Experimental pelvic inflammatory disease provoked by Chlamydia trachomatis and Mycoplasma hominis in grivet monkeys.
Pelvic inflammatory disease was produced by inoculation with Mycoplasma hominis and Chlamydia trachomatis directly into the fallopian tubes of grivet monkeys. The effects of various routes of infection were examined. The method of inoculation with the infecting agent influenced the resulting clinical spectrum. In these monkeys significant changes in humoral antibodies occurred with inflammation caused by both M. hominis and C. trachomatis. Development of cellular antibodies against M. hominis could be demonstrated in all experimentally infected monkeys, whereas no such antibodies could be detected in monkeys with chlamydia salpingitis. M. hominis in female grivet monkeys may spread from the cervix or the uterine cavity, probably via blood vessels and lymphatics, producing parametritis and "exosalpingitis." C. trachomatis may spread from the cervix via the uterine mucosa, producing endosalpingitis with destruction of the epithelium. The infection caused by M. hominis in the genital tract of female grivet monkeys resembles "nongonococcal" salpingitis while C. trachomatis produces infection resembling "gonococcal" salpingitis.
D000818:Animals; D000907:Antibodies, Bacterial; D002692:Chlamydia trachomatis / Q000276:immunology; D002522:Chlorocebus aethiops; D004195:Disease Models, Animal; D005260:Female; D007111:Immunity, Cellular; D008219:Lymphogranuloma Venereum; D009174:Mycoplasma / Q000276:immunology; D009175:Mycoplasma Infections; D000292:Pelvic Inflammatory Disease / Q000209:etiology* / Q000276:immunology / Q000382:microbiology
D000907:Antibodies, Bacterial