Schmidt Volker, Schlömer Julian, Lüken Caroline, Johne Reimar, Biere Barbara, Müller Hermann, Krautwald-Junghanns Maria-Elisabeth
Clinic for Birds and Reptiles, Faculty of Veterinary Medicine, University of Leipzig, An den Tierkliniken 17, D-04103 Leipzig, Germany.
Avian Dis. 2008 Sep;52(3):380-6. doi: 10.1637/8188-120407-Reg.
Pigeon circovirus (PiCV) infection and young pigeon disease syndrome (YPDS), associated with high morbidity and mortality, have been recognized in young racing pigeons from large portions of Central Europe. There exist a number of data indicating that YPDS is a consequence of PiCV infection and subsequent immunosuppression. In order to prove PiCV to be one of the crucial factors of YPDS, an experimental infection with PiCV was performed under controlled conditions. Twenty-four domestic pigeons (Columba livia forma domestica) were divided into two groups with 12 pigeons each; an infection group and a control group. All birds were between their fourth to eighth week of life. Pigeons in the infection group were infected both intramuscularly and orally with PiCV purified from naturally infected birds, while pigeons in the control group received a placebo. To test a possible influence of the PiCV infection on the immune system, the animals in both groups were vaccinated simultaneously, on the same day, against PMV-1 (Lasovac plus, IDT, Dessau-Tornau, Germany). Weekly virologic testing showed a viraemic period, and excretion of the infection virus, in pigeons in the infection group. Replication of PiCV could be proved on the basis of histologic findings of multiglobular inclusion bodies, mainly observed in macrophages of the bursa of Fabricius. A PiCV, genetically distinct from the experimental virus, was detected in the control group by polymerase chain reaction (PCR) testing, but any histologic findings comparable to the infection group were absent. None of the pigeons revealed clinical signs of illness, or hints that immunosuppression had occurred, regardless of their group. The absence of stressful conditions, considered as a trigger for the development of YPDS, may be responsible for the failure of disease reproduction in our infection model.
鸽圆环病毒(PiCV)感染与幼鸽病综合征(YPDS)相关,后者发病率和死亡率高,在中欧大部分地区的赛鸽幼鸽中已被确认。有多项数据表明,YPDS是PiCV感染及随后免疫抑制的结果。为证明PiCV是YPDS的关键因素之一,在可控条件下进行了PiCV实验性感染。24只家鸽(Columba livia forma domestica)分为两组,每组12只;一组为感染组,一组为对照组。所有鸽子均处于4至8周龄。感染组鸽子通过肌肉注射和口服从自然感染鸟类中纯化的PiCV进行感染,而对照组鸽子接受安慰剂。为测试PiCV感染对免疫系统的可能影响,两组动物在同一天同时接种针对PMV - 1(Lasovac plus,IDT,德国德绍 - 托尔瑙)的疫苗。每周病毒学检测显示感染组鸽子存在病毒血症期及感染病毒排泄情况。基于主要在法氏囊巨噬细胞中观察到的多球形体包涵体的组织学发现,可证明PiCV的复制。通过聚合酶链反应(PCR)检测在对照组中检测到一种与实验病毒基因不同的PiCV,但未发现与感染组可比的任何组织学发现。无论所属组别如何,所有鸽子均未表现出疾病的临床症状,也没有免疫抑制发生的迹象。被视为YPDS发病诱因的应激条件缺失,可能是我们的感染模型中疾病未能重现的原因。