Clinic for Birds, Reptiles, Amphibians and Fish, Justus Liebig University Giessen, Frankfurter Str. 144, 35392 Giessen, Germany.
Institute of Virology, Justus Liebig University Giessen, Schubertstr. 81, 35392 Giessen, Germany.
Avian Dis. 2020 Sep 1;64(3):247-253. doi: 10.1637/aviandiseases-D-19-00074.
In this study, we investigated the natural route of infection of psittacine bornavirus (PaBV), which is the causative agent of proventricular dilatation disease (PDD) in psittacines. We inoculated two infection groups through wounds with a PaBV-4 isolate. In nine cockatiels (Nymphicus hollandicus) we applied a virus suspension with a titer of 103 50% tissue culture infection dose (TCID50) via palatal lesions (Group P, P1-9). In a second group of three cockatiels, we applied a virus suspension with a titer of 104 TCID50 to footpad lesions (Group F, F1-3). In two cockatiels, the control (or "mock") group, we applied a virus-free cell suspension (Group M, M1-2) via palatal lesions. The observation period was 6 mo (Groups P and M) or 7 mo (Group F). We monitored PaBV-4 RNA shedding and seroconversion. At the end of the study, we examined the birds for the presence of inflammatory lesions, PaBV-4 RNA, and antigen in tissues, as well as virus reisolation of brain and crop material. We did not observe any clinical signs typical of PDD during this study. We also did not see seroconversion or PaBV RNA shedding in any bird during the entire investigation period, and virus reisolation was not successful. We only found PaBV-4 RNA in sciatic nerves, footpad tissue, skin, and in one sample from the intestine of Group F. In this group, the histopathology revealed mononuclear infiltrations mainly in skin and footpad tissue; immunohistochemistry showed positive reactions in spinal ganglia and in the spinal cord, and slightly in skin, footpad tissues, and sciatic nerves. In Groups P and M we found no viral antigen or specific inflammations. In summary, only the virus application on the footpad lesion led to detectable PaBV RNA, mononuclear infiltrations, and positive immunohistochemical reactions in tissues of the experimental birds. This could suggest that PaBV spreads via nervous tissue, with skin wounds as the primary entry route.
在这项研究中，我们研究了鹦鹉禽呼肠孤病毒（PaBV）的自然感染途径，该病毒是导致鹦鹉前胃扩张病（PDD）的病原体。我们通过伤口接种了两组感染群，接种的病毒是 PaBV-4 分离株。在 9 只玄凤鹦鹉（Nymphicus hollandicus）中，我们通过腭部病变（第 P 组，P1-9）应用了滴度为 10350%组织培养感染剂量（TCID50）的病毒悬液。在第二组的 3 只玄凤鹦鹉中，我们通过脚垫病变应用了滴度为 104TCID50 的病毒悬液（第 F 组，F1-3）。在两只玄凤鹦鹉（对照组或“模拟”组）中，我们通过腭部病变应用了不含病毒的细胞悬液（第 M 组，M1-2）。观察期为 6 个月（P 组和 M 组）或 7 个月（F 组）。我们监测 PaBV-4 RNA 的脱落和血清转换。研究结束时，我们检查了鸟类组织中是否存在炎症病变、PaBV-4 RNA 和抗原，以及脑和作物材料的病毒再分离情况。在整个研究过程中，我们没有观察到任何典型的 PDD 临床症状。我们也没有在任何一只鸟的整个调查期间看到血清转换或 PaBV RNA 的脱落，病毒再分离也没有成功。我们只在第 F 组的坐骨神经、脚垫组织、皮肤和肠道的一个样本中发现了 PaBV-4 RNA。在该组中，组织病理学显示主要在皮肤和脚垫组织中存在单核细胞浸润；免疫组织化学显示在脊髓节和脊髓中呈阳性反应，在皮肤、脚垫组织和坐骨神经中略有阳性反应。在 P 组和 M 组中，我们没有发现病毒抗原或特定的炎症。总的来说，只有在脚垫病变上应用病毒才能导致实验鸟类的组织中可检测到 PaBV RNA、单核细胞浸润和阳性免疫组织化学反应。这表明 PaBV 通过神经组织传播，皮肤伤口是主要的进入途径。
