A Case of Aseptic Meningitis Without Rash Possibly Associated With Varicella Vaccine

Abstract

Varicella-zoster virus (VZV) may cause aseptic meningitis in the pediatric age group. We describe a pediatric case of aseptic meningitis with a substantial increase of the paired serum antibody to VZV in which the child did not have skin rash during the course of illness. The patient was a 13-year-old boy without any history of exposure to VZV who was admitted with headache, vomiting, and low-grade fever. He had received one dose of varicella vaccine derived from the Oka/Biken strain (vOka) at the age of one year. Cerebrospinal fluid (CSF) analysis on admission revealed an elevated white blood cell count at 609/mm 3 with 99.6% mononuclear cells. As his symptoms resolved after lumbar puncture alone, he was discharged on the seventh day of hospitalization without receiving any specific medication. Serum VZV-IgG titer was found to be substantially elevated after two weeks. VZV infection and reactivations associated with vaccination, as well as past infections, should be included in the differential diagnoses of pediatric aseptic meningitis, even in the absence of skin rash in the entire course. Polymerase chain reaction (PCR) testing for VZV DNA in CSF should be performed in all cases, if available.

Varicella‐zoster virus‐related neurological complications: From infection to immunomodulatory therapies

“…143 VZV causes the meninges to become more amplified in the inflammatory cascade by eliciting an immunological response that is marked by the production of pro-inflammatory cytokines such as IL-6, TNF-α, and IFN-γ. 144 VZV infection may cause an inflammatory response, which can weaken the BBB and allow immune cells and inflammatory mediators to enter the brain and spinal cord. 145,146 Aseptic meningitis associated with VZV infection typically presents with symptoms such as headache, fever, neck stiffness, photophobia, and neurological deficits.…”

“…Reactivation of latent VZV inside the sensory ganglia may result in aseptic meningitis when the virus travels down sensory nerve fibres and invades the meninges 143 . VZV causes the meninges to become more amplified in the inflammatory cascade by eliciting an immunological response that is marked by the production of pro‐inflammatory cytokines such as IL‐6, TNF‐α, and IFN‐γ 144 . VZV infection may cause an inflammatory response, which can weaken the BBB and allow immune cells and inflammatory mediators to enter the brain and spinal cord 145,146 .…”