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Infection and Immunity, April 2009, p. 1442-1450, Vol. 77, No. 4
0019-9567/09/$08.00+0 doi:10.1128/IAI.01039-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Maria Damian,2
Awa Aïdara-Kane,3,
Yves Germani,4,
Arnaud Fontanet,5
Bernadette Coddeville,6
Yann Guérardel,6 and
Chantal Le Bouguénec1*
Institut Pasteur, Unité de Pathogénie Bactérienne des Muqueuses, F-75015 Paris, France,1 Cantacuzino Institute, Molecular Epidemiology Laboratory, Bucharest, Romania,2 Institut Pasteur Dakar, Laboratoire de Bactériologie Expérimentale, Dakar, Sénégal,3 Institut Pasteur, Unité des Maladies Infectieuses Opportunistes, Bangui, Central African Republic,4 Institut Pasteur, Unité d'Epidémiologie des Maladies Emergentes, F-75015 Paris, France,5 Laboratoire de Dynamique Structurale et Fonctionnelle, Université des Sciences et Technologies de Lille, UMR CNRS 8576, IFR 147, Villeneuve d'Ascq, France6
Received 20 August 2008/ Returned for modification 6 October 2008/ Accepted 14 January 2009
We previously suggested that the ability to metabolize deoxyribose, a phenotype encoded by the deoK operon, is associated with the pathogenic potential of Escherichia coli strains. Carbohydrate metabolism is thought to provide the nutritional support required for E. coli to colonize the intestine. We therefore investigated the role of deoxyribose catabolism in the colonization of the gut, which acts as a reservoir, by pathogenic E. coli strains. Molecular and biochemical characterization of 1,221 E. coli clones from various collections showed this biochemical trait to be common in the E. coli species (33.6%). However, multivariate analysis evidenced a higher prevalence of sugar-metabolizing E. coli clones in the stools of patients from countries in which intestinal diseases are endemic. Diarrhea processes frequently involve the destruction of intestinal epithelia, so it is plausible that such clones may be positively selected for in intestines containing abundant DNA, and consequently deoxyribose. Statistical analysis also indicated that symptomatic clinical disorders and the presence of virulence factors specific to extraintestinal pathogenic E. coli were significantly associated with an increased risk of biological samples and clones testing positive for deoxyribose. Using the streptomycin-treated-mouse model of intestinal colonization, we demonstrated the involvement of the deoK operon in gut colonization by two pathogenic isolates (one enteroaggregative and one uropathogenic strain). These results, indicating that deoxyribose availability promotes pathogenic E. coli growth during host colonization, suggest that the acquisition of this trait may be an evolutionary step enabling these pathogens to colonize and persist in the mammalian intestine.
Published ahead of print on 21 January 2009.
Present address: Institut Pasteur de Madagascar, Laboratoire d'Hygiène des Aliments et de l'Environnement, BP 1274 Ambatofotsikely, 101 Antananarivo, Madagascar.
Present address: World Health Organization, Department Food Safety, Zoonoses and Foodborne Diseases, 20, Avenue Appia, 1211 Geneva 27, Switzerland.
Present address: Institut Pasteur, Unité de Pathogénie Microbienne Moléculaire, F-75015 Paris, France.
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