Pathogenesis of urinary tract infection--experimental studies of vaginal resistance to colonization

Abstract

The review summarizes studies of vaginal colonization resistance against Escherichia coli in a primate model. The genital flora surrounding the urethral orifice exerts a strong colonization resistance. Amoxicillin profoundly disturbs the normal vaginal microflora, reduces its adherence to vaginal epithelial cells in vivo and promotes a persistent vaginal E. coli colonization. Certain cephalosporins may have a similar effect. The induced ecological changes mimic those seen in patients with recurrent urinary tract infections (UTI). Amoxicillin also promotes the spread of E. coli from rectum to vagina, which may be of clinical significance. Trimethoprim and nitrofurantoin do not have these effects. The natural colonization resistance could not clearly be correlated with the presence of lactobacilli, which were only transiently reduced by amoxicillin. The colonization resistance against E. coli could only partly be restored by vaginal instillation of lactobacilli, but was fully restored by flushing of the whole vaginal flora from a healthy monkey. Clinical observations suggest that accumulation of E. coli around the urethral orifice increases the risk of UTI. We conclude that antibiotics and other compounds that interfere with the normal genital flora may increase the risk of UTI. This should influence the choice of antibiotics in the treatment of UTI.