Spontaneous cardiomyopathy of young turkeys is characterized by sudden death due to cardiac arrest and is not related to other cardiomyopathies of poultry.
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. CK, 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.
Although 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 healthy 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 2–3 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 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. Hypoxia during incubation, transportation, or brooding has been associated with increased incidence, and enhanced ventilation during these periods appears to be critical. Practitioners have occasionally noted association of high levels of dietary (or drinking water) copper and increased incidence of spontaneous cardiomyopathy. Good brooding practices may reduce mortality, because overheating has also been postulated to increase the incidence of this disease.