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ACN Education Center

West Nile Virus: A Clinical Commentary for the Camp Healthcare Community

Ellen Reynolds, MSN, CPNP, Clinical Practice Chair
Holly Bauer, RN, Wisconsin Lions Camp
Originally published in CompassPoint, 12 (4), 6 - 8.

The appearance of West Nile Virus in recent years is perhaps the most well-documented introduction of a new, vector-borne human pathogen into the United States in this century. Because of the virus’ spread via mosquitoes, it is of particular concern for camps located in rural, wooded or wilderness areas. While the virus causes encephalitis and meningitis in serious cases, most cases are mild and require only symptomatic care. Education and prevention measures can help place concerns about the disease in proper perspective.

The purpose of this Clinical Commentary is multi-faceted. First, it is provided so that camp nurses and those concerned with camp health have accurate information about West Nile virus to date. Second, the Commentary describes a framework for camping’s response to this challenge. And finally, since this is an emerging problem, the Commentary recognizes that additional information may yet be determined that will change the recommendations brought forth in this discussion. Consequently, resources and references are provided so readers are able to check for updates. In addition, the spring issue of CompassPoint will carry a pre-summer update to this information.

INCIDENCE AND EPIDEMIOLOGY

West Nile virus was first isolated from an infected person and identified in the West Nile district of Uganda in 1937. Until 1999, the virus was found only in the Eastern Hemisphere. Infrequent human outbreaks, mostly associated with mild febrile illnesses, had been reported mostly in groups of soldiers, children, and healthy adults in Israel and Africa. Since the mid-1990s, the frequency and apparent clinical severity of West Nile virus outbreaks have increased (1). It is unclear whether this change is due to differences in the virus’s virulence or to changes in characteristics of the affected populations.

United States public health surveillance has documented persons with disease caused by West Nile virus since 1999, when it first appeared in New York City. These cases have been identified over an expanding geographic area:1 state in 1999, 3 in 2000, and 10 in 2001 (1). From 1 January to 10 October 2002, there were 2946 cases of West Nile virus identified in 35 states and the District of Columbia. These cases included 160 deaths (2). Certainly, the increase in reported cases is due in part to heightened awareness, surveillance, and testing.

West Nile virus is thought to be maintained in a cycle involving infected birds and vector mosquitoes. Many of the “bridge vectors” - mosquitoes that bite both birds and humans - likely become infected in late summer and then pose an infection threat to humans. West Nile virus can NOT be spread from human to human, nor from animal to humans. The peak of reported cases between 1999 and 2001 occurred in August and September (1). In warm or tropical climates, year round transmission is possible.

CLINICAL FEATURES

The incubation period of West Nile virus is estimated to range from three to 14 days. Most human infections are not clinically recognized simply because those affected may never feel very sick. A survey of serology in residents of New York City during the 1999 outbreak indicated that only approximately 20% of persons infected with West Nile virus had developed fever, and only half of those had visited a physician for this illness (3).

The range of symptoms associated with West Nile fever is poorly defined as reporting has focused on patients with more severe neurological disease. Mild disease is characterized as a febrile illness of sudden onset, often with general malaise, anorexia, headache, muscle aches, pains and weakness, nausea, vomiting, rash, and/or lymphadenopathy. The symptoms generally last three to six days. The most efficient diagnostic method is detection of IgM antibody to West Nile virus in patient serum or cerebrospinal fluid (1). Treatment is supportive, with no evidence of benefit from antimicrobial agents to date.

Advanced age has been found to be the most important risk factor in fatal cases. The presence of encephalitis, severe muscle weakness, and change in level of consciousness are also clinical factors associated with increased risk of fatality. Immunosuppressed patients are likely to be at additional risk. Few data exist regarding long-term outcomes for West Nile infection, but case analysis suggests that among those who require hospitalization, persistent symptoms including fatigue, memory loss, weakness, and depression are common (1).

West Nile virus encephalitis has recently been added to the list of designated reportable illnesses. Local public health departments should be notified of any confirmed cases. Recommended clinical and laboratory case definitions for West Nile virus are available at http://www.cdc.gov/ncidod/dvbid/westnile/resources/wnv-guidelines-apr-2001.pdf.

PREVENTION

Currently, prevention of West Nile virus infection is based on two strategies: reducing the number of mosquito vectors and preventing vector mosquitoes from biting humans. Many mosquitoes breed in small pools of standing water and have a limited flight range, so reducing mosquito populations in the immediate vicinity of human habitat and activity is useful. Property owners and municipalities can drain water from potential breeding sites, and coordinate plans for use of insecticides. Biological products, which consist chiefly of larvacidal bacteria, as well as pesticide chemicals may be used. More detailed information about pesticides and other mosquito control measures can be obtained from the US National Pesticide Information Center.

DEET (N,N-diethyl-3-methylbenzamide) is currently the most effective mosquito repellant available. It is available in many formulations and has an excellent safety profile. Products containing 10-50% DEET are considered sufficient to repel mosquitos, with concentrations greater than 50% demonstrating little additional efficacy. Manufacturer’s recommendations should be followed for periodic re-application of the repellant. The American Academy of Pediatrics recommends that repellants containing no more than 30% DEET be used in children, and that DEET not be used in infants under the age of two months (4). DEET can be applied to skin, pets, clothing, tents, bedrolls, and screens. While other products such as Skin-so-Soft, and citronella have mild repellant properties, the use of DEET should be promoted in order to prevent vector-borne infection.

IMPLICATIONS AND RECOMMENDATIONS FOR CAMPS

West Nile virus is presumed to be spreading in a pattern that will distribute it across North America at some point. Camps frequently are located in lake or woodland areas where mosquito populations flourish, and camps generally place emphasis on doing activities outside. So far, no one is recommending that people stay indoors, a strategy that would certainly minimize exposure to mosquitos. Yet camps do have a responsibility to provide the safest possible environment and program guidelines for their staff and campers. These guidelines should focus both on prevention strategies that minimize West Nile virus exposure and surveillance that identifies a potential case. In addition, camps should be prepared to provide information and resources to concerned parents and participants. Because this challenge has newly emerged, staying linked to reliable information will be critical.

With this in mind, the Association of Camp Nurses recommends the following risk reduction strategies for children’s camps.

I. Take actions that minimize the potential for mosquito bites during outdoor activity.

A. Encourage body cover (long pants, shirts, socks, hats) appropriate to the weather and activity. Shirts should be tucked in at the waist; socks should be pulled over pant legs.

B. Appropriately apply an insect repellant containing 10%-30% (recommended for children) to 50% DEET. Reapply per product directions throughout the duration of outdoor activity. Recommend spraying the repellant on clothing rather than skin when feasible. There is no need to apply DEET to the skin under clothing if it has been applied to that clothing. Avoid eye and mouth areas, as well as cuts, wounds, and irritated skin. Avoid using sprays in enclosed areas. Do not use DEET near food. Create related policies to ensure safe and consistent use of repellants such as supervision or application of repellants by counseling staff. Wash repellant off skin – with soap and water – when returning indoors, especially if repeated applications are used.

C. Educate staff – especially those who live with campers or who accompany groups of campers from activity to activity – to notice children who are getting bit by mosquitoes. Assess those campers for appropriate use of their repellent; take action based on that assessment. Be prepared to try a different repellent if the camper’s formulation is ineffective at repelling mosquitoes.

D. Avoid mosquito-rich habitats (e.g., wooded areas and marshes) during dusk and dawn periods, the peak biting time for many mosquitos. Avoid campouts near marshes and other wet areas or implement a plan to control for those mosquitos with commercial products.

E. Monitor the load of mosquitos in activity areas; note camper and/or staff comments that mosquitoes are typically heavy in certain areas. Act on this information.

F. Reduce human exposure to mosquitos’ long grass habitat by mowing paths of hiking trails; consider widening the trail to further limit exposure.

G. Review and adapt the camp schedule as necessary to avoid use of outdoor activity areas when mosquitos are heaviest.

II. Minimize the mosquito population and its access to human habitat.

A. Eliminate standing water around camp. Remember to consider potential breeding grounds such as gutters, old barrels, boats, and fire control buckets.

B. Keep window screens and doors in good repair.

C. Be aware of measures taken or recommended by local municipalities to decrease the mosquito population (e.g., pesticide spraying). Investigate the appropriateness of these actions for the camp.

III. Recognize clinically significant cases of West Nile virus disease.

A. Be aware of local guidelines for recognition of and testing for West Nile virus. In addition, work with the camp’s supervising physician to determine a case profile under which potential for WNV infection should be considered and educate camp administrative staff to this directive. Currently, only patients with signs and symptoms of neurological disease should be tested for West Nile virus. Patients with milder illnesses (e.g. fever and rash, fever and headache, lymphadenopathy) do not need to be tested for WNV (5). Bear in mind that West Nile is only one in the family of viruses that causes illness affecting the central nervous system. Other diseases include California, Eastern equine, Powassan, St Louis, Venezuelan equine, and Western equine encephalitis (4).

B. Immediately refer any camper or staff member with persistent high fever, altered mental status, focal neurological signs, significant muscle weakness, or other signs/symptoms suggestive of meningitis or encephalitis for physician evaluation.

C. Campers or staff with fever, general malaise, headache, body aches, and/or swollen lymph nodes should be monitored and treated symptomatically per the individual camp’s health care guidelines.

IV. Develop and implement a system to stay informed of developments regarding West Nile virus.

A. Suggested online resources:

1. Center for Disease Control: www.cdc.gov or call 1-888-246-2675.

2. US Food and Drug Administration: www.fda.gov or call 1-888-463-6332.

3. National Institute of Health: www.naid.nih.gov

4. US Environmental Protection Agency: www.epa.gov

5. American Mosquito Control Association: www.mosquito.org or call 1-732-932-0667.

B. Your State’s Department of Health (check with the State in which your camp is located).

C. Your camp’s supervising physician.

D. Camp specific resources:

1. Association of Camp Nurses (ACN): www.acn.org and CompassPoint.

2. American Camp Association (ACA): www.ACAcamps.org and CampLine.

The West Nile virus has the potential for causing serious illness in children and adults; the actual likelihood of infection is low. A combination of education and prevention strategies can have a significant impact on the perceived and actual risk of WNV infection to campers and staff.

1. Petersen, LR, & Marfin, AA (2002). West Nile virus: A primer for the clinician. Annals of Internal Medicine, 137(3), E173-E178.

2. Centers for Disease Control (2002). Website, http://ww.cdc.gov (click on West Nile Virus).

3. Mostashari F, Bunning ML, Kitsutani PT, Singer DA, Nash D, Cooper MJ, et al (1999). Epidemic West Nile encephalitis, New York, 1999: Results of a household-based seroepidemiological survey. Lancet. 2001;358:261-4.

4. Kristy Kennedy (2002). Calming West Nile fears. From American Academy of Pediatrics website http://www.aap.org/family/wnv-sept02.htm.

5. Zimmerman, RS (2002). PA Dept of Health: Health Alert # 31.

REVIEWERS

  • Mary Marugg, RN, Sonlight Christian Camp, Pagosa Springs, CO
  • Susan Van Cleve, RN, CPNP, MSN, PNP Program Director, University of Pittsburgh, PA
  • John J. LaBella, MD, pediatrictian, Children’s Community Pediatrics, Pittsburgh, PA