Abstract
The initial outbreak of West Nile virus (WNV) in North America was recognized in New York City in August 1999, with deaths reported in humans, horses, and numerous species of birds.8 Since then, the geographic distribution of WNV in North America has greatly increased, reaching Mexico in 2002, where a vast number of new potential hosts (avian, mammalian, reptilian) have been exposed to the disease. In Mexico, mosquito vectors are available throughout most of the year creating serious, long-term threats to human health, horses and vulnerable avian populations in the region.9
During the summer of 2002, the Agricultural Ministry of Mexico (SAGARPA) began to receive reports of encephalitis-like illness in horses from several different areas of Mexico, concurrent with reports of WNV encephalitis outbreaks in horses along the Texas border in the states of Coahuila, Tamaulipas and Chihuahua.1,2 Other suspected cases were reported from several southern Mexican states.2 In July 2002 antibodies to WNV were detected in horses in the state of Yucatan.8 The mode of entry of the virus into the Yucatan peninsula is unknown; however, the virus may have been brought in by migration because this area is a principal landfall of many species that migrate from the north-eastern and midwestern United States. Antibodies to WNV reported in certain species of migratory birds (gray catbird, rose-breasted grosbeak, and indigo bunting) supports this hypothesis.3,8 There is even a report in mid 2001 that neutralizing antibodies to WNV were detected in a bovine in the southern state of Chiapas.1,8
The first evidence of WNV transmission among birds in northern Mexico, was in March 2003, 796 birds representing 70 species were captured and assayed for antibodies to WNV. Nine birds had flavivirus-specific antibodies by epitope-blocking enzyme-linked immunosorbent assay; four were confirmed to have antibody to WNV by plaque reduction neutralization test.4 During 2003, several epizootics characterized by neurologic disease occurred on farms housing Crocodilus moreletii and C. acutus. Crocodilians may serve as an amplification host for this virus.5
In early 2003, a nation-wide surveillance network for the detection and prevention of WNV in zoological institutions was formed in conjunction with the Wild Life National Agency (Dirección General de Vida Silvestre) incorporating 33 institutions in the surveillance network and influencing a total of 85 zoos, aquariums and breeding facilities, from the Mexican Association of Zoological Parks and Aquariums (AZCARM). A specific protocol was put together and made available for these institutions in order to have a uniform approach to surveillance, diagnostics, case reporting and prevention of disease.
On May 5, 2003 a dead captive raven (Corvus corax) from a zoological park in the city of Villahermosa, Tabasco State, was analysed, and virus isolation of WNV was done on tissue samples at the CPA-SAGARPA biosafety level 3 facility in Mexico City.2 Phylogenetic studies indicate that this isolate, the first from Mexico, is related to strains from the central United States but has a relatively high degree of sequence divergence.2 Out of this isolate, a vaccine is being developed by the National Producer of Veterinary Biologics, mainly for the vaccination of horses in the army and for a cost-accessible product for mass vaccination (Hector Castell-Blanch personal communication).
Although WNV has already been detected in 13 states of Mexico, there is some difference in the impact of WNV in comparison with the USA experience, with a low rate of morbidity and mortality in both animals and humans. It has been hypothesized that extensive prior exposure to another flavivirus such as dengue (DEN), St. Louis encephalitis (SLEV), Venezuelan equine encephalitis (VEEV) or yellow fever virus, could attenuate the effects of WNV due to antigenic cross-reactivity of Flavivirus antibodies, especially after a second or sequential Flavivirus infection in the same host.11
For example, dengue and dengue hemorrhagic fever (DHF) have been present since 1982, when Mexico reported serotypes 1 and 2 and in 1995 serotypes 3 and 4 (hyperendemicity)7, an outstanding increase of DEN-3 circulation was identified10. Risk factors include the numbers of infected and susceptible human hosts, size of mosquito population, (Aedes aegypti) feeding habits, and temperature (which affects vector distribution, size, feeding habits, and extrinsic incubation period).6 There is also a Mexican isolate (200787/1983) which is antigenically unique by signature analysis with respect to all other dengue-2 topotype viruses. This strain is also unique in biologic behaviour (neurotropism) and is of epidemiologic significance in Mexico.10
The biologic and epidemiologic consequences of these mosquito-borne viruses co-circulating in the same ecosystem could either attenuate disease due to cross-protective antibodies or enhance disease due to immune enhancement. In the case of dengue, enhancement of virus replication by heterologous Flavivirus antibodies and T-cell activation are thought to occur in some patients during a second or sequential dengue infection, resulting in hemorrhagic fever or shock. In contrast, animal data indicate that prior infection with a heterologous Flavivirus reduces the severity of subsequent challenge with WNV. Results of experimental studies with rodents, monkeys, and pigs, suggest that heterologous Flavivirus antibodies protect against or modify subsequent infection with WNV.11
In the north-eastern region of the United States, the diagnosis of WNV infection has been relatively easy, since most people and animals were experiencing their first Flavivirus infection.11 However, as WNV spreads into geographic regions where people and animals have other pre-existing Flavivirus antibodies, the interpretation of diagnostic tests becomes more difficult, and the prediction of the consequences are more challenging.
Literature Cited
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