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The clinicopathological findings of mulberry heart disease in a piglet.

Introduction Selenium-vitamin E responsive conditions have a wide geographic distribution producing a variety of syndromes in poultry, domestic and laboratory animals (3). Feeding diets low in selenium to swine results in lesions of mulberry heart disease, hepatosis dietetica, skeletal muscle degeneration, exudative diathesis and ulceration of the pars esophagus (6). The clinical and pathological entities in swine are well documented (1, 10, 11). Changes in serum enzymes indicative of hepatic and muscular damage occur and are of diagnostic significance on an individual or herd basis (1, 2, 8). Changes in SGOT levels can be detected prior to clinical signs (5, 7), but CPK level is muscle specific and an increased level can be detected up to 21 days prior to the onset of symptoms (5). Treatment of the sow and/or piglet parenterally or in the ration has been used to control the effects of selenium and/or vitamin E deficiency (10, 11). Such treatment was also found to decrease the incidence of mastitis, metritis-agalactia, spraddle-legged and infertility syndromes in subsequent farrowings (10). Treatment also reduced losses of piglets from one to three days of age from colibacillosis and crushing (11).