West Nile Fever
Disease Details
Family Health Simplified
- Description
- West Nile Fever is a mosquito-borne viral infection that can cause flu-like symptoms and, in severe cases, neurological complications.
- Type
- West Nile fever is a viral infection. The causative agent, West Nile virus, is an RNA virus belonging to the Flavivirus genus. Human-to-human transmission through genetic means does not occur; it is primarily transmitted to humans through the bite of an infected mosquito, typically of the Culex species.
- Signs And Symptoms
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About 80% of those infected with West Nile virus (WNV) show no symptoms and go unreported. About 20% of infected people develop symptoms. These vary in severity, and begin 3 to 14 days after being bitten. Most people with mild symptoms of WNV recover completely, though fatigue and weakness may last for weeks or months. Symptoms may range from mild, such as fever, to severe, such as paralysis and meningitis. A severe infection can last weeks and can, rarely, cause permanent brain damage. Death may ensue if the central nervous system is affected. Medical conditions such as cancer and diabetes, and age over 60 years, increase the risk of developing severe symptoms.Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelitis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.
West Nile fever (WNF), which occurs in 20 percent of cases, is a febrile syndrome that causes flu-like symptoms. Most characterizations of WNF describe it as a mild, acute syndrome lasting 3 to 6 days after symptom onset. Systematic follow-up studies of patients with WNF have not been done, so this information is largely anecdotal. Possible symptoms include high fever, headache, chills, excessive sweating, weakness, fatigue, swollen lymph nodes, drowsiness, pain in the joints and flu-like symptoms. There may be gastrointestinal symptoms including nausea, vomiting, loss of appetite, and diarrhea. Fewer than one-third of patients develop a rash.
West Nile neuroinvasive disease (WNND), which occurs in less than 1 percent of cases, is when the virus infects the central nervous system resulting in meningitis, encephalitis, meningoencephalitis or a poliomyelitis-like syndrome. Many patients with WNND have normal neuroimaging studies, although abnormalities may be present in various cerebral areas including the basal ganglia, thalamus, cerebellum, and brainstem.
West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30 to 50 percent of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.
West Nile meningitis (WNM) usually involves fever, headache, stiff neck and pleocytosis, an increase of white blood cells in cerebrospinal fluid. Changes in consciousness are not usually seen and are mild when present.
West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).
West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, sometimes occurs.
West-Nile reversible paralysis, Like WNP, the weakness or paralysis is asymmetric. Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement. Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms. The prognosis for recovery is excellent.
Nonneurologic complications of WNV infection that may rarely occur include fulminant hepatitis, pancreatitis, myocarditis, rhabdomyolysis, orchitis, nephritis, optic neuritis and cardiac dysrhythmias and hemorrhagic fever with coagulopathy. Chorioretinitis may also be more common than previously thought.
Skin manifestations, specifically rashes, are common; however, there are few detailed descriptions in case reports, and few images are available. Punctate erythematous, macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems. A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection. - Prognosis
- While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60 to 90 days to recover. Patients with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple somatic complaints such as tremor, and dysfunction in motor skills and executive functions for over a year. People with milder symptoms are just as likely as people with more severe symptoms to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.
- Onset
- West Nile fever typically has an onset of symptoms between 2 to 14 days after being bitten by an infected mosquito.
- Prevalence
- The prevalence of West Nile fever varies significantly by region and year. It primarily affects areas in North America, Europe, Africa, the Middle East, and West Asia. In the United States, cases typically spike during mosquito season from summer through early fall. Specific prevalence figures may fluctuate annually depending on factors such as weather conditions, mosquito populations, and local control measures.
- Epidemiology
- WNV was first isolated from a feverish 37-year-old woman at Omogo in the West Nile District of Uganda in 1937 during research on yellow fever virus. A series of serosurveys in 1939 in central Africa found anti-WNV positive results ranging from 1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently identified in Egypt (1942) and India (1953), a 1950 serosurvey in Egypt found 90% of those over 40 years in age had WNV antibodies. The ecology was characterized in 1953 with studies in Egypt and Israel. The virus became recognized as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957. The disease was first noted in horses in Egypt and France in the early 1960s and found to be widespread in southern Europe, southwest Asia and Australia.The first appearance of WNV in the Western Hemisphere was in 1999 with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in College Point, Queens in New York City and was later spread to the neighboring states of New Jersey and Connecticut. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence. West Nile virus is now endemic in Africa, Europe, the Middle East, west and central Asia, Oceania (subtype Kunjin), and most recently, North America and is spreading into Central and South America.Outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), the Czech Republic (1997), Congo (1998), Russia (1999), the United States (1999 to 2009), Canada (1999–2007), Israel (2000) and Greece (2010).Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), and France (2000), Mexico (2003) and Sardinia (2011).Outdoor workers (including biological fieldworkers, construction workers, farmers, landscapers, and painters), healthcare personnel, and laboratory personnel who perform necropsies on animals are at risk of contracting WNV.In 2012, the US experienced one of its worst epidemics in which 286 people died, with the state of Texas being hard hit by this virus.
- Intractability
- West Nile fever is generally not considered intractable. Most individuals infected with the West Nile virus experience mild symptoms or are asymptomatic and recover without specific medical treatment. However, severe cases can occur, leading to neuroinvasive disease such as encephalitis or meningitis, which may require intensive medical care. The intractability of the disease could be a concern in these severe cases, but overall, West Nile fever itself is not deemed intractable.
- Disease Severity
- West Nile Fever can vary in severity. Most cases are mild and include symptoms such as fever, headache, body aches, and sometimes a skin rash or swollen lymph glands. However, in some cases, particularly in older adults or individuals with weakened immune systems, it can progress to severe diseases like West Nile encephalitis or meningitis, leading to neurological complications.
- Healthcare Professionals
- Disease Ontology ID - DOID:2366
- Pathophysiology
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Pathophysiology of West Nile Fever involves the following:
1. **Virus Entry and Spread:** The West Nile virus is primarily transmitted to humans through the bite of an infected mosquito. Once the virus enters the bloodstream, it can spread to various organs.
2. **Initial Immune Response:** The body's immediate immune response is activated, involving the innate immune system, which tries to limit viral replication.
3. **Viral Replication:** The virus primarily targets and replicates in cells of the monocyte-macrophage lineage and endothelial cells. This can lead to a viremia (presence of the virus in the blood).
4. **Crossing the Blood-Brain Barrier:** The virus can cross the blood-brain barrier, leading to inflammation in the central nervous system. This is particularly severe in some cases and can result in encephalitis or meningitis.
5. **Neuronal Infection and Inflammation:** Once in the brain, the virus can infect neurons, causing neuronal death and inflammation. This leads to the clinical symptoms of encephalitis, including fever, headache, and sometimes severe neurological complications such as seizures, paralysis, or coma.
6. **Adaptive Immune Response:** The adaptive immune system (including B cells and T cells) generates a more targeted response to the virus, producing antibodies and attacking infected cells to control and eventually clear the infection.
7. **Resolution or Chronic Effects:** In most individuals, the immune response successfully clears the virus, leading to recovery. However, in some cases, particularly in immunocompromised individuals or the elderly, the infection can lead to severe neurological damage or death. - Carrier Status
- Carrier status for West Nile Fever is associated with birds, which are the primary reservoirs of the virus. Mosquitoes, particularly Culex species, act as vectors transmitting the virus from infected birds to humans and other animals. Humans and horses are incidental hosts and do not develop high enough levels of the virus in their bloodstream to contribute to the transmission cycle.
- Mechanism
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West Nile fever is caused by the West Nile virus (WNV), which primarily spreads through the bite of an infected mosquito, particularly the Culex species. Its mechanism and molecular mechanisms are as follows:
**Mechanism:**
1. **Transmission**: The virus is transmitted to humans and animals through mosquito bites.
2. **Viral Entry**: Once WNV enters the bloodstream, it targets and infects various cell types, including dendritic cells, keratinocytes, and fibroblasts.
3. **Spread**: The virus can cross the blood-brain barrier and infect the central nervous system, leading to neurological complications in severe cases.
4. **Immune Response**: The immune system responds to the infection by producing antibodies and activating T-cells to clear the virus.
**Molecular Mechanisms:**
1. **Binding and Entry**: WNV binds to cell surface receptors, such as DC-SIGN, integrins, and glycosaminoglycans, facilitating viral entry via endocytosis.
2. **Replication**: After entry, the virus releases its positive-sense RNA genome into the host cell cytoplasm. This RNA acts as mRNA for the synthesis of viral proteins and as a template for RNA replication.
3. **Protein Translation**: Viral RNA is translated into a polyprotein, which is subsequently cleaved by viral and host proteases into structural (capsid, envelope) and non-structural proteins (NS1, NS3, NS5).
4. **Assembly and Release**: New viral particles are assembled in the endoplasmic reticulum, transported through the Golgi apparatus, and released from the host cell via exocytosis or budding.
5. **Host Response and Evasion**: WNV evades the immune response by inhibiting interferon signaling pathways, modulating apoptosis, and altering cytokine production to reduce host defense mechanisms.
Understanding these mechanisms aids in the development of therapeutic strategies and preventive measures against West Nile fever. - Treatment
- No specific treatment is available for WNV infection. Most people recover without treatment. In mild cases, over-the-counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases supportive care is provided, often in hospital, with intravenous fluids, pain medication, respiratory support, and prevention of secondary infections.
- Compassionate Use Treatment
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Compassionate use and experimental treatments for West Nile fever primarily involve investigational antiviral drugs and immunotherapies. Some of the treatments considered are:
1. **Ribavirin**: Although its effectiveness is not well-established, it has been considered in some cases.
2. **Interferons**: These are proteins that may help the immune system fight infections, and they have been considered for experimental use.
3. **Intravenous Immunoglobulin (IVIG)**: This treatment involves giving patients antibodies from donated blood plasma, which may help neutralize the virus.
4. **Monoclonal Antibodies**: Experimental treatments involving monoclonal antibodies specifically targeting the West Nile virus are under investigation.
These treatments are still largely experimental and may only be available through clinical trials or compassionate use programs. - Lifestyle Recommendations
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To prevent West Nile virus infection:
1. **Wear Protective Clothing**: Use long-sleeved shirts, long pants, and other protective clothing to cover your skin, especially during peak mosquito activity times (dawn and dusk).
2. **Use Mosquito Repellent**: Apply insect repellents containing ingredients such as DEET, picaridin, or oil of lemon eucalyptus to exposed skin and clothing.
3. **Eliminate Standing Water**: Remove any stagnant water around your home to reduce mosquito breeding sites. This includes buckets, flower pots, bird baths, and other containers.
4. **Install Screens**: Ensure that windows and doors are fitted with properly maintained screens to keep mosquitoes from entering your home.
5. **Limit Outdoor Activities**: Avoid outdoor activities during peak mosquito activity times, especially if you live in or travel to areas with known outbreaks.
6. **Support Community Measures**: Participate in or support local mosquito control programs to reduce mosquito populations in your area. - Medication
- There is no specific antiviral medication for West Nile fever. Treatment mainly involves supportive care to relieve symptoms, such as pain relievers for headaches and muscle aches, fever reducers, and fluids to prevent dehydration. In severe cases, hospitalization may be required for supportive treatments like intravenous fluids, pain management, and respiratory support.
- Repurposable Drugs
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Research into repurposing existing drugs for West Nile fever is ongoing. Some candidates include:
1. **Ribavirin** - An antiviral drug traditionally used to treat hepatitis C.
2. **Interferon alpha** - An immunomodulatory agent sometimes used in viral infections.
3. **IVIG (Intravenous Immunoglobulin)** - Provides passive immunity by supplying antibodies.
Clinical effectiveness for these drugs specifically for West Nile fever can vary, and they are under investigation. Always consult healthcare professionals for current treatment protocols. - Metabolites
- For West Nile fever, the specific metabolites associated with the virus and its metabolic impact on humans are not well-documented. Although various studies have looked into changes in host metabolism due to viral infections, precise metabolites related to West Nile virus have not been definitively identified. Research in this area is ongoing to better understand the biochemical pathways involved.
- Nutraceuticals
- Nutraceuticals have been explored for their potential to support the immune system and manage symptoms of West Nile fever, although there is no specific nutraceutical treatment for the disease. Substances like vitamin C, vitamin D, and echinacea are thought to boost immune function and may offer supportive care. However, these should not replace conventional medical treatments and preventive measures, such as mosquito control and repellents. Always consult healthcare professionals before starting any new supplements.
- Peptides
- West Nile Fever is primarily caused by the West Nile virus. Peptides, short chains of amino acids, are under investigation for their potential use in diagnostic tests and vaccines for West Nile virus. However, there are no specific therapeutic peptides currently approved for West Nile Fever. The term "nan" is not directly related to West Nile Fever; it might be a typo or irrelevant in this context. If further clarification is needed on "nan," please provide additional details.