The polymicrobial hypothesis of bacterial vaginosis causation: a reassessment.

The cause of bacterial vaginosis remains controversial. The two leading hypotheses are that Gardnerella vaginalis is the specific aetiologic agent versus the polymicrobial hypothesis that G. vaginalis acts in concert with other bacteria, principally anaerobes, to produce the disease. Here we reassess the prevailing polymicrobial hypothesis, finding it conceptually problematical. No host initiating factors as postulated have been identified, nor is there conclusive evidence that G. vaginalis lacks diagnostic specificity for the disease. The polymicrobial hypothesis, presupposing a unique disruption of vaginal microecology, is inconsistent with the epidemiological profile of the syndrome, which is that of a sexually transmitted disease. The epidemiological and clinical similarities between bacterial vaginosis and trichomoniasis suggest a similar pathogenetic process; i.e., primary causation by a specific agent, with secondary anaerobic activation and resultant amine production.

Vaginitis emphysematosa. A report of four cases.

It has been hypothesized that vaginitis emphysematosa is a manifestation of trichomonal or Gardnerella infection. In support of this etiologic concept, four cases of the disorder are described showing the apparent curative effect of treating the associated infection. The linkage of these and other reported cases with conditions of impaired immunity suggests that immunologic factors are involved in the pathogenesis.

Anovaginal fistula presenting as a vulvar ulcer. A report of two cases in postmenopausal women.

Two women in their early menopausal years were evaluated for a persistent ulcerative lesion located on the vulvar vestibular mucosa at the fourchette. In both cases the ulcer proved to be the vaginal orifice of a small anovaginal fistula of probable cryptogenic origin. Anovaginal fistula should be considered a possible diagnosis when an otherwise unexplained ulcerative lesion is encountered at or near the vaginal introitus.

Vaginitis. Reducing the number of refractory cases.

Therapeutic failure in vaginitis can be minimized if all cases are properly diagnosed and specific therapy is given. Use of wet mounts combined with liberal use of cultures, especially for Corynebacterium vaginale, should result in an accurate diagnosis in over 90% of cases. Treatment of choice for candidiasis is nystatin or miconazole nitrate applied topically. For trichomoniasis, metronidazole should be given orally to both sexual partners. Ampicillin, cephalexin, or cephradine are recommended for C vaginale infection.

Corynebacterium vaginale (Haemophilus vaginalis) in women with leukorrhea.

Corynebacterium vaginale was recovered from vaginal-cervical swab specimens in 164 of 288 women with leukorrhea and in four of 30 women without signs or symptoms of lower genital tract infection. The amount and character of the leukorrhea observed in association with C. vaginale infection were variable; in typical cases the discharge had the appearance of a thin paste. In a series of 100 patients studied to determine the apparent causes of leukorrhea, noninfectious causes were inferred in seven patients and no cause ascertained in six. Candida or other yeasts, C. vaginale, and Trichomonas vaginalis were identified alone or in combination in 87 patients; 53 had yeasts, 35 had C. vaginale, and 15 had T. vaginalis.

Epidemiologic characteristics of women infected with Corynebacterium vaginale (Haemophilus vainalis).

In a group of 184 women infected with Corynebacterium vaginale (Haemophilus vaginalis), 34% over age 30 were divorced or separated and 8% gave a history of induced abortion. Fifty-one percent were taking an oral contraceptive drug, as compared to 36% of 140 women in a control group. Various sexually transmitted diseases were diagnosed either concomitantly or at another time in 52% of women in the study group and 38% of those in the control group. The rate of cervical neoplasia (invasive carcinoma, carcinoma in situ, and dysplasia) was 13.6% in the study group and 5.7% in the control group, the rate in the study group being several times that in the general population. These and other available epidemiologic data support the conclusion that C vainale is transmitted sexually.

Viruses and cancer of the lower genital tract.

The importance of viruses as oncogenic agents in animals is well established. Recent work suggests that viruses may also be etiologically related to some human cancers. Herpes simplex virus type 2 (HSV-2) and the genital wart virus are prime suspects in carcinomas involving the female lower genital tract. In particular, a close association has been found between HSV-2 infection and cervical neoplasia in cytohistopathologic and seroepidemiologic studies. Preliminary results of prospective studies show further that women with genital herpetic infection are at increased risk of developing cervical neoplasia. Additional studies are also in progress on animal models, including subhuman primates, and efforts continue in the attempt to confirm the presence of viral genetic material or its expression in human cervical cancer cells. The possibility that human wart viruses have an oncogenic potential is suggested by clinicopathologic and electron microscopic observations. Further research is needed to ascertain the precise role of viruses in genital cancer.

[The present status of the theory of induction of carcinoma of the cervix in man by herpes virus (author's transl)]. / Der augenblickliche Stand der Herpesvirus-Zervixkarzinom-Theorie

A large body of evidence has accumulated during the past decade suggesting that HSV-2 infection of the cervix may be a major precursor of cervical carcinoma. A brief review of the more significant findings to date is presented.

Epidemiological studies relating genital herpetic infection to cervical carcinoma.

PIP: Epidemiological studies relating genital herpetic infection to cervical carcinoma are reviewed. The high frequency of herpes simplex virus type 2 (HSV-2) antibodies in young women (21 years or younger) with cervical carcinoma in situ and in women with dysplasia or carcinoma in situ, matched for various sexual attributes to control women, provide support for a causal relation. However, various laboratory, histopathological, and statistical problems associated with all epidemiological studies do not yet permit a firm conclusion as to the etiological role to the genital virus in cervical carcinogenesis. With the use of herpes-related cancer antigens or purified HSV-2 type-specific antigens, and with the possible development of protective HSV-2 vaccines, the application of epidemiological approaches may be necessary to provide the most finite evidence of causality.^ieng

Relation of cytohistopathology of genital herpesvirus infection to cervical anaplasia.

PIP: Cytological changes resulting from herpes simplex virus (HSV) were detected in 673 (.26%) of 279,589 cervicovaginal smears from an indigent hospital population. Histopathological features of HSV infection were observed in 45 of 126 biopsies taken from the group of 673. Most of the lesions were multifocal and were located on the squamocolumnar junction; diagnostic cells were found at the base of normal squamous epithelium or at the surface of anaplastic epithelium. The cytological and histological changes and diagnostic procedures for HSV infection are given in detail; cytological detection is 2/3 as sensitive as viral isolation. The presence of anaplasia in about 2/3 of the 673 HSV cases either before or at the same time as the detection of HSV suggests that anaplastic tissue is more susceptible to HSV infection. However, serological evidence showing HSV antibodies before the onset of cervical anaplasia, the recurring nature of HSV, and epidemiological evidence showing the age of acquisition of HSV to be 5-30 years before diagnosis of cervical cancer are all compatible with the view that HSV causes cervical cancer.^ieng