Matos Miguel, Dublecz Károly, Grafl Beatrice, Liebhart Dieter, Hess Michael
A Clinic for Poultry and Fish Medicine, Department for Farm Animals and Veterinary Public Health, University of Veterinary Medicine Vienna, Veterinaerplatz 1, 1210, Vienna, Austria.
B Department of Animal Science, Georgikon Faculty, University of Pannonia, Deak F. u. 16, H-8360 Keszthely, Hungary.
Avian Dis. 2018 Mar;62(1):57-64. doi: 10.1637/11755-092717-Reg.1.
The aim of the present study was to further unravel the pathophysiologic mechanisms of inclusion body hepatitis (IBH). In a first trial, the susceptibility of specific-pathogen-free (SPF) broilers to fowl aviadenovirus (FAdV) infections was investigated. Regardless of viral dose, route of infection, and susceptibility to disease on day 1, the 3-week-old SPF broilers showed resistance to IBH, with no mortality being recorded throughout the experiment. In a second trial, SPF broilers were orally infected at 3 weeks of age with a FAdV-E strain, and their digestive and metabolic processes were monitored. The birds' performance decreased from 7 days postinfection (dpi) onward, and hepato- and pancreatomegaly were found at necropsy at 4, 7, and 10 dpi and at 7 dpi, respectively. Clinical chemistry revealed transient hyperlipasemia at 4 dpi and hyperglycemia from 4 dpi onwards, with 25% of infected birds showing glycemia levels suggestive of diabetes mellitus. Histopathology findings included typical adenoviral hepatitis in the liver, while in the pancreas, inflammation characterized by multifocal infiltrations of lymphocytes, together with shrinkage of acinar cells, loss of acinar arrangement, and hyperplasia of islet cells, was noticed. Additionally, the pancreatic tissue had tendentiously lower levels of enzyme activity, and in the ileum, the digestibility of fat was significantly impaired. Hence, our data reinforce the concept of age-related resistance to experimentally induced IBH. Additionally, we demonstrated that FAdV-induced pancreatitis in broilers interferes with the digestive process and evolves into a dysmetabolic condition that resembles diabetes, affecting the health and zootechnical performance of birds, and therefore providing an important component of IBH pathogenesis.
本研究的目的是进一步揭示包涵体肝炎(IBH)的病理生理机制。在第一项试验中,研究了无特定病原体(SPF)肉鸡对禽腺病毒(FAdV)感染的易感性。无论病毒剂量、感染途径以及第1天的疾病易感性如何,3周龄的SPF肉鸡对IBH均表现出抗性,整个实验期间未记录到死亡情况。在第二项试验中,3周龄的SPF肉鸡经口感染FAdV-E毒株,并监测其消化和代谢过程。感染后7天(dpi)起鸡的生长性能下降,在4、7和10 dpi时尸检分别发现肝脏和胰腺肿大,在7 dpi时发现胰腺肿大。临床化学检测显示,4 dpi时出现短暂的高脂血症,4 dpi起出现高血糖,25%的感染鸡血糖水平提示患有糖尿病。组织病理学检查结果包括肝脏出现典型的腺病毒性肝炎,而在胰腺中,可见以淋巴细胞多灶性浸润为特征的炎症,同时伴有腺泡细胞萎缩、腺泡排列丧失和胰岛细胞增生。此外,胰腺组织的酶活性水平有下降趋势,在回肠中,脂肪消化率显著受损。因此,我们的数据强化了与年龄相关的对实验性诱导IBH的抗性这一概念。此外,我们证明FAdV诱导的肉鸡胰腺炎会干扰消化过程,并演变成类似糖尿病的代谢紊乱状态,影响鸡的健康和饲养性能,从而为IBH发病机制提供了一个重要组成部分。