Molecular characterization of methicillin-resistant Staphylococcus aureus from a fatal case of necrotizing fasciitis in an extremely low-birth-weight infant

Authors

  • K. O. Orii,

    1.  Department of Paediatirics, Gifu Prefectural General Medical Centre, Gifu
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  • Y. Iwao,

    1.  Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
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  • W. Higuchi,

    1.  Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
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  • T. Takano,

    1.  Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
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  • T. Yamamoto

    1.  Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
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Corresponding author and reprint requests: T. Yamamoto, Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, 757 Ichibanchou, Asahimachidori, Niigata, Japan
E-mail: tatsuoy@med.niigata-u.ac.jp

Abstract

Clin Microbiol Infect 2010; 16: 289–292

Abstract

Necrotizing fasciitis due to methicillin-resistant Staphylococcus aureus (MRSA) is an uncommon but life-threatening infection, and has mainly been reported as occurring in adults and the elderly. Recently, infant cases involving Panton–Valentine leukocidin (PVL)-positive community-acquired MRSA have been noted. Here, a case of fatal necrotizing fasciitis with sepsis and disseminated intravascular coagulation in an extremely low-birth-weight infant is described. The causative agent was the hospital-acquired MRSA New York/Japan clone carrying the spa variant gene and nine staphylococcal enterotoxin (SE) genes. These data suggest that a high-level combination of SEs and other virulence factors, but not PVL, could contribute to the pathogenesis of fatal necrotizing fasciitis.

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