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15 August 2004

Volume 190, Number 4
The Journal of Infectious Diseases 2004;190:727–738
© 2004 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2004/19004-0011$15.00
DOI: 10.1086/422697
MAJOR ARTICLE

Progress toward Characterization of the Group A Streptococcus Metagenome: Complete Genome Sequence of a Macrolide‐Resistant Serotype M6 Strain

David J. Banks,1,a

Stephen F. Porcella,1

Kent D. Barbian,1

Stephen B. Beres,1

Lauren E. Philips,1

Jovanka M. Voyich,1

Frank R. DeLeo,1

Judith M. Martin,2

Greg A. Somerville,1 and

James M. Musser1,3

1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana; 2Division of Allergy, Immunology, and Infectious Diseases, Department of Pediatrics, Children’s Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; 3Center for Human Bacterial Pathogenesis Research, Department of Pathology, Baylor College of Medicine, Houston, Texas

We describe the genome sequence of a macrolide‐resistant strain (MGAS10394) of serotype M6 group A Streptococcus (GAS). The genome is 1,900,156 bp in length, and 8 prophage‐like elements or remnants compose 12.4% of the chromosome. A 8.3‐kb prophage remnant encodes the SpeA4 variant of streptococcal pyrogenic exotoxin A. The genome of strain MGAS10394 contains a chimeric genetic element composed of prophage genes and a transposon encoding the mefA gene conferring macrolide resistance. This chimeric element also has a gene encoding a novel surface‐exposed protein (designated “R6 protein”), with an LPKTG cell‐anchor motif located at the carboxyterminus. Surface expression of this protein was confirmed by flow cytometry. Humans with GAS pharyngitis caused by serotype M6 strains had antibody against the R6 protein present in convalescent, but not acute, serum samples. Our studies add to the theme that GAS prophage–encoded extracellular proteins contribute to host‐pathogen interactions in a strain‐specific fashion.

Received 2 January 2004; accepted 5 March 2004; electronically published 20 July 2004.

Reprints or correspondence: Dr. James M. Musser, Dept. of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030 ().

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  • Present affiliation: Department of Microbiology, Immunology, and Molecular Genetics, University of California at Los Angeles, Los Angeles.

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