Serotypes of serious, sometimes fatal, streptococcal infections in Sweden during 1988-1989 were analyzed. The T1M1 type totally dominated, representing almost 70% of all group A streptococci from serious and uncomplicated infections at the peak of the outbreak. Immunoblots of isolates from various patient groups showed that all isolates produced high amounts of erythrogenic toxin (ET) B and high amounts of ET-C, whereas ET-A was released only in small amounts and from few isolates. ELISAs showed high antibody levels to these toxins and to the M1 antigen in patients with uncomplicated infections. Low antibody levels against M1 were seen in patients with bacteremia and in fatal cases; the latter also had low antibody levels against ET-B. It seems likely that a combination of production of large amounts of toxin and low antibody titers to it and to the M antigen of the infecting isolate are determining factors for the outcome of the infection. No signs of primary immune deficiency were noted.

No abstract

streptococcal plasminogen activator in the focus of infection and in the kidneys during the initial phase of experimental streptococcal glomerulonephritis.Strains of group A streptococci known to secrete the nephritis strain-associated protein (NSAP), a plasminogen activator, were studied for their ability to produce APSGN in rabbits. A tissue cage model was used to monitor the secretion of NSAP at the focus of infection and histopathological examination of kidney tissue was used to determine glomerular pathology. Animals infected with NSAP positive strains exhibited NSAP deposits in the glomerular tissue by day 7 in the absence of antibody to this molecule with progressive pathology indicative of APSGN three weeks later. Animals infected with the NSAP negative streptococcal strain exhibited no abnormal pathology. The ability of NSAP to bind to kidney tissue suggested that it has unique nephrotropic properties; and its ability to activate plasminogen to plasmin, possibly in situ, suggests that much of the pathological events associated with APSGN may be initiated by plasmin activity.

These data substantially add to the weight of evidence supporting the lack of non-clinical drug-induced pancreatic safety signals in animals exposed to GLP-1-based therapies.

SUMMARY. Group-B streptococci that possess a type-specific surface polysaccharide undergo phagocytosis only in the presence of antibodies to this, and complement. The snail Cepaea hortensis forms a lectin that is specific for sialic acid; treatment with this promoted the phagocytosis of a group-B streptococcus of serotype Ia (strain 090) in the absence of opsonic antibodies. The effect of the lectin was dose-dependent and required the presence of complement. The specificity of the lectin reaction for sialic acid was proved by the inhibition of phagocytosis by bovine submaxillary mucin. The participation of complement in the reaction was confirmed by demonstrating that C3 was bound to the surface of lectin-treated cells.