West Nile Virus

Updated: Mar 31, 2022
  • Author: Jess D Salinas, Jr, MD; Chief Editor: Elizabeth A Moberg-Wolff, MD  more...
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Practice Essentials

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, 3] However, wild birds are apparently the optimal hosts for harboring and replicating the virus.

Serologic testing to detect immunoglobulin M (IgM) antibodies is currently the best means [4] of diagnosing West Nile virus infection. The physical therapist can partially address the problems of increased muscle tone, weakness, decreased sensation, and poor endurance associated with the disease.

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, with the infection subsequently spreading throughout the North American continent. [5]

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 for persons with severe illness is 3-15%. Individuals older than 75 years are at particular risk. [2]

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]

A study by Hadler et al suggested that many US states may no longer have adequate surveillance systems for detecting and responding to outbreaks of West Nile virus. The investigators stated that although by 2004, with the aid of federal funding, well-developed West Nile virus surveillance systems existed in almost every state, by 2012, following a 61% decrease in federal funding, many health departments had reduced such surveillance and lacked a systematic, disease-based surveillance system for other arboviruses. [10]

Signs and symptoms of West Nile virus

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. [2]

Symptoms of more severe illness include severe muscle weakness, flaccid paralysis or increased muscle spasticity, photophobia, seizures, mental status changes, respiratory symptoms, and an erythematous, maculopapular, or morbilliform rash involving the neck, trunk, arms, or legs. [6, 11]

Diagnosis and management of West Nile virus

Serologic testing to detect immunoglobulin M (IgM) antibodies is currently the best means [4] of diagnosing West Nile virus infection.

In an estimated one third of infected individuals, magnetic resonance imaging (MRI) scans show notable enhancement in the leptomeninges and periventricular areas.

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.

Elderly patients who are severely deconditioned because of West Nile virus encephalitis may be predisposed to deep venous thrombosis (DVT). The inherent risk of having DVT is the development of a pulmonary embolus that can cause death. Prevention strategies include the use of thigh-high compression stockings, pneumatic compression devices, and subcutaneous, unfractionated or low–molecular weight heparins. Early mobilization and ambulation also may decrease the risk of DVT.

Individuals with severe illness secondary to West Nile virus infection are at increased risk of pulmonary complications in the rehabilitation setting. Individuals with encephalitis may have a decreased level of consciousness, or they may suffer from dysphagia related to their neurologic injury, predisposing them to aspiration pneumonia. Swallow evaluation can be performed to identify the problem and to help in implementing the appropriate diet and feeding techniques to decrease the risk of aspiration. Phrenic nerve palsy has been described; this complication could lead to decreased expansion of the lungs, further increasing the risk of atelectasis and nosocomial pneumonia. Deep-breathing exercises, use of an inspiratory spirometer, and early mobilization and ambulation help to decrease the risk of these complications occurring.

Patient education

For patient education information, see the Infections Center and the Brain and Nervous System Center, as well as West Nile Virus, Insect Bites, and Encephalitis.



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. [12] 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.




United States

The West Nile virus was introduced into the United States 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.

A large outbreak of West Nile virus infection in 2012 resulted in 5674 reported cases (51% of which were neuroinvasive), although the number of reported cases for 2013 dropped to 2469. In 2014, there were 2205 reported cases (61% of which were neuroinvasive), while in 2015, the number was 2175, with the incidence of neuroinvasive West Nile virus being 0.45 cases per 100,000 population nationally. [13, 14, 15, 16, 17, 18] In 2016, the number of US cases reported to the US Centers for Disease Control and Prevention (CDC) reached 2149, including 1309 neuroinvasive cases; the incidence of neuroinvasive disease was 0.41 per 100,000 population, comparable to the median incidence between 2002 and 2015. [19, 20] The infection data for 2018 was 2647 cases, including 1658 neuroinvasive disease cases. [21]  In total, 50,830 cases of West Nile virus were reported to the Centers for Disease Control and Prevention (CDC) between 1999 and 2018, including 24,657 cases of neuroinvasive disease. [21]

According to the CDC, in 2019 there were 1173 cases of domestic arbovirus disease reported for 47 states and the District of Columbia, with 971 of these (83%) being cases of West Nile virus. A classification of neuroinvasive disease was made for 633 (65%) of the West Nile virus cases, the incidence—0.19 cases per 100,000 population—being 53% below the median annual incidence for 2009-2018. [22]


The West Nile virus is most commonly identified in Asia, Africa, and the Middle East and is endemic in those parts of the world. [23] In the 1990s, outbreaks of West Nile virus encephalitis were reported in Algeria, the Czech Republic, France, Romania, Russia, and Israel. [2] In the Americas, since its introduction into the United States, in 1999, the West Nile virus has spread to Canada and into South America. [24]


Reports indicate that less than 1% of persons who are infected with the West Nile virus develop severe illness; of individuals who have severe illness secondary to the infection, 3-15% die.

Severe disease particularly affects the elderly. Advanced age is by far the greatest risk factor for neurologic disease, long-term morbidity, and death, especially in persons older than 75 years. In 2019, among US patients with West Nile virus neuroinvasive disease who died, the median age was 73 years. [14, 22]

The total number of reported deaths from the West Nile virus in the United States between 1999 and 2016 was 2017 (4% of cases), including 1888 from neuroinvasive disease. [19]


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.