Urinary Tract Infection Research Today is a free monthly online journal that collates and summarizes the latest research about Urinary Tract Infection, including details on uti, causes, prevention, diet, treatment.

Utilization of an intracellular bacterial community pathway in Klebsiella pneumoniae urinary tract infection and the effects of FimK on type 1 pilus expression.

Rosen DA, Pinkner JS, Jones JM, Walker JN, Clegg S, Hultgren SJ

Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA.

Klebsiella pneumoniae is an important cause of urinary tract infection (UTI), but little is known about its pathogenesis in vivo. The pathogenesis of the K. pneumoniae cystitis isolate TOP52 was compared to that of the uropathogenic Escherichia coli (UPEC) isolate UTI89 in a murine cystitis model. Bladder and kidney titers of TOP52 were lower than those of UTI89 at early time points but similar at later time points. TOP52, like UTI89, formed biofilm-like intracellular bacterial communities (IBCs) within the murine bladder, albeit at significantly lower levels than UTI89. Additionally, filamentation of TOP52 was observed, a process critical for UTI89 evasion of neutrophil phagocytosis and persistence in the bladder. Thus, the IBC pathway is not specific to UPEC alone. We investigated if differences in type 1 pilus expression may explain TOP52's early defect in vivo. The type 1 pilus operon is controlled by recombinase-mediated (fimE, fimB, and fimX) phase variation of an invertible promoter element. We found that K. pneumoniae carries an extra gene of unknown function at the 3' end of its type 1 operon, fimK, and the genome lacks the recombinase fimX. A deletion mutant of fimK was constructed, and TOP52 Delta fimK had higher titers and formed more IBCs in the murine cystitis model than wild type. The loss of fimK or expression of E. coli fimX from a plasmid in TOP52 resulted in a larger phase-ON population and higher expression levels of type 1 pili and gave TOP52 the ability to form type 1-dependent biofilms. Complementation with pfimK decreased type 1 pilus expression and biofilm formation of TOP52 Delta fimK and decreased UTI89 biofilm formation. Thus, K. pneumoniae appears programmed for minimal expression of type 1 pili, which may explain, in part, why K. pneumoniae is a less prevalent etiologic agent of UTI than UPEC.

Published 20 June 2008 in Infect Immun, 76(7): 3337-45.
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