West Nile Virus: A Clinical Commentary for the Camp Healthcare
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.
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
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
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
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
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.
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.
- 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