Abstract
Descriptions of a venereal disease syndrome resembling gonorrhea have been present throughout much of recorded history. Despite the development of effective chemotherapeutic agents and recent intense efforts by epidemiologists to control gonorrhea, gonococcal infections have become one of the most prevalent of all bacterial infections. In 1965, there were 324,925 cases of gonorrhea reported to the Center for Disease Control. In 1970, there were 670,268 reported cases of gonorrhea and in 1975, there were 991,162 reported cases of gonorrhea (1,2). | One of the problems associated with this continuing rise in the incidence of gonorrhea is the lack of knowledge concerning factors which influence the acquisition of the gonococcus. It has been estimated that the risk of a male acquiring gonorrhea by contact with an infected female is approximately 22% (3). Various factors which may influence this acquisition rate have been suggested, but very little data exist. Among the possibilities being investigated are factors such as anatomical variations of the genital tract, degree of sexual excitation of the female, use of oral contraceptives, and decreased use of mechanical contraceptives. The fluctuations in the composition of the normal endocervical flora associated with the menstrual cycle may also influence the acquisition of gonococcal infections. Although the hormone controlled variations in the environment of the female genital tract have been fairly well documented, the direct effects of the "microbial shifts" associated with hormonal changes on susceptibility to infection have not been extensively studied. A considerable volume of data has been gathered in studies on the normal flora residing in other body sites that suggest the normal flora may play a role in resistance to infection. Many in vitro bacterial antagonisms have been demonstrated to occur between components of the normal flora and potential human pathogens. Investigators have hypothesized that these in vitro antagonsims may play an important role in maintaining a stable indigenous flora and thus contribute to "non-specific" factors of host resistance to infection. Clinical studies have been performed to evaluate the protective role, in vivo, of indigenous flora demonstrated to be antagonistic in vitro to a particular pathogenic organism. Despite this large interest in bacterial antagonisms, little has been done to study the role normal endocervical flora might play in the acquisition of gonococcal infections. Since bacterial interference has been shown to play a protective role in various other disease states, it was hypothesized that interactions occurring between the normal endocervical flora and Neisseria gonorrhea (GC) might be involved in resistance to infection. Therefore, this study was designed to determine the ability of components of the endocervical flora to antagonize the growth of GC in vitro and to examine various factors which might influence the occurrence of these organisms in vivo. The data obtained were analyzed on the basis of culture status of the women (presence or absence of GC), time during the menstrual cycle at which the woman was cultured, and use of oral contraceptives (birth control pills). Information obtained from data analyses was then used to speculate on the role which the inhibitory endocervical flora might play in resistance to gonorrhea.