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Journal of Clinical Microbiology, April 2006, p. 1257-1261, Vol. 44, No. 4
0095-1137/06/$08.00+0 doi:10.1128/JCM.44.4.1257-1261.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Penny Clark,10
George G. Rhoads,11
Carl E. Frasch,12
James Troendle,1
Patricia Moyer,1 and
John F. Bohnsack2
National Institute of Child Health and Human Development, National Institutes of Health,1 Center for Biologics Research and Review, Food and Drug Administration, Department of Health and Human Services, Bethesda, Maryland,12 Department of Pediatrics,2 Genome Center, University of Utah Health Sciences Center, Salt Lake City, Utah,5 Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee,3 Division of Microbiology, Joshi-Eiyoh University, Saitama, Japan,4 Children's Hospital Medical Center of Northern California, Oakland, California,6 University of Alabama at Birmingham, Birmingham, Alabama,7 Baylor College of Medicine, Houston, Texas,8 Columbia University Health Sciences, New York, New York,9 University of Florida, Gainesville, Florida,10 University of Dentistry and Medicine of New Jersey, Piscataway, New Jersey,11
Received 3 November 2005/ Returned for modification 17 December 2005/ Accepted 22 January 2006
This study compares the phylogenetic lineages of invasive serotype III group B streptococci (GBS) to those of colonizing strains in order to determine lineages associated with invasive disease. Isolates from 29 infants with early-onset disease (EOD) and from 196 colonized infants, collected in a prospective, multicenter study, were assigned a sequence type (ST) by multilocus sequence typing. Overall, 54.5% of the isolates were in the ST-19 complex, and 40.4% were in the ST-17 complex. Invasive strains were more likely to be in the ST-17 complex than were colonizing strains (59% versus 38%, P = 0.03). After we adjusted for potential confounders, the ST-17 complex was more likely to be associated with EOD than were other lineages (odds ratio = 2.51, 95% confidence interval = 1.02 to 6.20). These data support the hypothesis that ST-17 complex GBS are more virulent than other serotype III GBS.
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