Morphology of acute myopathy associated with influenza B infection.
Calf muscle samples were obtained from 12 children with transient incapacitating myalgia and proved infection of the upper respiratory tract with influenza virus, type B. In all except one, light microscopy revealed isolated segmental muscle fiber degeneration and necrosis without frank myositis. Ultrastructural studies revealed that in zones of segmental necrosis, the sarcolemma was lysed but the basement membrane was intact. Focal degenerative changes included myofibrillar disarray with disruption/loss of the sarcoplasmic reticulum, glycogen depletion accompanied by mitochondriopathy, subsarcolemmal mitochondrial aggregates, activation of satellite cells, and focal filopodial transformation of the sarcolemma. The primary event in the pathogenesis of focal muscle fiber necrosis is likely to be biochemical and was not elucidated, but the focal sarcolemmal and T-tubule changes and mitochondriopathy suggest that destabilization of cell membranes may play a critical role. Sarcolemmal filopodia may be a marker for a specific type of membrane injury, but we were unable to establish that influenza virus has a direct role in its genesis.
D002648:Child; D006801:Humans; D009981:Influenza B virus; D007251:Influenza, Human / Q000150:complications / Q000473:pathology*; D008854:Microscopy, Electron; D008931:Mitochondria, Muscle / Q000648:ultrastructure; D009132:Muscles / Q000648:ultrastructure*; D009135:Muscular Diseases / Q000209:etiology / Q000473:pathology*; D009210:Myofibrils / Q000648:ultrastructure; D012508:Sarcolemma / Q000648:ultrastructure; D014771:Virion / Q000648:ultrastructure