Schiff D, Rosenblum M K
Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
Hum Pathol. 1998 Mar;29(3):215-22. doi: 10.1016/s0046-8177(98)90038-7.
Although herpes simplex encephalitis (HSE) is not regarded as an opportunistic infection, the occurrence of HSE in immunocompromised patients has been documented and the suggestion made that unusual clinical and neuropathologic features characterize the disorder in this population. To further characterize HSE as it affects the immunodeficient, the authors reviewed the clinical and pathological findings in three immunocompromised patients with autopsy-proven HSE. Two patients had cancer (one with lymphoma and another with glioblastoma multiforme), one was known to be human immunodeficiency virus-type 1 (HIV-1)-seropositive and a second was suspected of harboring underlying HIV-1 infection. Two were receiving dexamethasone at onset of HSE. All had fever, mental status changes and new, focal neurological deficits or worsening of established deficits. Cerebrospinal fluid (CSF) pleocytosis was absent or minimal and head computerized tomographic (CT) scans, performed in all cases, were unrevealing. No patient was clinically suspected of having HSE, only one received acyclovir (for concurrent mucocutaneous herpes) and HSE played a major role in all deaths. Autopsy revealed an unusual form of HSE characterized by a noninflammatory, pseudoischemic histological presentation and the unexpected persistence of viral antigens in abundance despite survival beyond the clinical stage during which inflammatory responses usually peak and productive brain infection wanes. The incidence of HSE in the immunocompromised may be underestimated. Preexistent neurological disease, a noninflammatory CSF profile and negative CT scan may confound the diagnosis in this population, a typical clinical presentation notwithstanding. Increased clinical suspicion, the use of magnetic resonance imaging and polymerase chain reaction analysis of CSF for herpes simplex virus nucleic acid sequences may permit more rapid diagnosis and treatment. The absence of inflammatory infiltrates in some fatal cases of HSE suggests that an intact immune response is not requisite to the devastating neurological injury characteristic of this disorder.
虽然单纯疱疹性脑炎（HSE）不被视为机会性感染，但免疫功能低下患者发生HSE的情况已有记录，并且有人提出该人群中这种疾病具有不寻常的临床和神经病理学特征。为了进一步描述HSE对免疫缺陷患者的影响，作者回顾了3例经尸检证实为HSE的免疫功能低下患者的临床和病理结果。2例患者患有癌症（1例为淋巴瘤，另1例为多形性胶质母细胞瘤），1例已知为人类免疫缺陷病毒1型（HIV-1）血清阳性，另1例怀疑存在潜在的HIV-1感染。2例在HSE发病时正在接受地塞米松治疗。所有患者均有发热、精神状态改变以及新出现的局灶性神经功能缺损或原有缺损加重。脑脊液（CSF）细胞增多症不存在或轻微，所有病例均进行了头部计算机断层扫描（CT），但均未发现异常。临床上没有患者被怀疑患有HSE，只有1例接受了阿昔洛韦治疗（用于并发的黏膜皮肤疱疹），HSE在所有死亡病例中都起了主要作用。尸检显示HSE的一种不寻常形式，其特征为非炎症性、假性缺血性组织学表现，并且尽管已度过炎症反应通常达到高峰且脑实质感染减弱的临床阶段，但病毒抗原仍意外大量持续存在。免疫功能低下患者中HSE的发病率可能被低估。既往存在的神经系统疾病、非炎症性脑脊液检查结果以及CT扫描阴性可能会使该人群中的诊断变得复杂，尽管有典型的临床表现。提高临床怀疑度、使用磁共振成像以及对脑脊液进行单纯疱疹病毒核酸序列的聚合酶链反应分析可能有助于更快速地诊断和治疗。HSE某些致命病例中缺乏炎症浸润表明，完整的免疫反应并非这种疾病所特有的毁灭性神经损伤的必要条件。
