The Arginine Catabolic Mobile Element Is Not Associated with Enhanced Virulence in Experimental Invasive Disease Caused by the Community-Associated Methicillin-Resistant Staphylococcus aureus USA300 Genetic Background
The Arginine Catabolic Mobile Element Is Not Associated with Enhanced Virulence in Experimental Invasive Disease Caused by the Community-Associated Methicillin-Resistant Staphylococcus aureus USA300 Genetic Background
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DOI：
10.1128/iai.00256-09
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发表时间：
2009-07-01
影响因子：
3.1
通讯作者：
Daum, Robert S.
中科院分区：
文献类型：
--
作者：
Montgomery, Christopher P.;Boyle-Vavra, Susan;Daum, Robert S.
USA300 已成为美国大多数社区中主要的社区相关耐甲氧西林金黄色葡萄球菌 (CA-MRSA) 遗传背景。这种遗传背景占主导地位的原因尚不清楚，但最近在 USA300 基因组中发现的精氨酸分解代谢移动元件 (ACME) 的存在被认为是一种可能性。分析了存在或不存在 ACME 的 CA-MRSA 临床分离株 (USA300) 和 USA300 野生型/ACME 缺失突变体对的整体调节基因的体外表达和毒力因子的产生。在坏死性肺炎和皮肤感染的啮齿动物模型中比较了这些分离株的毒力。无论是否存在 ACME，测试的分离株中介导毒力的所选基因（hla、lukSF-PV、agr、saeRS）的表达没有显着差异。 ACME 阳性分离株的培养上清液中的 α-溶血素丰度高于 ACME 阴性分离株，但蛋白 A 的水平没有显着差异。根据死亡率、体内细菌存活率和肺部病理严重程度评估，ACME 的存在与坏死性肺炎大鼠模型中毒力的增加无关。在皮肤感染模型中，ACME 的存在也与皮肤坏死增加无关。我们的结论是，ACME 对于 CA-MRSA USA300 肺炎或皮肤感染的啮齿动物模型中的毒力来说并不是必需的。
USA300 has become the predominant community-associated methicillin (meticillin)-resistant Staphylococcus aureus (CA-MRSA) genetic background in most U. S. communities. The reasons for the dominance of this genetic background are unclear, but the presence of the recently identified arginine catabolic mobile element (ACME) in the USA300 genome has been advocated as one possibility. CA-MRSA clinical isolates (USA300) differing in the presence or absence of ACME and a USA300 wild-type/ACME deletion mutant pair were analyzed for in vitro expression of global regulatory genes and production of virulence factors. The virulence of these isolates was compared in rodent models of necrotizing pneumonia and skin infection. There was no significant difference in the expression of selected genes mediating virulence (hla, lukSF-PV, agr, saeRS) among the isolates tested, regardless of the presence of ACME. There was a higher abundance of alpha-hemolysin in culture supernatants among ACME-positive isolates than among ACME-negative isolates, but there was no significant difference in the levels of protein A. The presence of ACME was not associated with increased virulence in a rat model of necrotizing pneumonia, as assessed by mortality, in vivo bacterial survival, and severity of lung pathology. Nor was the presence of ACME associated with increased dermonecrosis in a model of skin infection. We conclude that ACME is not necessary for virulence in rodent models of CA-MRSA USA300 pneumonia or skin infection.