West nile virus infection

West Nile virus infection

M L BUNNING, T M WILSON AND R A BOWEN
Rinderpest

Introduction

West Nile (WN) virus infection is a mosquito-borne illness of animals and humans. Previously seen only in Africa, Asia and Europe, it now appears to be endemic in eastern North America where the first human, animal and bird cases were identified in New York City, USA, in 1999.1

West Nile virus (WNV) was first isolated in the West Nile district of Uganda in 1937.36 The first recorded and most noteworthy human epidemics occurred in Israel during 1951–1954, and again in 1957. In South Africa the largest human epidemic ever recorded occurred in 1974. Epidemics of West Nile encephalitis in humans were reported in southern France in 1962, in south-eastern Romania in 1996, and in south-central Russia in 1999. However, since the mid-1990s a new epidemiological trend has occurred with increasing frequency whereby outbreaks in both humans and horses are being reported simultaneously (e.g. Romania 1996; Morocco 1996; Tunisia 1997; Italy 1998; Russia, the USA and Israel 1999; and Israel, France and the USA 2000).14, 20, 27, 42

The recent introduction of WNV into the Western Hemisphere (USA and Canada) has renewed interest into the disease, and is resulting in a plethora of novel research into many aspects of the disease, some of which will be discussed in this chapter.

Aetiology

West Nile virus is an enveloped virus approximately 45 nm in diameter and containing a linear single-stranded RNA genome. 32 It was originally classified as a member of the group-B arboviruses and subsequently placed in the Flavivirus genus within the family Togaviridae. More recently, however, the flaviviruses (including WNV) have been classified as constituting a genus within the family Flaviviridae.43 West Nile virus is a flavivirus belonging taxonomically within the Japanese encephalitis sero-complex; this group also includes the closely related Japanese encephalitis (JE), Kunjin, Murray Valley encephalitis and St. Louis encephalitis (SLE) viruses.19

West Nile virus shares a close antigenic relationship with the other viruses of the Japanese encephalitis sero-complex as well as eight other viruses of the Flaviviridae comprising the West Nile subgroup or complex of viruses (Figure 91.1). Significant differences in nucleotide sequences between WNV isolates from different parts of the world have been documented and, more recently, it has been shown using both polyclonal and monoclonal sera, that there is significant antigenic variation among strains isolated within the same geographic region.6, 9

Epidemiology

West Nile virus cycles primarily between different species of mosquitoes and wild birds, both of which vary according to specific geographic area. This cycle represents the major endemic transmission cycle (Figure 91.2). Epidemic cycles occur when a host of variables relating to climate conditions, susceptible vertebrate hosts, and invertebrate numbers are favourable.

In the Old World, WNV has been isolated from vertebrates and/or arthropods in 18 countries within the Ethiopian, Palaearctic and Oriental regions, ranging from Portugal at its western limit of distribution to India in the east (Figure 91.3).20 As the outbreak in the New World (western hemisphere) continues to move south and west across the North American continent, numerous novel species of susceptible vertebrate and invertebrate hosts will undoubtedly be identified. Already in 2001, 15 species of mosquitoes, 55 species of birds, and seven species of mammals have been identified as hosts of WNV in North America.26

Migratory birds in the Old World have long been suspected as the principal hosts for introducing WNV into new regions. Because outbreaks of disease in temperate regions generally occur during late summer or early fall, coinciding with the arrival of large concentrations of migratory birds and dense populations of mosquitoes.28, 33, 35, 38 This is also considered to be the case in North America where, after its introduction in 1999, the virus spread along established flyways used by migratory birds.33 Unlike the 1999 epidemic in New York City during which large numbers of dead and dying birds, especially crows, were observed,5 the Old World epidemics of WNV had few concurrent reports noting deaths of infected birds.20

Figure 91.1 Geographic distribution of the Japanese encephalitis sero-complex, 2000. (By courtesy of Centers for Disease Control and Prevention, USA)

Figure 91.2 West Nile virus transmission cycle. (Redrawn from figure by courtesy of Centers for Disease Control and Prevention, USA)

West Nile virus has been isolated from a large number of birds and mammals in nature. Serosurveys have indicated the presence of WNV antibody in humans, a wide variety of wild and domestic bird species, wild mammals such as lemurs, chimpanzees, rodents and bats, and domestic mammals such as camels, horses, mules, donkeys, goats, cattle, water buffalo, sheep, and pigs.19 Birds are considered to be the primary reservoir and amplifying hosts for WNV, based on frequency of virus isolation, serologic surveys, and the experimental demonstration of viraemia sufficient to infect engorging mosquitoes.19

The recognition of WNV in North America during 1999 was the first indication that the virus was present in the Western Hemisphere. Continuing widespread virus activity in the...

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