ARCHIVED - Canada Communicable Disease Report

1 October 2007

Encephalitis in the Summer: A Case of Snowshoe Hare (California Serogroup) Virus Infection in Nova Scotia

V Meier-Stephenson, BSC, PhD, (1), JM Langley, MSc, MD, FRCPC, (1,2,3), M Drebot, MSc, PhD, (4), H Artsob, PhD (4)

1. Faculty of Medicine, Dalhousie University, Halifax, NS

2. Department of Pediatrics, Dalhousie University, Halifax, NS

3. Department of Community Health and Epidemiology, Dalhousie University, Halifax, NS

4. Zoonotic Diseases and Special Pathogens Branch, National Mircobiology Laboratory, Public Health Agency of Canada, Winnipeg, MB

Snowshoe hare (SSH) virus is one of approximately 10 viruses classified under the California (CAL) serogroup of viruses. The members of this serogroup are linked serologically by genetic characterization and by a common mechanism of transmission to humans: mosquito bites. Humans may acquire infection through mosquito bites resulting in asymptomatic to mild febrile illness and a variety of neurologic syndromes. CAL serogroup viruses are now recognized as the second leading cause of arbovirus-associated neurological disease in North America.

In Canada, CAL serogroup virus activity has been demonstrated in all provinces and territories, and human disease due to SSH and Jamestown Canyon viruses has been documented⁽¹⁾. These agents are carried by Aedes and Culiseta mosquito species and infect a wide variety of animals, including squirrels, chipmunks, hares, deer, moose, cattle, horses and swine⁽²⁾.

Although most patients with CAL-associated viral encephalitis recover fully, some long-standing neurologic sequelae have been reported, in particular for the La Crosse virus⁽³⁾. We report a case of viral encephalitis during the summer in a pre-school child from a wooded area of Halifax, Nova Scotia, that was due to SSH.

Case presentation

A 3-year-old boy was brought into the emergency department of a children's hospital in August with a 1-day history of headache and fever. He had no prior health problems except for upper respiratory tract infection in the previous week. His parents reported that the illness began when the child was playing. They noted that he stopped moving and started holding his head in the right frontal area. The temperature at home was measured at 38° C. He was reported as being febrile, anorexic and complaining of a headache over the next 24 hours. He progressively lost interest in play, vomited several times, was distressed and described as "not being himself". There was no history of trauma, travel outside the Maritime provinces or animal exposure. The family had recently moved to a new house on a forested plot near a pond.

On examination, the boy was febrile (40° C), pale, quiet and preferred to lie still. He did not appear to recognize his parents. There were no focal findings on neurologic examination and no meningismus. There were multiple excoriated mosquito bites on the lower extremities. Lumbar puncture showed clear, colourless cerebrospinal fluid with a leukocyte count of 67 x 106/L and erythrocyte count of 2 x 106/L; the Gram stain was negative. Empiric antimicrobial therapy was given until culture of the cerebrospinal fluid was sterile at 48 hours. PCR (polymerase chain reaction) testing of spinal fluid for enterovirus and herpesvirus was negative. During his stay he had significant headache, irritability and anorexia, and was febrile several times daily with a temperature up to 40° C. On the second hospital day he had a generalized tonic-clonic seizure following a period of decreased responsiveness, which was arrested with anticonvulsants. A computed tomography scan was normal, except for small lateral ventricles, suggesting some brain swelling. On the fourth hospital day his fever abated, he began to drink and eat, and became interested in play.

Testing for arboviruses was negative for antibodies to Eastern Equine, Western Equine, West Nile, St. Louis, Powassan and dengue viruses. Acute phase serum taken 3 days after the onset of illness was positive for SSH IgM and IgG antibodies using an antibody capture enzyme-linked immunosorbent assay and immunofluorescence antibody testing. A convalescent phase sample was obtained 25 days after illness onset, fix and plaque reduction neutralization testing confirmed the presence of SSH-specific antibodies in the patient's serum and a greater than four-fold rise in antibody titre in acute (1:320) and convalescent samples (1:5120).

When the patient was seen in the clinic 2 weeks after discharge his parents reported that he was completely well, and physical examination was normal.

Discussion

Between 1978 and 1989, at least one symptomatic infection due to a CAL serogroup virus was recognized every year in Canada with a total of over 20 cases; most of these were attributable to SSH virus(1). Although it has been many years since a viral encephalitis infection due to CAL serogroup viruses was reported in Canada(4-8), our 2006 case shows that that these agents continue to circulate during the mosquito season. Transovarial transmission of CAL serogroup viruses in Aedes species mosquitoes appears to be a very effective mechanism for adaptation of these viruses to the Canadian ecosystem.

While febrile and neurological disease due to arbovirus infection has gained a greater profile with the recent incursion of West Nile virus, CAL serogroup viruses should not be overlooked in the differential for such a presentation (Table 1). No etiologic diagnosis is found for most cases of presumed infectious encephalitis, but a systematic approach to laboratory confirmation can lead to a confirmed or probable agent in up to 40% of patients⁽⁹⁾. This report attempts to raise awareness and the index of suspicion for such encephalitic cases arising in the summer and early fall, when mosquitoes are in their greatest numbers. Prevention of mosquito bites by avoiding exposure, wearing protective clothing, using insect repellent and eliminating mosquito breeding sites is recommended to prevent arboviral infection.

Table 1. Cases of California encephalitis virus infection in Canada

Acknowledgements

The authors would like to acknowledge the valuable technical assistance of Dr. Maya Andonova of the Zoonotic Diseases and Special Pathogens Branch, National Microbiology Laboratory, Public Health Agency of Canada.

References

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