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Infection and Immunity, November 2005, p. 7597-7601, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7597-7601.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Dra/AfaE Adhesin of Uropathogenic Dr/Afa⁺ Escherichia coli Mediates Mortality in Pregnant Rats

Departments of Obstetrics and Gynecology,¹ Microbiology and Immunology,² Neuroscience and Cell Biology, University of Texas—Medical Branch at Galveston, Galveston, Texas,³ Unite de Pathogenie Bacterienne des Muqueuses, Institut Pasteur, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France,⁴ Department of Neonatal Infectious Diseases, Chair of Neonatology, Poznan University of Medical Science, Poznan, Poland,⁵ Department of Pathology and Laboratory Medicine, Children's Mercy Hospital, Kansas City, Missouri⁶

Received 2 March 2005/ Returned for modification 2 June 2005/ Accepted 4 August 2005

Escherichia coli bearing adhesins of the Dr/Afa family frequently causes urogenital infections during pregnancy in humans and has been associated with mortality in pregnant rats. Two components of the adhesin, Dra/AfaE and Dra/AfaD, considered virulence factors, are responsible for bacterial binding and internalization. We hypothesize that gestational mortality caused by Dr/Afa⁺ E. coli is mediated by one of these two proteins, Dra/AfaE or Dra/AfaD. In this study, using afaE and/or afaD mutants, we investigated the role of the afaE and afaD genes in the mortality of pregnant rats from intrauterine infection. Sprague-Dawley rats, on the 17th day of pregnancy, were infected with the E. coli afaE⁺ afaD and afaE afaD⁺ mutants. The clinical E. coli strain (afaE⁺ afaD⁺) and the afaE afaD double mutant were used as positive and negative controls, respectively. The mortality rate was evaluated 24 h after infection. The highest maternal mortality was observed in the group infected with the afaE⁺ afaD⁺ strain, followed by the group infected with the afaE⁺ afaD strain. The mortality was dose dependent. The afaE afaD double mutant did not cause maternal mortality, even with the highest infection dose. The in vivo studies corresponded with the invasion assay, where the afaE⁺ strains were the most invasive (afaE⁺ afaD strain > afaE⁺ afaD⁺ strain), while the afaE mutant strains (afaE afaD⁺ and afaE afaD strains) seemed to be noninvasive. This study shows for the first time that the afaE gene coding for the AfaE subunit of Dr/Afa adhesin is involved in the lethal outcome of gestational infection in rats. This lethal effect associated with AfaE correlates with the invasiveness of afaE⁺ E. coli strains in vitro.

Editor: V. J. DiRita