MOUSE INTRAVAGINAL INFECTION WITH TRICHOMONAS-VAGINALIS AND ROLE OF LACTOBACILLUS-ACIDOPHILUS IN SUSTAINING INFECTION

Recent work with a mouse model of Trichomonas vaginalis infection indicated that only 25% of mice harbor Lactobacillus spp. and that T. vaginalis infection rates fall rapidly after 7 days postinfection. In women infected with T. vaginalis, there is a disruption of the Lactobacillus population, which usually predominates. In an attempt to establish a better mouse intravaginal infection that resembles human disease, we established Lactobacillus acidophilus in estrogenized BALB/c mice. T. vaginalis was then inoculated intravaginally into mice previously infected with L. acidophilus and into mice in an untreated group. From 52 mice, 50-mu-l vaginal washes were collected, cultured, and examined daily for live trichomonads after inoculation. Although initial infectivity in the two groups was comparable (79 to 83%), L. acidophilus-infected mice showed greater duration of infection. At day 24 postinfection, 69% of L. acidophilus-infected mice were still infected with T. vaginalis compared with only 11% of untreated mice (P = 0.002). The addition of L. acidophilus did not significantly alter the resident mouse vaginal flora. By the addition of L. acidophilus, the mouse will be valuable for studying factors involved in T. vaginalis infectivity and pathogenicity.