Pakpinyo S, Ley D H, Barnes H J, Vaillancourt J P, Guy J S
Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh 27606, USA.
Avian Dis. 2002 Apr-Jun;46(2):360-9. doi: 10.1637/0005-2086(2002)046[0360:POEECI]2.0.CO;2.
Enteropathogenic Escherichia coli (EPEC) previously were identified in poult enteritis-mortality syndrome (PEMS)-affected turkeys and associated as a cause of this disease. In the present study, the prevalence of EPEC in PEMS-affected turkeys was examined retrospectively with archived tissues and intestinal contents collected from 12 PEMS-affected turkey flocks in 1998. Formalin-fixed intestinal tissues were examined by light and electron microscopy for attaching and effacing (AE) lesions characteristic of EPEC, and frozen (-75 C) intestinal contents were examined for presence of EPEC. Escherichia coli isolates were characterized on the basis of epithelial cell attachment, fluorescent actin staining (FAS) test, and presence of E. coli attaching/effacing (EAE), shigalike toxin (SLT) type I, SLT II, and bundle-forming pilus (BFP) genes by polymerase chain reaction procedures. EPEC isolates were examined for pathogenicity and ability to induce AE lesions in experimentally inoculated young turkeys. AE lesions were identified by light microscopy in Giemsa-stained intestines from 7 of 12 PEMS-affected turkey flocks. Lesions consisted of bacterial microcolonies attached to epithelial surfaces with epithelial degeneration at sites of attachment and inflammatory infiltration of the lamina propria. Electron microscopy confirmed the identity of AE lesions in six of seven flocks determined to have AE lesions by light microscopy. EPEC were identified in 4 of 12 flocks on the basis of the presence of EAE genes a nd absence of SLT I and SLT II genes; all isolates lacked BFP genes. EPEC isolates produced AE lesions and variable mortality in turkeys coinfected with turkey coronavirus. In total, EPEC were associated with 10 of 12 (83%) naturally occurring PEMS cases on the basis of identification of AE lesions and/or EPEC isolates. These findings provide additional evidence suggesting a possible role for EPEC in the pathogenesis of PEMS.
肠致病性大肠杆菌（EPEC）此前在患家禽肠炎-死亡综合征（PEMS）的火鸡中被鉴定出来，并被认为是该疾病的病因之一。在本研究中，利用1998年从12个受PEMS影响的火鸡群收集的存档组织和肠道内容物，对受PEMS影响的火鸡中EPEC的流行情况进行了回顾性研究。通过光学显微镜和电子显微镜检查福尔马林固定的肠道组织，寻找EPEC特有的黏附与抹消（AE）损伤，检查冷冻（-75℃）肠道内容物中是否存在EPEC。根据上皮细胞黏附、荧光肌动蛋白染色（FAS）试验以及通过聚合酶链反应程序检测大肠杆菌黏附/抹消（EAE）、I型志贺样毒素（SLT）、SLT II和束状菌毛（BFP）基因的存在情况，对大肠杆菌分离株进行鉴定。对EPEC分离株在实验接种的幼龄火鸡中的致病性和诱导AE损伤的能力进行了检测。通过光学显微镜在12个受PEMS影响的火鸡群中的7个群的吉姆萨染色肠道中鉴定出了AE损伤。损伤表现为附着在上皮表面的细菌微菌落，附着部位上皮变性，固有层有炎性浸润。电子显微镜证实了在通过光学显微镜确定有AE损伤的7个群中的6个群中存在AE损伤。根据EAE基因的存在以及SLT I和SLT II基因的缺失，在12个群中的4个群中鉴定出了EPEC；所有分离株均缺乏BFP基因。EPEC分离株在用火鸡冠状病毒共同感染的火鸡中产生了AE损伤和不同程度的死亡率。总体而言，根据AE损伤和/或EPEC分离株的鉴定，EPEC与12例自然发生的PEMS病例中的10例（83%）有关。这些发现提供了更多证据，表明EPEC在PEMS发病机制中可能发挥作用。
