West Nile Encephalitis: What it could mean to Canadian paediatricians in the summer of 2000

In August and September 1999, New York, New York, and its surrounding areas experienced the first outbreak of West Nile (WN) viral encephalitis ever recorded in North America or the western hemisphere. Initially, the first laboratory-confirmed cases were reported to be due to St Louis encephalitis (SLE) virus, a closely related flavivirus. However, molecular characterization of the infecting agent and testing of patients' sera using both SLE and WN antigens resulted in definitive evidence that the outbreak was due to the WN virus. The WN virus was originally isolated in 1937 from the blood of a febrile patient in the region of West Nile, Uganda. The virus had been previously documented in at least 17 countries, with a geographic distribution that included Africa and Eurasia. The WN virus is transmitted through the bite of a mosquito, which has become infected by feeding on a viremic bird. Multiple species of mosquitoes can serve as vectors for the virus in the bird-mosquito-bird cycle, which can spill over into the human population and into domestic animal populations such as horses. Birds are effective reservoirs of the virus, and can serve as amplifying hosts that can allow sufficient numbers of infected mosquitoes to build up, which could then cause large scale outbreaks in humans. Clinical disease can occur in some infected bird species. For example, in the New York City area, thousands of American crows and some fish crows, as well as several exotic bird species at a zoological park, died from WN infection during the outbreak. Birds and/or mosquitoes infected with the WN virus were also identified in New Jersey, Connecticut and Maryland. There is no documented evidence that the WN virus is transmitted directly from person to person or from bird to person. Once the outbreak was identified in New York City, health authorities promptly introduced citywide aerial and ground application of malathion and the pyrethroid-based insecticides, resmethrin and sumethrin, to control the mosquito population. In addition, many standing water sources, which could harbour mosquito larvae, were treated or eliminated. With these control measures and the changing season from summer to fall, the outbreak subsided. The total number of confirmed cases of WN encephalitis in New York City and environs was 62, including seven deaths; approximately 45 patients were in New York City itself. One of the fatalities was a 75-year-old Canadian resident who returned to Toronto from New York City five days before the onset of symptoms. More than 60% of the patients with the WN virus were older than 65 years of age. Only two cases occurred in children (one child was five years of age and the other child was 15 years of age). The New York City Department of Health investigated approximately 700 possible cases. The New York City Department of Health conducted a population-based serological survey in October 1999 in northern Queens (a district of New York City), in collaboration with the United States Centers for Disease Control and Prevention (CDC), to assess how many people in northern Queens may have been exposed to the WN virus during last year's outbreak. Households were selected at random, and a total of 677 persons agreed to participate anonymously by completing interviews and volunteering blood samples. Nineteen anonymous blood samples (2.6%) tested positive for previous infection with the WN virus. Based on this result, it is estimated that between 1.2% (533) and 4.1% (1903) persons in the surveyed area (total population 46,220) were likely to have been exposed to the WN virus. The ability of the WN virus to remain viable over the winter was confirmed when it was isolated in three of 69 mosquito pools collected from sheltered sites in New York City. In addition, the WN virus was detected in a dead red-tailed hawk found in the New York City area in the late winter and early spring, and more recently in dead crows in Rockland County outside of New York City. The WN virus generally causes a somewhat milder disease than that caused by the SLE virus, although WN outbreaks in the 1990s have shown an increased incidence of encephalitis in patients than had been previously documented. Symptoms can be unapparent to mild. Symptoms range from a slight fever and headache to rapid onset of severe headache, high fever, stiff neck, muscle weakness and disorientation, three to 12 days following the bite of an infected mosquito. Illness is more common and more severe in adults than in children. Fatalities are more frequent in the elderly, although serious illness may occur in paediatric populations. The outbreak in New York City is the first recognized introduction of the WN virus into the western hemisphere. The short and long term consequences of this event are unknown. Many critical questions remain unanswered. Will the WN virus gain a foothold in the Americas? If so, will the WN virus move as far north as Canada? Will the WN virus move into unanticipated reservoirs, such as ticks? Will the WN virus spread beyond the initial outbreak area (eg, will it become established in southern ecologies)? If it is established, will the WN virus cause repeated outbreaks or will it simply maintain a low profile in most years? Investigations revealed that a large number of migratory and nonmigratory bird species became infected with the WN virus. If the virus has moved via birds migrating south to the southern United States, Central or South America or the Caribbean, and it is maintained in bird-mosquito-bird cycles there, it could theoretically move back in the spring or summer to northern ecologies such as those found in southern Ontario, southern Quebec, or eastern or western Canada, where appropriate mosquito vectors are well established. Health Canada convened a multidisciplinary working group meeting in Ottawa on February 10 and 11, 2000, to assess the risk of the WN virus being introduced into Canada and to plan for possible courses of action. Effective monitoring for the WN virus will require a multidisciplinary effort, with cooperation among many agencies, including the Canadian Cooperative Wildlife Health Centre (CCWHC), Canadian Wildlife Service, Health Canada, Canadian Food Inspection Agency, provincial veterinarians, provincial public health agencies, provincial departments of agriculture and food, and entomologists, as well as partners in the United States, such as the CDC and the National Wildlife Health Center. A national multidisciplinary committee, along with several specific working groups, has developed three levels of surveillance activities for detecting and responding to the possible introduction of the WN virus into Canada. The plans, listed below, include implementing human, animal and mosquito surveillance, developing appropriate laboratory testing capacities, and generating information and/or fact sheets for various target audiences and the general public. By the end of May 2000, provinces from Saskatchewan to the east coast will have placed sentinel chickens at several strategic sites within key localities. The sentinel chickens will be bled periodically, and blood samples will be analyzed for evidence of WN virus infection (ie, the presence of WN virus antibodies) at both provincial and federal laboratories. The provinces listed above are also collecting, speciating and pooling mosquitoes, usually collected from locations near the sentinel chicken sites. These mosquito pools will be stored for further analysis should WN virus activity be detected. A program of enhanced passive surveillance of dead birds to be examined for possible WN virus infection was undertaken under the leadership of the CCWHC. In general, members of the public are asked to notify local authorities about dead birds. The dead birds will be collected and sent to a regional office of the CCWHC or to selected provincial veterinarians for pathological examination. Provinces are establishing active or enhanced passive surveillance for human cases of viral encephalitis. Provincial public health authorities will increase clinician awareness and, in some cases, are conducting active, hospital-based sentinel surveillance. Paediatricians who care for patients with a presumptive diagnosis of viral encephalitis should be aware of the WN virus as a possible etiological agent. If surveillance measures indicate that the WN virus entered Canada in the spring or summer of 2000, there will be intensified surveillance and epidemiological investigation in any area where activity has been detected. Depending on the circumstances and geographical location, any one of the surveillance methods described above could be expanded. In addition, surveillance could be expanded to include the testing of peridomestic birds. Planning is currently underway to develop criteria for when and where control measures may be undertaken. Specific control and prevention interventions will require a multidisciplinary approach to take into consideration public health and environmental concerns. It must be stressed that the basic surveillance measures described above will be used in different combinations at different times, and with varying degrees of intensity, according to perceived levels of risk. Uncertainty regarding the introduction and possible spread of the WN virus in Canada dictates the need for a flexible, robust response capacity at both provincial and federal levels, with extensive collaboration with Canada's clinicians, veterinarians, virologists, laboratory diagnostic experts, entomologists and wildlife experts.

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