德國(guó)研究人員23日在英國(guó)《柳葉刀傳染病》期刊上報(bào)告說(shuō)，本次德國(guó)腸出血性大腸桿菌疫情致病菌的菌株是10年前僅在德國(guó)現(xiàn)身過(guò)的一種大腸桿菌的克隆變種。這種病菌結(jié)合了腸出血性大腸桿菌和腸聚集性大腸桿菌的基因特性,，因此具有更大危害性。
明斯特大學(xué)當(dāng)天發(fā)布的新聞公報(bào)說(shuō),，該校醫(yī)學(xué)院衛(wèi)生研究所所長(zhǎng)卡希領(lǐng)導(dǎo)的研究小組分析了從德國(guó)17個(gè)城市共80名患者排泄物中分離出的菌株的遺傳物質(zhì)特性,，發(fā)現(xiàn)所有這些菌株都屬于血清型O104：H4型,、序列型678型大腸桿菌,。與此非常類似的大腸桿菌以往僅于2001年在德國(guó)兩名患者身上出現(xiàn)過(guò),，這次卻出人意料地在德國(guó)造成大流行。
研究小組還指出,，本次暴發(fā)菌株都有與不同毒性相關(guān)的13個(gè)編碼基因，包括腸出血性大腸桿菌常見(jiàn)的志賀毒素2的編碼基因和與出血性腹瀉相關(guān)的基因,，還有與病菌黏附性相關(guān)的菌毛和黏附蛋白,。
本次暴發(fā)菌株與2001年的分離菌株相比差別微小，主要是有了更多的抗生素耐藥基因,，同時(shí)又缺少了腸道聚集黏附大腸桿菌耐熱腸毒素1基因,。卡希認(rèn)為,，上述基因的增減是病原性大腸桿菌變異的常見(jiàn)現(xiàn)象,。
卡希說(shuō)，與腸聚集性大腸桿菌類似,，本次暴發(fā)菌進(jìn)入腸道后會(huì)成群聚集黏附在腸細(xì)胞上,，形態(tài)如同“磚墻”一般。這時(shí)候病菌排出的志賀毒素往往會(huì)以迄今尚不明了的機(jī)理進(jìn)入血液循環(huán),，并優(yōu)先選擇腎細(xì)胞和腦內(nèi)皮細(xì)胞附著,，造成腎和腦損壞，從而導(dǎo)致嚴(yán)重的溶血性尿毒綜合征甚至使患者死亡,。
卡希強(qiáng)調(diào),，目前這種病菌尚有許多未解之謎：是否僅僅是因?yàn)閹追N致病因素結(jié)合就使其有如此強(qiáng)的進(jìn)攻性？到底需要多少病菌能造成感染,？人類對(duì)這種病菌沒(méi)有免疫能力是否是因?yàn)檫@種幾乎是無(wú)中生有的病菌以前從未與人接觸過(guò),？入侵人體之前，這種病菌又在何種群落生境中生存,？
據(jù)德國(guó)負(fù)責(zé)匯總疫情的羅伯特科赫研究所23日公布的最新疫情通報(bào),，德國(guó)一個(gè)月來(lái)腸出血性大腸桿菌感染病例累計(jì)達(dá)3688例，其中患溶血性尿毒綜合征的重癥病例所占比例超過(guò)22%,，遠(yuǎn)高于以往腸出血性大腸桿菌流行中不到10%的重癥患者比例,。截至22日,，德國(guó)累計(jì)死亡患者已達(dá)42人。不過(guò)近兩周來(lái)德國(guó)新增病例已明顯減少,。（生物谷Bioon.com）
生物谷推薦原文出處：
The Lancet doi:10.1016/S1473-3099(11)70165-7
Characterisation of the Escherichia coli strain associated with an outbreak of haemolytic uraemic syndrome in Germany, 2011: a microbiological study
Martina Bielaszewska MD , Alexander Mellmann MD , Wenlan Zhang MD , Robin Kck MD , Angelika Fruth PhD , Andreas Bauwens PhD , Georg Peters MD , Prof Helge Karch PhD
Background
In an ongoing outbreak of haemolytic uraemic syndrome and bloody diarrhoea caused by a virulent Escherichia coli strain O104:H4 in Germany (with some cases elsewhere in Europe and North America), 810 cases of the syndrome and 39 deaths have occurred since the beginning of May, 2011. We analysed virulence profiles and relevant phenotypes of outbreak isolates recovered in our laboratory.
Methods
We analysed stool samples from 80 patients that had been submitted to the National Consulting Laboratory for Haemolytic Uraemic Syndrome in Münster, Germany, between May 23 and June 2, 2011. Isolates were screened with standard PCR for virulence genes of Shiga-toxin-producing E coli and a newly developed multiplex PCR for characteristic features of the outbreak strain (rfbO104, fliCH4, stx2, and terD). Virulence profiles of the isolates were determined with PCR targeting typical virulence genes of Shiga-toxin-producing E coli and of other intestinal pathogenic E coli. We sequenced stx with Sanger sequencing and measured Shiga-toxin production, adherence to epithelial cells, and determined phylogeny and antimicrobial susceptibility.
Findings
All isolates were of the HUSEC041 clone (sequence type 678). All shared virulence profiles combining typical Shiga-toxin-producing E coli (stx2, iha, lpfO26, lpfO113) and enteroaggregative E coli (aggA, aggR, set1, pic, aap) loci and expressed phenotypes that define Shiga-toxin-producing E coli and enteroaggregative E coli, including production of Shiga toxing 2 and aggregative adherence to epithelial cells. Isolates additionally displayed an extended-spectrum β-lactamase phenotype absent in HUSEC041.
Interpretation
Augmented adherence of the strain to intestinal epithelium might facilitate systemic absorption of Shiga toxin and could explain the high progression to haemolytic uraemic syndrome. This outbreak demonstrates that blended virulence profiles in enteric pathogens, introduced into susceptible populations, can have extreme consequences for infected people.
Funding
German Federal Ministry of Education and Research, Network Zoonoses.
