Snowshoe Hare Virus Emerges in a Pediatric Meningoencephalitis Cluster in Whistler
A summer cluster of snowshoe hare virus meningoencephalitis in Whistler, British Columbia, exposed how easily an arboviral neuroinfection can hide inside routine emergency workups. Three children from the same community presented within days of one another with culture-negative meningoencephalitis, yet the diagnosis remained invisible until clinicians recognized the epidemiologic link and expanded testing after discharge.
The pattern fits the biology of California serogroup viruses. These are mosquito-borne orthobunyaviruses that circulate across Canada and the northern United States, with transmission concentrated during mosquito season and a short incubation period of about 3 to 7 days. In healthy children, the illness can begin as fever, headache, or seizures and then progress to meningoencephalitis, a course that mimics herpesvirus infection, enteroviral meningitis, migraine, or other common pediatric neurologic syndromes.
The clinical consequence is straightforward: if the exposure history is not connected to local vector ecology, the virus stays hidden.
Shared Geography, Shared Timing, Shared Diagnostic Blind Spots
All three children lived in Whistler and developed symptoms in July and August 2024. Their onset dates were within 1 week of one another, and each had an initial first-tier infectious diseases evaluation that failed to identify a cause. That combination of timing and geography is hard to explain by chance alone, especially in a mosquito season when California serogroup viruses circulate silently and viremia may already be waning by the time cerebrospinal fluid is collected.
Standard testing did not solve the problem. Reverse transcription PCR can distinguish among California serogroup viruses, but sensitivity is limited because viremia is low and transient in immunocompetent patients. Serology is more sensitive, yet IgM cross-reactivity between snowshoe hare virus and Jamestown Canyon virus complicates interpretation. The result is a diagnostic dead zone: molecular testing may be negative, screening serology may be ambiguous, and the decisive neutralizing antibody comparison often comes only later.
Case 1: Headache, Opening Pressure, and a False Lead From Epstein-Barr Virus
The first child, a 12-year-old girl with no underlying conditions, initially presented with a 3-day history of severe bilateral pulsatile headache, photophobia, phonophobia, abdominal pain, and emesis. She was first presumed to have migraine and discharged. Her symptoms worsened, and by day 5 she returned with headache severe enough to wake her from sleep.
Neuroimaging did not reveal a structural explanation. Head CT, CT venogram, and brain MRI were unremarkable, shifting attention toward inflammatory or infectious meningitis. Lumbar puncture on day 6 showed elevated opening pressure at 33.4 cm H2O and a cerebrospinal fluid nucleated cell count of 250 × 10^6 cells/L. Empiric ceftriaxone, vancomycin, and acyclovir were started after the tap, a common move when bacterial and herpesviral etiologies remain in play.
The routine workup was unrevealing. CSF and blood cultures stayed negative, the BioFire Meningitis/Encephalitis CSF Panel was negative, and CSF Epstein-Barr virus nucleic acid testing was negative. A transient EBV IgM reactivity created a misleading trail, but repeat serology 6 weeks later was negative for both IgM and IgG, making a false-positive initial result the most plausible explanation. She improved clinically, completed 10 days of ceftriaxone for culture-negative meningitis, and left the hospital with only mild residual headache. Retrospective California serogroup testing later showed neutralizing antibody titers most consistent with probable snowshoe hare virus meningoencephalitis, although the titers did not meet the 4-fold change required for confirmed infection. Serum RT-PCR was negative, and insufficient residual CSF remained for additional molecular testing.
Seizures, Cortical Inflammation, and a Clearer Serologic Signal
The second child, a 3-year-old girl with strabismus and a prior neurologic history that included mild hypoxic ischemic encephalopathy and a single focal seizure 1 year earlier, arrived in early August with fever, decreased energy, three hemiclonic focal seizures, and Todd’s paresis. Her course was more dramatic from the start. EEG testing showed focal seizure activity from the right posterior quadrant and later posterior quadrant slowing, while her subsequent symptoms included visual hallucinations, balance problems, and speech difficulty.
Imaging again pointed toward encephalitis rather than a localized abscess or stroke. MRI demonstrated abnormal signal in the right perirolandic cortex, right insular cortex, and bilateral thalami, with scattered sulcal enhancement. CSF showed a mildly elevated nucleated cell count of 12 × 10^6 cells/L. Extensive testing for bacterial, herpesviral, fungal, leptospiral, rickettsial, and other viral etiologies was negative, and acyclovir was stopped after herpes simplex virus PCR returned negative.
Retrospective serology solved the case far more cleanly than acute testing did. Acute and convalescent samples showed a 32-fold rise in snowshoe hare virus PRNT titers, meeting criteria for infection. RT-PCR on serum collected on day 5 of symptoms was negative, again illustrating how quickly the molecular window can close. She was discharged after 12 days on seizure medication and later recovered fully, with no further seizures at 3-month follow-up.
Why Pediatric Arboviral Encephalitis Can Hide in Plain Sight
This cluster matters because the bedside presentation did not announce the cause. Instead, it imitated more familiar pediatric diagnoses: migraine, culture-negative meningitis, herpes encephalitis, and seizure disorders. In each child, the decisive clue was not a single laboratory result but the combination of shared residence, overlapping symptom onset, and summer mosquito exposure in a region where California serogroup viruses circulate.
The pathophysiology fits the observed syndrome. After mosquito inoculation, transient viremia may seed the central nervous system, producing meningeal inflammation, encephalopathy, seizures, and sometimes elevated intracranial pressure. Because the acute viral burden may already be low by the time children reach hospital care, negative PCR cannot exclude infection. Serology remains essential, but cross-reactivity means neutralization assays still carry the most weight when cases are adjudicated retrospectively.
The investigators’ conclusion is grounded in that diagnostic reality. SSHV infection is likely underrecognized and underreported, and neuroinvasive disease may be missed when initial panels do not include the correct arbovirus or when clinicians stop after a negative first-line result. During mosquito season in North America, especially in children and young adults with unexplained meningoencephalitis, SSHV belongs on the differential diagnosis even when routine testing is unrevealing.
The unresolved question is not whether the virus can cause severe pediatric neurologic disease. This cluster shows that it can. The remaining issue is how many similar cases are being labeled as idiopathic meningitis or nonspecific viral encephalitis before serologic follow-up ever happens.