RESISTANCE OF GROUP B STREPTOCOCCI (GBS) TO KILLING BY OXYGEN METABOLITES

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Known risk factors for early onset GBS sepsis include lack of specific antibody, density of maternal colonization and prematurity. An additional proposed risk factor, is decreased production of microbicidal oxygen metabolites by phagocytes of susceptible newborns(NB). However, GBS lack catalase, produce and release H2O2, and thus should be readily killed by phagocytes with a diminished respiratory burst. Surprisingly, CBS III were equally or more resistant than Staph aureus (SA) to reagent H2O2(60 min assay, n=5-7): log10 cfu/ml at none, 10−3M, 5×10−3M, 10−2M H2O2 for GBS=7.1,7.3,5.9,3.1* and for SA=7.2,6.6,4.5*,4.4*-(*p < 0.001 vs none). Results with other strains of GBS were similar; Group A strep were more susceptible. Neither GBS nor SA were killed in 60 min by a xanthine oxidase-acetaldehyde - Fe++ - EDTA system by a flux of 0.7 nmoles O2/ml/min; both were killed by 3.5 nmoles O2/ml/min. Killing of both was inhibited by omission of Fe++ or EDTA and by addition of mannitol, catalase or superoxide dismutase, suggesting that hydroxyl radical (OH·) played a major role in microbicidal activity and was active at concentrations T 2 log10 less than H2O2. Although GBS lacked catalase, GBS compared to SA contained more glutathione(G) (68.2 vs 0.2 nmoles/mg) and G reductase (44.2 vs 1.3 nmoles/mg/min); SOD and G peroxidase were comparable. G may protect GBS from H2O2 and OH: Defective phagocyte production of oxygen radicals, particularly OH· as reported by Ambruso(Ped 64:722,1979), may contribute to the NB's susceptibility to GBS.