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1 September 2005

Volume 192, Number 5
The Journal of Infectious Diseases 2005;192:760–770
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19205-0007$15.00
DOI: 10.1086/430618
MAJOR ARTICLE

Genome Sequence of a Serotype M28 Strain of Group A Streptococcus: Potential New Insights into Puerperal Sepsis and Bacterial Disease Specificity

Nicole M. Green,1,2,3,a

Shizhen Zhang,2,a

Stephen F. Porcella,1,a

Michal J. Nagiec,2

Kent D. Barbian,1

Stephen B. Beres,2

Rance B. LeFebvre,3 and

James M. Musser1,2

1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, Montana; 2Center for Human Bacterial Pathogenesis Research, Department of Pathology, Baylor College of Medicine, Houston, Texas; 3Department of Pathology, Microbiology, and Immunology, University of California—Davis, Davis

Puerperal sepsis, a major cause of death of young women in Europe in the 1800s, was due predominantly to the gram‐positive pathogen group A Streptococcus. Studies conducted during past decades have shown that serotype M28 strains are the major group A Streptococcus organisms responsible for many of these infections. To begin to increase our understanding of their enrichment in puerperal sepsis, we sequenced the genome of a genetically representative strain. This strain has genes encoding a novel array of prophage virulence factors, cell‐surface proteins, and other molecules likely to contribute to host‐pathogen interactions. Importantly, genes for 7 inferred extracellular proteins are encoded by a 37.4‐kb foreign DNA element that is shared with group B Streptococcus and is present in all serotype M28 strains. Proteins encoded by the 37.4‐kb element were expressed extracellularly and in human infections. Acquisition of foreign genes has helped create a disease‐specialist clone of this pathogen.

Received 29 October 2004; accepted 26 January 2005; electronically published 29 July 2005.

Reprints or correspondence: Dr. James M. Musser, Center for Human Bacterial Pathogenesis Research, Dept. of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030 ().

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  • Financial support: National Institute of Allergy and Infectious Diseases (grant UO1‐60595 to J.M.M.).

  • The first 3 authors contributed equally to the work.

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