Western equine encephalitis (WEE) is defined as acute brain inflammation with possible meningeal involvement in encephalitis.
It is a viral disease that is caused due to the Western equine encephalitis virus. It belongs to the Togaviridae family and the Alphavirus genus.
Mosquitoes are the main vector of the disease with birds as reservoirs. Alphaviruses are 60-65 nm spherical viruses with glycoprotein shell and lipid bilayer.
Horses and humans do not have enough virus in their blood to infect mosquitoes.
Symptoms range from mild to severe neurological disease. In severe cases it shows high fever, headache, and confusion.It may be observed that small and wild mammals also spread the virus.
Epidemiology
It is commonly seen in western states and Canadian provinces west of the Mississippi and Rocky Mountains.
Study of WEE in northern California found independent strain evolution and minimal region movement.Summer bird C tarsalis cycle leads to infections from viral amplification in spring.
During epidemic years with the worst in 1941 in the western US and Canada to cause 300000 encephalitis cases in mules and 3336 in humans.
Mosquitoes spread quickly with high larval and weather factors causes epidemics.WEE more common in males than females based on study.
Anatomy
Pathophysiology
WEE virus is a neurotropic alphavirus causes encephalitis with viral symptoms but without rash.Severe stages of WEE involve diffuse CNS involvement with damage caused due to immunologically active cells enters brain parenchyma and perivascular areas.
Autopsy findings of vascular inflammation, endothelial proliferation, thrombosis, and perivascular cuffing. Apoptosis is mainly in glial and inflammatory cells.
A virus moves from mosquitoes into the host’s subcutaneous skin. It does not transfer through aerosol route may be transmitted.
A virus binds tissue receptors undergoes endocytosis to produce RNA and protein. High inoculum leads to viremia and CNS entry through endothelial cells.
Etiology
Causes of WEE are:
Causative Agent
Transmission Cycle
Reservoir Hosts
Amplification Cycle
Incidental Hosts
Target Organs
Immune Response
Genetics
Prognostic Factors
Young children face higher risk of severe neurological issues such as encephalitis, seizures, and deficits.
Western equine encephalitis patients without neurologic signs have good prognosis.
Patients with seizures are likely to develop a subsequent lifetime seizure disorder.
Reported neurologic sequelae include developmental delay, motor impairments, and residual behavioural problems.
Infants more susceptible to illness with 30% of infected children face neurological complications.
Clinical History
Detailed information including presenting symptoms and medical history of patient should be gathered.
The incubation period in humans ranges from 5 to 10 days after the bite of an infected mosquito.
Physical Examination
Musculoskeletal Examination
Neurological Examination
Head and Neck Examination
Dermatologic Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Mild to Moderate symptoms are:
Fever, headache, malaise, and muscle ache
Severe symptoms are:
Confusion, disorientation, seizures, photophobia, and neck stiffness
Differential Diagnoses
Leptospirosis
Subarachnoid Hemorrhage
Superficial Thrombophlebitis
Toxoplasmosis
Mycoplasma Infections
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Triple antibiotic therapy for bacterial coverage with acyclovir for empirical herpes treatment.
Pharmacologic therapy includes use of antipyretics, analgesics, and anticonvulsants agents.
Surgery is not an option for this disease, except for specific neurologic procedures for severe complications.
Monitoring Western equine encephalitis infection in wild or sentinel birds can help identify infection sources.
Environmental agencies can now use advanced techniques like indirect enzyme immunoassay for easier screening.
Skin treatment not good repellent but can cause insect death. Permethrin rinse on clothing effective in preventing insect bites.
WEE vaccine exists but is not widely used but effective against some variants.
Western equine encephalitis (WEE) is defined as acute brain inflammation with possible meningeal involvement in encephalitis.
It is a viral disease that is caused due to the Western equine encephalitis virus. It belongs to the Togaviridae family and the Alphavirus genus.
Mosquitoes are the main vector of the disease with birds as reservoirs. Alphaviruses are 60-65 nm spherical viruses with glycoprotein shell and lipid bilayer.
Horses and humans do not have enough virus in their blood to infect mosquitoes.
Symptoms range from mild to severe neurological disease. In severe cases it shows high fever, headache, and confusion.It may be observed that small and wild mammals also spread the virus.
It is commonly seen in western states and Canadian provinces west of the Mississippi and Rocky Mountains.
Study of WEE in northern California found independent strain evolution and minimal region movement.Summer bird C tarsalis cycle leads to infections from viral amplification in spring.
During epidemic years with the worst in 1941 in the western US and Canada to cause 300000 encephalitis cases in mules and 3336 in humans.
Mosquitoes spread quickly with high larval and weather factors causes epidemics.WEE more common in males than females based on study.
WEE virus is a neurotropic alphavirus causes encephalitis with viral symptoms but without rash.Severe stages of WEE involve diffuse CNS involvement with damage caused due to immunologically active cells enters brain parenchyma and perivascular areas.
Autopsy findings of vascular inflammation, endothelial proliferation, thrombosis, and perivascular cuffing. Apoptosis is mainly in glial and inflammatory cells.
A virus moves from mosquitoes into the host’s subcutaneous skin. It does not transfer through aerosol route may be transmitted.
A virus binds tissue receptors undergoes endocytosis to produce RNA and protein. High inoculum leads to viremia and CNS entry through endothelial cells.
Causes of WEE are:
Causative Agent
Transmission Cycle
Reservoir Hosts
Amplification Cycle
Incidental Hosts
Target Organs
Immune Response
Young children face higher risk of severe neurological issues such as encephalitis, seizures, and deficits.
Western equine encephalitis patients without neurologic signs have good prognosis.
Patients with seizures are likely to develop a subsequent lifetime seizure disorder.
Reported neurologic sequelae include developmental delay, motor impairments, and residual behavioural problems.
Infants more susceptible to illness with 30% of infected children face neurological complications.
Detailed information including presenting symptoms and medical history of patient should be gathered.
The incubation period in humans ranges from 5 to 10 days after the bite of an infected mosquito.
Musculoskeletal Examination
Neurological Examination
Head and Neck Examination
Dermatologic Examination
Mild to Moderate symptoms are:
Fever, headache, malaise, and muscle ache
Severe symptoms are:
Confusion, disorientation, seizures, photophobia, and neck stiffness
Leptospirosis
Subarachnoid Hemorrhage
Superficial Thrombophlebitis
Toxoplasmosis
Mycoplasma Infections
Triple antibiotic therapy for bacterial coverage with acyclovir for empirical herpes treatment.
Pharmacologic therapy includes use of antipyretics, analgesics, and anticonvulsants agents.
Surgery is not an option for this disease, except for specific neurologic procedures for severe complications.
Monitoring Western equine encephalitis infection in wild or sentinel birds can help identify infection sources.
Environmental agencies can now use advanced techniques like indirect enzyme immunoassay for easier screening.
Skin treatment not good repellent but can cause insect death. Permethrin rinse on clothing effective in preventing insect bites.
WEE vaccine exists but is not widely used but effective against some variants.
Infectious Disease
Increase water management in farming areas with irrigation scheduling for drainage.
Containers should be removed or cover that collect rainwater and serve as breeding sites.
In high-risk areas, individuals at high risk should wear protective clothing, use mosquito repellent, and avoid mosquito-prone areas to prevent WEE.
Apply larvicides to water bodies that cannot be drained or eliminated.
Install screens on windows and doors of homes to prevent mosquitoes from entering indoor spaces.
Proper awareness about WEE should be provided and its related causes with management strategies.
Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort.
Infectious Disease
Phenytoin:
It inhibits the spread of seizure and activity of brain stem centers is responsible for the tonic phase of grand mal seizures.
Western equine encephalitis (WEE) is defined as acute brain inflammation with possible meningeal involvement in encephalitis.
It is a viral disease that is caused due to the Western equine encephalitis virus. It belongs to the Togaviridae family and the Alphavirus genus.
Mosquitoes are the main vector of the disease with birds as reservoirs. Alphaviruses are 60-65 nm spherical viruses with glycoprotein shell and lipid bilayer.
Horses and humans do not have enough virus in their blood to infect mosquitoes.
Symptoms range from mild to severe neurological disease. In severe cases it shows high fever, headache, and confusion.It may be observed that small and wild mammals also spread the virus.
It is commonly seen in western states and Canadian provinces west of the Mississippi and Rocky Mountains.
Study of WEE in northern California found independent strain evolution and minimal region movement.Summer bird C tarsalis cycle leads to infections from viral amplification in spring.
During epidemic years with the worst in 1941 in the western US and Canada to cause 300000 encephalitis cases in mules and 3336 in humans.
Mosquitoes spread quickly with high larval and weather factors causes epidemics.WEE more common in males than females based on study.
WEE virus is a neurotropic alphavirus causes encephalitis with viral symptoms but without rash.Severe stages of WEE involve diffuse CNS involvement with damage caused due to immunologically active cells enters brain parenchyma and perivascular areas.
Autopsy findings of vascular inflammation, endothelial proliferation, thrombosis, and perivascular cuffing. Apoptosis is mainly in glial and inflammatory cells.
A virus moves from mosquitoes into the host’s subcutaneous skin. It does not transfer through aerosol route may be transmitted.
A virus binds tissue receptors undergoes endocytosis to produce RNA and protein. High inoculum leads to viremia and CNS entry through endothelial cells.
Causes of WEE are:
Causative Agent
Transmission Cycle
Reservoir Hosts
Amplification Cycle
Incidental Hosts
Target Organs
Immune Response
Young children face higher risk of severe neurological issues such as encephalitis, seizures, and deficits.
Western equine encephalitis patients without neurologic signs have good prognosis.
Patients with seizures are likely to develop a subsequent lifetime seizure disorder.
Reported neurologic sequelae include developmental delay, motor impairments, and residual behavioural problems.
Infants more susceptible to illness with 30% of infected children face neurological complications.
Detailed information including presenting symptoms and medical history of patient should be gathered.
The incubation period in humans ranges from 5 to 10 days after the bite of an infected mosquito.
Musculoskeletal Examination
Neurological Examination
Head and Neck Examination
Dermatologic Examination
Mild to Moderate symptoms are:
Fever, headache, malaise, and muscle ache
Severe symptoms are:
Confusion, disorientation, seizures, photophobia, and neck stiffness
Leptospirosis
Subarachnoid Hemorrhage
Superficial Thrombophlebitis
Toxoplasmosis
Mycoplasma Infections
Triple antibiotic therapy for bacterial coverage with acyclovir for empirical herpes treatment.
Pharmacologic therapy includes use of antipyretics, analgesics, and anticonvulsants agents.
Surgery is not an option for this disease, except for specific neurologic procedures for severe complications.
Monitoring Western equine encephalitis infection in wild or sentinel birds can help identify infection sources.
Environmental agencies can now use advanced techniques like indirect enzyme immunoassay for easier screening.
Skin treatment not good repellent but can cause insect death. Permethrin rinse on clothing effective in preventing insect bites.
WEE vaccine exists but is not widely used but effective against some variants.
Infectious Disease
Increase water management in farming areas with irrigation scheduling for drainage.
Containers should be removed or cover that collect rainwater and serve as breeding sites.
In high-risk areas, individuals at high risk should wear protective clothing, use mosquito repellent, and avoid mosquito-prone areas to prevent WEE.
Apply larvicides to water bodies that cannot be drained or eliminated.
Install screens on windows and doors of homes to prevent mosquitoes from entering indoor spaces.
Proper awareness about WEE should be provided and its related causes with management strategies.
Appointments with a physician and preventing recurrence of disorder is an ongoing life-long effort.
Infectious Disease
Phenytoin:
It inhibits the spread of seizure and activity of brain stem centers is responsible for the tonic phase of grand mal seizures.
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