萬古霉素是最后防線的抗生素，已有十幾株金黃色葡萄球菌對其產(chǎn)生耐受,，研究人員測定了這些耐受菌的基因組序列,，結(jié)果顯示：每株菌獨(dú)立地出現(xiàn)耐藥性，有一些共同特征,，從而有助于它們獲得萬古霉素抗性和逃避人類系統(tǒng)免疫防御,。
在美國，耐甲氧西林金黃色葡萄球菌（MRSA)是醫(yī)院內(nèi)獲得性感染的一種主要病因,，最新數(shù)據(jù)顯示,，它在2005年引起1.8萬人死亡。嚴(yán)重的多重耐藥性MRSA感染需要用萬古霉素治療,。從2002年以來,，在美國已記錄有12例耐萬古霉素金黃色葡萄球菌（VRSA）的病例,，這使人們更加擔(dān)心，如果萬古霉素耐受變得普遍,，葡萄球菌感染可能無法治療,。大多數(shù)VRSA情況發(fā)生在肢體感染的糖尿病患者，以存在多種類型細(xì)菌為特點(diǎn),，包括萬古霉素耐受的腸球菌,。
該研究比較了這12株VRSA的遺傳差別，最后發(fā)現(xiàn),，它們的共同祖先出現(xiàn)在50多年以前,，正好在萬古霉素耐受出現(xiàn)之前；萬古霉素耐受不是在人與人之間傳播,，而是重復(fù)出現(xiàn)在每例VRSA病例里,；每一株VRSA菌株獲得一點(diǎn)稱為轉(zhuǎn)座子Tn1546的遺傳物質(zhì)。
所有VRSA菌株都屬于葡萄球菌的CC5家族或CC5進(jìn)化枝,，而CC5進(jìn)化枝通常見于抗生素耐受的醫(yī)院內(nèi)獲得性感染,，缺乏制造天然抗生素定居因子的能力，這就是它們?yōu)槭裁茨芘c腸球菌共存的原因,。CC5菌株能制造一些蛋白質(zhì),，這些蛋白質(zhì)可瓦解人大量的免疫應(yīng)答而使細(xì)菌興旺發(fā)達(dá)，從而增強(qiáng)混合感染中耐受因子從腸球菌轉(zhuǎn)移至葡萄球菌的優(yōu)勢,。
為什么VRSA的人與人傳播沒有變得普遍,？基因組也提供了相關(guān)線索，CC5菌株沒有制造或抵制抗生素殖民化因子的能力,，在遇到任何天然出現(xiàn)的葡萄球菌時處于劣勢,，因?yàn)樘烊怀霈F(xiàn)的葡萄球菌通常生活在皮膚上，能產(chǎn)生抗生素定居因子,。（生物谷bioon.com）
doi:10.1128/mBio.00112-12
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Comparative genomics of vancomycin-resistant Staphylococcus aureus strains and their positions within the clade most commonly associated with methicillin-resistant S. aureus hospital-acquired infection in the United States
Veronica N. Kos, Christopher A. Desjardins, Allison Griggs, Gustavo Cerqueira, Andries Van Tonder, Matthew T. G. Holden, Paul Godfrey, Kelli L. Palmer, Kip Bodi, Emmanuel F. Mongodin, Jennifer Wortman, Michael Feldgarden, Trevor Lawley, Steven R. Gill, Brian J. Haas, Bruce Birren and Michael S. Gilmore
Methicillin-resistant Staphylococcus aureus (MRSA) strains are leading causes of hospital-acquired infections in the United States, and clonal cluster 5 (CC5) is the predominant lineage responsible for these infections. Since 2002, there have been 12 cases of vancomycin-resistant S. aureus (VRSA) infection in the United States-all CC5 strains. To understand this genetic background and what distinguishes it from other lineages, we generated and analyzed high-quality draft genome sequences for all available VRSA strains. Sequence comparisons show unambiguously that each strain independently acquired Tn1546 and that all VRSA strains last shared a common ancestor over 50 years ago, well before the occurrence of vancomycin resistance in this species. In contrast to existing hypotheses on what predisposes this lineage to acquire Tn1546, the barrier posed by restriction systems appears to be intact in most VRSA strains. However, VRSA (and other CC5) strains were found to possess a constellation of traits that appears to be optimized for proliferation in precisely the types of polymicrobic infection where transfer could occur. They lack a bacteriocin operon that would be predicted to limit the occurrence of non-CC5 strains in mixed infection and harbor a cluster of unique superantigens and lipoproteins to confound host immunity. A frameshift in dprA, which in other microbes influences uptake of foreign DNA, may also make this lineage conducive to foreign DNA acquisition.
