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1.  Differentiation Between Women With Vulvovaginal Symptoms Who are Positive or Negative for Candida Species by Culture 
Objective: To investigate whether clinical criteria could differentiate between women with vulvovaginitis who were culture positive or negative for vaginal Candida species.
Methods: Vulvovaginal specimens were obtained from 501 women with a vaginal discharge and/or pruritis. Clinical information and wet mount microscopy findings were obtained. All specimens were sent to a central laboratory for species identification.
Results: A positive culture for Candida species was obtained from 364 (72.7%) of the specimens. C. albicans was identified in 86.4% of the positive cultures, followed by C. glabrata in 4.5%, C. parapsilosis in 3.9%, C. tropicalis in 2.7% and other Candida species in 1.4%.Women with a positive Candida culture had an increased utilization of oral contraceptives (26.1% vs. 16.8%, p = 0.02) and antibiotics (8.2% vs. 0.7%, p = 0.001), and were more likely to be pregnant (9.1% vs. 3.6%, p = 0.04) than the culture-negative women. Dyspareunia was more frequent in women without Candida (38.0% vs. 28.3%, p = 0.03) while vaginal erythema (p = 0.01) was more common in women with a positive Candida culture.
Conclusions: Although quantitative differences were observed, the presence of vaginal Candida vulvovaginitis cannot be definitively identified by clinical criteria.
PMCID: PMC1784657  PMID: 11916179
3.  Vulvar Vestibulitis—A Complex Clinical Entity 
Objective: This study aims to determine the pathophysiology of vulvar vestibulitis and to evaluate currently used treatment options.
Methods: Two hundred twenty women with vulvar vestibulitis were seen between October 1987 and March 1995. Every patient had vulvar pain when they attempted intercourse, 75% had excessive vaginal discharge, 36.4% had constant or recurring vulvar burning, and 10.9% had symptoms suggestive of cystitis. All were cultured for the presence of Candida albicans. One hundred sixty-one (73.2%) were also tested for vaginal IgE and prostaglandin E2 (PGE2); 72 (32.7%) had a vulvar biopsy performed as well.
Results: A wide range of variants were noted: 53 (24.1%) had a human papilloma virus (HPV) infection, 25 (11.4%) had a Candida vulvovaginitis, 43 (19.5%) had a vaginal allergy, 15 (6.8%) had vaginal PGE2 present, 14 (6.4%) had elevated urinary oxalate excretion, and 29 (13.2%) had a variety of diagnosed variants. In 81 (36.8%) no underlying diagnosis was made. This understates the numbers and varieties of vulvar vaginal diagnoses, for not all patients received a vaginal fluid analysis, a vulvar biopsy, or a 24 h urine screen for oxalates. A variety of medical and operative interventions was used. Symptoms were relieved in 65.9% of patients. The degree of sueeess varied. Successful outcomes were achieved in 14.3% of patients using a low oxalate diet and calcium citrate supplementation, 16% with anti-Candida treatment, 48.1% with antihistamines, 77% with vulvar injection of interferon, 83% with operative removal of inflamed vulvar tissue, and a posterior colporrhaphy used to cover the cutaneous defect.
Conclusions: The diagnosis of vulvar vestibulitis is easy to make. An etiology for this chronic condition will not be achieved in every patient. A majority of patients can get relief by a variety of medical and operative interventions.
PMCID: PMC2364514  PMID: 18476106
5.  Immune Recognition of the 60kD Heat Shock Protein: Implications for Subsequent Fertility 
The 60kD heat shock protein (hsp60) is a highly conserved protein and a dominant antigen of most pathogenic bacteria. In some women, chronic or repeated upper genital tract infections with Chlamydia trachomatis, and possibly with other microorganisms, induces immune sensitization to epitopes of hsp60 that are present in both the microbial and human hsp60. Once a woman becomes sensitized to these conserved epitpes, any subsequent induction of human or bacterial hsp60 expression will reactivate hsp60-sensitized lymphocytes and initiate a pro-inflammatory immune response. Hsp60 is expressed during the early stages of pregnancy, by both the embryo and the maternal decidua. We examined, therefore, whether women who were sensitized to hsp60 experienced less successful pregnancy outcomes compared to women who were not sensitized to this antigen. In women undergoing in vitro fertilization (IVF), the presence of cervical IgA antibodies reactive with the C. trachomatis hsp60 correlated with implantation failure after embryo transfer. Further analysis revealed that an immunodominant epitope for these IgA antibodies was an hsp60 epitope shared between C. trachomatis and man. In subsequent studies of women not undergoing IVF, cervical IgA antibodies to the human hsp60 were identified in 13 of 91 reproductive age women. This antibody was most prevalent in those women with a history of primary infertility (p = 0.003). In addition, cervical anti-hsp60 IgA correlated with the detection of the pro-inflammatory cytokines interferon-γ (p = 0.001) and tumor necrosis factor-α (p = 0.02) in the cervix. Conversely, women with proven fertility had the highest prevalence of the anti-inflammatory cytokine, interleukin 10, in their cervices (p = 0.001). In an analysis of serum samples in a third study, women with a history of two or more consecutive first trimester spontaneous abortions had a higher prevalence (p = 0.01) of IgG antibodies to the human hsp60 (36.8%) than did age matched fertile women (11.1%) or women with primary infertility (11.8%). Immune sensitization to epitopes expressed by the human hsp60 may reduce the probability of a successful pregnancy outcome due to reactivation of hsp60-reactive lymphocytes, induction of a pro-inflammatory cytokine response and interference with early embryo development and/or implantation.
PMCID: PMC2364488  PMID: 18476087
6.  Immune Regulation in the Male Genital Tract 
Spermatozoa are not produced until puberty, long after the establishment of tolerance to self-antigens. Therefore, sperm-specific antigens are immunogenic in men. Most men, however, do not produce antibodies to their own gametes. Development of mechanisms to prevent or limit autoimmune responses to spermatozoa were essential for preservation of reproductive capacity. Tight junctions between adjacent Sertoli cells, as part of the blood-testis barrier, prevent sperm-immune cell contact. In some portions of the genital tract this barrier is thin or incomplete. Immune mechanisms have evolved to actively suppress the autoimmune response to spermatozoa within the genital tract. Unlike in the circulation where CD4+ helper T lymphocytes predominate, CD8+ suppressor/cytotoxic T lymphocytes are the most prominant T cells in the epididymis and vas deferens. In addition, spermatozoa suppress pro-inflammatory lymphocyte immune responses, possibly by inducing production of anti-inflammatory cytokines. Antisperm antibody production is induced in the male genital tract when a local infection or disruption in the genital tract physical barrier leads to an influx of CD4+ T cells. In response to induction of a productive immune response, two additional mechanisms downregulate humoral immunity within the genital tract. T lymphocytes possessing the γσ form of the antigen receptor (γσ T cells) are concentrated in the male genital tract and in semen. These cells become activated and proliferate in men with evidence of sperm autoimmunity. Activated γσ T cells inhibit production of antibodies by activated B lymphocytes, thereby limiting antisperm antibody production. Heat shock proteins (hsps) are also present in semen in association with infection and antisperm antibody formation. Hsp gene transcription leads to inhibition of transcription of the genes coding for pro-inflammatory cytokines and, conversely, to activation of γσ T cells. Activated γσ T cells also promote hsp synthesis. The mechanisms to inhibit immunity to sperm may hinder effective immune elimination of microoganisms in the male genital tract.
PMCID: PMC2364484  PMID: 18476083
7.  Immune Pathogenesis of Asymptomatic Chlamydia trachomatis Infections in the Female Genital Tract 
Chlamydia trachomatis (CT) infections of the female genital tract, although frequently asymptomatic, are a major cause of fallopian-tube occlusion and infertility. Early stage pregnancy loss may also be due to an unsuspected and undetected CT infection. In vitro and in vivo studies have demonstrated that this organism can persist in the female genital tract in a form undetectable by culture. The mechanism of tubal damage as well as the rejection of an embryo may involve an initial immune sensitization to the CT 60 kD heat shock protein (HSP), followed by a reactivation of HSP-sensitized lymphocytes in response to the human HSP and the subsequent release of inflammatory cytokines. The periodic induction of human HSP expression by various microorganisms or by noninfectious mechanisms in the fallopian tubes of women sensitized to the CT HSP may eventually result in tubal scarring and occlusion. Similarly, an immune response to human HSP expression during the early stages of pregnancy may interfere with the immune regulatory mechanisms required for the maintenance of a semiallogeneic embryo.
PMCID: PMC2364440  PMID: 18476043
8.  Pregnancy Outcome Following Pelvic Infection 
To determine whether a previous pelvic infection has an effect on the outcome of a subsequent pregnancy, we identified women with a diagnosis of pelvic inflammatory disease (PID), amnionitis, and postpartum or postabortal endometritis-salpingitis by a retrospective chart review of all patients admitted to the Department of Obstetrics and Gynecology at The New York Hospital-Cornell Medical Center between 1975 and 1977 and between 1985 and 1988. Antimicrobial regimens effective against Chlamydia trachomatis were initiated in 1985. Controls were randomly selected patients presenting during the same time period for routine examinations who had normal Pap smears and no infections. Both groups were comparable for age, race, gravity, and parity. Differences were evaluated by chi square analysis, using the Yates correction factor. We identified 183 women with a history of the above infections who subsequently conceived, and 82 controls. There were no differences in outcome between the two index groups. Term vaginal deliveries occurred in 14.2% of the women with a prior pelvic infection and in 56% of the controls (P < 0.001). Among the 97 women who had had PID, 21 (21.6%) had a spontaneous abortion in the subsequent pregnancy, as opposed to 6 (7.3%) of the controls (P = 0.013). In addition, eight of the women with PID (but no controls) went into preterm labor (P = 0.021). An increased incidence of preterm labor (P = 0.001) was also observed in women with a history of amnionitis. A history of endometritis was not associated with an increased prevalence of abnormal outcome in subsequent pregnancies. PID and amnionitis may adversely affect the outcome of subsequent pregnancies.
PMCID: PMC2364674  PMID: 18476199

Results 1-8 (8)