Aseptic Meningitis Due to Varicella-Zoster Virus: Serum Antibody Levels and Local Synthesis of Specific IgG, IgM, and IgA

Abstract

We used an indirect enzyme immunoassay to describe the evolution of serum levels and the intrathecal production of IgG, IgA, and IgM antibodies to varicella-zoster virus (VZV) in eight patients with a syndrome of acute aseptic meningitis (AAM) and evidence of intrathecal production of VZV-specific IgG antibodies. Four of the eight patients showed no cutaneous zoster while hospitalized. Our results suggested an etiologic relation between VZV and AAM in all cases. Furthermore, we observed some differences in the pattern of evolution of antibodies in serum and cerebrospinal fluid in relation to the presence or absence of cutaneous lesions in our patients. These differences could reflect different pathogenic mechanisms in the spread of VZV to the central nervous system and in the production of the AAM syndrome.

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

“…Serum IgG antibody titers were all 1: 1,280, which meant the presence of immunity for them but they were lacking specificity due to heterotypic reactivity occasionally seen between them [ 13], Recent infection of VZV was also not proved serologically because serum of acute stage could not be obtained and serum IgM was not detected. Detec tion of antibodies to VZV in the CSF is also a reliable means of diagnosis of CNS involvement of HZ [11], But in our patient, CSF IgG and IgM antibodies were not detected and thus not helpful for diagnosis.…”

“…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.…”

“…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. When skin lesions are not typical for the HZ or in rare instances o f'zoster sine herpete' in which skin lesions fail to ensue, HZ can be diagnosed serologically by detecting at least a fourfold rise in the IgG antibody titers between acute and convalescent serum [12] or by demonstration of virus-specific IgM antibody which is a reliable indicator of recent infection or reactivation [11], But not all patients with zoster develop IgM antibodies to VZV dur ing the course of the disease [11]. In our case, IgG and IgM antibodies to three types of herpes virus group were measured with commercially available ELISA.…”

Infections of the Nervous System Caused by Varicella-Zoster Virus: A Review

“…(6) specific IgG antibody activity in CSF when the albumin ratio CSF/serum was <0.0075 [75], (7) ratio of antibody titer CSF/serum to total IgG or IgA concentration CSF/serum (antibody to immunoglob ulin index. Iab:Ig) >2.0 [92], (8) significant VZV antibody activity in CSF when compared with the antibody activity against another virus (i.e.. measles virus or CMV) which is taken as reference; this is measured by the ratio of anti-VZV titer CSF/serum that must be 2-4 times higher than the ratio for the reference agent to indicate intrathecal antibody production [108,109], (9) specific antibody activity in CSF higher than in a selected dilution of serum when samples are tested by capture EIA for VZV-specific IgG or IgA antibody [110], and (10) multisubclass pattern for the VZV-specific IgG detected in CSF [111,112].…”

“…Virus recovery is more frequent among the immunocompromised [87][88][89], but in normal patients it is an uncommon finding, occur ring only at a very early stage of neurological disease [90][91][92][93]. Isolation procedures may render negative results even when viral particles are present in the CSF, as seen by electron microscopy [94], Neurological syndromes af ter the primary VZV infection are immunc-mediated and virus is already cleared from the CSF when the disease starts.…”