Bryan Larsen

Vaginal flora in health and disease.

This chapter has portrayed the normal vaginal flora as a range of microbial species that associates in a stable way with human vaginal epithelium. The human vagina provides these microorganisms with the physical and chemical environment that allows them to use this tissue as a normal habitat. Because the relationship of the normal flora to the underlying tissue is that of an ecosystem, the components of this system are in dynamic equilibrium. Consequently, a change in the environmental conditions provided by the vaginal epithelium will result in changes in the population density or the species composition of the normal flora. Although the microbial flora appears to provide a benefit to the host by reducing the probability of colonization by exogenous microorganisms, it may participate in various undesirable symptoms, including various types of vaginitis or postoperative, postabortion, and post-Caesarean section infections, and upper tract invasion after lower tract infection. All future attempts to understand vaginitis in all its manifestations necessarily must include recognition of the importance of the normal flora because all types of vaginitis are superimposed on an existing endogenous microbial flora.

Vaginal microbial flora: practical and theoretic relevance.

&NA; The bacterial flora of the female reproductive tract is a focal point for the study of infectious disease in obstetrics and gynecology, as it is recognized that many pelvic infections involve bacteria resident on the cervical‐vaginal epithelium. The vaginal flora contains a large variety of bacterial species, including aerobic and anaerobic organisms, as revealed by modern microbiologic methods. Recent studies have indicated that certain organisms commonly involved in pelvic infections, particularly those following genital tract surgery, namely Escherichia coli and Bacteroides fragilis, appear to be underrepresented in relationship to the infectious complications they cause. A possible explanation of this phenomenon has been suggested based on the finding that traumatic events in the reproductive tract, including parturition, surgery, and invasive malignancy, result in increased colonization by organisms commonly involved in pelvic infections. Other changes in the flora related to the hosts hormonal milieu were identified and are generally less profound than those related to trauma. We have reviewed some of the newer aspects of our understanding of the genital flora, such as quantitation of the vaginal flora, which should continue to improve our understanding of the role of the genital tract flora in disease states.

Vaginal Microbial Flora: Composition and Influences of Host Physiology

Abstract The normal bacterial flora of the female genital tract is composed of various aerobic and anaerobic bacteria. Because the normal flora may be a source of disease-causing organisms or may i...

Estrogen effects on Candida albicans: a potential virulence-regulating mechanism.

Three Candida albicans strains were tested in the presence of 17-beta-estradiol (10-6 M and 10-9 M) for increased growth and for enhanced survival during incubation at nonpermissive temperatures. All 3 test organisms showed increased growth in the presence of estradiol compared with estrogen-free controls. Likewise, all 3 strains, when treated with estradiol, survived incubation at 48 degrees C better than did controls. Cytoplasmic extracts were probed with an anti-hsp90 antibody, and results suggested that intracellular hsp90 was up-regulated in the presence of 10-9 M 17-beta-estradiol. The results were confirmed by reverse-transcriptase polymerase chain reaction with primers specific for C. albicans hsp90. A kinetic study revealed that peak hsp90 expression occurred within 2 h of exposure to 17-beta-estradiol. In addition, estrogen increased the amount of cdr1 (Candida multidrug resistance) mRNA compared with cells not treated with estrogen. Coumarin and phenol also up-regulated hsp90 and cdr1 mRNAs, indicating that the estrogen-sensing and -response systems in C. albicans may lack specificity.

The Bacterial Flora of the Female Rat Genital Tract

Summary A study of the genital micro-flora in virgin female rats of reproductive age has demonstrated that alpha and nonhe-molytic streptococci, Pasteurella pneumotro-pica, diphtheroid bacilli, Staphylococcus epi-dermidis, and Proteus mirabilis are the predominant genital organisms. The pH of the rat vagina was demonstrated to be near neutrality. It is suggested that the higher pH in the rat vagina as compared to the human vagina may account for some of the differences between human and rat genital micro-flora. A. J. Markovetz is the recipient of a Development Award-Research Career Program (5KO4 GM14681) from the National Institute of General Medical Sciences. The assistance of Marilyn J. Ohm in identifying anaerobic bacteria for this study is gratefully acknowledged.

Bacterial growth inhibition by amniotic fluid: I. In vitro evidence for bacterial growth-inhibiting activity

Abstract By measuring bacterial growth spectrophotometrically, it has been demonstrated that amniotic fluid fails to support the growth of Escherichia coli, Streptococcus faecalis , and Staphylococcus aureus . Dilution of amniotic fluid in water prior to addition of an inoculum of Escherichia coli results in a loss of inhibition. Comparable results are obtained whether growth is monitored by plate count or spectrophotometry. Plate-count studies revealed that amniotic fluid may be diluted to 30 per cent of its original concentration and still retain enough inhibitory activity to maintain bacterial counts at a lower level than for an equivalent inoculum in distilled water. Growth of Escherichia coli in amniotic fluid is inversely related to amniotic fluid concentration. Amniotic fluid does not fail to support bacterial growth because of nutritional inadequacy but contains some material which suppresses bacterial growth.

Host-parasite interactions during pregnancy.

The point that host defense against infectious disease is exceedingly complex scarcely needs further emphasis. We have tried to show that pregnancy is a state which has the potential for altering any of the many facets of host defense, and in some instances presented evidence that pregnancy does alter resistance to infection. Some diseases are either more severe during pregnancy or more prevalent during pregnancy, suggesting a softening of the host defenses. However, both monocytic and polymorphonuclear leucocyte phagocytic systems seem to be more active during pregnancy. Transferrin is increased in pregnancy. The immune system in pregnancy is either normal or slightly depressed. A number of other factors have been mentioned for which no information exists as to the effect pregnancy has on them. Despite the information reviewed, it is not possible to say that pregnancy has a net positive or negative effect on host defense; the effect, if any, depends ostensibly on the disease entity. That the host defenses may be somewhat enhanced by pregnancy while susceptibility to certain diseases is increased is paradoxical and serves to underscore the fact that our understanding of host defense in pregnancy is abysmally deficient. Probably no concept is made more clear by this paper than the idea that in the area of host defense in pregnancy there is as much space as any researcher may choose to fill.

Host resistance to intraamniotic infection.

In this review the mechanisms whereby amniotic fluid serves to protect the fetus from microbial disease have considered. It appears from the data reviewed that the principal mode of antibacterial action of amniotic fluid is bacteriostasis. Thus, the host is able to cope with a small number of organisms introduced into the amniotic cavity; however when the amniotic fluid is grossly contaminated the host resistance capacity of the amniotic fluid may be overwhelmed. This may be understood best by the quantitative description of disease theroized by Theobald Smith (94). Smith suggested that disease was a function of the number of organisms with which a host is initially infected multiplied by the virulence of the organism. The effects of the number and virulence of the organism in producing disease is lessened by the hosts resistance capacity. This concept of disease is summarized by the equation: Disease equals (number) (virulence)/resistance. Although these parameters do not possess numeric values, it is possible to see at least conceptually their interplay with respect to intrauterine infection. For example, the number of organisms reaching the amniotic fluid may be increased by various modes, namely maternal viremia or bacteremia; premature rupture of the fetal membranes, antenatal vaginal examination and possibly intrauterine fetal monitoring. While these circumstances may result in increased rate of infection, some reports conversely indicate that minimal bacterial contamination in the amniotic fluid is not an extraordinary occurrence and may not result in any maternal or fetal complication (73,74). The intrinsic host resistance capacity of the amniotic fluid likewise represents an important part of the Smith equation for disease. We have found that amniotic fluids may vary in antibacterial efficacy from almost no inhibitory activity to profound bactericidal activity (90). Obviously, the likelihood of the production of disease by an equivalent inoculum of a particular organism would be quite different depending upon the intrinsic inhibitory capacity of the amniotic fluid. The measurement of the inhibitory capacity of amniotic fluid holds some promise for enabling a physician to determine which patients may be at special risk of intrauterine infection.

Bacterial growth inhibition by amniotic fluid: II. Reversal of amniotic fluid bacterial growth inhibition by addition of a chemically defined medium

Abstract By measuring the growth of E. coli spectrophotometrically, it has been possible to determine that a chemically defined medium supported growth of this organisms; however, when amniotic fluid was added to chemically defined medium before inoculation with the test organism, enhanced growth was observed although amniotic fluid alone failed to support detectable growth of E. coli . Reversal of bacterial growth inhibition in amniotic fluid was found to be related to phosphate in chemically defined medium. The reversal of growth inhibition was demonstrated with various phosphate containing compounds. It is proposed that phosphate interacts with a bacterial growth inhibitor in amniotic fluid which results in the loss of its bacterial growth-inhibiting ability.

Relationship of Fungal Vaginitis Therapy to Prior Antibiotic Exposure

Objective: To address the putative association of antibiotic use and subsequent yeast vaginitis in a population of non-pregnant women. Methods: Three hundred and sixteen women who received medical care in rural family medicine clinics enrolled in this study. Participants were pre-menopausal and non-pregnant and were followed until they used a course of antifungal therapy for vaginitis, became pregnant or moved from the catchment area. At entry subjects were free of vaginitis symptoms and had taken no antibiotics for 30 days. Patients were followed by repeated review of clinic records, hospital records and telephone or personal interviews. Data collection included documentation of episodes of antifungal treatment for vulvovaginal candidiasis and confirmed antibiotic treatment or credible history of antibiotic use prior to the use of antifungal therapy. Physician-reported uses of antibiotic and antifungal as well as patient-reported uses of these were recorded. Results: There were four reported cases of antifungal therapy following within a month of antibiotic use, in contrast to 484 antibiotic uses not followed by antifungal use. If time of observation was extended to 6 months from antibiotic use, there were 13 uses of antifungal therapy after antibiotics and 475 uses of antibiotics not followed by antifungal therapy. Conclusion: Our results cast doubt on the association of antibiotics as a putative cause of yeast vulvovaginitis.