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Year : 2012  |  Volume : 28  |  Issue : 2  |  Page : 158
 

New paradigms of urinary tract infection


Medical Microbiology, Postgraduate Institute of Medical Education & Research, Sector-12, Chandigarh, India

Date of Web Publication13-Jul-2012

Correspondence Address:
Manisha Biswal
Assistant Professor, Medical Microbiology, Postgraduate Institute of Medical Education & Research, Sector-12, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Biswal M. New paradigms of urinary tract infection. Indian J Urol 2012;28:158

How to cite this URL:
Biswal M. New paradigms of urinary tract infection. Indian J Urol [serial online] 2012 [cited 2023 Mar 30];28:158. Available from: https://www.indianjurol.com/text.asp?2012/28/2/158/98456


A growing number of studies indicate that many recurrent urinary tract infections (UTIs) may in effect be relapses caused by the resurgence of intracellular bacterial reservoirs that can persist for many weeks to months within the urothelium. In the recent years, the ability of uropathogenic  Escherichia More Details coli (UPEC) to form both extra- and intracellular biofilm-like communities within the bladder has been proven beyond doubt. Bacteria in biofilms offer high resistance to the action of antibiotics compared to bacteria in planktonic stage. UPEC also persist inside host urothelial cells in a more quiescent state, sequestered within late endosomal compartments. This property, in addition, renders them to antibiotics that primarily target actively replicating bacterial cells.

Under experimental conditions bladder cell-culture assays, only a few antibiotics, including nitrofurantoin and the fluoroquinolones ciprofloxacin and sparfloxacin, have been shown to be able to eliminate intracellular bacteria. Such findings have received corroborative evidence in mice UTI model systems in which although these antibiotics reached concentrations in the urine specimens that far exceeded minimal inhibitory doses, UPEC reservoirs in bladder tissues were not effectively eradicated. The persistence of UPEC within the bladder is probably a result of a combination of biofilm formation, entry of UPEC into a quiescent or semiquiescent state within host cells, as well as the stalwart permeability barrier function associated with the bladder urothelium. These and related observations indicated that recurrent UTIs in many individuals, including those who receive antibiotic treatments, may in actuality be relapses caused by the resurgence of UPEC from intracellular bacterial reservoirs. Epidemiological studies lend credence to this possibility, demonstrating that the bacteria responsible for recurrent UTIs are identical to the microbes that caused the initial acute infections in a significant proportion of patients. In light of these findings, it has been suggested that more penetrant antibiotics might better eliminate UPEC reservoirs from the bladder and consequently reduce the incidence of chronic and recurrent UTIs. The authors of the paper entitled "New Paradigms of Urinary Tract Infections: Implications for Patient Management" have reviewed the new insights into the mechanism and role of UPEC in UTI and the implications of therapy thereof.




 

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