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Infection and Immunity, April 2007, p. 1565-1576, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.01496-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Native Microbial Colonization of Drosophila melanogaster and Its Use as a Model of Enterococcus faecalis Pathogenesis
,
Christopher R. Cox1,2 and
Michael S. Gilmore1*
Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts,1
Oklahoma Center for Neurosciences, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma2
Received 18 September 2006/
Returned for modification 22 November 2006/
Accepted 31 December 2006
Enterococci are commensal organisms of the gastrointestinal (GI) tracts of a broad range of mammalian and insect hosts, but they are also leading causes of nosocomial infection. Little is known about the ecological role of enterococci in the GI tract consortia. To develop a tractable model for studying the roles of these organisms as commensals and pathogens, we characterized the Drosophila melanogaster microflora and examined the occurrence of enterococci in the gastrointestinal consortium of Drosophila. In a survey of laboratory-reared Drosophila and wild-captured flies, we found that Drosophila was naturally colonized by representatives of five bacterial phyla. Among these organisms were several species of enterococci, including Enterococcus faecalis, Enterococcus faecium, Enterococcus gallinaraum, and Enterococcus durans, as well as a previously detected but uncultured Enterococcus species. Drosophila could be cured of enterococcal carriage by antibiotic treatment and could be reassociated with laboratory strains. High-level colonization by a well-characterized strain expressing the enterococcal cytolysin was found to be detrimental to Drosophila compared to the effect of an isogenic, noncytolytic control. The anatomical distribution of enterococci in the Drosophila GI tract was determined by immunohistochemical staining of thin sections of naturally colonized and reassociated flies.
* Corresponding author. Mailing address: The Schepens Eye Research Institute, 20 Staniford St., Boston, MA 02114. Phone: (617) 912-7448. Fax: (617) 912-0115. E-mail:
mgilmore{at}vision.eri.harvard.edu.
Published ahead of print on 12 January 2007.
Editor: V. J. DiRita
Supplemental material for this article may be found at http://iai.asm.org/.
Infection and Immunity, April 2007, p. 1565-1576, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.01496-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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