GENITAL AND SYSTEMIC IMMUNE-RESPONSES IN A MURINE MODEL OF TRITRICHOMONAS-FETUS INFECTION

A reliable laboratory animal model would be useful for the study of im mune responses to trichomoniasis, a sexually transmitted disease of hu man beings and cattle. Murine models are available, but pretreatment w ith estrogen is used, which may influence immune responses. To evaluat e whether vaginal trichomoniasis could be established in nonestrogeniz ed mice ana to define the immune responses associated with the infecti on. CD1 and BALB/c mice were studied with or without estrogen treatmen t prior to inoculation with Tritrichomonas foetus. Tritrichomonas foet us was cultured from the vagina and uterus of both estrogen treated an d untreated control mice for up to 26 wk. The infection was sustained better in BALB/c than in CD1 mice, suggesting that the former strain w as most susceptible. In CD1 mice, infection was sustained less well in estrogen-treated than in untreated control mice, but there was no dif ference between treatment groups of BALB/c mice. IgA and Ige antibodie s in vaginal secretions. uterine secretions, and serum specific for a surface antigen of T. foetus (TF1.17) were measured by enzyme-linked i mmunosorbent assay. In infected CD1 mice, vaginal IgA and IgG antibodi es were detected by 8 wk postinoculation (PI). In infected BALB/c mice , vaginal IgA and Ige antibodies were detected by 12 wk PI. Uterine Ig G responses predominated over IgA in estrogen-treated and untreated CD 1 and BALB/c mice. There were high levels of IgG, but relatively no Ig A in the sera of CD1 and BALB/c mice. Overall, the highest IgA respons e was in the vaginal secretions of infected CD1 mice, and some animals of this strain cleared the infection. These results show that a chron ic trichomonad infection was established in mice without prior treatme nt with estrogen. The infection was associated with antibody responses in reproductive secretions and serum. This animal model will be usefu l in studying immunization to protect against trichomoniasis in mice n ot immunocompromised by estrogen.