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禽致病性大肠杆菌(APEC)

[Avian pathogenic Escherichia coli (APEC)].

作者信息

Ewers Christa, Janssen Traute, Wieler Lothar H

机构信息

Institut für Mikrobiologie und Tierseuchen Freie Universität, Berlin.

出版信息

Berl Munch Tierarztl Wochenschr. 2003 Sep-Oct;116(9-10):381-95.

Abstract

Infections with avian pathogenic Escherichia coli (APEC) cause colibacillosis, an acute and mostly systemic disease resulting in significant economic losses in poultry industry worldwide. Avian colibacillosis is a complex syndrome characterized by multiple organ lesions with airsacculitis and associated pericarditis, perihepatitis and peritonitis being most typical. Environmental factors as well as the constitution of poultry or initial viral infections influence the outcome of APEC-infections. However, several challenge experiments in chickens proofed the role of virulent APEC strains as the single aetiological agent. Currently serotypes O1:K1, O2:K1 and O78:K80 are recognized as the most prevalent, however the number of published serotypes is increasing. In addition, single APEC isolates vary profoundly in virulence, and knowledge about the molecular basis of this variability is still scarce. Known virulence factors of APEC are adhesins (F1- and P-fimbriae), iron acquisition systems (aerobactin and yersiniabactin), hemolysins (hemolysinE and temperaturesensitive hemagglutinin), resistance to the bactericidal effects of serum and phagocytosis (outer membrane protein, iss protein, lipopolysaccharide, K/1)-capsule and colilcin production) as well as toxins and cytotoxins (heat stable toxin, cyto-/verotoxin and flagella toxin). Esperimental studies have shown that the respiratory tract, principally the gas-exchange region of the lung and the interstitium of the air sacs are the most important sites of entry for avian pathogenic E. coli. APEC strains adhere to the epithelial cells of air sacs presumably through F1-fimbriae. After colonization and multiplication the bacteria enter the bloodstream, and the temperature-sensitive hemagglutinin (tsh) seems to be important int his step. After invading the bloodstream APEC cause a septicemia resulting in massive lesins in multiple internal organs and in sudden death of the birds. The ability of the bacteria to acquire iron and the resistance to the bactericidal effects of serum, predominantly conferred by the increased serum survival (iss)--protein, enables APEC to multiply quickly in their hosts. Iss is regarded a specific genetic marker for avian pathogenic E. colistrains. A critical review of the literature published so far on APEC reveals, that these pathotypes are not defined appropriately. This findings urge investigations on the population structure of APEC, enabling the establishment of appropriate diagnostic tools and avoiding the obsolete use of serotyping for APEC diagnosis. So far more than 20 APEC strains have been investigated in animal experiments, explaining contrary published results. Thus, the lack of knowledge in pathogenicity and in immunity of APEC infections urges further experimental studies. As APEC share not only identical serotypes with human pathogens but also specific virulence factors, their zoonotic potential is under consideration.

摘要

禽致病性大肠杆菌(APEC)感染可引发大肠杆菌病,这是一种急性且多为全身性的疾病,在全球家禽业造成重大经济损失。禽大肠杆菌病是一种复杂的综合征,其特征为多个器官出现病变,气囊炎以及相关的心包炎、肝周炎和腹膜炎最为典型。环境因素以及家禽的体质或初始病毒感染会影响APEC感染的结果。然而,多项针对鸡的攻毒实验证明了强毒APEC菌株作为单一病原体的作用。目前,O1:K1、O2:K1和O78:K80血清型被认为是最常见的,但已公布的血清型数量正在增加。此外,单个APEC分离株的毒力差异很大,而关于这种变异性分子基础的知识仍然匮乏。APEC已知的毒力因子包括黏附素(F1和P菌毛)、铁获取系统(气杆菌素和耶尔森菌素)、溶血素(溶血素E和温度敏感血凝素)、对血清杀菌作用和吞噬作用的抗性(外膜蛋白、iss蛋白、脂多糖、K/1 - 荚膜和大肠杆菌素产生)以及毒素和细胞毒素(热稳定毒素、细胞/维罗毒素和鞭毛毒素)。实验研究表明,呼吸道,主要是肺的气体交换区域和气囊间质,是禽致病性大肠杆菌最重要的侵入部位。APEC菌株可能通过F1菌毛黏附在气囊上皮细胞上。在定植和繁殖后,细菌进入血液,温度敏感血凝素(tsh)在这一步似乎很重要。侵入血液后,APEC引发败血症,导致多个内部器官出现大量病变并使禽类突然死亡。细菌获取铁的能力以及对血清杀菌作用的抗性,主要由血清存活增强蛋白(iss)赋予,使APEC能够在宿主体内快速繁殖。Iss被认为是禽致病性大肠杆菌菌株的一个特异性遗传标记。对迄今为止发表的关于APEC的文献进行批判性综述发现,这些致病型没有得到恰当定义。这一发现促使对APEC的种群结构进行研究,以便建立合适的诊断工具并避免在APEC诊断中过时地使用血清分型。到目前为止,已有20多种APEC菌株在动物实验中得到研究,这解释了已发表的相互矛盾的结果。因此,对APEC感染的致病性和免疫性缺乏了解促使进一步开展实验研究。由于APEC不仅与人类病原体具有相同的血清型,还具有特定的毒力因子,其人畜共患病潜力受到关注。

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