Nervous system complications of herpes zoster: immunofluorescent demonstration of varicella-zoster antigen in CSF cells

Abstract

(Gold, 1966;Joncas et al., 1968;Djupesland et al., 1976;Hotson and Pedley, 1976). The VZ antigen has been demonstrated in CSF cells in one case of herpes zoster meningitis (Shoji et al., 1976).As CNS involvement in herpes zoster is not infrequent, and morbidity and mortality are not

Varicella zoster virus meningitis with hypoglycorrhachia in the absence of rash in an immunocompetent woman

“…VZV isolation from CSF or stool is rare, and VZV is an exclusively human virus that does not produce disease after experimental infection of mice (Wroblewska et al, 1982). More recently, proof that VZV can cause serious neurological disease, often in the absence of rash, has been based on serologic analyses to detect VZV-specific antibodies (Shoji et al, 1976), as well as intracellular antigen in patients with zoster meningoencephalitis, cranial and spinal radiculoneuritis (Peters et al, 1979), and intrathecal production of anti-VZV antibodies (Martinez-Martin et al, 1985; Echevarria et al, 1987). Most recently, combined PCR and antibody testing revealed that VZV causes 5% to 27% of all aseptic meningitis (Koskiniemi et al, 2001; Hausfater et al, 2004; Kupila et al, 2006; Frantzidou et al, 2008), which is not altogether surprising because PCR has already shown that VZV causes zoster sine herpete (Gilden et al, 1994), vasculopathy (Gilden et al, 1996), acute (Gilden, 1994) and recurrent (Gilden et al, 2009) myelopathy, acute cerebellar ataxia (Moses et al, 2006; Ratzka et al, 2006), and retinal necrosis (el Azazi et al, 1991; Galindez et al, 1996), all without rash.…”

A Case of Herpes Zoster Myelitis: Positive Magnetic Resonance Imaging Finding

“…The incidence and severity of HZ is greatly increased in persons with defective cel lular immunity such as advancing age, lymphoproliféra tive malignancies and immunosuppressive treatment [8], In these circumstances, dissemination and serious complications of HZ are also more frequent [8,9], How ever, our patient had no evidence of underlying malig nancy and was younger than the other patients with HZ myelitis reported in the literature [5][6][7], It is likely that the clinical manifestations of HZ infection are deter mined by a complex interplay of host-defense defects, activation of latent agents and environmental exposure The pathogenesis of HZ myelitis has been thought as a direct viral invasion because inclusion bodies and VZV particles were found in glial cells, and the virus was iso lated from the spinal cord of patients with zoster myelitis [5], Isolation of the VZV from the CSF or demonstration of the VZV antigen in CSF cells by immunofluorescence is a confirmative evidence for viral central nervous sys tem (CNS) infection but it is rarely successful [ 10,11], Therefore, the diagnosis is usually made on the clinical ground when characteristic CNS symptoms develop in the context of HZ. The association was clear in our case because the interval between the exanthem and the onset of neurologic symptoms was as short as 3 days.…”

Role of the virology laboratory in diagnosis and management of patients with central nervous system disease

“…In one study, myelitis occurred as an unusual complication of VZV infection (1 of 1,210 cases) (147), as does herpes ophthalmicus with contralateral hemiplegia. Even in uncomplicated VZV infection, the CSF may show pleocytosis and increased protein concentration (112 (19,21). Although on a worldwide basis mumps remains the second leading cause of aseptic meningitis and encephalomyelitis (20,42,44,116,146), the incidence has decreased dramatically in the United States with the introduction of large-scale immunization.…”