Adle-Biassette H, Bourhy H, Gisselbrecht M, Chrétien F, Wingertsmann L, Baudrimont M, Rotivel Y, Godeau B, Gray F
Département de Pathologie (Neuropathologie), Hôpital Henri Mondor, Créteil, France.
Acta Neuropathol. 1996 Oct;92(4):415-20. doi: 10.1007/s004010050538.
A 46-year-old man was bitten by a dog in Mali; anti-rabies vaccination was incomplete. Three months later he was admitted to hospital with fever and diarrhea. Human immunodeficiency virus (HIV) serology was positive and CD4 count was 70/mm3. His status worsened rapidly with confusion hydrophobia and hypersialorrhea. Despite anti-rabies serotherapy and vaccination, he died suddenly 12 days after admission. Immunofluorescence on cerebral tissue samples established rabies encephalitis. Neuropathology showed mild encephalitis with occasional Babès nodules and rare perivascular mononuclear cuffs. Intraneuronal Negri inclusion bodies were remarkably diffuse and abundant. They were clearly demonstrated by immunocytochemistry and electron microscopy. Apoptotic neurons were identified in the brain stem and hippocampus in the vicinity of inflammatory foci. In contrast, apoptosis could not be demonstrated in non-inflammatory areas, even where Negri bodies were numerous. There was no associated HIV encephalitis or opportunistic infection. The occurrence of rabies encephalitis in AIDS represents a random association, but is probably not exceptional as rabies is endemic in many countries and the AIDS epidemic is spreading worldwide. In this case, although the incubation duration and clinical presentation were comparable to those in classical rabies the T-cell-mediated immunosuppression may account for the weak inflammatory reaction and unusually abundant viral multiplication. This observation confirms that all those at risk for rabies, particularly immunocompromised patients, should receive complete anti-rabies treatment including vaccines and specific immunoglobulins, as soon as possible after infection.
一名46岁男子在马里被狗咬伤；抗狂犬病疫苗接种未完成。三个月后，他因发热和腹泻入院。人类免疫缺陷病毒（HIV）血清学检测呈阳性，CD4细胞计数为70/mm³。他的病情迅速恶化，出现意识模糊、恐水症和唾液分泌过多。尽管进行了抗狂犬病血清疗法和疫苗接种，但他在入院12天后突然死亡。脑组织样本的免疫荧光检查确诊为狂犬病脑炎。神经病理学显示轻度脑炎，偶见巴贝斯结节和罕见的血管周围单核细胞套袖。神经元内的内基小体明显弥漫且丰富。通过免疫细胞化学和电子显微镜清晰地显示了这些小体。在脑干和海马体的炎症病灶附近发现了凋亡神经元。相比之下，在非炎症区域即使内基小体很多也未发现凋亡现象。未发现相关的HIV脑炎或机会性感染。艾滋病患者发生狂犬病脑炎是一种随机关联，但可能并不罕见，因为狂犬病在许多国家流行，且艾滋病疫情正在全球蔓延。在这种情况下，尽管潜伏期和临床表现与经典狂犬病相似，但T细胞介导的免疫抑制可能是炎症反应较弱和病毒异常大量增殖的原因。这一观察结果证实，所有有感染狂犬病风险的人，特别是免疫功能低下的患者，在感染后应尽快接受包括疫苗和特异性免疫球蛋白在内的完整抗狂犬病治疗。
