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Male guinea pigs were infected with the chlamydial agent of guinea pig inclusion conjunctivitis (GPIC) by intraurethral injection of chlamydiae or by placement of a drop of chlamydial suspension on the meatus of the extruded penis. Transient urethritis and cystitis were observed in animals infected by either method. The production of cystitis by the drop-on technique indicated that chlamydiae are able to ascend the urethra and that the bladder may be a target organ of chlamydial infection. When infected animals were immunosuppressed with cyclophosphamide, the number of guinea pigs with cystitis was increased, and chlamydiae could be detected in the bladder for as long as 50 days after infection. In contrast, GPIC was not detected in the bladders of untreated animals after day 18.

Female guinea pigs were treated daily with 1 mg of beta-estradiol-3-benzoate intramuscularly beginning 14 days before intravaginal inoculation with the chlamydial agent of guinea pig inclusion conjunctivitis and continuing during the course of the infection. Treatment with estradiol was found to markedly influence the course of genital infection with the chlamydial agent of guinea pig inclusion conjunctivitis, producing infections of greater intensity and longer duration than those in control animals. Moreover, pathogenesis was altered in that ascending infection was observed, resulting in endometritis, cystic salpingitis, and cystitis. Infection in the controls was limited to the cervix and vagina. Estradiol treatment increased the apparent number of infected cells in the cervix and vagina as detected by histopathology and immunofluorescent staining. Humoral and cell-mediated immune responses to the chlamydial agent of guinea pig inclusion conjunctivitis were comparable in estradiol-treated and untreated animals. These data indicate that hormonal manipulation may have profound effects on the course of chlamydial genital infections.

Female guinea pigs were given daily doses of a combination of oral contraceptive (OC) agents, consisting of mestranol and norethynodrel suspended in sesame oil or distilled H2O, and were infected in the genital tract with the chlamydial agent of guinea pig inclusion conjunctivitis (GPIC). Counts of chlamydial inclusions in cells of vaginal smears collected during infection, showed prolongation and enhancement of infection in OC-treated animals as compared with controls. Appearance of IgG and IgA antibodies to GPIC in genital secretions, as determined by enzyme-linked immunosorbent assay (ELISA), was also delayed in OC-treated animals as compared with controls. OC-treated infected animals were killed on days 15 and 43, and gross pathological evidence for ascending infection culminating in salpingitis was found in all of five and four of five animals, respectively. On the other hand, among untreated infected controls on each sacrifice day, only one of five animals had any evidence for ascending infection. Chlamydiae were detected by light and electron microscopy in fallopian tube tissue collected on day 15 following OC-treatment but not in tissue from control animals.

Female guinea pigs were experimentally infected in the genital tract with the strain of Chlamydia psittaci that causes guinea pig inclusion conjunctivitis. Chlamydiae were found frequently in superficial squamous epithelial cells of the exocervix, along with heavy involvement at the squamocolumnar junction. In this zone chlamydiae were observed in columnar cells, but inflammation and chlamydial inclusions were not observed in true endocervical epithelium. These observations were supported by results of immunofluorescence microscopy. Electron micrographs revealed typical chlamydiae within surface epithelial cells at the squamocolumnar junction; various stages of the growth cycle (elementary, reticulate, and intermediate bodies) were also present. Cytopathologic features were not remarkable, but peripheral distribution of organelles, rarefaction of the cytoplasm, and loss of microvilli were observed.

A new animal model for the study of genital infections caused by Chlamydia trachomatis has been developed. Female mice were successfully infected after intravaginal inoculation with the C. trachomatis agent of mouse pneumonitis. Evidence for infection was obtained by detection of chlamydial inclusions in smears of cervical scrapings treated with Giemsa stain. Chlamydiae were observed in sections of cervical tissues examined by light and electron microscopy as well as by immunofluorescence microscopy. An antibody response to the agent of mouse pneumonitis was also demonstrated in sera after infection. The mouse model of genital infection with the agent of mouse pneumonitis offers an opportunity to investigate many questions related to pathogenesis and immunity associated with C. trachomatis genital infections.