Sudden death in cattle, especially calves, is a common problem of farm practice. Some cases are associated with significant cardiac lesions; in others, although necropsy suggests
cardiac failure to be the cause of death, histological examination of H & E sections fails to demonstrate conclusively the site and nature of the lesion. We have studied 26 animals which died suddenly and in which the only pathological abnormalities detected were definite or equivocal myocardial
necrosis. Three types of
necrosis were identified: myodegeneration, contraction band
necrosis and coagulation
necrosis. Vacuolation of myocytes occurred in control hearts only in the sub-endocardial myocardium, but was found more extensively in diseased hearts.
Paraffin sections of myocardium stained by von Kóssa's method or by haematoxylin-
basic fuchsin-
picric acid improved the detection of myocardial
necrosis. Some myocardium was examined by electron microscopy which detected early myocardial
necrosis in some equivocal cases and defined the nature of the lesion in more advanced cases. Early changes were an increase in the number of type A mitochondrial inclusions which did not contain significant quantities of
calcium but which increased in number after death, albeit to a lesser degree, even in control material. This was followed by deposition of electron-dense granules and spicules (Type B inclusions) and totally electron-opaque mitochondria in association with contraction band
necrosis. X-ray microanalysis showed type B inclusions and electron-opaque mitochondria to have peaks for
calcium. It is suggested that myocardial cell death in animals having such lesions resulted from mitochondrial
calcium overload. The findings are discussed in relation to nutritional
myopathies of ruminants and human
myocardial disease associated with
sudden death, and to experimental myocardial ischaemia.