Rapid molecular genetic subtyping of serotype M1 group A Streptococcus strains

Serotype M1 group A Streptococcus, the most common cause of invasive disease in many case series, generally have resisted extensive molecular subtyping by standard techniques (e.g., multilocus enzyme electrophoresis, pulsed-field gel electrophoresis). We used automated sequencing of the sic gene enc...

Full description

Saved in:
Bibliographic Details
Published inEmerging infectious diseases Vol. 5; no. 2; pp. 254 - 263
Main Authors Hoe, N, Nakashima, K, Grigsby, D, Pan, X, Dou, S J, Naidich, S, Garcia, M, Kahn, E, Bergmire-Sweat, D, Musser, J M
Format Journal Article
LanguageEnglish
Published United States Centers for Disease Control and Prevention 01.03.1999
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Serotype M1 group A Streptococcus, the most common cause of invasive disease in many case series, generally have resisted extensive molecular subtyping by standard techniques (e.g., multilocus enzyme electrophoresis, pulsed-field gel electrophoresis). We used automated sequencing of the sic gene encoding streptococcal inhibitor of complement and of a region of the chromosome with direct repeat sequences to unambiguously differentiate 30 M1 isolates recovered from 28 patients in Texas with invasive disease episodes temporally clustered and thought to represent an outbreak. Sequencing of the emm gene was less useful for M1 strain differentiation, and restriction fragment length polymorphism analysis with IS1548 or IS1562 as Southern hybridization probes did not provide epidemiologically useful subtyping information. Sequence polymorphism in the direct repeat region of the chromosome and IS1548 profiling data support the hypothesis that M1 organisms have two main evolutionary lineages marked by the presence or absence of the speA2 allele encoding streptococcal pyrogenic exotoxin A2.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1080-6040
1080-6059
DOI:10.3201/eid0502.990210