West Nile encephalitis☆
Article Outline
- Abstract
- Epidemiology
- Etiology/possible pathways
- Pathophysiology
- Clinical manifestations
- Diagnosis
- Management
- Prognosis and follow-up
- References
- Copyright
Abstract
After the New York outbreak of West Nile Virus encephalitis in the summer of 1999, awareness that vulnerable children and adolescents may be at risk for this mosquito-borne viral infection intensified. The Nurse Practitioner can play an invaluable critical role to recognize and diagnose this arthropod-borne virus. Pathophysiology, vector transmission, clinical manifestations and laboratory findings are discussed in this article. Emphasis is placed on the PNP's role of providing anticipatory guidance concerning prevention of outbreaks and physical management that focuses on the elimination of mosquito-breeding areas, reducing personal exposure, and biological control of mosquito populations. J Pediatr Health Care. (2002). 16, 278-281.
Approximately two-thirds of the presumed cases of viral encephalitis have unknown causes. Most acute cases in the USA are due to herpes simplex virus (HSV), enteroviruses, and arthropod-borne viruses. Only arboviruses cause epidemics of viral encephalitis, and they are linked to mosquito and tick vectors. Most predominant in temperate areas, arboviruses can cause fatal encephalitis in humans and horses as well as some domestic and wild birds. West Nile Virus (WNV) was initially isolated in 1937 in the blood of a Ugandan woman who suffered from a febrile illness. The first outbreak was reported in 1950 in Israel (Day & Tabachnik, 1999). It is currently one of the world's most widely distributed arboviruses and has caused meningoencephalitis outbreaks in Romania in 1996, and in Russia in 1999 (Tyler, 2001), as well as a cluster of encephalitis cases in the New York City (NYC) area in 1999 [Center for Disease Control (CDC), 2001b; Day & Tabachnick, 1999; Nash et al., 2001]. As of July 2001, WNV cases have been documented in the USA from New Hampshire to Florida and from the Atlantic states west to Ohio (CDC, 2001c).
A characteristic of WNV is unexpected deaths in bird and horse populations before human symptoms begin. Although WNV studies have focused on older people, it has relevance in surveillance for potential pediatric outbreaks. Studies during the outbreak of 1999 generally overlooked pediatric patients with meningitis. This is significant because milder pediatric cases of WNV infection may have been overlooked or pediatric encephalitis cases may have been incorrectly attributed to enteroviruses. Although some may have recovered without significant morbidity, other children with undiagnosed cases of WNV may have suffered mortality and significant morbidity. This in turn may have also placed children with immunocompromise or chronic conditions such as diabetes at higher risk because surveillance was not heightened in the pediatric population. It would be prudent for reports of future outbreaks to include the spectrum of clinical manifestations as well as the degree to which the pediatric population is affected with WNV (CDC, 2001a). Therefore, consideration should be given to including WNV in differentials for children with acute febrile illness of unknown cause, especially during mosquito seasons (Meek, 2002).
Epidemiology
The incidence of WNV is seasonal (Tyler, 2001). In areas where infected mosquitoes are present, one per 100-1,000 mosquitoes is infected; one person per 100 people bitten by an infected mosquito may develop severe manifestations (CDC, 2001b). Of 719 patients with clinical syndromes of meningitis or encephalitis in NYC during the summer of 1999, 9% had laboratory evidence of WNV. Symptoms peaked at mid-late August (Nash et al., 2001). It should be noted that the incidence was based on severe WNV symptomatology, and that counting people with mild and nonspecific symptoms would have exhausted staff and laboratory resources during surveillance (CDC, 2001a). Since it has become permanently established in the western hemisphere, WNV can be transmitted at any time due to differing temperatures in northern and southern climates, particularly in the Gulf States (CDC, 2001a-b). It is likely to spread geographically and cause additional outbreaks of WNV encephalitis (CDC, 2001a,c; Nash et al., 2001).
Etiology/possible pathways
The genetic relatedness between the 1999 NYC virus and the 1998 Israel virus strongly suggests that the NYC virus originated in the Middle East (Nash et al., 2001). The virus was most likely introduced to this country by an infected migratory or imported bird. Mosquitoes were the responsible vectors for spreading the virus to other birds and humans. Although it has been associated with tick bites in Africa and Asia, there is no tick vector evidence in the USA (CDC, 2001b; Day & Tabachnik, 1999; Tyler, 2001). Other plausible introduction possibilities include the existence of low-level transmission cycles in the northeastern USA for several years. A hot summer supports higher levels of mosquito populations, and this may have led to the NYC 1999 outbreak of WNV. Also, a recent human traveler from Africa or Eastern Europe could have re-entered the country with a very high viral load and then transmitted the virus to additional mosquitoes. It is possible that infected mosquitoes may have traveled on an international flight, or they may have been accidentally released from a scientific experiment or through intentional bio-terrorism (Day & Tabachnik, 1999). The possibility of transmission through blood transfusions, breast-feeding, and organ transplants is under investigation
Pathophysiology
In a continuously widening geographical area, WNV has been isolated in mosquitoes, over 4,000 birds, many horses, and a few small mammals (Tyler, 2001). Of over 3,000 species of mosquitoes worldwide, only two species were found to have WNV. These were the common urban mosquito, Culex pipens, and the flood water mosquito, Aedes vexans. Culex pipens breeds in stagnant water from late May through the year's first frost, and feeds mostly on birds and occasionally on humans. The virus endures in over-wintering mosquitoes (CDC, 2001b; Day & Tabachnik, 1999; Talan, Moran & Pinner, 2000). The mechanism that permits this unusual survival during the winter's cold temperatures is unknown (Craven & Roehrig, 2001).
Infected parent Culex mosquitoes can vertically transmit the WNV to their offspring (Talan, Moran, & Pinner, 2000). Located in mosquito salivary glands, the virus is injected into hosts when the mosquito bites. WNV then multiplies within the host and can cause illness when it crosses the blood-brain barrier. Birds are considered to be the primary host and humans to be dead-end hosts (Meek, 2002; Tyler, 2001). Thus, WNV is not spread directly from bird-to-humans or human-to-human. Although WNV has been isolated in 18 native USA bird species, the crow is the most sensitive and their deaths are sentinel to geographic distribution and potential human outbreaks (CDC, 2001b).
Clinical manifestations
After being bitten by an infected mosquito, incubation is 3-15 days. Manifestations can be clinical or subclinical and are generally mild in healthy children and adults. Symptoms are usually sudden and range from slight fever, headache, lymphadenopathy and petechial rash, to sudden onset of high fever, severe headache, nuchal rigidity, disorientation, muscle weakness, coma, and, rarely, death (CDC, 2001b; Day & Tabachnik, 1999; Nash et al., 2001). Neurological manifestations can include diminished reflexes, diffuse flaccid paralysis, abnormal cranial nerve function, and low incidence of seizures that are absent in other encephalitis forms. Lymphocytopenia that is rarely seen in viral encephalitis may be evident (CDC, 2001b; Nash et al., 2001; Tyler, 2001). Manifestations can also include decreased strength and hyporeflexia, nausea, vomiting, and altered mental status. The reported skin manifestation in 19% of the patients during the 1999 NYC outbreak was an erythematous macopapular or morbilliform rash of the neck, trunk, and/or extremities. Most infections are subclinical with overt disease in approximately 1 of 100 infections. Very young children and those with compromised immune systems and/or diabetes mellitus are also more likely to exhibit serious manifestations and significant risk factors for death (Craven & Roehrig, 2001; Nash et al., 2001; Szilak & Minamoto, 2000). Underlying conditions such as hypertension may enhance passage of WNV across the blood-brain barrier and predispose patients to neurologic complications (Nash et al., 2001). Box 1 provides a summary of clinical symptoms.
Diagnosis
A detailed general history should include questions concerning chronic conditions that may predispose to immunocompromise. In addition to a detailed history of the course and severity of manifestations, possible exposure to mosquitoes should be included. This exposure can encompass outdoor activities such as gardening, especially in evening hours (Nash et al., 2001), camping, and outdoor sports such as golf. Questions should also be asked concerning the degree of fever, the presence of headache or rash, and neurological findings such as nuchal rigidity, disorientation, and muscle weakness. A complete general physical examination and neurological assessment should follow the history, and should include vital signs. Close attention should focus on skin rash, muscle weakness, nuchal rigidity as well as other neuropathological findings suggestive of encephalitis, mental status, and lymphadenopathy. Those clients with severe manifestations should be hospitalized and supportive treatment given while diagnosis is pursued through laboratory testing. Differential diagnoses include viral encephalitis, viral meningitis, atypical Guillain-Barre Syndrome, and aseptic meningitis.
Diagnosis in 1999 was primarily based on the presence of IgM antibodies against WNV in cerebrospinal fluid, or, if that were negative, by the presence of serum IgM antibodies (usually a fourfold rise) against WNV (Meek, 2002) and neutralizing antibodies (Nash et al., 2001; Szilak & Minamoto, 2000; Tyler, 2001). Most reliably, cerebrospinal fluid is strongly diagnostic for WNV with protein of at least 40 mg/deciliter or WBC of at least 5/cubic millimeter, negative Gram's stain, and negative bacterial culture (Nash et al., 2001). Additionally, positive serum ELISA for IgM and IgG against WNV as well as St. Louis encephalitic virus (CDC, 2001a; Nash et al., 2001) are also reliably diagnostic. Patients will most probably have a relatively normal CBC. With reference to radiological or imaging tests, CT scans show no evidence of acute disease, however MRI may show enhancement of leptomeninges, and/or periventricular areas (Nash et al., 2001). See Box 2 for a summary of diagnostic indicators.
Management
Treatment for WNV encephalitis is supportive with IV fluids, respiratory support as needed, and antimicrobials to prevent secondary infections or while waiting for culture results (CDC, 2001b; Craven & Roehrig, 2001). A third-generation cephalosporin is the probable drug of choice (Baraff, 2000). To prevent outbreaks, physical management focuses on the elimination of mosquito-breeding areas, reducing personal exposure, and biological control of mosquito populations. The PNP can provide guidance in these areas not only during primary or chronic care visits, but also in school-based health centers as well as during consultations with schools, daycare providers, and community organizations such as camps. Physical protective measures such as getting rid of outdoor containers that can collect water, and checking areas for proper drainage, should be stressed to property owners. This includes draining areas where stagnant water can collect, such as birdbaths, rain gutters, flowerpots, and trashcan lids. Window and door screens should be in good repair. Leaking outdoor faucets and pipes should be repaired, outdoor pools should be properly chlorinated, and plastic wading pools should be drained at least once a week. Birdbath water should also be changed weekly. Grass and shrubs should be well trimmed (Town of Greenwich, 2000).
Information concerning pesticide sprays can be found at the Environmental Protection Agency (EPA) website (CDC, 2001b). Bacillus Thuringiensis Israelensis (BTI) insecticides can be safe to treat mosquito-breeding sites. If water areas have fish, frogs or amphibians that can eat mosquito larvae, they do not need to be treated with BTI. This insecticide can also be found as solid “dunks,” which are placed monthly into small ponds and water-collecting sites such as flowerpots, roof gutters, and rain barrels. While floating, the solid BTI releases long-term larvacide to the water's surface. Because they work on the surface where mosquito larvae are hatched, the dunks can be used regardless of the water's depth. Parents should be instructed to read the packaging materials before using. Children should be prevented from playing in and drinking the pond water.
Local Health Departments should be contacted for lists of licensed pesticide applicators if property is to be treated with an insecticide. The skin of infants and children should not be sprayed with DEET. However, clothing can be sprayed with 35% DEET. Complete Protection Time (CPT) after being personally sprayed with 5% DEET is approximately 2 hours, while 24% DEET is 4 hours (Day & Tabachnik). Ultrasound devices and Vitamin B will not prevent mosquito bites (CDC, 2001b).
Gambusia affinis is another environmentally friendly form of mosquito control. Known as the “mosquito fish,” this small guppy-like fish has a voracious appetite for mosquito larvae and can eat several hundred daily. They can be used to stock small ornamental ponds as well as larger ponds on golf courses, unused unchlorinated pools, reservoirs, swamps, creeks and animal watering troughs. Mosquito fish inhabit shallow water, as well as reed areas which are also preferred sites for mosquitoes and their larvae (Fattigfish, 2001; Owen, 1995; Shasta Mosquito and Vector Control District, 2001).
It is recommended that the PNP counsel children and their families to avoid outdoor activities at dawn and dusk when mosquitoes are most active. They should wear long pants and shirts, and wear mosquito repellent when outdoors. Playpens and carriages can be covered with mosquito netting when outdoors. When camping, use tents with mosquito-proof netting, and do not camp near stagnant/standing water areas (CDC, 2001b; Day & Tabachnik, 1999; Town of Greenwich, 2000). Children and families should be cautioned to not pick up dead birds and animals with bare hands; they should use plastic bags or gloves and place carcasses in garbage cans (CDC, 2001b). Dead birds and small animals should be reported to the local Department of Health (Nash et al., 2001).
Prognosis and follow-up
Prognosis and follow-up is dependent on the severity of WNV manifestations. Protocol should follow that for encephalitis. Surveillance methods include vigilance in spotting clusters of unusual cases of encephalitis (Tyler, 2001) and the use of established mosquito and vector control programs. A vaccine for this pathogen is not available, and it is generally accepted that the cost of widespread vaccination would be prohibitively expensive (Day & Tabachnik, 1999). Since 1% of mosquitoes carry the virus, and only 1% of bitten people will develop WNV encephalitis, chances of severe infection are small. However, very young children and those who are immunocompromised or have conditions such as diabetes have higher risk factors for WNV encephalitis. Currently there have been no documented episodes of teratogenicity. Subsequent immunity is believed to be life-long with some waning over the years (CDC, 2001b; Day & Tabachnik, 1999).
By including WNV in the differential, the PNP can play an integral role in vigilance and recognition of clusters of unusual illness. Additionally, the PNP can provide critical and swift response for vulnerable children and adolescents. Those who are immunocompromised and who are exposed to mosquitoes should be carefully monitored for WNV encephalitis. Symptomatic clients should be hospitalized for supportive treatment and conclusive diagnosis. During consultations, adults may voice concern about the safety of children who may be bitten by mosquitoes. They may also be concerned about personal risk, especially during pregnancy. The PNP can provide accurate information and anticipatory guidance regarding risk factors and preventive measures. With emphasis on prevention and physical management that eliminates mosquito-breeding areas, reduces personal exposure, and biologically controls mosquito populations, future outbreaks may be prevented.
Symptoms are usually sudden and range from:
Detailed general history focused on:
Complete physical exam including neurological assessment focused on:
Laboratory findings:
Radiological/imaging tests:
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☆ Reprint requests: Therese W. Harrison, MSN, RN, PNP, 573 Manhattan Ave., Thornwood, New York 10594. e-mail: seamist573@aol.com
PII: S0891-5245(02)00061-5
doi:10.1067/mph.2002.128084
© 2002 National Association of Pediatric Nurse Practitioners. Published by Elsevier Inc. All rights reserved.
