Spontaneous cardiomyopathy of young turkeys is characterized by sudden death due to cardiac arrest. It has been suggested that the condition should be called spontaneous cardiomyopathy to distinguish it from round heart disease of chickens, a different syndrome that is rarely recognized today.

The exact etiology of spontaneous cardiomyopathy in turkeys is unknown. However, studies using furazolidone to produce dilated cardiomyopathy in turkeys have indicated altered membrane transport resulting in myocardial failure. Creatine kinase, glycolysis, glycogen, myofibril, Krebs cycle enzymes, fatty acid oxidation, and soluble proteins are all reduced. The calcium-transport ATPase activity of the sarcoplasmic reticulum is increased. This pattern of biochemical changes is consistent with ischemia playing a role in the pathogenesis of spontaneous cardiomyopathy in turkeys.

While most deaths occur during the brooding period, the ratio of heart weight to body weight of affected birds is increased throughout the growing period. The chronic cardiac insufficiency causes reduced growth rate, resulting in attacks on affected birds by their normal cohorts. In affected turkeys surviving to market age, body weights are reduced an average of 3 lb (1.4 kg). Some outbreaks of the condition have been associated with hypoxia during incubation of the eggs or during transportation of poults from the hatchery to the brood farm. It is possible that stratification of air in poorly-ventilated facilities without circulation fans may similarly contribute to heart damage with subsequent expression of this disease later in life.

Most deaths from spontaneous cardiomyopathy occur during the first 4 wk of life, with mortality peaking at 2 wk. Many poults die suddenly, but some may have ruffled feathers, drooping wings, and a general unthrifty appearance. They may show labored, gasping breathing before death. After 3 wk of age, mortality is sporadic. Characteristically, the affected poult in the first 4 wk of life has a greatly enlarged heart due to dilatation of both ventricles, congested lungs, and a swollen liver. Ascites, anasarca, pulmonary edema, and hydropericardium may or may not be present. In older poults, enlarged hearts are due to marked hypertrophy of the ventricles in addition to dilatation. Histologically, lesions of abnormal hearts are nonspecific and include congestion, damage of the myofibrils of the cardiocytes, and focal infiltration by lymphocytes.

Generally, diagnosis is based on history and gross findings at necropsy; although an ECG can be used, it is of little practical use. Sodium and polychlorinated biphenyls or related compounds may produce similar syndromes.

No treatment is available. Good brooding practices may reduce mortality. Any toxins should be eliminated. Incubation, transportation, and early brooding ventilation conditions should be reviewed.

Last full review/revision March 2012 by Billy M. Hargis, DVM, PhD, DACPV