SWINE

Ionophore toxicity in pigs

Josepha DeLay, Maria Spinato

Over a 6-day period, bodies or field postmortem samples of nursery pigs from 4 herds were submitted to the AHL. The clinical complaints ranged from weak and fading pigs, to animals that were stumbling or recumbent and demonstrated unspecified neurologic signs. Up to 30% morbidity and 20% mortality was reported in some herds. Antibiotic therapy was unsuccessful in resolving clinical signs in those herds that carried out this treatment.

Discussion among several of the swine veterinarians involved in these cases identified a common feed source, and further investigation determined that an ionophore had been added inadvertently to feed containing tiamulin. At postmortem, no significant gross lesions were evident in the pigs, however all animals had microscopic lesions involving striated muscle, with sparing of myocardium. Acute-to-subacute myodegeneration varied in severity among individual animals, and targeted skeletal muscle, as well as diaphragm and tongue in some animals. In addition to ionophore toxicosis, nutritional myopathy caused by selenium and/or vitamin E deficiency is a differential diagnosis for this histologic lesion; however selenium levels were assessed to be normal by liver mineral analysis.

Tiamulin potentiation of the toxic effects of ionophores in swine is well recognized and has been documented previously. Tiamulin is thought to inhibit normal cytochrome P450 activity and ionophore metabolism. Confirmation of ionophore toxicosis requires analysis of the source feed or stomach content (in cases where the suspect feed is still being fed), and tissues cannot be tested for ionophores. Species differences exist for susceptibility to ionophore toxicosis, and swine are moderately sensitive to this toxin. Comparatively, horses are highly sensitive to ionophore toxicosis, and chickens are relatively insensitive.

Muscle lesions were minimal in follow-up muscle samples taken 4 weeks following ionophore exposure from pigs in a 5th affected herd, indicating that recovery may be possible in some animals if the source of the offending ionophore is removed before muscle injury is overwhelming.

These cases demonstrate the value of communication among practitioners, and between practitioners and diagnosticians, in solving disease problems. This event also highlights the importance of including muscle from several sites among formalin-fixed histology samples from field postmortems. In pigs, myopathy can easily be confused clinically with neurologic disease, and a diagnosis of myopathy will be missed if muscle samples are not included for histologic evaluation.   AHL

References

Roder JD. Ionophore toxicity and toxicosis. Vet Clin North Am Food Anim Pract2011;27:305-314.

Szucs G, et al. Biochemical background of toxic interaction between tiamulin and monensin. Chem Biol Interact 2004;147:151-161.

Van Vleet JF, et al. Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and /or vitamin E. Am J Vet Res 1987;48:1520-1524.

Van Vleet JF, Ferrans VJ. Ultrastructural alterations in skeletal muscle of pigs with acute monensin mycotoxicosis. Am J Pathol 1984;14:461-471.

Figure 1. Myodegeneration in skeletal muscle of affected pig. Numerous swollen myocytes with sarcolemmal contraction bands and vacuolation (arrows).

Figure 2. Normal skeletal muscle in age-matched nursery pig. Intact, happy myocytes.