Worrell J T, Cockerell C J
Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, USA.
Am J Dermatopathol. 1997 Apr;19(2):133-7. doi: 10.1097/00000372-199704000-00006.
Cutaneous herpesvirus infection is a common viral disorder manifest by epidermal and/or mucosal vesicle formation. Though it is believed that the virus most likely resides in regional sensory ganglia following primary infection and that cutaneous involvement represents reactivation of a latent infection, the histopathology of cutaneous nerves in sites of disease has not been well characterized. In order to assess and characterize the pathologic changes of these nerves, we retrospectively examined 54 cases of cutaneous and mucosal herpesvirus infection as defined by the presence of diagnostic multinucleate epithelial giant cells that demonstrated viral cytopathic effect. Dermal nerves were evaluable in 48 of 54 cases. All cases showed perineural inflammation that consisted of a dense mixed lymphocyte-polymorphonuclear cell infiltrate. Twenty-six cases exhibited intraneural infiltrations accompanied by Schwann cell hypertrophy with nuclear eosinophilia and pyknosis. Frank neuronal necrosis was present in 21 cases, with viral cytopathic effect evident within neurons of four cases. The degree of peri- and intraneural inflammation correlated with the severity of the inflammatory response within the dermis in most cases; however, in eight cases there was inflammatory involvement of neurovascular structures distant from and out of proportion to dermal and epidermal changes. Immunoperoxidase staining using a polyvalent antibody to human herpesvirus was performed in two cases and demonstrated viral antigen within nerve twigs. This pattern of peripheral nerve twig inflammation, along with the occurrence of more distant neural involvement, may prove to have diagnostic implications and serve as a clue in the recognition of cutaneous herpesvirus infection, particularly in cases with subtle or absent epidermal alteration. Furthermore, the presence of inflammation within and around nerves as well as degenerative changes suggest that nerve twigs are not passive conduits for viral spread but may be directly involved in infection.
皮肤疱疹病毒感染是一种常见的病毒性疾病，表现为表皮和/或黏膜水疱形成。尽管人们认为病毒在初次感染后很可能潜伏在局部感觉神经节中，而皮肤受累代表潜伏感染的重新激活，但疾病部位皮肤神经的组织病理学特征尚未得到充分描述。为了评估和描述这些神经的病理变化，我们回顾性研究了54例皮肤和黏膜疱疹病毒感染病例，这些病例通过诊断性多核上皮巨细胞的存在来定义，这些巨细胞显示出病毒细胞病变效应。54例中有48例真皮神经可评估。所有病例均显示神经周围炎症，由密集的混合淋巴细胞-多形核细胞浸润组成。26例出现神经内浸润，伴有施万细胞肥大，核嗜酸性变和核固缩。21例出现明显的神经元坏死，4例神经元内可见明显的病毒细胞病变效应。在大多数情况下，神经周围和神经内炎症程度与真皮内炎症反应的严重程度相关；然而，在8例中，远离真皮和表皮变化且与之不成比例的神经血管结构出现了炎症累及。对2例进行了使用抗人疱疹病毒多价抗体的免疫过氧化物酶染色，在神经小枝内显示出病毒抗原。这种周围神经小枝炎症模式，以及更远处神经受累的发生，可能具有诊断意义，并可作为识别皮肤疱疹病毒感染的线索，特别是在表皮改变不明显或不存在的病例中。此外，神经内和神经周围炎症的存在以及退行性改变表明，神经小枝不是病毒传播的被动管道，而是可能直接参与感染。
