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Infection and Immunity, November 2002, p. 6481-6484, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.6481-6484.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Type 1 Fimbria- and P Fimbria-Specific Adherence in Colonization of the Neurogenic Human Bladder by Escherichia coli

Richard A. Hull,1,2* William H. Donovan,3,4 Michael Del Terzo,5 Colleen Stewart,6 Margaret Rogers,4 and Rabih O. Darouiche2,6

Department of Molecular Virology and Microbiology,1 Center for Prostheses Infections, Department of Physical Medicine and Rehabilitation, Baylor College of Medicine,2 Department of Physical Medicine and Rehabilitation,3 Division of Urology, Department of Medicine, University of Texas Medical School,5 The Institute for Rehabilitation and Research,4 Spinal Cord Injury and Medical Services, Infectious Disease Section, Veterans Affairs Medical Center, Houston, Texas6

Received 22 April 2002/ Returned for modification 29 June 2002/ Accepted 14 August 2002

Recent clinical studies suggest that the deliberate colonization of the human bladder with a prototypic asymptomatic bacteriuria-associated bacterium, Escherichia coli 83972, may reduce the frequency of urinary tract infection in individuals with spinal cord injuries. However, the mechanism by which E. coli 83972 colonizes the bladder is unknown. We examined the role in bladder colonization of the E. coli 83972 genes papG and fimH, which respectively encode P and type 1 receptor-specific fimbrial adhesins. E. coli 83972 and isogenic papG{Delta} and papG{Delta} fimH{Delta} mutants of E. coli 83972 were compared for their capacities to colonize the neurogenic human bladder. Both strains were capable of stable colonization of the bladder. The results indicated that type 1 class-specific adherence and P class-specific adherence, while implicated as significant colonization factors in experiments that employed various animal model systems, were not required for colonization of the neurogenic bladder in human beings. The implications of these results with regard to the selection of potential vaccine antigens for the prevention of urinary tract infection are discussed.


* Corresponding author. Mailing address: Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-4926. Fax: (713) 798-5402. E-mail: rhull{at}bcm.tmc.edu.

Editor: V. J. DiRita


Infection and Immunity, November 2002, p. 6481-6484, Vol. 70, No. 11
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.11.6481-6484.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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