Nakamura K, Mase M, Yamaguchi S, Shibahara T, Yuasa N
National Institute of Animal Health, Ibaraki, Japan.
Avian Dis. 1999 Jul-Sep;43(3):414-23.
The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.
对从日本患有心包积水综合征（HPS）的鸡中分离出的4型腺病毒所导致的死亡率和病理学变化，在无特定病原体（SPF）鸡中进行了研究。将1日龄至15月龄的SPF鸡通过肌肉注射、口服和滴鼻接种来自患有HPS的鸡的肝脏匀浆或分离出的4型腺病毒。死亡前无临床症状。所有1日龄雏鸡组的死亡率均为100%，无论接种物或接种途径如何。接种肝脏匀浆的4周龄鸡死亡率也为100%。接种HPS腺病毒细胞培养物的5周龄鸡死亡率为40%。肌肉注射和口服接种肝脏匀浆的7月龄母鸡死亡率分别为75%和25%。肌肉注射接种肝脏匀浆的15月龄母鸡死亡率为70%。大体病变为心包积水以及肝脏肿胀和充血，偶尔有瘀点出血。组织学上，肝脏有弥漫性或多灶性肝坏死和出血，肝细胞内可见核内包涵体。在脾脏中，红髓内含有红细胞和黄色色素的巨噬细胞显著。在肺中，整个肺实质有中度弥漫性巨噬细胞浸润，这些巨噬细胞含有黄色色素。1日龄接种雏鸡的胰腺中有腺泡多灶性坏死并有核内包涵体。在1日龄接种雏鸡的肌胃、腺胃、十二指肠、盲肠、肾脏和肺中也可见核内包涵体。免疫组织化学显示，各器官的核内包涵体对I群禽腺病毒呈阳性反应。从患有HPS的鸡的肝脏中分离到了腺病毒。本研究表明，HPS腺病毒能够在SPF雏鸡甚至成年鸡中再现HPS病变和死亡率，并且它是一种高致病性毒株。
