最新研究顯示,引起肺炎和腦膜炎的細(xì)菌會(huì)非??焖俚馗念^換面,,靈敏地產(chǎn)生對(duì)抗菌素和疫苗的抵抗力。
古往今來(lái),,肺炎鏈球菌一直是造成人類(lèi)死亡的一個(gè)主要原因,。出現(xiàn)在全世界的肺炎鏈球菌西班牙23F菌株是一個(gè)對(duì)多種抗菌素有抵抗力的特別棘手的菌株。幸運(yùn)地是,,這一世系的菌株分離物自1984年以來(lái)已經(jīng)在全世界多個(gè)地點(diǎn)被收集起來(lái),,Nicholas Croucher及其同事利用這些收集的菌株來(lái)仔細(xì)地剖析其演變過(guò)程。該國(guó)際性研究團(tuán)隊(duì)用高通量測(cè)序技術(shù)對(duì)200多個(gè)分離株的基因組進(jìn)行了測(cè)序和比較,。
結(jié)果顯示,,自1984年以來(lái),該細(xì)菌已經(jīng)用重組(即在細(xì)胞分裂時(shí)將基因組做混合改組)和堿基置換(這是將個(gè)體DNA“字母”進(jìn)行調(diào)換的突變)這兩種方法已經(jīng)翻轉(zhuǎn)了其約四分之三的基因組,。這一敏捷的基因變化使得該病原體能夠躲避諸如疫苗和抗菌素等公共健康措施的影響,。在一則相關(guān)的觀點(diǎn)欄目中,Mark C. Enright 與Brian G. Spratt將這一研究方法的功效與先前研究的功效進(jìn)行了對(duì)比,。
先前的研究所分析的只是每個(gè)分離物中的少許基因,。而最近的這一研究顯示了細(xì)菌在非常短的時(shí)期中是如何變化的,這對(duì)人們理解和預(yù)測(cè)病原體對(duì)新的抗菌素和疫苗的反應(yīng)是重要的,。(生物谷Bioon.com)
原文出處:
Science Vol. 331 no. 6016 pp. 430-434 DOI: 10.1126/science.1198545
Rapid Pneumococcal Evolution in Response to Clinical Interventions
Nicholas J. Croucher1, Simon R. Harris1, Christophe Fraser2, Michael A. Quail1, John Burton1, Mark van der Linden3, Lesley McGee4, Anne von Gottberg5, Jae Hoon Song6, Kwan Soo Ko7, Bruno Pichon8, Stephen Baker9, Christopher M. Parry9, Lotte M. Lambertsen10, Dea Shahinas11, Dylan R. Pillai11, Timothy J. Mitchell12, Gordon Dougan1, Alexander Tomasz13, Keith P. Klugman4,5,14, Julian Parkhill1, William P. Hanage2,15, and Stephen D. Bentley1,*
Epidemiological studies of the naturally transformable bacterial pathogen Streptococcus pneumoniae have previously been confounded by high rates of recombination. Sequencing 240 isolates of the PMEN1 (Spain23F-1) multidrug-resistant lineage enabled base substitutions to be distinguished from polymorphisms arising through horizontal sequence transfer. More than 700 recombinations were detected, with genes encoding major antigens frequently affected. Among these were 10 capsule-switching events, one of which accompanied a population shift as vaccine-escape serotype 19A isolates emerged in the USA after the introduction of the conjugate polysaccharide vaccine. The evolution of resistance to fluoroquinolones, rifampicin, and macrolides was observed to occur on multiple occasions. This study details how genomic plasticity within lineages of recombinogenic bacteria can permit adaptation to clinical interventions over remarkably short time scales.