Ear, Nose, and Throat Specialists Offer Primer on West Nile Virus
In 1999, West Nile virus (WNV) appeared in New York City, marking the most significant beginning of a new, vector-borne human pathogen in the United States over the past century. Throughout North American history, rapid expansion of various modes of travel and commerce have led to the introduction of such vector-borne human pathogens as dengue, yellow fever, plague and malaria. Now, it is West Nile Virus that has captured the attention of infectious disease officials as well as the American public.
In 2003 alone, this illness afflicted more than 9800 individuals resulting in 264 deaths. The wide range of symptoms includes malaise, anorexia, nausea, vomiting, headache, myalgia, and dysphasia, as well affecting the lymph nodes. Patients will seek treatment from their primary care provider; but the ear, nose, and throat specialist may also be required to offer care with those diagnosed with this disorder.
Two U.S. Air Force otolaryngologist—head and neck surgeons are offering their colleagues a primer on West Nile virus, designed specifically to meet the needs of the specialty. The authors of “West Nile Virus: A Primer for the Otolaryngologist,” are Peter G. Michaelson, MD, Captain, USAF, MC, Eric A. Mair, MD, Colonel, USAF, MC, both from the Department of Otolaryngology—Head and Neck Surgery, Wilford Hall USAF Medical Center, San Antonio, TX. Their report is being presented at the American Academy of Otolaryngology-Head and Neck Surgery Foundation Annual Meeting & OTO EXPO, being held September 19-22, 2004, at the Jacob K. Javits Convention Center, New York City, NY.
A summary of the subject matter being provided to otolaryngologist—head and neck surgeons follow:
Epidemiology: How closer examination of the affected birds showed differing degrees of both meningoencephalitis and myocarditis, while all tested negative for the most probable avian pathogens. Isolation of a virus specific to the birds’ tissues showed similarities to West Nile virus and proved genetically identical to the virus recovered from human victims of the New York outbreak. Although previous outbreaks of WNV around the world had not been uncommon, this 1999 appearance in New York City represented its first major manifestation in the continental United States.
Virology: That WNV is a flavivirus, composed of single-stranded RNA, which incorporates an envelope glycoprotein on its surface responsible for virus—host cell binding. As a member of the Japanese encephalitis virus serocomplex, WNV is closely related to several other flaviviruses also associated with human encephalitis—St Louis encephalitis, Murray Valley encephalitis and Kunjin virus.
Although evidence exists that the virus may have originated in the Middle East, it is still unclear how the virus finally arrived in the United States. With the viral load in humans being extremely low, transmission by an infected international traveler is highly unlikely. A more plausible culprit would be migrating birds or perhaps infected adult mosquitoes or larvae inadvertently transported on a transcontinental aircraft.
Transmission: WNV infection most commonly occurs through the bite of the infected culicine mosquito. Transmission occurs from infected birds with adequate viral loads to mosquitoes during a blood meal, with recent literature showing infection in 146 species of bird (with crows and blue jays being most susceptible) and 29 species of mosquito in the United States. Humans, horses and the majority of other mammals carry a low and brief virus in the bloodstream incapable of infecting others, to include a biting mosquito. However, the role of the human as a “dead end” host has come into question with multiple newly described modes of transmission, to include blood transfusion, organ transplantation, breast-feeding, transplacental transmission and laboratory acquisition.
Clinical presentation: Approximately 80 percent of those infected with WNV will have an infection without the presence of symptoms, produce an immune response, and probably never know they were infected. The vast majority displaying infection will experience West Nile fever, a mild illness that follows an incubation period of three to 14 days. This illness, which is self-limiting, lasts approximately a week and produces a fever with constitutional signs and symptoms. These complaints include headache, backache, myalgias and anorexia, also includes conditions commonly seen by the otolaryngologist, such as a roseolar (red patches) or maculopapular rash involving primarily the head, neck and trunk, which occurs in about half of these patients. Dysphagia, or difficulty in swallowing, may be a concurrent complaint in up to half of affected patients, impacting both patient comfort and nutrition.
Laboratory findings/Diagnostic measures: Due to a low human indication of virus in the bloodstream, isolation of the virus is difficult, and diagnosis is usually dependent on IgM recognition. Studies can be performed on serum or cerebrospinal fluid (CSF) with a 90 percent IgM enzyme-linked immunosorbent assay (ELISA) detection rate beginning on the eighth day following infection). This is the most simple, cost-effective way to confirm a suspected diagnosis. IgM antibodies to WNV may persist for more than six months; therefore a positive ELISA does not always signify a recent infection (unless it’s related to analogous symptoms).
If testing is conducted at private laboratories, the health department or Centers for Disease Control (CDC) will often confirm results in their own laboratories before officially reporting WNV cases. CDC will finally report a case of WNV once a state officially reports and verifies that case to CDC.
Management: Patients with WNV should be hospitalized, the appropriate specialists consulted, and supportive care given, to include when necessary ventilatory support. To date, no clear benefit from the administration of ribavirin, interferon alfa, pyrazidine, steroids or other agents has been documented. Recently, WNV encephalitis has been added to the list of designated nationally notifiable arboviral encephalitides, with aseptic meningitis reportable in some jurisdictions.
Prevention: Due to the lack of an effective medicinal cure and on-going research in potential vaccines, control of WNV depends on both clinical and public health preventative measures. A growing surveillance system must be matched with attempts to lower the number of vector mosquitoes as well as the possibility of those mosquitoes biting humans. Stagnant water found in containers or other objects serves as a breeding site for mosquitoes, and eliminating these sites decreases possible-breeding locations for the host who have a limited flight range. Larvicides and other pesticides may be administered by trained personnel, and when used properly are associated with rare potential adverse heath affects. Interestingly, backyard “bug zappers” or carbon dioxide-baited devices have not been proven to significantly reduce the number of mosquito bites.
Additional personnel protective measures include wearing long-sleeved shirts and pants as well as regular application of insect repellants containing DEET to skin and permethrin to clothes. DEET-containing repellants, which are more effective than any currently available non-DEET formulations (to include citronella), show a maximum effectiveness at 50 percent concentration, with no added benefit for higher strengths. This repellant, which should be washed off the skin once inside, has an excellent safety record and is safe to use in infants over two months and pregnant females. Permethrin, a synthetic pyrethroid, can be used in addition to DEET with directed application to clothing, tents, mosquito nets and other fabric.
Other public health measures, to include the reporting of dead birds to local and state health departments as well as reporting human infections to the appropriate health departments are also crucial.