Clinical spectrum and prognosis of neurological complications of reactivated varicella-zoster infection: the role of immunosuppression.

Immunosuppressed patients are at higher risk for developing herpes zoster (HZ), and neurological complications are frequent in them. However, the influence of immunosuppression (IS) on the severity and prognosis of neurological complications of varicella-zoster virus (VZV) reactivation is unknown. We studied retrospectively patients with neurological complications due to VZV reactivation who attended our hospital between 2004 and 2019. We aimed to assess the clinical spectrum, potential prognostic factors, and the influence of the immune status on the severity of neurological symptoms. A total of 98 patients were included (40% had IS). Fifty-five patients (56%) had cranial neuropathies which included Ramsay-Hunt syndrome (36 patients) and cranial multineuritis (23 patients). Twenty-one patients developed encephalitis (21%). Other diagnosis included radiculopathies, meningitis, vasculitis, or myelitis (15, 10, 6, and 4 patients, respectively). Mortality was low (3%). At follow-up, 24% of patients had persistent symptoms although these were usually mild. IS was associated with severity (defined as a modified Rankin scale greater than 2) (odds ratio, 4.23; 95% confidence interval, 1.74-10.27), but not with prognosis. Shorter latency between HZ and neurologic symptoms was the only factor associated with an unfavorable course (death or sequelae) (odds ratio, 0.82; 95% confidence interval, 0.71-0.95). In conclusion, the clinical spectrum of neurological complications in VZV reactivation is wide. Mortality was low and sequelae were mild. The presence of IS may play a role on the severity of neurological symptoms, and a shorter time between HZ and the onset of neurological symptoms appears to be a negative prognostic factor.

Varicella-zoster virus-specific cell-mediated immunity in Ramsay Hunt syndrome.

OBJECTIVES/HYPOTHESIS: The etiology of Ramsay Hunt syndrome (Hunt syndrome) is reactivation of latent varicella-zoster virus (VZV) in the geniculate ganglion of the facial nerve, leading to neuritis. Although the mechanism of the VZV reactivation is unclear, one possibility is that the reactivation involves a low level of VZV-specific cell-mediated immunity (CMI). The aim of this study was to clarify the characteristics of the VZV-specific CMI in Hunt syndrome compared to that in Bell's palsy, and to obtain clues to its role in the development of Hunt syndrome. STUDY DESIGN: Prospective study. METHODS: We determined the median spot numbers and examined VZV-specific CMI in patients with Hunt syndrome and with Bell's palsy using interferon-γ enzyme-linked immunospot (ELISPOT) assays. We analyzed the relationship between the value of VZV-specific CMI and days from disease onset. RESULTS: The median spot number in Hunt syndrome (87.3 spot-forming cells [SFCs]/4 × 10(5) peripheral blood mononuclear cells [PBMCs]) was higher than that in Bell's palsy (62.3 SFCs/4 × 10(5) PBMCs). Hunt syndrome showed a strong relationship between the ELISPOT count and days from onset (r = 0.65). Within the first 5 days from onset, no ELISPOT counts higher than 80 SFCs/4 × 10(5) PBMCs were observed. On the other hand, no correlation was observed between the ELISPOT count and days from onset in patients with Bell's palsy (r = -0.19). CONCLUSIONS: These results suggest that VZV-specific CMI in Hunt syndrome is low at disease onset and increases rapidly thereafter. Consequently, reduced VZV-specific CMI may play an important role in the reactivation of VZV in the facial nerve, leading to Hunt syndrome.

[Herpes zoster oticus: symptom constellation and serological diagnosis]. / Untersuchungen zum Zoster oticus.

BACKGROUND: Herpes zoster oticus is a rare illness with cutaneous symptoms (eruptions) and a colored picture of brain nerve failures. The clinical symptoms, the symptom constellation, diagnostics and therapy, however, have been examined till now only in few studies. PATIENTS AND METHODS: In this study 91 cases of a zoster oticus were looked at in retrospect from the complete archives of the university ENT clinic Jena/Germany in the period from 1932 to 2001. Inclusion criterion was the occurrence eruptions in the ear region. The demographic data, subjective and objective symptoms, the symptom constellations, diagnostic methods and the therapy were arranged. RESULTS: Women (68.1 %) were concerned more frequently than men (31.9 %). The average illness age was 51.2 days. The prodromal stage lasted for 2.2 days in the average. Earache (50.2 %) and headache (11.0 %) were the most frequent first symptoms. No prodroma appeared in 27.5 % of the cases. The facial nerve (86.8 %) was most frequently affected, the vestibular nerve in 76.9 % and the cochlear nerve in 36.3 %. Other brain nerve damages were extremly rare. The therapy success was identical with regard to the brain nerve regeneration at all times. A positive antibody titer for VZV-IgM and/or IgA or an IgG is a sign for an acute infektion. VZV-IgA antibody titers appeared more constantly, frequent and early than an IgM. CONCLUSIONS: Women have a greater risk of falling ill at a zoster oticus than men. Although more than 72 hours is behind the beginning of the symptoms in this study, treatment with virostatic drugs should always be carried out in zoster oticus. Different therapy methods do not have any influence to the success therapy of the therapy. The facial nerve showed the best cure trend. A postzosteric pain develops approximately the half of the cases at the zoster oticus. The serological diagnostic is not necessary in clinically clear cases.

Rapid strip assay for detection of anti-herpes simplex virus antibodies: application to prediction of varicella-zoster virus reactivation in patients with acute peripheral facial palsy.

Varicella-zoster virus (VZV) reactivation causes acute peripheral facial palsy in the majority (88%) of patients who lack anti-herpes simplex virus (HSV) antibodies, suggesting that an absence of anti-HSV antibodies is a reliable serological marker for the diagnosis of VZV reactivation in patients who are diagnosed initially as idiopathic peripheral facial palsy (Bell's palsy) [Furuta et al., 2000] Clinical Infectious Diseases]. A simple and rapid immunoassay for detection of anti-HSV antibodies based on HSV type 1 glycoprotein D was developed by modifying the conventional Western blot technique. The assay was evaluated by comparing the results with those of conventional Western blot. In total, 100 sera obtained from patients with acute peripheral facial palsy were tested and judged blindly by two investigators. Twenty-four of 26 HSV-seronegative sera were obtained from patients with VZV reactivation (Ramsay Hunt syndrome or zoster sine herpete). The sensitivity of the assay was over 95% and the specificity was 100%. The two investigators agreed on the diagnosis in 99 of the 100 sera. These results indicate that the rapid strip assay is applicable to prediction of VZV reactivation in patients diagnosed clinically with Bell's palsy before zoster lesions appear or PCR using saliva samples indicates VZV reactivation.

Impaired specific cellular immunity to the varicella-zoster virus in patients with herpes zoster oticus.

The possible involvement of depression on cellular immunity in reactivation of varicella-zoster virus (VZV) in herpes zoster oticus was investigated. The subjects comprised 59 cases of herpes zoster oticus, 33 cases of herpes zoster sine herpete (ZSH) with facial paralysis, and 205 cases of Bell's palsy. The transformation rate of lymphocytes to phytohaemagglutinin in herpes zoster oticus tended to be lower than that in Bell's palsy. In skin tests with purified protein derivatives of tuberculin, the positivity rate in herpes zoster oticus was significantly lower than that in Bell's palsy (p < 0.015). In skin tests using VZV antigen the positivity rate in herpes zoster oticus and ZSH were significantly lower than that of Bell's palsy (p < 0.001 and p < 0.015, respectively). Thus, it was noted that cellular immunity, especially specific cellular immunity against VZV, was significantly depressed in herpes zoster oticus and ZSH. We consider that depression of specific cellular immunity plays an important role in triggering reactivation of VZV and onset of these diseases.