Updated: Nov 6, 2009
The West Nile virus is one of the many members of the genus Flavivirus that are known to cause human disease. The life cycle of the West Nile virus involves the microbe's transmission from nonhuman animals to humans by way of Aedes, Culex, or Anopheles mosquitoes. The West Nile virus can infect horses, birds, dogs, and other mammals.1,2 However, wild birds are apparently the optimal hosts for harboring and replicating the virus.
The West Nile virus has been reported in Africa, Asia, Europe, the Middle East, and North America. In 1999, the first cases of West Nile virus disease were reported in New York City, and the infection has been spreading throughout the North American continent ever since.3 In 2002, a total of 3,389 cases were reported in the United States.4,5 Approximately 55% of these cases were from the Midwest (Illinois, Michigan, Ohio, Indiana).
The West Nile virus causes serious manifestations in approximately 1% of persons who are infected, with increased morbidity and mortality in individuals older than 50 years. In hospitalized patients in New York City, neurologic sequelae of the West Nile virus included severe muscle weakness, with approximately 10% of patients developing a complete flaccid paralysis.6,7,8 One in 150 West Nile virus infections results in encephalitis or meningitis, and the mortality rate from severe illness is 3-15%. Individuals older than 75 years are at particular risk.1
As the elderly population increases and the distribution of the West Nile virus spreads nationwide, a growing number of infected individuals may require comprehensive inpatient rehabilitation to overcome the virus's disabling effects.9
Examining the ways in which the West Nile virus may cross the blood-brain barrier to infect the nervous system, Verma et al infected primary human brain microvascular endothelial (HBMVE) cells with NY99, a neurovirulent strain of the virus.10 The authors noted that the virus did not have a cytopathic effect on the HBMVE cells. Increased mRNA (messenger ribonucleic acid) and protein expression of the tight-junction protein claudin-1 and of 2 cell adhesion molecules (vascular cell adhesion molecule and E-selectin) were seen 2-3 days after cellular infection, the same time at which West Nile virus replication had peaked.
The study provided evidence that infection of HBMVE cells by the West Nile virus enables the cell-free virus to enter the central nervous system without disturbing the barrier's integrity. In addition, the authors suggested that cell adhesion molecules may help to traffic West Nile virus – infected immune cells into the central nervous system.
In the Western hemisphere, West Nile virus infection originated in 1999, in New York City. Since then, the disease has occurred with greater frequency in the Southern, Midwestern, and Western states. Symptoms of the infection first appear in the population in early June, with the peak incidence occurring in late August and tapering through early November.
The West Nile virus is most commonly identified in Asia, Africa, and the Middle East and is endemic in those parts of the world. In the 1990s, outbreaks of West Nile virus encephalitis were reported in Algeria, the Czech Republic, France, Romania, Russia, and Israel.1
There is no known predisposition related to a particular ethnic group.
There is no known sex predilection. Men and women are affected equally.
In the United States, the elderly are particularly disposed to illness from West Nile virus infection.
Mosquito bites may or may not be present in an infected person. A history of travel to or from an area that is known to harbor the virus is common.
The incubation period for the West Nile virus is postulated to be approximately 5-15 days. Symptoms of mild infection may last 3-6 days and include fever in 20% of cases. Other symptoms include nausea, anorexia, malaise, myalgia, headache, backache, rash, eye pain, and vomiting.1
Symptoms of more severe illness include severe muscle weakness, flaccid paralysis, photophobia, seizures, mental status changes, respiratory symptoms, and an erythematous, maculopapular, or morbilliform rash involving the neck, trunk, arms, or legs.6,11 The severity of the illness is related to the degree of central nervous system invasion by the virus.
Signs of encephalitis and meningoencephalitis may be seen. These include mental status changes, such as confusion, stupor, or coma. Other findings include positive Brudzinski and Kernig signs, papilledema, cranial nerve involvement (eg, facial weakness, double vision, visual loss, decreased taste sensation), motor strength weakness, decreased sensation, hyperreflexia, and positive pathologic reflexes (eg, Babinski sign, Hoffman sign).
The West Nile virus is transmitted to humans by the bite of an infected mosquito. Typically, warm climates and the summer months provide an ideal environment for mosquitoes to breed.1 Multiple mosquito bites and greater exposure to environments with a large mosquito population increase the risk of infection. However, some cases have been linked to organ transplantation, breastfeeding, and (possibly) blood transfusions.12
Acute Poliomyelitis
Guillain-Barre Syndrome
Multiple Sclerosis
Postpolio Syndrome
Vertebrobasilar Stroke
Bacterial meningitis
Viral meningitis
Ischemic stroke
Hemorrhagic stroke
Brain abscess
Brain tumor
Cat-scratch disease
Herpes simplex
Herpes simplex encephalitis
Myasthenia gravis
Hypoglycemia
Leptospirosis
Subarachnoid hemorrhage
Tick-borne diseases, Lyme
Tick-borne diseases, Rocky Mountain spotted fever
Toxoplasmosis
Tuberculosis
Autopsy findings in some patients with West Nile virus infection reveal mononuclear inflammation that extensively involves the medulla, with some involvement of the cranial nerve roots.15 However, these findings are not diagnostic for the infection.
Brain injury from West Nile virus encephalitis or meningitis can result in cognitive, gross motor, and fine motor delays. Because infected patients have varying degrees of functional deficits, treatment programs must be individualized. Comprehensive rehabilitation using a team consisting of a physiatrist, nurse, physical therapist, occupational therapist, speech therapist, social worker/case manager, and neuropsychologist achieves best outcomes.
The physical therapist can partially address the problems of increased muscle tone, weakness, decreased sensation, and poor endurance. Mobility training, transfer training, and gait training are usually implemented, with range of motion and proper positioning attended to as well. Physical therapists are also important in providing exercises for muscle reeducation and for the improvement of strength, endurance, coordination, and balance, with the goal of returning the patient to independent function.
Occupational therapy focuses on the activities of daily living (ADLs), including bathing, dressing, feeding, and hygiene maintenance. Occupational therapists provide a program to maximize the use of the arms and hands with functional activities; they also address the cognitive issues that affect daily independent function. (See also Further Outpatient Care.)
Patients may develop dysarthria, dysphagia, or aphasia. A structured speech therapy program may improve their ability to swallow, help them recover speech and language function, and prevent complications, such as aspiration pneumonia. (See also Further Outpatient Care.)
No surgical indications are reported at this time.
Ongoing research is being pursued into the direct treatment of West Nile virus meningoencephalitis with interferon alpha and intravenous immunoglobulin G (Omr-IgG-am).
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West Nile virus, West Nile symptoms, West Nile virus symptoms, WNV, , West Nile fever, West Nile encephalitis, West Nile virus mosquitoes, West Nile fever, West Nile infection, mosquito bites, mosquitoes, mosquitoes, mosquitoes
Jess D Salinas Jr, MD, Medical Director, Lake Mary Clinic, National Pain Institute, LLC; Associate Medical Director, Winter Park Clinic, National Pain Institute, LLC
Jess D Salinas Jr, MD is a member of the following medical societies: American Academy of Pain Management, American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Society of Interventional Pain Physicians, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
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Monica L Steiner, MD, Clinical Assistant Professor, Program Director, Department of Orthopedics and Rehabilitation, Loyola University Medical Center
Monica L Steiner, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Elizabeth A Moberg-Wolff, MD, Associate Professor and Pediatric PM&R Fellowship Director, Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin; Program Director, Tone Management and Mobility, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin
Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
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Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Clinical guidelines:
Interim guidelines for the evaluation of infants born to mothers infected with West Nile virus during pregnancy. Centers for Disease Control and Prevention - Federal Government Agency [U.S.]. 2004 Feb 27. 4 pages. NGC:003471
The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Infectious Diseases Society of America - Medical Specialty Society. 2008 Aug 1. 25 pages. NGC:007083
Clinical trials:
Treatment of West Nile Virus With MGAWN1 (PARADIGM)
VRC 300: Screening of Healthy Volunteers for Clinical Trials of Investigational Vaccines to Prevent Infectious Diseases
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