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Infection and Immunity, November 2005, p. 7772-7774, Vol. 73, No. 11
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.11.7772-7774.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Fang Teng,1,2
Kavindra V. Singh,1,2 and
Barbara E. Murray1,2,3*
Center for the Study of Emerging and Re-Emerging Pathogens,1 Division of Infectious Diseases, Department of Internal Medicine,2 Department of Microbiology and Molecular Genetics, The University of Texas Medical School, Houston, Texas3
Received 13 April 2005/ Returned for modification 18 May 2005/ Accepted 29 July 2005
In the current study, the gls24 disruption mutant TX10100, previously shown to be more sensitive to bile salts and attenuated in a mouse peritonitis model, showed an approximately fivefold higher 50% infective dose than wild-type OG1RF in a rat endocarditis model. When administered as a mixture, TX10100, unlike a downstream glsB mutant, was significantly outnumbered by OG1RF in vegetations, organs, and blood, despite being inoculated in greater numbers. These results indicate that gls24 is important in the pathogenesis of enterococcal endocarditis.
Present address: Catedra de Infectologia, Facultad de Ciencias Medicas, Universidad Nacional de Rosario, Rosario, Argentina.
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