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This 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 the role of ischemia 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. Market body weights of affected birds are reduced an average of 3 lb. Some outbreaks of the condition have been associated with hypoxia during incubation of the eggs.
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, the 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 the 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 and incubation conditions reviewed.
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