AB S T R A C T The opsonophagocytic requirements of human sera containing endogenous complement for a variety of type Ia, and group B streptococcal strains were defined. Significant reduction (290%) in colonyforming 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 gg/ml), whereas bacterial growth occurred in 25 sera with low levels of specific antibody (mean, 2.1 ug/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 la 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 pathwaymediated 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 agammaglobulinernic 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 Ta capsular polysac-

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.

The role of complement and antibody in the opsonophagocytosis of type II group B streptococci (type II GBS) was defined with sera from healthy adults and two populations with theoretical susceptibility to type II GBS infection--neonates and insulin-dependent diabetics. Significant opsonophagocytosis (bactericidal index, greater than or equal to 90%) of five clinical isolates of type II GBS lacking components of protein antigen c was demonstrated by each of 12 adult sera, as well as by agammaglobulinemic serum, a result indicating that opsonophagocytosis can proceed by antibody-independent activation of the classic complement pathway. Strains containing components of protein antigen c were somewhat more resistant to opsonin-binding activity. Four of 10 neonatal sera and nine of 15 diabetic sera exhibited inefficient opsonophagocytosis. Some of the adult sera with either high or low concentrations of specific antibody to type II GBS promoted opsonophagocytosis via the alternative complement pathway, but this response was not observed with neonatal sera. The addition of sufficient amounts of specific antibody to type II GBS to neonatal and adult diabetic sera in vitro, however, promoted efficient opsonophagocytosis via the alternative pathway.

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The usefulness of Phadebact streptococcus reagents for the detection of group B streptococcal antigen in cerebrospinal fluid was evaluated in 54 infants with meningitis and in 22 normal infants. Antigens was detected by slide coagglutination in 19 (82.6%) and by countercurrent immunoelectrophoresis in 20 (87.0%) of 23 cerebrospinal fluid specimens from infants with group B streptococcal meningitis at admission. After initiation of antimicrobial therapy, antigen could be detected in 11 of 19 (by slide coagglutination) and 7 of 18 (by countercurrent immunoelectrophoresis) cerebrospinal fluids. False-positive reactions were noted by slide coagglutination in one infant with S. bovis meningitis and one with group B streptococcal bacteremia without meningitis; none occurred with countercurrent immunoelectrophoresis. The commercial availiability, simplicity, sensitivity (82.6%), and specificity (96.4%) of the Phadebact slide coaggluatination test for detecting group B streptococcal antigen in cerebrospinal fluid suggest that it may be useful for the early and rapid diagnosis of group B streptococcal meningitis.