Many women get only one urinary tract infection (UTI) in their lifetime, but others get repeat episodes. Recurrent UTI is associated with inflammatory diseases such as rheumatoid arthritis and type 1 diabetes. Vaginal infections, especially bacterial vaginosis, are also associated with UTI. What makes some women susceptible?
A research team based in Canada wants to find out. For their initial study, they identified 22 women with recurrent UTI and 17 healthy controls. They examined blood, urine, and vaginal samples taken at a time when each subject was free of UTI symptoms. Their findings include significant differences between the immune system characteristics and vaginal flora of women with and without recurrent UTI.
Genetic differences appear to be part of the problem. A family history of UTI is a risk factor, and the blood tests showed abnormalities in the immune systems of women with recurrent UTI. These women may have a chronic, low-grade infection. When the symptoms of UTI return, they are typically caused by the same strain of bacteria. Chronic infection is associated with chronic inflammation, which can explain the association with rheumatoid arthritis and type 1 diabetes.
Another problem is the types of bacteria that populate the vaginal walls. The bacteria that cause UTI generally start in the intestines. A decisive step toward UTI is colonization of the vagina by uropathogenic species. The vaginal samples in the Canadian study showed that healthy women without recurrent UTI have vaginal flora dominated by Lactobacillus bacteria. The most common species observed in the Canadian study were L. iners, L. crispatus, and L. gasseri. For women with recurrent UTI, the vaginal samples showed significantly more bacteria with potential to cause infections, including Staphylococcus, Clostridium, Fusobacterium, and Streptococcus strains.
Based on these findings, the Canadian team concluded that:
1. Lactobacillus bacteria in the vagina have a protective effect against UTI.
2. Susceptibility to repeat infections is associated with a defect in translating the immune response into an effective defense by T-cell activity.