Vaginal Microecology and the Pathogenesis of Urinary Tract Infections
نویسنده
چکیده
Vaginal colonisation with E. coli appears to be an important prerequisite for the development of UTI. Whereas colonisation with P fimbriated strains has been clearly shown to predispose to pyelonephritis, virulence factors which predispose to cystitis have not been so clearly identified. Several host genetic and behavioural factors have been found to be associated with increased colonisation with E. coli and other uropathogens and subsequent UTI. Such factors include having the blood group antigen nonsecretor phenotype which is associated with increased E. coli vaginal colonisation, using spermicidal contraceptive products which increase E. coli vaginal colonisation probably through adverse effects on lactobacilli, exposure to certain antimicrobials which facilitate coliform colonisation through adverse effects on the anaerobic flora, and use of oestrogen products which appear to enhance E. coli adherence to vaginal and uroepithelial cells. Increased knowledge about these and other factors which influence the vaginal microecology is important if we are to develop safe and effective strategies to prevent UTI. For example, we can expect a reduction in the risk of vaginal colonisation with uropathogens and subsequent UTI by a decrease in the use of spermicide-containing products and use when appropriate of antimicrobials that have less impact on the anaerobic rectal and vaginal flora, such as trimethoprim, trimethoprimsulfamethoxazole, nitrofurantoin, or fluoroquinolones. In postmenopausal women, topical oestrogens clearly help normalise the flora and reduce the risk of recurrent UTIs. Further research is needed to evaluate the feasibility and effectiveness of re-establishing vaginal colonisation with lactobacilli, especially H2O2-producing strains, and whether recolonization can reduce the risk of UTI. In addition, a better understanding of the vaginal microecology and immunity is necessary in order develop a safe and effective vaccine to prevent UTI.
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Cloning of synthetic gene including antigens against Urinary Tract Infections in pET28a+ vector
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