Weissenböck H, Suchy A, Holzmann H
Institute of Pathology and Forensic Veterinary Medicine, University of Veterinary Medicine, Vienna, Austria.
Acta Neuropathol. 1998 Apr;95(4):361-6. doi: 10.1007/s004010050811.
Eight dogs originating from different regions of Austria [all of them known as tick-borne encephalitis (TBE) areas] with severe neurological signs were either euthanatized or died spontaneously. Tick-borne encephalitis virus (TBEV) antigen was detected in the brains of five of these dogs by immunohistology, but not in the others. All of the dogs, however, had identical neuropathological changes. There were moderate lymphohistiocytic meningitis, widespread neuronal necroses, karyorrhexis of glial cells, numerous neuronophagic nodules, and extensive microgliosis. In the cerebellum, loss of Purkinje cells and proliferation of microglial cells in the molecular layer were found. All brain regions showed numerous perivascular cuffs consisting of lymphocytes, macrophages, plasma cells and, occasionally, red blood cells. The blood-derived cells were not restricted to the perivascular spaces but diffusely infiltrated the neuropil. The most severe changes were localized in the neuroparenchyma surrounding the fourth ventricle. Lesions were less severe in basal ganglia, thalamus, mesencephalon, nuclei of pons and medulla oblongata. Moderate lesions were found in the gray matter of neocortex and allocortex, hippocampus and molecular and Purkinje cell layers of the cerebellum. White matter was slightly to moderately affected. The choroid plexus was free of inflammation. Due to rapid virus clearance mechanisms in this disease, antigen was not detectable in all cases. Neuropathological changes identical with those of immunohistologically proven cases justified the diagnosis TBE in these cases. In addition, the neuropathological diagnosis was supported by the origin of the affected dogs from endemic areas, the seasonal occurrence of the disease and a clinical history of a highly febrile neurological disease with short duration.
来自奥地利不同地区（均为已知的蜱传脑炎疫区）的8只出现严重神经症状的犬，要么被实施安乐死，要么自行死亡。通过免疫组织学方法在其中5只犬的大脑中检测到了蜱传脑炎病毒（TBEV）抗原，而其他犬未检测到。然而，所有这些犬都有相同的神经病理学变化。存在中度淋巴细胞性组织细胞性脑膜炎、广泛的神经元坏死、神经胶质细胞核固缩、大量噬神经结节以及广泛的小胶质细胞增生。在小脑，发现浦肯野细胞缺失以及分子层中小胶质细胞增生。所有脑区均可见由淋巴细胞、巨噬细胞、浆细胞以及偶尔的红细胞组成的大量血管周围套袖状浸润。血液来源的细胞并不局限于血管周围间隙，而是弥漫性浸润神经纤维网。最严重的变化位于第四脑室周围的神经实质。基底神经节、丘脑、中脑、脑桥核和延髓的病变较轻。在新皮质和旧皮质的灰质、海马以及小脑的分子层和浦肯野细胞层发现中度病变。白质受到轻度至中度影响。脉络丛无炎症。由于该疾病中病毒的快速清除机制，并非所有病例都能检测到抗原。与免疫组织学证实的病例相同的神经病理学变化证明了这些病例中蜱传脑炎的诊断。此外，患病犬来自疫区、疾病的季节性发生以及高热性神经系统疾病的短期临床病史支持了神经病理学诊断。
