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1 September 2005

Volume 192, Number 5
The Journal of Infectious Diseases 2005;192:771–782
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19205-0008$15.00
DOI: 10.1086/432514
MAJOR ARTICLE

Evolutionary Origin and Emergence of a Highly Successful Clone of Serotype M1 Group A Streptococcus Involved Multiple Horizontal Gene Transfer Events

Paul Sumby,1,2

Steve F. Porcella,1

Andres G. Madrigal,1,a

Kent D. Barbian,1

Kimmo Virtaneva,1

Stacy M. Ricklefs,1

Daniel E. Sturdevant,1

Morag R. Graham,1,a

Jaana Vuopio‐Varkila,3

Nancy P. Hoe,1 and

James M. Musser1,2

1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana; 2Center for Human Bacterial Pathogenesis Research, Department of Pathology, Baylor College of Medicine, Houston, Texas; 3National Public Health Institute, Helsinki, Finland

To better understand the molecular events involved in the origin of new pathogenic bacteria, we studied the evolution of a highly virulent clone of serotype M1 group A Streptococcus (GAS). Genomic, DNA‐DNA microarray, and single‐nucleotide polymorphism analyses indicated that this clone evolved through a series of horizontal gene transfer events that involved (1) the acquisition of prophages encoding streptococcal pyrogenic exotoxin A and extracellular DNases and (2) the reciprocal recombination of a 36‐kb chromosomal region encoding the extracellular toxins NAD+‐glycohydrolase (NADase) and streptolysin O (SLO). These gene transfer events were associated with significantly increased production of SLO and NADase. Virtual identity in the 36‐kb region present in contemporary serotype M1 and M12 isolates suggests that a serotype M12 strain served as the donor of this region. Multiple horizontal gene transfer events were a crucial factor in the evolutionary origin and emergence of a very abundant contemporary clone of serotype M1 GAS.

Received 26 January 2005; accepted 1 April 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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  • Data depositions: GenBank accession number for MGAS5005 genome, CP000017.

    Potential conflicts of interest: none reported.

    Financial support: National Institutes of Health (grant UO1‐AI‐060595).

  • Present affiliations: Boston University School of Medicine, Boston, Massachusetts (A.G.M.); Canadian Centre for Human and Animal Health, Winnipeg, Canada (M.R.G.).

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