Bette J. Webb

Antimicrobial susceptibility of group B streptococci isolated from a variety of clinical sources.

The minimal inhibitory concentration of 10 antibiotics for 244 isolates of group B streptococci was determined. Susceptibility to penicillin G, ampicillin, cephalothin, chloramphenicol, and carbenicillin was uniform. Tetracycline and bacitracin resistance among these isolates was frequent (87.5 and 97.9%, respectively). Three strains (1.2%) failed to be inhibited by 100 μg of lincomycin or clindamycin per ml. Susceptibility of these 244 strains to the agents tested was unrelated to source of the isolate, year of isolation, or strain serotype. No apparent change in the suceptibility of group B streptococci to penicillin G has occurred during the past 2 decades.

Antibody-independent Classical Pathway-mediated Opsonophagocytosis of Type Ia, Group B Streptococcus

The opsonophagocytic requirements of human sera containing endogenous complement for a variety of type Ia, and group B streptococcal strains were defined. Significant reduction (>==90%) in colony-forming units was noted after a 40-min incubation for the highly encapsulated, mouse-passed prototype strain 090 by sera containing moderate to high concentrations of antibody to type Ia polysaccharide (mean, 16.5 mug/ml), whereas bacterial growth occurred in 25 sera with low levels of specific antibody (mean, 2.1 mug/ml). This absolute requirement for a critical amount of specific antibody in promoting opsonophagocytic killing of strain 090 was not found when 18 fresh clinical type Ia isolates were tested. In antibody-deficient and agammaglobulinemic sera, respectively, mean reductions in colony-forming units of 94 and 95% were seen for fresh clinical isolates, whereas strain 090 was not killed by polymorphonuclear leukocytes in the presence of these sera. All strains required a considerable amount of specific antibody for alternative pathway-mediated opsonophagocytosis. That opsonophagocytic killing of clinical type Ia isolates was mediated by the classical pathway in a nonantibody-dependent fashion was shown when MgEGTA chelation of agammaglobulinemic serum or use of serum deficient in C2 resulted in bacterial growth. The addition of C2 to C2-deficient serum restored bactericidal activity of this serum. These experiments indicate that substances other than the exposed surface of the type Ia capsular polysaccharide initiate classical pathway-mediated opsonophagocytosis of clinical isolates of type Ia, group B streptococci by human sera in the absence of immunoglobulin. Perhaps, a deficiency in classical complement pathway function is critical to the susceptibility of neonates to type Ia, group B streptococcal disease.

Group B streptococcal colonization and antibody status in lower socioeconomic parturient women

This investigation was undertaken to determine the prevalence of group B streptococcal vaginal and throat colonization among lower socioeconomic pregnant women and the antibody concentration to the capsular polysaccharide antigen of type III group B streptococcus in their sera. Group B streptococci were recovered from 28.6 per cent of the 112 women studied; vaginal colonization was detected in 23.4 per cent, throat colonization in 4.7 per cent, and colonization at both sites in 0.9 per cent of the patients, respectively. Among these isolates of group B streptococci, serotypes III (39.5 per cent) and II (30.3 per cent) predominated. No differences were found between colonized and noncolonized women with respect to age, race, marital status, or parity. The majority of all women studied had low concentration of antibody in serum (less than 1.0 microgram per milliliter). However, women with isolation of type III group B streptococci from cultures at the time sera were collected had significantly higher concentrations than did women without group B streptococci from cultures at the time sera were collected had significantly higher concentrations than did women without group B streptococcal colonization.

Lack of stimulation of isohemagglutinin antibodies byimmunization with group B streptococcal (Type III) vaccine

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895 ANTIBODY-INDEPENDENT CLASSICAL PATHWAY (CP)-MEDIATED OPSONOPHAGOCYTOSIS (OP) OF TYPE Ia GROUP B STREPTOCOCCI (IaGBS)

Since invasive IaGBS disease rarely occurs beyond the early neonatal period, heat-labile serum factors rather than type-specific antibody (SpAb) could be critical to host defense against la GBS. The OP requirements for prototype strain,090, and 18 fresh clinical isolates were assessed in an assay employing human PMN, serum containing endogenous complement, and 3×106 CFU/ml of IaGBS. Significant OP of 090 (>90% reduction in CFU) occurred after 40 min. incubation in 6 sera containing high levels of SpAb, while bacterial growth was noted in 25 sera with low levels. The mean OP for 090 was compared to that for 18 clinical isolates in 3 representative sera. OP was similar in serum with high SpAb levels (94% vs 97%). However, in low SpAb and agammaglobulinemic sera, respectively, OP was 94% (range, 83-98%) and 95% (range, 77-99%) for 18 clinical isolates, while 090 grew in these sera. Absorption of serum with high SpAb with Ia polysaccharide antigen (Ag) completely inhibited OP for 090, but did not effect that for clinical isolates. All strains required high SpAb levels for alternative pathway recruitment. Serum deficient in C2 and SpAb did not promote OP of clinical isolates of IaGBS until reconstituted with C2. These findings that OP of clinical isolates of IaGBS is CP-mediated in a non-SpAb dependent fashion indicate that substances other than Ia capsular Ag, such as polar glycophospholipids, may initiate CP activation in the absence of immunoglobulin G.