Severe myopathy in lambs
Felipe Reggeti, Andrew Brooks, Nick Schrier, James Dykeman, Tracy Van Raaij
Animal Health Laboratory, University of Guelph, Guelph, ON (Reggeti, Brooks, Schrier, Van Raaij); Miller Vet Services(Dykeman)
AHL Newsletter 2020;24(4):8.
Twenty 2 to 3-week-old lambs from a herd of 120 ewes died after showing clinical signs consistent with lethargy and diarrhea. The lambs were offered a new “starter” ration, as well as medicated pellets as a free choice creep feed (lasalocid sodium 36 mg/kg), and an undetermined amount of a mineral mix, also fed to the adults. The owner reported that the losses coincided with offering the starter, and that the animals did not seem to like it very much. Clinical signs improved after treatment with Amprol, Baycox and Biomycin, but approximately half of the affected animals developed posterior paresis.
Three live lambs were submitted to the AHL for diagnostic evaluation. Blood samples were drawn before euthanasia and forwarded to the Clinical Pathology laboratory. Complete blood counts (CBC) identified neutrophilia and thrombocytosis in all samples, consistent with inflammatory disease, which was further supported by elevated haptoglobin concentrations (acute phase response). Serum creatine kinase (CK) and aspartate aminotransferase (AST) were significantly elevated in 2 animals, with the highest concentrations being CK: 310,400 U/L (reference interval 23-313 U/L) and AST: 19,751 U/L (reference interval 23-313 U/L). These findings indicated cellular damage with leakage of intracellular muscle enzymes into plasma.
On postmortem examination, there was gross evidence of diffuse myopathy (Fig. 1). On histopathology, the 2 animals with the highest CK and AST concentrations had very severe extensive skeletal muscle necrosis and mineralization. A few granular casts were noted in the renal medulla, possibly due to myoglobinuric nephrosis.
Based on laboratory results and postmortem findings, the main differential diagnoses were nutritional myopathy and toxic myopathy; appropriate samples were submitted to the AHL Toxicology laboratory for further testing. Liver selenium levels were adequate, but serum vitamin E concentrations were sub-optimal. The starter feed and the mineral mix were tested for ionophores; namely, monensin, narasin and salinomycin. Results were below the detection limits of the method for the starter feed, but monensin was present in the mineral mix at 58 ppm which was not supposed to be medicated, according to the product’s label. Monensin was also identified in the ruminal contents of one of the lambs at 5.8 ppm.
Markedly elevated serum CK and AST concentrations and extensive muscle necrosis appeared to be too severe for nutritional myopathy alone. CK levels in acute nutritional muscular dystrophy in lambs have been reported to be higher than 1000 IU/L and commonly between 5000-10,000 IU/L, although they may be higher in some cases. AST commonly increases to 2000-3000 IU/L (1). These observations, along with inadvertent exposure to monensin, raised concerns for ionophore toxicity; however, toxicity could not be confirmed because the amount of the ionophore consumed could not be determined. Since the recommended dose of monensin in feed for sheep is 11 mg/kg to 22 mg/kg (0.0011% to 0.0022%) (2), identification of 5.8 ppm monensin in the rumen seemed to be a safe level. However, these results only confirmed exposure, as any residues present in the rumen would depend on the amount of feed ingested, homogeneity of the ration, and time between exposure and sample collection (i.e. progression of ingesta to the lower GI tract, absorption and excretion).
Although a definitive cause for the severe myopathy in this case could not be determined, the losses stopped when the feed and mineral mix were removed and replaced with a new ration that the lambs seemed to accept better. This observation further suggested a possible association with the feed and mineral mix; nevertheless, multiple factors might have contributed, including young age/rapid growth rate, reduced protection against oxidative damage (presumptive vitamin E deficiency), and additive effect of the ionophore antibiotics lasalocid and monensin. AHL
Figure 1. Striated skeletal muscle myopathy, as indicated by white discoloration of the muscle fibers (arrows).
References
1. Radostits OM, Gay CC, Hinchcliff KW, Contstable, PD. Chapter 30 - Diseases associated with nutritional deficiencies. In: Veterinary Medicine: A textbook of the diseases of cattle, horses, sheep, pigs and goats, 10th ed. Radostits OM et al, eds. Elsevier, 2007:1746.
2. Monensin – Medicating ingredient brochure, Canadian Food Inspection Agency, June 29 2020. https://www.inspection.gc.ca/animal-health/livestock-feeds/medicating-ingredients/mib/monensin-mos-/eng/1331053867503/1331053926592#a8