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West Nile Fever: Here to Stay and Spreading

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West Nile Fever: Here to Stay and Spreading EMERGING INFECTIONS JAMES PILE, MD Department of General Internal Medicine, Cleveland Clinic West Nile fever: Here to stay and spreading ■ ABSTRACT EST NILE VIRUS is the cause of the latest W and most well-publicized of the emerg- The ultimate extent of West Nile virus’s range in North ing infectious disease, West Nile fever, and it America is uncertain but is likely to expand in 2001. Spread appears to be here to stay. It has been a source chiefly by night-biting Culex mosquitoes, the virus results in of anxiety in affected areas, particularly New York City and the northeastern United States, infection that most often is asymptomatic or causes a self- since the first cases were reported in 1999. limited febrile illness. The elderly, however, are prone to Although fewer severe human cases were develop neurologic manifestations, including potentially reported in 2000 than in 1999, the virus sur- fatal encephalitis. vived the winter and demonstrated an impres- sive ability to spread geographically in 2000, a ■ KEY POINTS phenomenon most authorities expect to con- tinue in 2001.1,2 Movement of the virus to Birds are the primary “amplifying” hosts of West Nile virus, states and provinces adjacent to areas already and many bird species are capable of this role. affected is likely this year, with more extensive spread possible. Common symptoms include myalgia, headache, fatigue, and This article briefly reviews the background arthralgia. The elderly are at highest risk for neurologic of West Nile virus disease, its chief manifesta- symptoms. tions, and current guidelines for preventing the disease in humans. Testing serum samples in both the acute and the ■ convalescent stages is important to confirm West Nile virus ANOTHER EMERGING INFECTIOUS DISEASE disease, yet it is often not done. Much attention has been given to so-called The use of repellents is especially important for the elderly, emerging infectious diseases—illnesses either as they are at markedly disproportionate risk of developing previously undescribed or presenting in areas severe disease. where they were not known to be endemic. Since the mid-1970s, these have included acquired immunodeficiency syndrome (AIDS), Lyme disease, Ebola virus infection, ehrlichiosis, dengue fever, hantavirus pul- monary syndrome, new-variant Creutzfeldt- Jakob (“mad cow”) disease, and Nipah virus encephalitis. In the late summer of 1999, West Nile virus, previously not reported in the Western Hemisphere, was added to this list when it caused an outbreak of meningoencephalitis in the New York City area. Initially, it was CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 6 JUNE 2001 553 Downloaded from www.ccjm.org on September 28, 2021. For personal use only. All other uses require permission. WEST NILE FEVER PILE unclear whether the virus would establish Over time the distribution of human West itself in North America, but this now appears Nile infection was found to include much of to be the case. Africa and the Middle East, as well as parts of Europe, the former Soviet Union, and the ■ CLASSIFICATION AND LIFE CYCLE Indian subcontinent, with sporadic reports of outbreaks from areas with little or no previ- West Nile is an RNA virus of the flavivirus ously recognized disease.7–9 family, which includes members ranging from dengue to hepatitis C. West Nile belongs to Clinical manifestations the Japanese encephalitis complex, which also West Nile fever was initially considered a uni- includes the agents of St. Louis encephalitis versally mild, self-limited disease, marked by and Murray Valley encephalitis. several days of fever and other “flu-like” symp- The only primary “amplifying” hosts (ie, toms. Marberg and colleagues6 described a able to sustain naturally occurring infection) group of 70 members of the Israeli armed are birds, with many bird species capable of forces hospitalized with West Nile fever in this role. Even though migratory birds have 1953. In addition to fever, the illness was char- long been suspected as critical agents in out- acterized by headache (80%), ocular pain breaks of this and other arthropod-borne (45%), backache (40%), and diarrhea (30%). viruses (“arboviruses”), the link remains con- Other stigmata of disease included lym- jectural because of the difficulty in determin- phadenopathy (90%), conjunctival injection ing the intensity and duration of viremia in (60%), rash (50%), and splenomegaly (20%). naturally infected wild birds. Old World birds The disease was typically abrupt in onset, infected with West Nile virus have tradition- lasted 3 to 5 days in most patients, and left ally shown little or no evidence of disease. A some patients with a prolonged period of variety of mammalian species may be infected, weakness and fatigue.6 The experience of oth- but all, including humans, exhibit brief, low- ers has largely confirmed the signs and symp- level viremia and appear to serve only as toms outlined in this report, with most illness Encephalitis “dead-end” hosts. characterized by an incubation period of 2 to is only the Many types of ornithophilic mosquitoes 6 days, followed by onset of fever and a vari- act as vectors for the spread of West Nile virus, ety of constitutional complaints. The fever tip of the although certain species seem most important may have a biphasic pattern similar to dengue iceberg in transmission, chiefly of the Culex genus (C fever (acute illness lasting several days, spon- pipiens in Europe, C univittatus in Africa). taneous remission, then recurrence). Rash, when present, is generally maculopapular or ■ PREVIOUS REPORTS OF WEST NILE FEVER roseolar. Pain with eye movement, lym- phadenopathy, gastrointestinal complaints, The virus was initially isolated from the blood and myalgias are all commonly reported. of a febrile, mildly ill woman in the West Nile Laboratory studies are generally nonspecific, region of Uganda in 1937 and was noted by although lymphopenia is usually noted. the original investigators to cause encephalitis Subclinical and minimally symptomatic in rhesus monkeys.3 During the ensuing 15 infections are common.4,10,11 years, the disease was found to be endemic in Egypt and the cause of sporadic summertime Neurologic manifestations epidemics in Israel.4 In the 1950s, West Nile virus showed that it Serologic evidence of disease was found in could cause neurologic disease, although up to 60% of people in specific age groups in rarely. Investigators at Memorial Sloan- the Nile Delta during early studies, with Kettering Cancer Center, hoping that the approximately 40% of adults from the same virus might have an antitumor effect, experi- region seropositive in a more recent report.4,5 mentally infected patients who had advanced Attack rates in closed (especially military) cancer. They found that 9 of 78 evaluable populations in Israel in the 1950s were some- patients developed evidence of encephalitis times impressively high (60% or greater).4,6 (altered mental status, abnormal deep tendon 554 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 68 • NUMBER 6 JUNE 2001 Downloaded from www.ccjm.org on September 28, 2021. For personal use only. All other uses require permission. reflexes, and “abnormal twitching”), but most encephalitis to a hospital in Queens prompted patients did not have significant muscular a physician there to contact the New York weakness. Presumably, the frequency of neuro- City Department of Health, which quickly logic symptoms in these patients was at least recognized six patients with mental status partially explained by their underlying malig- changes, profound weakness, and an axonal nancies.12 pattern on electromyography. New cases con- An outbreak of West Nile fever occurred tinued to appear, with eight of the earliest- in two nursing homes in Israel in 1957, with reported cases occurring in people living in a 12 cases of suspected meningoencephalitis, 4 4-square-mile area of northern Queens and of which were fatal.13 Apart from a limited southern Bronx. number of published cases, however, neuro- An arbovirus was suspected as the cause, logic involvement in West Nile fever contin- and serum and cerebrospinal fluid (CSF) from ued to be largely unappreciated for many patients were consistent with St. Louis years. More recently, however, multiple larger encephalitis virus by immunoglobulin M outbreaks of meningoencephalitis have (IgM) capture enzyme-linked immunosorbent occurred, prompting greater awareness of assay (ELISA).16 However, bird “die-offs” had more severe disease. been noted, beginning shortly before the onset of human cases, affecting exotic birds at Larger outbreaks of meningoencephalitis the Bronx and Queens zoos and also native An outbreak of West Nile fever took place in crows. Avian mortality is not a feature of St. several Algerian oases in 1994, with 50 cases Louis encephalitis virus infection, prompting of neurologic involvement and 8 deaths.9 An suspicion that infection was due to another outbreak of meningoencephalitis due to West flavivirus. Subsequent genomic analysis of the Nile virus occurred in southern Russia late in virus at the US Centers for Disease Control the summer of 1999, with 1,000 cases and 40 and Prevention (CDC) and at the University deaths.14 The best-described large epidemic of California-Irvine confirmed that it was in took place in August 1996 in the vicinity of fact West Nile virus.16,17 Bucharest, Romania, with 352 laboratory- Although it remains unclear how West Bird die-offs confirmed cases of meningoencephalitis and Nile virus migrated to the
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