By Stan Deresinski, MD, FACP
WNV was first detected in Uganda in 1937 with subsequent appearances in Asia, the Middle East, and Eastern Europe. With the exception of a 1957 nursing home outbreak in Israel in which a number of those affected developed infections of the central nervous system (CNS), it generally produced sporadic mild febrile illness, with occasional outbreaks. This pattern changed after 1996 with the occurrence in Israel of outbreaks associated with more severe illness and frequent CNS involvement, a pattern followed by the US experience. This similarity of clinical illness is no surprise since the virus detected in 1999 in New York is virtually genetically identical to that isolated from a dead goose found in Israel in 1998.
While the numbers of cases of WNV infection in the United States were relatively small from 1999 through 2001, in 2002 an epidemiologic explosion occurred with 4156 cases, including 284 deaths, in 44 states plus the District of Columbia.1
WNV also demonstrated new methods of transmission and novel clinical syndromes. In addition to its usual mode of transmission by the bite of mosquitoes, WNV has been transmitted by percutaneous inoculation in laboratory accidents, by transfusion of blood products, via transplanted organs, via breast milk, and by the transplacental route.2 The FDA hopes to introduce blood screening procedures this summer.
The most remarkable clinical findings have been the frequent occurrence of profound muscular weakness and of movement disorders. A syndrome closely resembling that of paralytic polio is, like that due to polio virus, the result of infection of anterior horn cells.3 The observed movement disorders include tremors, myoclonus, and Parkinson’s-like findings.
Diagnosis depends upon antibody tests and genome detection by polymerase chain reaction. Treatment remains supportive, although both ribavirin and interferon alpha are active against the virus in vitro. A therapeutic trial examining the safety of the latter agent received FDA approval in January of this year. This study, whose principal investigator is at New York Hospital in Queens, will enroll 40 patients with WNV encephalitis.
It is believed that yellow fever virus and its vector were introduced into the Americas in the 16th or 17th centuries as the result of the slave trade. The US Congress was driven from Philadelphia in the summer of 1793 by a yellow fever epidemic. Although eradicated from North America, yellow fever persists in tropical South America. Centuries later, another flavivirus, WNV, has found its way to the Americas and is in expansive mode, surprising us with some of its manifestations. It’s time to get ready for the 2003 version of WNV infection in North America. At the same time, we should begin to look ahead—Could Japanese encephalitis virus, yet another flavivirus, make its way into North America?
Dr. Deresinski is Clinical Professor of Medicine, Stanford; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center, Calif.
2. Deresinski S. West Nile virus—Multiple modes of transmission. Infectious Disease Alert. 2003;22:57-59.
3. Leis AA, et al. West Nile poliomyelitis. Lancet Infect Dis. 2003;3:9-10.