The microbiological flora of the lower female genital tract provides a dynamic, complex example of microbial colonization, the regulation of which is not fully understood. When an exogenous bacterial species, with its array of virulence factors, is introduced into the host, disease does not always occur. Conversely, under selected conditions, commensal endogenous bacteria-for example, Gardnerella vaginalis and group B streptococci-can participate in disease processes. Disease caused by both exogenous and endogenous bacteria correlates positively with a markedly increased level of bacterial replication. The key question is what determines the quantity of a given bacterium at any given time. For disease to occur, exogenous or endogenous bacteria that possess pathogenic prerequisites must attain replicative dominance. Their ability to do so is potentially governed by inhibitory or synergistic interrelationships with other microbes.

Objective: The purpose of this study was to analyze the ability of septicemic and nonsepticemic isolates of group B streptococci (GBS) to inhibit in vitro the principal bacterial groups found in the normal bacterial flora of the female genital tract.Methods: The target groups were composed of 1) 10 strains each of the following: viridans streptococci, nonhemolytic streptococci (not group B or D), group A streptococci, GBS, peptostreptococci, coagulase-negative staphylococci, Staphylococcus aureus, and Gardnerella vaginalis; 2) 9 strains of enterococci; 3)9 strains of group C or G streptococci; 4) 7 strains of lactobacilli; and 5) 7 strains of diphtheroids. All target groups were tested for inhibition by a test panel of either a group of 10 or 41 GBS isolates. If the GBS isolates failed to inhibit a target group, that group was tested for its ability to inhibit the GBS test panel.Results: The GBS test panel did not inhibit the growth of coagulase-negative staphylococci or S. aureus but uniformly inhibited groups A, B, C, and G streptococci, lactobacilli, and G. vaginalis. One of the 7 strains of diphtheroids was inhibited by 37 of the 41 GBS isolates; the other 6 strains of diphtheroids were uniformly inhibited. Variable inhibition by GBS was observed with viridans streptococci, nonhemolytic (not group B or D) streptococci, peptostreptococci, and enterococci; however, inhibition or noninhibition was uniform for a given target strain against the entire GBS test panel. The 23 GBS isolates obtained from septicemic neonates or adults did not differ from the 18 nonsepticemic isolates in their ability to inhibit other species of streptococci or other gram-positive or gram-variable constituents of the bacterial flora of the female genital tract. When converse testing was done, all 10 GBS isolates were uniformly inhibited by coagulase-negative staphylococci and by the majority of enterococci, but were not inhibited by S. aureus.Conclusions: These studies suggest that GBS may be significant regulators of other [3-hemolytic streptococci, diphtheroids, lactobacilli, and G. vaginalis within the bacterial flora of the female genital tract. Moreover, the absence of GBS in the vaginal flora may be the result of mediation by coagulase-negative staphylococci and selected strains of enterococci. (C)

Analysis of 240 consecutive vaginal swabs using the compatibility profile technique revealed that only 2 bacteria have the ability to be a sole isolate and as such a candidate to be a major aerobic regulator of the bacterial flora of the female genital tract (BFFGT). Compatibility profiles of Lactobacillus and Gardnerella vaginalis have shown that these organisms shared compatibility profiling for the majority of the normal bacterial constituents of the female genital tract. Dominance disruption appears to come from the addition of compatible co‐isolates and presumed loss of numerical superiority. These phenomena appear to be the keys to reregulation of BFFGT. Lactobacillus appears to be the major regulator of both G. vaginalis and anaerobic bacteria. When additional organisms are added to the bacterial flora, they may add to or partially negate the inhibitory influence of Lactobacillus on the BFFGT. Inhibitor interrelationships appear to exist between coagulase‐negative staphylococci and Staphylococcus aureus and the group B streptococci (GBS) and other beta hemolytic streptococci. Facilitating interrelationships appear to exist between S. aureus and the GBS and selected Enterobacteriaceae. Infect Dis. Obstet. Gynecol. 5:303–309, 1997. © 1998 Wiley‐Liss, Inc.

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