Myofiber damage accompanying intramuscular parasitism by Sarcocystis muris.

Myofiber degeneration which results from Sarcocystis infection exhibits a number of fine structural features suggestive of other myopathies and several well-defined fine structural features not characteristic of other myopathies. Some of these fine structural features are similar to those observed in intramuscular infections of Trichinella spiralis, another muscle parasite. Major alterations of the myofibrillar contractile apparatus occur at the periphery of the membrane bound parasitophorous vacuole which include splitting and fragmentation of the myofibrils at the longitudinal ends of the parasitophorous vacuole and Z line dissolution at the radial periphery. Membranous structural elements including mitochondria, sarcoplasmic reticulum and T system components become disarrayed as the myofibrils degenerate. Some minor hypertrophy of the sarcoplasmic reticulum occurs in conjunction with initial fragmentation of the myofibrils bu no major dilation or hypertrophy has been observed. There is a distinctive membranous organization of the interface of the parasitophorous vacuole. The presence of pycnotic and fragmenting nuclei, sarcolemmal invaginations with accompanying fibrous connective tissue invasion and large areas of undifferentiated cytoplasm suggest the ultimate necrosis and destruction of infected myofibers. The similarity between morphological features of myofibrillar degeneration accompanying intramuscular Sarcocystis muris infections and those associated with a variety of myopathies resulting from other causes suggests that a common mechanism of muscle response to damage might result in the observed structural degeneration.