, recumbency and death, and pathologically by focal degenerative cardiomyopathy, skeletal muscle necrosis, and congestive heart failure may warrant a presumptive diagnosis of ionophore toxicity. Confirmatory diagnosis will require considerations of differential diagnoses and laboratory assays to determine the specific ionophore involved. Presently, there is no antidote or treatment for toxicoses induced by the ionophores. Judicious use, avoidance of overdosing, and adherence to species recommendation will help prevent the occurrence of adverse effects associated with this class of compounds.

Mass poisoning in cattle, palm doves and mink caused by the coccidiostat dibutyltin dilaurate.

Poisoning caused by dibutyltin dilaurate (DBTD) was diagnosed in cattle, mink, and palm doves. The accidental addition of a DBTD premix to calf concentrates at levels up to 25000 ppm on 18 farms caused poisoning in 1000 cattle, of which 171 died and 287 were slaughtered. High concentrations of tin were found in the cattle tissues and precluded their consumption by humans. Palm doves ingesting concentrates containing 12500 ppm DBTD on one farm were also poisoned and had high concentrations of tin in tissues. Mink were inadvertently fed a vitamin-mineral supplement containing about 1700 ppm DBTD. They appeared the most suceptible of the three species to this compound.

Monensin poisoning in Brazilian horses.

Three outbreaks of monensin poisoning caused 12 deaths in 16 horses. The illnesses were associated with the ingestion of the same batch of a commercial ration labeled for feeder calves which contained 180 +/- 20 ppm sodium monensin. The morbidity rate was 100% and lethality was 60%, 75%, and 100%. Clinical signs were tachycardia and cardiac arrythmia, groaning, incoordination, sudoresis, recumbency, and paddling movements with the limbs before death. Two horses had dark discolored urine (myoglobinuria). Serum levels of creatine phosphokinase activity were increased. Main necropsy findings were in the skeletal muscles and myocardium.