IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Regué, M.
Right arrow Articles by Tomás, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Regué, M.
Right arrow Articles by Tomás, J. M.

 Previous Article  |  Next Article 

Infection and Immunity, January 2004, p. 54-61, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.54-61.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

A Gene, uge, Is Essential for Klebsiella pneumoniae Virulence

Miguel Regué,1 Beatriz Hita,1 Nuria Piqué,1 Luis Izquierdo,2 Susana Merino,2 Sandra Fresno,2 Vicente Javier Benedí,1,{dagger} and Juan M. Tomás2*

Departamento de Microbiología, Facultad de Biología, Universidad de Barcelona, 08071 Barcelona,2 Departamento de Microbiología y Parasitología Sanitarias. División de Ciencias de la Salud, Facultad de Farmacia, Universidad de Barcelona, 08028 Barcelona, Spain1

Received 28 May 2003/ Returned for modification 30 June 2003/ Accepted 15 September 2003

Klebsiella pneumoniae strains typically express both smooth lipopolysaccharide (LPS) with O antigen molecules and capsule polysaccharide (K antigen) on the surface. A single mutation in a gene that codes for a UDP galacturonate 4-epimerase (uge) renders a strain with the O-:K- phenotype (lack of capsule and LPS without O antigen molecules and outer core oligosaccharide). The uge gene was present in all the K. pneumoniae strains tested. The K. pneumoniae uge mutants were unable to produce experimental urinary tract infections in rats and were completely avirulent in two different animal models (septicemia and pneumonia). Reintroduction of the single uge wild-type gene in the corresponding mutants completely restored the wild-type phenotype (presence of capsule and smooth LPS) independently of the O or K serotype of the wild type. Furthermore, complemented uge mutants recovered the ability to produce experimental urinary tract infections in rats and virulence in the septicemia and pneumonia animal models.

* Corresponding author. Mailing address: Departamento de Microbiología. Facultad de Biología. Universidad de Barcelona. Diagonal 645, 08071 Barcelona, Spain. Phone: 34-934021486. Fax: 34-93-4110592. E-mail: juant{at}porthos.bio.ub.es.

Editor: D. L. Burns

{dagger} In memoriam.

Infection and Immunity, January 2004, p. 54-61, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.54-61.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2004 by the American Society for Microbiology. All rights reserved.