A 46-year-old female presenting with worsening headache, nuchal rigidity and a skin rash in varicella zoster virus meningitis: A case report

Department of Medicine, Division of Infectious Diseases, Island University Hospital 475 Seaview Ave., Staten Island, NY 10305 USA.
Cases Journal 09/2009; 2(9):6299. DOI: 10.4076/1757-1626-2-6299
Source: PubMed


Varicella zoster virus causes two distinct clinical diseases. Varicella is the primary infection and results from exposure of a person susceptible to the virus. The virus remains latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in the elderly and immuno-compromised, varicella zoster virus reactivates and can cause a wide range of neurologic disease, including herpes zoster ('shingles'), postherpetic neuralgia, vasculopathy, myelopathy, retinal necrosis, cerebellitis, and zoster sine herpete. Herpes zoster is associated with numerous neurologic complications and varied presentations. Patients who have a dermatomal distribution of varicella zoster virus and who have headaches should be considered to have VZV meningitis. Virologic confirmation requires testing the cerebrospinal fluid for varicella zoster virus deoxyribonucleic acid via polymerase chain reaction. The application of polymerase chain reaction to the cerebrospinal fluid can be used to detect varicella zoster virus deoxyribonucleic acid and, therefore, infections of the central nervous system. We present a case report of a 46-year-old female who initially presented with worsening headache, nuchal rigidity, fever, and a skin rash, who was subsequently found to have varicella zoster meningitis.

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    ABSTRACT: Primary infection with varicella-zoster virus (VZV), an exclusively human neurotropic α-herpesvirus, causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), dermatomal distribution pain, and rash on an erythematous base in one to three dermatomes. Zoster develops anywhere on the body. Skin lesions resolve within 1-2 weeks while complete cessation of pain usually takes 4-6 weeks. Unfortunately, zoster can be followed by chronic pain (postherpetic neuralgia), meningoencephalitis, cerebellitis, cranial nerve palsies, vasculopathy, myelopathy, and inflammatory eye disease. VZV reactivation also produces chronic radicular pain without rash (zoster sine herpete). In fact, all neurologic and ocular disorders listed above may also develop without rash. This review covers clinical, laboratory, and pathologic features of neurologic complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system and the potential value of examining saliva for VZV DNA in patients with neurologic disease without rash. Additional perspectives are provided by discussions of the VZV genome, latency, pathogenesis, and immunity, and of the value of immunization of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.
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