A urinary tract infection (UTI) (also known as acute cystitis or bladder infection) is an infection of the urinary tract. In the lower urinary tract it is called cystitis (a bladder infection), and in the upper urinary tract it is known as pyelonephritis (a kidney infection).
When having UTI at the lower urinary tract, the most common symptoms are: painful urination, urgency and/or frequent urination. For a UTI in the upper urinary tract, the same symptoms can be experienced, in addition to fever and flank pain.
- UTIs in women are mainly due to an emergence of commensal uropathogens such as E. coli, Proteus sp., Klebsiella sp. andPs. aeruginosa [CHAN 1985], [REID 1990] but E. coli is the main incriminated bacterium. A correlation was established between its port in the urethra and a bladder infection [REID 1990]. From the rectum, the uropathogens go back up to the vagina and then to the urethra and the bladder [REID 2006].
- The susceptibility of some women to urinary tract infections could be genetic, but few researchers study their immune status.
- CADIEUX P.A. et al. explained the case of indirect development of a urinary tract infection by the bacterium Prevotella bivia generally responsible for bacterial vaginosis. Indeed, this bacterium produces amine which increases pH. Thus, the lactic acid synthesized by lactobacilli and which initially has an antibacterial activity, becomes a carbon source for E. coli UPEC and Prevotella. This could explain some cases of urinary tract infections despite a high number of lactobacilli in the vagina [CADIEUX 2009].
Adhesion of the uropathogen E.coli
By using the techniques of vital staining of uroepithelial cells and mucopolysaccharides which form the mucus layer, it has been shown that bacteria adhere to mucopolysaccharides [REID 1982].
The uroepithelial cells can be isolated from urine and their susceptibility to the adhesion of E. coli varies during the menstrual cycle and during pregnancy [REID 1983]. In fact, the cells in urine collected at t=10 days of the menstrual cycle (before ovulation) are more receptive to uropathogens [CHAN 1985].
The adhesion of certain E. coli strains is increased when uroepithelial cells are covered with mucus. However, other strains adhere indifferently to cells covered with mucus or not, which suggests that two different mechanisms ensure the adhesion of E. coli [REID 1983].
The strains of E. coli with adhesins insensitive to the addition of mannose are those of serotype O regularly found in urinary tract infections.
Electron microscopy confirms that 67% of these strains also have fibrils, but strains without fibrils adhere as effectively to uroepithelial cells [CHAN 1984].
A labelling technique of E. coli by fluorescent antibodies was developed to study the in vitro adhesion of this germ to uroepithelial cells and in vivo in women with urinary tract infections. Similar results can be obtained with methylene blue, but they depend on the experience of the examiners.
The authors believed that patients with symptoms of urinary tract infections, but whose urine contains less than 103 cells /ml, can be examined to detect the presence of E. coli by this method. This marking can also be used to study bacterial colonisation in the mucous membranes and catheters. To be close to reality, the colonisation experiments are performed in urine [REID 1984].
In vitro, the flora of the urinary tract – that is to say isolated from cervical, vaginal and distal urethra surfaces – of healthy women exercises an antagonism of adhesion of uropathogens to uroepithelial cells [REID 1985] but its inhibitory capacity varies during the menstrual cycle [CHAN 1985, REID 1983].
It has been shown that antibodies are produced against uropathogens but they do not provide effective protection. In general, dendritic cells are mobilized in the urinary epithelium. They present bacterial antigens to T cells for the development of an immune response against a new infection: is there deficiency of adaptive immune responses provided by lymphocytes in women with recurrent urinary tract infections? To answer this question, vaginal, urinary and blood samples were collected during the period of remission of 22 women with recurrent urinary tract infections and 17 healthy women (control group). In women with recurrent urinary tract infections (UTI), blood monocytes and myeloid dendritic cells produce a lot of IL-12 but, paradoxically, the polarization of T cells is not observed; therefore, it seems that this synthesis of IL-12 does not result in an activation of T cells, a phenomenon usually observed in healthy women. In the vaginal mucosa, the rate of VEGF (Vascular Endothelial Growth Factor) involved in tissue repair is lower in women with recurrent urinary tract infections than in healthy women. Few sick women have detectable levels of MCP-1 cytokine involved in the mobilization of monocytes and dendritic cells. Even during the period of remission, the Nugent score of women with recurrent UTIs is higher than that of healthy women (4.6 versus 1.7). The authors concluded that a deficient immune system associated with abnormal vaginal microbiota could contribute to increased susceptibility to urinary tract infections [KIRJAVAINEN 2009].
Most of the patients suffering from urinary tract infections (UTI) consulting a doctor are prescribed low-dose antibiotics for a long time. However, a certain resistance of E. Coli to amoxicillin was observed and the study of the vaginal flora showed that it is not restored after an antibiotic therapy [REID 1990]. Therefore, recurrences are frequent.
Antibiotic therapy helps eradicate uropathogens contained in the urine but uroepithelial cells remain receptive to the adhesion of pathogens during and after treatment. The consequence is a re-infection of the urinary tract and, thus, relapses [REID 1988]. Uropathogens predominate in the urethra and the vaginal orifice [REID 1990]. In addition, the coaggregation of uropathogens promotes the formation of biofilms which give bacteria the resistance to antibiotics and mechanisms of host defence [REID, MCGRARTY et al. 1990] [REID, BRUCE et al. 1990].
Vaccination was developed for germs other than E. coli. Thus, according to Professor Reid, the use of probiotics could be a new approach in the prevention of recurrent UTIs by restoring the urovaginal flora [REID 1999].
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REID G., McGROARTY J.A., DOMINGUE P.A.G., CHOW A.W., BRUCE A.W., EISEN A. & COSTERTON J.W. Coaggregation of urogenital bacteria in vitro and in vivo. Current Microbiology, 1990, 20, 47-52.
REID G., BRUCE A.W., COOK R.L. & LLANO M. Effect of urogenital flora of antibiotic therapy for urinary tract infection. Scand. J. Infect. Dis., 1990, 22(1), 43-47.
REID G. & BRUCE A.W. Probiotics to prevent urinary tract infection: the rationale and evidence. World J. Urol., 2006, 24(1), 28-32.
REID G., BRUCE A.W. & BEHESHTI M. Effect of antibiotic treatment on receptivity of uroepithelial cells to uropathogens. Can. J. Microbiol., 1988, 34, 3, 327-331.
REID G., BRUCE A.W., McGROARTY J.A., CHENG K.J. & COSTERTON J.W. Is there a role for Lactobacilli in prevention of urogenital and intestinal infections? Clinical Microbiology Review, 1990, 3, 4, 335-344.
REID G. Potential preventive strategies and therapies in urinary tract infection. World J. Urol., 1999, 17(6), 359-363.
CADIEUX P.A., BURTON J.P., DEVILLARD E. & REID G. Lactobacillus by-products inhibit the growth and virulence of uropathogenic Escherichia coli. Journal of Physiology and Pharmacology, 2009, 60, suppl.6, 13-16.
KIRJAVAINEN P.V., PAUTLER S., BAROJA M.L., ANUKAM K., CROWLEY K., CARTER K. & REID G. Abnormal immunological profile and vaginal microbiota in women prone to urinary tract infections. Clinical and Vaccine Immunology, 2009, 16, 1, 29-36.
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