Ewers Christa, Antão Esther-Maria, Diehl Ines, Philipp Hans-C, Wieler Lothar H
Institute of Microbiology and Epizootics, Philippstrasse 13, 10115 Berlin, Germany.
Appl Environ Microbiol. 2009 Jan;75(1):184-92. doi: 10.1128/AEM.01324-08. Epub 2008 Nov 7.
Although research has increasingly focused on the pathogenesis of avian pathogenic Escherichia coli (APEC) infections and the "APEC pathotype" itself, little is known about the reservoirs of these bacteria. We therefore compared outbreak strains isolated from diseased chickens (n = 121) with nonoutbreak strains, including fecal E. coli strains from clinically healthy chickens (n = 211) and strains from their environment (n = 35) by determining their virulence gene profiles, phylogenetic backgrounds, responses to chicken serum, and in vivo pathogenicities in a chicken infection model. In general, by examining 46 different virulence-associated genes we were able to distinguish the three groups of avian strains, but some specific fecal and environmental isolates had a virulence gene profile that was indistinguishable from that determined for outbreak strains. In addition, a substantial number of phylogenetic EcoR group B2 strains, which are known to include potent human and animal extraintestinal pathogenic E. coli (ExPEC) strains, were identified among the APEC strains (44.5%) as well as among the fecal E. coli strains from clinically healthy chickens (23.2%). Comparably high percentages (79.2 to 89.3%) of serum-resistant strains were identified for all three groups of strains tested, bringing into question the usefulness of this phenotype as a principal marker for extraintestinal virulence. Intratracheal infection of 5-week-old chickens corroborated the pathogenicity of a number of nonoutbreak strains. Multilocus sequence typing data revealed that most strains that were virulent in chicken infection experiments belonged to sequence types that are almost exclusively associated with extraintestinal diseases not only in birds but also in humans, like septicemia, urinary tract infection, and newborn meningitis, supporting the hypothesis that not the ecohabitat but the phylogeny of E. coli strains determines virulence. These data provide strong evidence for an avian intestinal reservoir hypothesis which could be used to develop intestinal intervention strategies. These strains pose a zoonotic risk because either they could be transferred directly from birds to humans or they could serve as a genetic pool for ExPEC strains.
尽管研究越来越关注禽致病性大肠杆菌(APEC)感染的发病机制以及“APEC致病型”本身,但对于这些细菌的储存宿主却知之甚少。因此,我们通过测定从患病鸡中分离出的暴发菌株(n = 121)与非暴发菌株(包括来自临床健康鸡的粪便大肠杆菌菌株(n = 211)及其环境中的菌株(n = 35))的毒力基因谱、系统发育背景、对鸡血清的反应以及在鸡感染模型中的体内致病性,对它们进行了比较。总体而言,通过检测46种不同的毒力相关基因,我们能够区分这三组禽类菌株,但一些特定的粪便和环境分离株的毒力基因谱与暴发菌株的无法区分。此外,在APEC菌株(44.5%)以及来自临床健康鸡的粪便大肠杆菌菌株(23.2%)中,鉴定出了大量的系统发育EcoR B2组菌株,已知该组包括强大的人和动物肠道外致病性大肠杆菌(ExPEC)菌株。对所有三组测试菌株均鉴定出了相当高比例(79.2%至89.3%)的血清抗性菌株,这使得这种表型作为肠道外毒力的主要标志物的实用性受到质疑。对5周龄鸡进行气管内感染证实了许多非暴发菌株的致病性。多位点序列分型数据表明,在鸡感染实验中具有毒力的大多数菌株属于不仅在鸟类而且在人类中几乎专门与肠道外疾病相关的序列类型,如败血症、尿路感染和新生儿脑膜炎,这支持了大肠杆菌菌株的毒力不是由生态栖息地而是由系统发育决定的假说。这些数据为禽类肠道储存宿主假说提供了有力证据,该假说可用于制定肠道干预策略。这些菌株构成了人畜共患病风险,因为它们要么可以直接从鸟类传播给人类,要么可以作为ExPEC菌株的基因库。