کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3500512 1234502 2006 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Complete genome sequence of USA300, an epidemic clone of community-acquired meticillin-resistant Staphylococcus aureus
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی پزشکی و دندانپزشکی (عمومی)
پیش نمایش صفحه اول مقاله
Complete genome sequence of USA300, an epidemic clone of community-acquired meticillin-resistant Staphylococcus aureus
چکیده انگلیسی

SummaryBackgroundUSA300, a clone of meticillin-resistant Staphylococcus aureus, is a major source of community-acquired infections in the USA, Canada, and Europe. Our aim was to sequence its genome and compare it with those of other strains of S aureus to try to identify genes responsible for its distinctive epidemiological and virulence properties.MethodsWe ascertained the genome sequence of FPR3757, a multidrug resistant USA300 strain, by random shotgun sequencing, then compared it with the sequences of ten other staphylococcal strains.FindingsCompared with closely related S aureus, we noted that almost all of the unique genes in USA300 clustered in novel allotypes of mobile genetic elements. Some of the unique genes are involved in pathogenesis, including Panton-Valentine leucocidin and molecular variants of enterotoxin Q and K. The most striking feature of the USA300 genome is the horizontal acquisition of a novel mobile genetic element that encodes an arginine deiminase pathway and an oligopeptide permease system that could contribute to growth and survival of USA300. We did not detect this element, termed arginine catabolic mobile element (ACME), in other S aureus strains. We noted a high prevalence of ACME in S epidermidis, suggesting not only that ACME transfers into USA300 from S epidermidis, but also that this element confers a selective advantage to this ubiquitous commensal of the human skin.InterpretationUSA300 has acquired mobile genetic elements that encode resistance and virulence determinants that could enhance fitness and pathogenicity.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 367, Issue 9512, 4–10 March 2006, Pages 731–739
نویسندگان
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