کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3373074 1219280 2009 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Community-associated meticillin-resistant Staphylococcus aureus as a cause of hospital-acquired infections
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروبیولوژی و بیوتکنولوژی کاربردی
پیش نمایش صفحه اول مقاله
Community-associated meticillin-resistant Staphylococcus aureus as a cause of hospital-acquired infections
چکیده انگلیسی

SummaryThe worldwide emergence of community-associated meticillin-resistant Staphylococcus aureus (CA-MRSA) during the last decade represents a significant change in the biology of MRSA strains and is changing the epidemiology of MRSA infections. CA-MRSA infections are caused by strains belonging to lineages distinct from HA-MRSA. In the community, CA-MRSA strains typically cause skin and soft tissue infections in children and younger adults. However, CA-MRSA strains increasingly cause healthcare-acquired infections including surgical site infections, ventilator-associated pneumonia and bacteraemia. A mathematical model showing the influence of MRSA transmission in the community on the prevalence of MRSA in hospitals is presented. The increasing prevalence of MRSA in the community also results in an increase in community-onset MRSA (CO-MRSA) among S. aureus bacteraemia and other invasive infections. These patients do not have typical risk factors for MRSA. Such changes may have profound implications for the choice of empirical therapy for serious infections where S. aureus is a possible cause. The new and potentially very large reservoir of MRSA in production animals with subsequent transmission to humans represents an additional serious threat to the control of MRSA both in general and as a cause of healthcare-acquired infections. CA-MRSA is thus a matter of serious concern and should be suppressed.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Hospital Infection - Volume 73, Issue 4, December 2009, Pages 364–370
نویسندگان
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