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Rapid Emergence of a New Clone Impacts the Population at Risk and Increases the Incidence of Type emm89 Group A Streptococcus Invasive Disease.
Teatero, Sarah; Coleman, Brenda L; Beres, Stephen B; Olsen, Randall J; Kandel, Christopher; Reynolds, Olivia; Athey, Taryn B T; Musser, James M; McGeer, Allison; Fittipaldi, Nahuel.
Afiliación
  • Teatero S; Public Health Ontario, Toronto, Canada.
  • Coleman BL; Department of Laboratory Medicine and Pathobiology, University of Toronto, Canada.
  • Beres SB; Mount Sinai Hospital, Toronto, Canada; and.
  • Olsen RJ; Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Texas.
  • Kandel C; Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Texas.
  • Reynolds O; Department of Laboratory Medicine and Pathobiology, University of Toronto, Canada.
  • Athey TBT; Mount Sinai Hospital, Toronto, Canada; and.
  • Musser JM; Public Health Ontario, Toronto, Canada.
  • McGeer A; Public Health Ontario, Toronto, Canada.
  • Fittipaldi N; Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Texas.
Open Forum Infect Dis ; 4(2): ofx042, 2017.
Article en En | MEDLINE | ID: mdl-28470020
ABSTRACT

BACKGROUND:

Invasive group A Streptococcus (iGAS) disease caused by type emm89 strains has been increasing worldwide, driven by the emergence of an epidemic clonal variant (clade 3 emm89). The clinical characteristics of patients with emm89 iGAS disease, and in particular with clade 3 emm89 iGAS disease, are poorly described.

METHODS:

We used population-based iGAS surveillance data collected in metropolitan Toronto, Ontario, Canada during the period 2000-2014. We sequenced the genomes of 105 emm89 isolates representing all emm89 iGAS disease cases in the area during the period and 138 temporally matched emm89 iGAS isolates collected elsewhere in Ontario.

RESULTS:

Clades 1 and 2 and clade O, a newly discovered emm89 genetic variant, caused most cases of emm89 iGAS disease in metropolitan Toronto before 2008. After rapid emergence of new clade 3, previously circulating clades were purged from the population and the incidence of emm89 iGAS disease significantly increased from 0.14 per 100000 in 2000-2007 to 0.22 per 100000 in 2008-2014. Overall, emm89 organisms caused significantly more arthritis but less necrotizing fasciitis than strains of the more common type emm1. Other clinical presentations were soft tissue and severe respiratory tract infections. Clinical outcomes did not differ significantly between emm89 clades overall. However, clade 3 emm89 iGAS disease was more common in youth and middle-aged individuals.

CONCLUSIONS:

The rapid shift in emm89 iGAS strain genetics in metropolitan Toronto has resulted in a significant increase in the incidence of emm89 iGAS disease, with noticeably higher rates of clade 3 disease in younger patients.
Palabras clave

Texto completo: 1 Base de datos: MEDLINE Tipo de estudio: Etiology_studies / Incidence_studies / Risk_factors_studies Idioma: En Revista: Open Forum Infect Dis Año: 2017 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Tipo de estudio: Etiology_studies / Incidence_studies / Risk_factors_studies Idioma: En Revista: Open Forum Infect Dis Año: 2017 Tipo del documento: Article