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Infection and Immunity, August 2001, p. 4858-4869, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.4858-4869.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Directional Gene Movement from Human-Pathogenic to Commensal-Like Streptococci

Awdhesh Kalia,1 Mark C. Enright,2 Brian G. Spratt,3 and Debra E. Bessen1,*

Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut,1 and Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY,2 and Department of Infectious Disease Epidemiology, Imperial College School of Medicine, University of London, St. Mary's Campus, London W2 1PG,3 United Kingdom

Received 1 March 2001/Returned for modification 19 April 2001/Accepted 1 May 2001

Group A streptococci (GAS) are highly pathogenic for humans, and their closest genetic relatives, group C and G streptococci (GCS and GGS, respectively), are generally regarded as commensals, although they can be found in association with human disease. As part of an effort to better understand the evolution of virulence, the phylogenetic relationships between GAS, GCS, and GGS were examined. The nucleotide sequence was determined for an internal portion of seven housekeeping (neutral) loci among >200 isolates of GAS and 34 isolates of GCS or GGS obtained from human subjects. Genotypic analysis failed to show support for the separation of GCS and GGS into two distinct populations. Unlike GAS, there was poor concordance between emm type and genetic relatedness among GCS and GGS. All housekeeping genes within GAS displayed relatively low levels of sequence diversity. In contrast, individual GCS and GGS strains had mosaic genomes, containing alleles at some loci that were similar or identical to GAS alleles, whereas the alleles at other loci were about 10 to 30% diverged. The data provide evidence for a history of recent interspecies transfer of neutral genes that exhibits a strong net directionality from GAS donors to GCS and GGS recipients. A model for the evolution of GAS and of GCS and GGS is described.

* Corresponding author, Mailing address: Yale University School of Medicine, Department of Epidemiology & Public Health, 60 College Street, Box 208034, New Haven, CT 06520-8034. Phone: (203) 785-4480. Fax: (203) 737-4285. E-mail: debra.bessen{at}yale.edu.

Infection and Immunity, August 2001, p. 4858-4869, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.4858-4869.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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