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| NO OF CASES ARE LISTED IN EACH ACTIVE STATE |
In late summer 1999, the first domestically acquired human cases of West Nile (WN) encephalitis
were documented in the U.S.1-6 The discovery of virus-infected, overwintering mosquitoes during
the winter of 1999-2000 presaged renewed virus activity for the following spring and precipitated
early season vector control and disease surveillance in New York City (NYC) and the surrounding
areas. These surveillance efforts were focused on identifying and documenting WN virus (WNV)
infections in birds, mosquitoes and equines as sentinel animals that could alert health officials to
the occurrence of human disease. Surveillance tracked the spread of WNV throughout much of
the U.S. between 2000 and 2002. By the end of 2002, WNV activity had been identified in 44
states and the District of Columbia. The 2002 WNV epidemic and epizootic reported human cases of
WN disease (including 2,942 meningoencephalitis cases and 284 deaths), 16,741 dead birds, 6,604
infected mosquito pools, and 14,571 equine cases. The 2002 WNV epidemic was the largest
recognized arboviral meningoencephalitis epidemic in the Western Hemisphere and the largest WN
meningoencephalitis epidemic ever recorded. Significant human disease activity was recorded in
Canada for the first time, and WNV activity was also documented in the Caribbean basin and Mexico.
In 2002, 4 novel routes of WNV transmission to humans were documented for the first time: 1) blood
transfusion, 2) organ transplantation, 3) transplacental transfer, and 4) breast-feeding.
WNV is a member of the family Flaviviridae (genus Flavivirus).
WNV is a member of the family Flaviviridae (genus Flavivirus). Serologically, it is a member of the
Japanese encephalitis virus antigenic complex, which includes St. Louis, Japanese, Kunjin, and
Murray Valley encephalitis viruses. WNV was first isolated in the WN province of Uganda in
1937. Human and equine outbreaks have been recorded in portions of Africa, southern Europe,
North America, and Asia.
Although it is still not known when or how WNV was introduced into North America, international
travel of infected persons to New York, importation of infected birds or mosquitoes, or migration of
infected birds are all possibilities. In humans, WNV infection usually produces either asymptomatic
infection or mild febrile disease, sometimes accompanied by rash, but it can cause severe and
even fatal diseases in a small percentage of patients. The human case-fatality rate in the U.S. has
been 7% overall, and among patients with neuroinvasive WNV disease, 10%.
WNV has been transmitted principally by Culex species mosquitoes, the usual vectors of SLE virus.
Thirty-six species of mosquitoes have been shown to be infected with WNV. This wide variety of
WNV-infected mosquito species has widened this virus’ host-range in the U.S.: 27 mammalian
species have been shown to be susceptible to WNV infection and disease has been reported in 20
of these (including humans and horses). It must be remembered, however, that the detection of
WNV in a mosquito species is necessary but not sufficient to implicate that species as a competent
vector of WNV.
were documented in the U.S.1-6 The discovery of virus-infected, overwintering mosquitoes during
the winter of 1999-2000 presaged renewed virus activity for the following spring and precipitated
early season vector control and disease surveillance in New York City (NYC) and the surrounding
areas. These surveillance efforts were focused on identifying and documenting WN virus (WNV)
infections in birds, mosquitoes and equines as sentinel animals that could alert health officials to
the occurrence of human disease. Surveillance tracked the spread of WNV throughout much of
the U.S. between 2000 and 2002. By the end of 2002, WNV activity had been identified in 44
states and the District of Columbia. The 2002 WNV epidemic and epizootic reported human cases of
WN disease (including 2,942 meningoencephalitis cases and 284 deaths), 16,741 dead birds, 6,604
infected mosquito pools, and 14,571 equine cases. The 2002 WNV epidemic was the largest
recognized arboviral meningoencephalitis epidemic in the Western Hemisphere and the largest WN
meningoencephalitis epidemic ever recorded. Significant human disease activity was recorded in
Canada for the first time, and WNV activity was also documented in the Caribbean basin and Mexico.
In 2002, 4 novel routes of WNV transmission to humans were documented for the first time: 1) blood
transfusion, 2) organ transplantation, 3) transplacental transfer, and 4) breast-feeding.
WNV is a member of the family Flaviviridae (genus Flavivirus).
WNV is a member of the family Flaviviridae (genus Flavivirus). Serologically, it is a member of the
Japanese encephalitis virus antigenic complex, which includes St. Louis, Japanese, Kunjin, and
Murray Valley encephalitis viruses. WNV was first isolated in the WN province of Uganda in
1937. Human and equine outbreaks have been recorded in portions of Africa, southern Europe,
North America, and Asia.
Although it is still not known when or how WNV was introduced into North America, international
travel of infected persons to New York, importation of infected birds or mosquitoes, or migration of
infected birds are all possibilities. In humans, WNV infection usually produces either asymptomatic
infection or mild febrile disease, sometimes accompanied by rash, but it can cause severe and
even fatal diseases in a small percentage of patients. The human case-fatality rate in the U.S. has
been 7% overall, and among patients with neuroinvasive WNV disease, 10%.
WNV has been transmitted principally by Culex species mosquitoes, the usual vectors of SLE virus.
Thirty-six species of mosquitoes have been shown to be infected with WNV. This wide variety of
WNV-infected mosquito species has widened this virus’ host-range in the U.S.: 27 mammalian
species have been shown to be susceptible to WNV infection and disease has been reported in 20
of these (including humans and horses). It must be remembered, however, that the detection of
WNV in a mosquito species is necessary but not sufficient to implicate that species as a competent
vector of WNV.
A disease like the West Nile Virus is tricky for doctors to diagnose. In fact, 80 percent of
those with the virus show no symptoms. And for the remaining people that are effected
by the virus, symptoms can seem like many other illnesses. Dr. James Dungan says, "You
really aren't going to be able to tell the difference from one mosquito to the next. Then
symptoms that you could show up with can be very vague. Might just be a flu-like illness,
fever, headaches, stuff you can see with many different types of illnesses.
those with the virus show no symptoms. And for the remaining people that are effected
by the virus, symptoms can seem like many other illnesses. Dr. James Dungan says, "You
really aren't going to be able to tell the difference from one mosquito to the next. Then
symptoms that you could show up with can be very vague. Might just be a flu-like illness,
fever, headaches, stuff you can see with many different types of illnesses.
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