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Infection and Immunity, March 2004, p. 1230-1239, Vol. 72, No. 3
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.3.1230-1239.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Contribution of Long Polar Fimbriae to the Virulence of Rabbit-Specific Enteropathogenic Escherichia coli

Hayley J. Newton,1 Joan Sloan,1 Vicki Bennett-Wood,2,3 Louise M. Adams,2,3 Roy M. Robins-Browne,2,3 and Elizabeth L. Hartland1,2,4*

Australian Bacterial Pathogenesis Program, Department of Microbiology, Monash University, Victoria 3800,1 Microbiological Research Unit, Murdoch Childrens Research Institute and Royal Children's Hospital, Parkville 3052,2 Australian Bacterial Pathogenesis Program, Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia,3 Centre for Molecular Microbiology and Infection, Department of Biological Sciences Flowers Building, Imperial College London, London SW7 2AZ, United Kingdom4

Received 3 September 2003/ Returned for modification 12 November 2003/ Accepted 8 December 2003

Enteropathogenic Escherichia coli (EPEC) is a major of cause of diarrhea among children in developing countries. Although EPEC is a human specific pathogen, some related strains are natural pathogens of animals, including laboratory-bred rabbits. We have identified two chromosomal loci in rabbit-specific EPEC (REPEC) O15:H- strain 83/39, which are predicted to encode long polar fimbriae (LPF). lpfR154 was identical to a fimbrial gene cluster, lpfO113, identified previously in enterohemorrhagic E. coli (EHEC) O113:H21. The second locus, lpfR141, comprised a novel sequence with five predicted open reading frames, lpfA to lpfE, that encoded long fine fimbriae in nonfimbriated E. coli ORN103. The predicted products of lpfR141 shared identity with components of the lpfABCC'DE gene cluster from EHEC O157:H7, and the fimbriae were similar in morphology and length to LPF from EHEC O157:H7. Interruption of lpfR141 resulted in significant attenuation of REPEC 83/39 for rabbits with respect to the early stages of colonization and severity of diarrhea. However, there was no significant difference in the number of bacteria shed at later time points or in overall body weight and mortality rate of rabbits infected with lpfR141 mutant strains or wild-type REPEC 83/39. Although rabbits infected with the lpfR141 mutants did not develop severe diarrhea, there was evidence of attaching and effacing histopathology, which was indistinguishable in morphology, location, and extent compared to rabbits infected with wild-type REPEC 83/39. The results suggested that lpfR141 contributes to the early stages of REPEC-mediated disease and that this is important for the development of severe diarrhea in susceptible animals.

* Corresponding author. Mailing address: Department of Microbiology, Monash University, Victoria 3800, Australia. Phone: (61) 3-9905-4323. Fax: (61) 3-9905-4811. E-mail: Liz.Hartland{at}med.monash.edu.au.

Editor: B. B. Finlay

Infection and Immunity, March 2004, p. 1230-1239, Vol. 72, No. 3
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.3.1230-1239.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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