Fatal Encephalitis and Myocarditis
During 1999 and 2000, a disease outbreak of West Nile (WN) virus occurred in humans, horses, and wild and zoological birds in the northeastern USA. In our experiments, WN virus infection of young domestic geese (Anser anser domesticus) caused depression, weight loss, torticollis, opisthotonus, and death with accompanying encephalitis and myocarditis. Based on this experimental study and a field outbreak in Israel, WN virus is a disease threat to young goslings and viremia levels are potentially sufficient to infect mosquitoes and transmit WN virus to other animal species.
West Nile (WN) virus belongs to the family Flaviviridae in the Japanese encephalitis (JE) serocomplex group and is transmitted through various species of adult Culex mosquitos to a variety of mammals and birds. WN virus was not recognized in North America until the fall of 1999, when an epizootic began with the death of a wild American Crow (Corvus brachyrhynchos) in New York; an additional 194 deaths in wild birds were confirmed with WN virus infections that fall. Most birds that died were from the order Passeriformes; corvids (crows and jays) accounted for >80% of deaths. Simultaneously, WN virus emerged as a cause of 62 cases of encephalitis with seven fatalities in humans and 25 cases of neurologic disease in horses in New York City or on Long Island.
WN virus has not affected commercial chickens (Gallus gallus domesticus) or turkeys (Meleagridis gallopavo), which are predominantly raised indoors with low potential for exposure to mosquito vectors. Furthermore, experimental studies in chickens and turkeys inoculated subcutaneously with a New York WN virus isolate had low viremia titers and no clinical disease. However, natural WN virus infections were associated with severe neurologic signs and death in 160 of 400 8- to 10-week-old domestic geese from a flock in Israel. The role of domestic geese as a WN virus reservoir in the Israel outbreak is unknown, but goose infection rates in the Sindbis District of the northern Nile Valley were 27%, similar to rates in buffed-back herons (Bubulcus ibis ibis), doves (Streptopelia senegalensis senegalensis), and domesticated pigeons (Columbia livia) and twice the rate in domesticated chickens and ducks (Anas platyrhynchos), suggesting that geese may have a role in local WN virus ecology. The U.S. WN virus is closely related to WN virus isolates obtained from humans with encephalitis in Romania (1996) and geese in Israel (1998). We report the experimental reproduction of neurologic disease and death in young domestic geese with a WN virus isolated from an American crow on Long Island.
During 1999 and 2000, a disease outbreak of West Nile (WN) virus occurred in humans, horses, and wild and zoological birds in the northeastern USA. In our experiments, WN virus infection of young domestic geese (Anser anser domesticus) caused depression, weight loss, torticollis, opisthotonus, and death with accompanying encephalitis and myocarditis. Based on this experimental study and a field outbreak in Israel, WN virus is a disease threat to young goslings and viremia levels are potentially sufficient to infect mosquitoes and transmit WN virus to other animal species.
West Nile (WN) virus belongs to the family Flaviviridae in the Japanese encephalitis (JE) serocomplex group and is transmitted through various species of adult Culex mosquitos to a variety of mammals and birds. WN virus was not recognized in North America until the fall of 1999, when an epizootic began with the death of a wild American Crow (Corvus brachyrhynchos) in New York; an additional 194 deaths in wild birds were confirmed with WN virus infections that fall. Most birds that died were from the order Passeriformes; corvids (crows and jays) accounted for >80% of deaths. Simultaneously, WN virus emerged as a cause of 62 cases of encephalitis with seven fatalities in humans and 25 cases of neurologic disease in horses in New York City or on Long Island.
WN virus has not affected commercial chickens (Gallus gallus domesticus) or turkeys (Meleagridis gallopavo), which are predominantly raised indoors with low potential for exposure to mosquito vectors. Furthermore, experimental studies in chickens and turkeys inoculated subcutaneously with a New York WN virus isolate had low viremia titers and no clinical disease. However, natural WN virus infections were associated with severe neurologic signs and death in 160 of 400 8- to 10-week-old domestic geese from a flock in Israel. The role of domestic geese as a WN virus reservoir in the Israel outbreak is unknown, but goose infection rates in the Sindbis District of the northern Nile Valley were 27%, similar to rates in buffed-back herons (Bubulcus ibis ibis), doves (Streptopelia senegalensis senegalensis), and domesticated pigeons (Columbia livia) and twice the rate in domesticated chickens and ducks (Anas platyrhynchos), suggesting that geese may have a role in local WN virus ecology. The U.S. WN virus is closely related to WN virus isolates obtained from humans with encephalitis in Romania (1996) and geese in Israel (1998). We report the experimental reproduction of neurologic disease and death in young domestic geese with a WN virus isolated from an American crow on Long Island.