Invasive Group A Streptococcal Infections in North Carolina: Epidemiology, Clinical Features, and Genetic and Serotype Analysis of Causative Organisms | Zendy

Deanna L. Kiska | Zendy; Barbara Thiede | Zendy; Judy Caracciolo | Zendy; Michele Jordan | Zendy; Dwight R. Johnson | Zendy; Edward L. Kaplan | Zendy; Robert P. Gruninger | Zendy; Jacob A. Lohr | Zendy; Peter H. Gilligan | Zendy; Floyd W. Denny | Zendy

Open Access

Invasive Group A Streptococcal Infections in North Carolina: Epidemiology, Clinical Features, and Genetic and Serotype Analysis of Causative Organisms

Author(s) -

Deanna L. Kiska,

Barbara Thiede,

Judy Caracciolo,

Michele Jordan,

Dwight R. Johnson,

Edward L. Kaplan,

Robert P. Gruninger,

Jacob A. Lohr,

Peter H. Gilligan,

Floyd W. Denny

Publication year - 1997

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/516540

Subject(s) - serotype , pulsed field gel electrophoresis , microbiology and biotechnology , toxic shock syndrome , biology , polymerase chain reaction , virulence , exotoxin , fasciitis , group a , streptococcus , molecular epidemiology , virology , genotype , bacteria , medicine , staphylococcus aureus , gene , genetics , toxin , surgery

During 1994 and 1995, an increase in the number and severity of group A streptococcal (GAS) infections was noted in North Carolina. Ninety-six patients had GAS recovered from blood and other sterile body fluids, abscesses, and soft tissue. The overall case fatality rate was 11% but was much higher in patients with toxic shock syndrome (55%) and necrotizing fasciitis (58%). Recent invasive GAS isolates were compared with pre-1994 invasive isolates and temporally related pharyngeal isolates by M protein serotyping, pulsed field gel electrophoresis (PFGE), and polymerase chain reaction amplification of the streptococcal pyrogenic exotoxin A gene. Serotypes M1 and M3 accounted for 50% of recent invasive isolates (1994-1995) and 58% of pharyngeal isolates (1994). The latter isolates demonstrated PFGE patterns that were identical to invasive M1 and M3 strains, suggesting that pharyngeal infections may have served as a reservoir for virulent GAS clones.

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