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法氏囊参与火鸡出血性肠炎发病机制的证据。

Evidence for bursal involvement in the pathogenesis of hemorrhagic enteritis of turkeys.

作者信息

Fadly A M, Nazerian K

出版信息

Avian Dis. 1982 Jul-Sep;26(3):525-33.

PMID:6293443
Abstract

The pathogenesis of hemorrhagic enteritis in turkey poults infected with hemorrhagic enteritis virus (HEV) at 3 days or at 2 or 5 weeks of age was compared with pathogenesis in poults that had been chemically bursectomized neonatally and exposed to cell-culture-propagated virus at 2 or 5 weeks of age. Conventional poults exposed to HEV at 2 or 5 weeks developed clinical disease, and mortality ranged from 38% to 100%. In addition to the splenic and intestinal lesions usually seen with HEV infection, the pancreas, bursa of Fabricius, and thymus were also affected. In contrast, although they were free from detectable maternal antibody, poults infected with HEV at 3 days of age failed to develop clinical disease or mortality; however, virus was demonstrated by histological and electron microscopic examinations in spleens of these poults. Neonatal chemical bursectomy completely prevented the clinical signs, gross lesions, and mortality induced by HEV in poults at 2 or 5 weeks of age. These findings strongly suggest that an intact bursa is necessary for HEV to induce disease in turkeys.

摘要

将3日龄、2周龄或5周龄感染出血性肠炎病毒(HEV)的火鸡雏鸡的出血性肠炎发病机制,与新生期经化学法切除法氏囊并在2周龄或5周龄接触细胞培养增殖病毒的火鸡雏鸡的发病机制进行了比较。2周龄或5周龄接触HEV的传统火鸡雏鸡出现临床疾病,死亡率在38%至100%之间。除了通常在HEV感染时可见的脾脏和肠道病变外,胰腺、法氏囊和胸腺也受到影响。相比之下,尽管3日龄感染HEV的火鸡雏鸡没有可检测到的母源抗体,但它们并未出现临床疾病或死亡;然而,通过组织学和电子显微镜检查在这些火鸡雏鸡的脾脏中发现了病毒。新生期化学法切除法氏囊完全预防了2周龄或5周龄火鸡雏鸡由HEV诱导的临床症状、肉眼病变和死亡。这些发现强烈表明,完整的法氏囊是HEV在火鸡中诱导疾病所必需的。

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