Although identified in Africa, West Asia, and the Middle East in 1937, West Nile virus (WNV) did not make it to the United States and the western part of the world until 1999. The first outbreak of WNV in the United States occurred in New York City, but since then almost every state has reported the illness. In 2002, WNV struck in epidemic proportions in the western hemisphere, extending from the United States to Canada, Mexico, and the Caribbean.1 The largest meningoencephalitis epidemic related to WNV also occurred in 2002. That year, the first cases of WNV transmission via blood transfusion, organ transplantation, pregnancy, and breast feeding were reported. Because of the epidemic and the new cases of transmission, the Centers for Disease Control and Prevention (CDC) began an extensive surveillance and education campaign to try to control the virus.
WNV Origins
In the early years of WNV, named so from the first documented case in 1937 in the West Nile district of Uganda, the disease was asymptomatic or a very mild, febrile illness without neurologic symptoms. The first cases of neurologic manifestations occurred in Israel in 1957. Then, beginning in 1996, the cases of neurologic disease and death increased in frequency with outbreaks occurring in 1996 in Romania, 1999 in Russia, 2000 in Israel, and in 2002 as previously stated. The reasons for the change in the disease pattern and frequency are unknown, but may be due to changes in the virus itself.
West Nile virus is an arboviral virus. Arbovirus is derived from arthropod-borne viruses. These viruses are spread from arthropods such as mosquitoes and ticks to vertebrate animals. The term arbovirus refers to a group of viruses-Togaviridae, Flaviviridae, and Bunyaviridae-which cause encephalitis in humans. West Nile virus is in the family Flaviviridae.
It is thought that WNV was brought to the United States from either infected humans or infected birds. Even though most WNV infections in humans are asymptomatic, the epidemic of 2002 and subsequent deaths that occurred related to the virus led the CDC to begin surveillance of birds and mosquitoes, as well as human cases, in order to track WNV activity. In 2004, 40 states reported almost 2,500 cases of WNV illness. Of these reported cases, there were approximately 80 deaths attributable to the virus. Most of the cases were in the western United States. Approximately 200 potential blood donors were found to have the virus, with less than one-third of these potential blood donors going on to develop WNV illness. Over 7,000 birds tested were infected with the virus.
Because of the invasion of WNV into the United States in 1999, guidelines for surveillance, prevention, and control of WNV were developed and originally published in 2001 and revised in 2003. The guideline, "Epidemic/Epzootic West Nile Virus in the United States: Guidelines for Surveillance, Prevention, and Control," can be found in its entirety at http://www.guidelines.gov.2 The guideline developers include the CDC, the Department of Health and Human Services, the Division of Vector-Borne Infectious Diseases, the National Center for Infectious Diseases, and the Public Health Service. Following is a brief summary of the guideline as it pertains to primary care providers (PCP).
Surveillance
Surveillance is the first part of the guideline. Human surveillance can be both passive and active. In areas where WNV is not considered active, cases of encephalitis should be made known to PCPs, among others, so that a high degree of suspicion can be maintained. Meningitis and encephalitis from WNV cannot necessarily be differentiated from other causes of the same illness based on clinical presentation alone. Patient history, including time of year (summer and fall), outdoor exposure, rain, exposure to standing water, and history of mosquito bites may alert the PCP to obtain immunoglobulin M (IgM) antibodies to WNV. Antibody testing can include samples of serum or cerebrospinal fluid (CSF). Serum samples may yield false-positives if the patient was immunized against related viruses such as yellow fever or Japanese encephalitis, or if he was recently infected with a similar virus such as St. Louis encephalitis or dengue, or the patient had an asymptomatic infection of WNV within the past 6 months. Immunoglobulin M antibodies to WNV can remain in the serum up to 6 months post infection.
Active surveillance occurs when the area is known to harbor active WNV. The local health department in conjunction with the CDC will help PCPs identify patients who are suspicious for WNV illness and then help obtain appropriate diagnostic laboratory testing.
In suspected cases of severe WNV illness, IgM antibodies, using IgM antibody-capture, enzyme-linked immunosorbent assay (MAC-ELISA) can be found in the CSF on the first day of illness. Serum measurements may also be helpful during the acute phase. ELISA or other neutralization tests can be used to check serum samples for seroconversion from acute to convalescent phases. Acute phase is considered from day 0 through day 8 and convalescent is usually measured at days 14 through 21. Obtaining both samples increases the predictive value, especially if the acute sample was negative. Total white blood cell counts may be normal or elevated with lymphocytopenia and anemia. Hyponatremia may also be present on an electrolyte panel, especially if the patient has encephalitis. The plaque reduction neutralization test is the most specific test to distinguish false-positive results from the MAC-ELISA.
Prevention and Control
After surveillance, the guideline discusses prevention and control of WNV and stresses that the most effective prevention and control program is a comprehensive mosquito management program. A major aspect of the program is reduction of mosquitoes, especially breeding. Reduction begins with each citizen through education regarding the relationship between mosquito breeding and standing water. All dwellings should have rain gutters, bird baths, planting pots, tires, children's swimming pools, or other sources of standing water emptied frequently or treated to deter mosquito infestations, if appropriate. Information on ways in which to reduce mosquitoes in and around the home can be placed in the office for your patients.
When management of standing water is not sufficient to keep the mosquito population down, chemical control may be necessary. Insecticides can be used on unhatched mosquitoes or adult mosquitoes. All chemicals used should meet Environmental Protection Agency guidelines and consumers should be informed about proper handling, storage, and disposal of pesticides. Because insects can develop resistance to insecticides, ongoing monitoring and surveillance for resistance should be carried out by the appropriate local public health facility. In some cases, biological control can be utilized. Biological control uses the specific mosquito or by-product of the mosquito to carry out pest control. The goal of biological control is to be more target-specific in pest control, only eliminating the targeted pest.
Another extremely important part of the mosquito management program is the ability to identify when mosquitoes with WNV are on the rise in the community long before a case of WNV transmission to a human host occurs. In general, surveillance activities have allowed communities to know several days to 2 or more weeks in advance when outbreaks of WNV may be expected to occur in humans unless specific precautions are taken. As PCPs, it is important to stay informed through the local health department and other health and welfare agencies regarding WNV potential. In the United States, WNV has been reported from mid-July through early December, with peak incidence in late August through early September.
Besides understanding mosquito habits, prevention of WNV requires prevention of mosquito bites. Important points to know include peak "biting" times for mosquitoes and what type of insect repellant to use. In general, mosquitoes are most prevalent from dusk to dawn, and N,N-diethyl-m-toluamide or N,N-diethyl-3-methylbenzamide (DEET)-type repellants used on both the skin and clothing are the best types of insect repellants to use. DEET can be safely used on anyone over the age of 2 months. In general, products containing over one-half DEET are not necessary. The percentage of DEET within a product rates the product as to how long its protection will last. Products close to one-quarter DEET last up to 5 hours and those with 7% last approximately 2 hours. The American Academy of Pediatrics recommends that no more than 30% DEET should be used on children and the preferred amount is 10% or less. Children should not handle the spray cans, and DEET products should be applied to children by an adult, who will spray her hands and then rub the product onto the child. Lotions can also be used. The adult should thoroughly wash hands after touching the DEET. DEET products are safe for pregnant and breastfeeding women. More information on DEET and other pesticides can be obtained from the National Pesticide Information Center at 1-800-858-7378, http://www.npic.orst.edu, or http://www.epq.gov/pesticides/factsheets/insectrp.htm. Other tips for prevention of mosquito bites include covering body parts with clothing as much as possible while outside and avoiding going outside during peak biting times.
Risk
Persons over 50 years of age are at increased risk of death from WNV. People whose job requires them to work outdoors are also at a greater risk than the general population. Homeless individuals or those who live in homes that do not have adequate window and door screens are also at an increased risk to be in contact with mosquitoes infected with WNV. As a PCP, be sure to alert these individuals of their increased risk and educate them regarding mosquito surveillance and the use of DEET or other approved human insect repellants.
In individuals bitten by a mosquito carrying WNV, 80% of these individuals will be asymptomatic. In the remaining 20% of individuals, various presentations of acute infection will develop. The incubation period for WNV is between 2 to 14 days with the average being 2 to 6 days. Symptoms may include fever, headache, fatigue, malaise, abdominal pain, vomiting, diarrhea, adenopathy, eye pain, and an erythematous, maculopapular rash mainly on the torso. These symptoms are generally considered mild and should resolve in a few days. The mild disease is also known as West Nile fever. Less than 1% of individuals with WNV develop severe neurologic symptoms leading to West Nile meningitis, West Nile encephalitis, West Nile meningoencephalitis, and West Nile poliomyelitis. Symptoms of severe disease include high fever, headache, neck rigidity, stupor, confusion, disorientation, coma, seizures, tremors, muscle weakness, blindness, paresthesia, and/or paralysis. Severe symptoms can last several weeks or may even become permanent. In general, since WNV is a viral illness, most cases are only symptomatically treated. Treatment with ribavirin and interferon alpha has not proven successful.3 Any person with neurologic involvement should be hospitalized to insure adequate respiratory and neurologic support. The most common cause of death in those hospitalized with severe WNV disease is neuronal dysfunction, respiratory failure, or cerebral edema.
In order to prevent panic, be sure to educate patients about prevention. Prevention is the mainstay of avoiding the illness. Also, be sure that patients know that most people who contract WNV either have no symptoms or will develop "flu-like" symptoms that generally last 3 to 6 days. Once contracted, immunity for WNV may be lifelong. For more information on WNV, go to the CDC Web site at http://www.cdc.gov/westnile.
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