Spontaneous bacterial peritonitis caused by Neisseria gonorrhoeae. Evidence for a transfallopian route of infection.

We describe the clinical and laboratory features of a case of spontaneous bacterial peritonitis caused by Neisseria gonorrhoeae in a sexually active woman with Laennec's cirrhosis, ascites, and asymptomatic cervical gonorrhea. Treatment of the infection with high-dose parenteral penicillin was associated with resolution of the infection. This first report of spontaneous gonococcal peritonitis provides highly suggestive evidence that the transfallopian route is a mechanism whereby bacteria may enter the peritoneal cavity. Appropriate cultures for this organism should be included when a woman with chronic liver disease, who is sexually active, presents with spontaneous peritonitis.

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.

Clinical and pathogenetic implications of histopathology in childhood polydermatomyositis.

Childhood dermatomyositis is a distinct subset of dermatomyositis with highly variable outcome. We reviewed our experience with 29 patients observed over 22 years and attempted to correlate tissue manifestation with outcome. Distinctive vascular lesions included non-necrotizing vasculitis and a unique spectrum of endovascular injury producing temporary or permanent occlusion of small arteries and capillaries. Vessels with noninflammatory endovasculopathy were often reactive with fluorescein-conjugated antisera to IgM, C3d, and/or fibrin. Lesions linked to endovascular injury include infarction, zonal myopathy, and loss of capillary network. We were able to identify half of the children destined to have persistent morbidity on the basis of severity of vasculopathy in pretreatment muscle-biopsy specimens. Our observations support a central role for endothelial cell injury in the pathogenesis of childhood dermatomyositis, suggest a basis for assessing the efficacy of therapy, and provide a focus for investigation of basic mechanisms.

Cylindrical spirals in a familial neuromuscular disorder.

Cylindrical spirals are unique membranous structures that were detected in skeletal muscle of a mother and one of her two children; all three have percussion myotonia but no evidence of weak or wasted skeletal muscles. Muscle cramps, stiffness, posteffort muscle tightness, myotonic lid lag, and the cylinders appear or progress with age, but the disorder is asymptomatic in the children and only mildly incapacitating in the mother. The cylinders are 8 mu long and 1 mu wide, are composed of spiraling double-laminate membrane resembling myelin, and are derived from abnormal subsarcolemmal tubulovesicular structures that are interpreted as pathological T-tubes.