manifested as fever with a variety of other conditions, including rash, arthralgia, myalgia, headaches, and gastrointestinal symptoms.

Since the 1990s, however, there have been reports of increased incidence and severity of WNV illness (Solomon and Cardosa 2000). New neurologic and ophthalmologic manifestations of West Nile encephalitis have been recognized each year since the virus first reached North America in 1999 (Cunha 2004). A small but significant proportion of cases of West Nile neurologic disease (WNND) have led to death, particularly among the elderly. These recent, marked changes in the epidemiology of WNV illness led the committee to include it in this chapter even though the long-term adverse health outcomes of WNV usually are manifest during the acute illness.

Alarm triggered by the sudden change in the incidence and severity of WNV illness must be tempered by the understanding that severe WNV disease remains rare. Only 0.7% of people who become infected with West Nile virus in the United States develop severe neurologic disease, and more than one-third of these recover fully within a year (Klee et al. 2004; Mostashari et al. 2001). About 20% of infected people develop traditional, self-limited West Nile fever, and about 80% are asymptomatic, whereas only 1 in 150 develops neurologic manifestations.

Transmission of West Nile Virus Infection

Although WNV is found in several species of mosquitoes, the vast majority of infections are transmitted by Culex spp. (Campbell et al. 2002). These highly ornithophilic vectors transmit the virus among its natural reservoir: birds. Detected in more than 275 species of birds, WNV is particularly virulent for the family Corvidae, which includes crows and jays. The virus amplifies itself in birds’ bloodstream to a trillion or more virions per milliliter. Mammals are end-stage hosts and may develop disease but do not develop high enough viremia to contribute significantly to the virus’s epidemic spread.

WNV is transmissible from human to human through blood transfusions, transplanted organs, the placenta, and breastfeeding (CDC 2002). Between June and December 2003, WNV nucleic acid amplification testing (NAT) was performed on about 6 million units of blood, which resulted in the removal of at least 818 viremic blood donations. However, even with NAT testing, there were 6 cases of transfusion-associated WNV infection due to low levels of virus not detected by the testing method (minipools from 6-16 donations were used rather than individual testing) (CDC 2004c).

Endemicity in Southwest and South-Central Asia

WNV has been reported in Afghanistan, Pakistan, Iran, and other countries in southwest and south-central Asia (Arsen'eva 1982; Hubalek and Halouzka 1999; Naficy and Saidi 1970; Sugamata et al. 1988; Wilson 1991). In Afghanistan, antibodies to WNV were found in Kunduz, Heart, Bamyan, and Helmand provinces (Arsen'eva 1982). In neighboring Pakistan, 50-65% of the population of Karachi reportedly had antibodies to WNV in 1983 and 1985; new infections were identified in 13% of the population during those years (Sugamata et al. 1988). Similarly, a serum survey conducted in northeastern Iran in the late 1960s found that 30% of surveyed subjects had antibodies to WNV (Naficy and Saidi 1970).



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