Acute cerebellitis and concurrent encephalitis associated with parvovirus B19 infection.

C nervous system (CNS) infections caused by parvovirus B19 (PVB19) have been rarely documented, especially the involvement of the cerebellum. We describe an immunocompetent girl with acute cerebellitis associated with PVB19 infection. A 5-year-old girl was hospitalized because of seizures of the upper extremities after a 3-day history of fever. On arrival, consciousness was disturbed (Glasgow coma scale: E2V1M4). Laboratory findings on admission included white blood cells 10.6 ×10/L, blood glucose 74 mg/dL and sodium 130 mmol/L. Cerebrospinal fluid (CSF) examination showed 229 cells/μL with predominance of polymorphonuclear cells, 144 mg/dL protein and 56 mg/dL glucose. A brain computed tomography image was normal. The patient began treatment with intravenous ceftriaxone, panipenem/ betamipron, dexamethasone and acyclovir. Owing to persistent consciousness disturbance, methylprednisolone therapy was added on the fourth day in a dose of 30 mg/kg for 3 days. Electroencephalography on the sixth day showed high-voltage delta activity in the bilateral occipital regions, leading to the diagnosis of encephalopathy. On the sixth day, brain diffusionweighted magnetic resonance images (see Fig. A, Supplemental Digital Content 1, http://links.lww.com/INF/B90) showed marked hyperintensity in the bilateral dentate nuclei in the cerebellum, suggesting a diagnosis of acute cerebellitis. These dentate nuclear lesions disappeared on the 10th day, and instead hyperintensity in the cerebellar hemisphere became prominent (see Fig. B, Supplemental Digital Content 1, http://links.lww.com/INF/B90). Thereafter, the patient could gradually follow simple verbal instructions, could sit alone on the 16th day, and could walk with a wide stance on the 26th day. Mutism had remained until the 20th day. Three months later, slurred speech and intention tremor persisted. A follow-up magnetic resonance study 6 months later showed cerebellar atrophy (see Fig. C, Supplemental Digital Content 1, http://links.lww.com/ INF/B90). On the 10th day, maculopapular rash appeared, extending to the face and extremities, suggesting erythema infectiosum. This was confirmed by elevation of serum PVB19 IgM and IgG antibodies (11.63 and 7.79 titers, respectively) using enzyme immunosorbent assay. Polymerase chain reaction analyses detected PVB19 DNA in the CSF (4.5 × 10 copies/mL) and in the plasma (2.8 × 10 copies/mL) samples stored from the time of admission. Polymerase chain reaction was also applied for herpes simplex virus 1 and 2, human herpes virus (HHV) 6, 7 and 8, varicellazoster virus, cytomegalovirus, Epstein-Barr virus, JC virus and BK virus, showing negative results for all viruses examined except for HHV6 (5.5 × 10 and 3.5 × 10 copies/mL in the CSF and plasma, respectively). Serologically, HHV6-IgG antibody was positive and HHV6-IgM antibody was negative, findings consistent with history of exanthema subitum. Collectively, cerebellitis and concurrent encephalitis were likely caused by CNS PVB19 infection with reactivation of latent HHV6. It is important to note that clinical and radiologic features in our patient were consistent with those of rotavirus-associated cerebellitis. Takanashi et al documented 11 such cases and proposed it as a novel clinicoradiologic entity because of the homogeneous characteristics. Although rotavirus predominated as causative pathogens, adenovirus type 3, HHV-6 and influenza virus have also been reported. Among 31 childhood PVB19 CNS infections, only 2 developed ataxia, but their cerebellar involvement was not radiologically demonstrated. Thus, this is the first describing PVB19 as a cause for this novel type of cerebellitis and suggests a wider entity and a common mechanism.