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Enhanced resistance to streptococcal infection induced in mice by cell wall mucopeptide.

The streptococcal cell wall mucopeptide when injected into mice either intraperitoneally or intravenously enhances the resitance to subsequent challenge with virulent Group A streptococci. Rabbits which are injected intravenously with solubilized mucopeptide develop a fever response which has a resemblance to that achieved with endotoxin. Mice which survive 6 to 7 weeks after challenge with virulent Group A streptococci yield at autopsy search Group A streptococci serologically identical to the challenge organisms. A preparative dose of cell walls injected into mice prior to challenge diminished this late recovery of streptococci. Group A-variant streptococci were recovered from mice which survived challenge and carried the organisms for several weeks. Filterable bacterial forms, which grew on L form media, were recovered from infected mice. The serologic type of the L forms was identical to that of the challenge organisms.

Animals↗

Histopathologic changes in kidney and liver correlate with streptococcal pyrogenic exotoxin B production in the mouse model of group A streptococcal infection.

Previous studies show that isogenic mutants deficient in streptococcal pyrogenic exotoxin B (SPE B) cause less mortality and skin tissue damage than wild-type strains of Streptococcus pyogenes when inoculated into mice via an air pouch. In this study, the growth and dissemination of bacteria, pathologic changes in various organs, and their correlation with SPE B production were examined. Bacterial numbers in the air pouch from wild-type strain NZ131-infected mice increased at 48 h, while those from speB mutant SW510-infected mice continuously reduced. Mice infected with NZ131 developed bacteremia and greater dissemination in the kidney, liver, and spleen; those infected with SW510 showed either no or slight bacteremia and dissemination. Co-inoculation of SW510 with recombinant SPE B showed a higher bacterial count in the air pouch, bacteremia, and organ dissemination compared to co-inoculation with a C192S mutant lacking protease activity. The histopathologic changes examined showed lesions in kidney and liver in the NZ131-infected but not in SW510-infected mice. The elevation in sera of BUN, AST, and ALT correlated positively with renal and liver impairment. Taken together, SPE B produced during S. pyogenes infection plays a pathogenic role. A direct effect of SPE B on vessel permeability change was also demonstrated.

Alanine Transaminase↗

Systemic group D streptococcal infection in newborn infants.

Thirteen cases of group D streptococcal neonatal sepsis and/or meningitis were identified at the Cincinnati Children's Hospital from 1970 to 1976. Ages at onset of disease ranged from 1 to 25 days. The most frequent symptoms were fever (five cases), lethargy (five cases), and respiratory difficulty (four cases). Blood cultures for seven infants were positive; CSF cultures for five infants were positive; and CSF and blood cultures for one infant were both positive. In 12 patients, parenteral antibiotic therapy consisted of a penicillin and an aminoglycoside. One infant with a severe meningomyelocele died. The other 12 infants showed a rapid clinical response with seven patients improving within 48 hours of the start of therapy. Infection with group D streptococcus results in a low-grade systemic disease in both full-term and premature infants that responds favorably to appropriate therapy.

Ampicillin↗

Invasive streptococcal infections in the era before the acquired immune deficiency syndrome: a 10 years' compilation of patients with streptococcal bacteraemia in North Yorkshire.

Significant streptococcal (non-pneumococcal, non-enterococcal) bacteraemia was detected in 100 patients in two Health Districts of North Yorkshire in the decade 1978-1988. Patients with these infections accounted for 11% of the total 902 patients in the districts in whom bacteraemia was diagnosed during the period. Infection was most often seen with beta-haemolytic streptococci (52 patients) comprising Lancefield group A (Streptococcus pyogenes) (20 patients), group B (13), group C (5), group G (9), haemolytic Streptococcus milleri and non-groupable streptococci (5). The wide variety of serious infections included cellulitis, abscess, septicaemia, pneumonia, septic arthritis, necrotising fasciitis, acute endocarditis and mycotic aneurysm. Of these 52 patients, 21 (40%) died. alpha-Haemolytic streptococcal bacteraemia was diagnosed in 38 patients of whom 24 (63%) suffered from endocarditis and three (8%) died. Three of ten patients with non-haemolytic or anaerobic streptococcal bacteraemia died also. Six of the 100 patients with streptococcal bacteraemia had concomitant acute virus infections. Of the total 56 patients with infective endocarditis diagnosed in the districts during the period, streptococci were responsible in 30 (54%) of them. The predisposing factors, clinical features and outcome of the infections are described and discussed.

Adult↗