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Monensin toxicity in ostriches on a farm in northern Greece

(Vitamin E Selen; Schering-Plough Animal Health), and a single dose of 25 g sodium propionate (Cevalactyl; Ceva), diluted in 500 ml of drinking water. All the birds, including those showing no clinical signs, received multivitamins and essential amino acids (Amovit Polvo; Laboratories Ovejero), diluted to 0·5 g/l drinking water for seven days. Artificial feeding was instituted for the birds with decreased appetite, and each day the farmer encouraged the recumbent ostriches to move and rise, in order to prevent injury to the muscles, tendons and nerves of the affected birds. Serum biochemical analysis of blood samples obtained from the six affected birds on the day of the clinical examination and from one adult female ostrich on the farm, which was used as a control because it had not received the diet with the new mixture of vitamins and minerals, showed that the serum activities of the enzymes creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) were very high in the affected ostriches compared with those of the control bird (Table 1). Analysis of samples of the new mixture of vitamins and trace minerals and the concentrate feed revealed concentrations of monensin of 3790 ppm and 190 ppm, respectively. Of the six affected birds that were treated, four (one male and three females) recovered within two weeks of treatment; the other two females died one week after the onset of clinical signs. The development of non-pathognomonic clinical signs in association with the history of a feed change related-problem was suggestive of a toxic aetiology. The detection of extremely high serum activities of the enzymes AST, CK and LDH in the affected birds indicated acute muscle myopathy (Lumeij 1994). Poisoning due to botulism, sodium chloride, furazolidone and other medicines, as well as mycotoxicosis and poisoning by the ingestion of toxic plants, have all been recorded in farmed ostriches (Huchzermeyer 1999), but acute myopathy is not a feature of any of these conditions. Nutritional myopathy associated with selenium or vitamin E deficiency in ostriches has been reported only in chicks and juveniles (Aganga and others 2003). Capture myopathy associated with severe muscular exertion has been reported in ratites (Jensen and others 1992), but in the present case no unaccustomed exercise preceded the onset of clinical signs. Degenerative myopathy can also follow prolonged recumbency in farmed ostriches (Shakespeare 1995, Huchzermeyer 1999), but in this case, the clinical history and signs suggested that the muscle damage preceded the recumbency rather than being the result of it. Moreover, the very high serum activity of AST, CK and LDH was indicative of acute myopathy. The recovery and quantitative analysis of the toxin in either the feed or the stomach or intestinal contents of an affected animal or bird is essential for a final diagnosis (Donoho 1984, Hamar and others 2002). In the present case, the diagnosis of monensin toxicity was confirmed by the detection of monensin in the breeder feed and the mixture of vitamins and trace minerals. It was presumed that the vitamin/mineral mix was the primary source of monensin because of the higher monensin concentration in the mixture. The fact that new clinical cases ceased to occur immediately after the withdrawal of the suspected premix and the vitamin/mineral mix supports the diagnosis. Two incidents of monensin toxicity in ostriches have been reported worldwide, one in the USA (Gregory and others 1992) and the other in the UK (Baird and others 1997). In both cases the monensin was accidentally added to the ostrich diets and proved to be very toxic, causing very high morbidity and mortality at much lower levels (27 ppm and 49 ppm) than were detected in the present study. Moreover, the clinical signs recorded in the previous incidents were similar to those found in the present case and were indicative of acute myopathy. Veterinary Record (2007) 161, 628-629