Western Equine Encephalitis

Overview


Western equine encephalitis (WEE) is a viral infection transmitted by mosquitoes, caused by the Western equine encephalitis virus, which belongs to the Togaviridae family. While most cases are asymptomatic or mild, presenting with symptoms like fever, chills, fatigue, and muscle aches, some infections can escalate to severe complications, including acute inflammation of the brain (encephalitis) and the surrounding membranes (meningitis). This activity focuses on diagnosing and treating WEE, emphasising the importance of a collaborative approach from the interprofessional team in managing affected patients.

What is Western Equine Encephalitis?


The reason for Western Equine Encephalitis is a mosquito-borne viral infection caused by the Western equine encephalomyelitis virus, a member of the Alphavirus genus within the Togaviridae family. Found throughout America, this virus can lead to encephalitis in both humans and horses. WEE virus transmission cycles between vertebrate hosts and mosquito vectors.

In certain regions, human and equine infections typically appear regularly from mid-summer to late autumn, although in tropical regions, cases may occur year-round due to climate conditions that favour mosquito activity.

In horses, WEE infection presents with symptoms such as fever, loss of appetite, and depression, and in severe cases, it can advance to hyperexcitability, blindness, ataxia, profound lethargy, recumbency, seizures, and potentially death, with mortality rates below 30%. Birds, particularly passerine species, serve as the primary virus reservoirs, though most avian infections are subclinical. However, the virus can cause illness in poultry, game birds, and ratites.

Humans and horses are considered incidental, dead-end hosts for the WEE virus. Effective vaccines for WEE are available and are known for their safety and ability to stimulate immunity.

Western Equine Encephalitis Symptoms


Eastern, Western, and Venezuelan equine encephalitis viruses primarily impact the nervous system and can present with a range of non-specific clinical signs. Key symptoms to watch for include impaired vision, fever, changes in behaviour, severe depression, often referred to as "sleeping sickness", circling or head-pressing, difficulty swallowing, muscle twitching, seizures, paralysis, and even, sudden death.

In contrast, clinical signs of West Nile virus infection can vary but may include lying down with an inability to rise, lack of coordination, weakness in the hind limbs, behavioural changes, fever, depression, loss of appetite, difficulty in swallowing, muscle tremors, excessive sweating, head pressing, and teeth grinding.

Western Equine Encephalitis Causes


Alphavirus is responsible for Western Equine encephalitis and belongs to the Togaviridae family, which also includes several viruses linked to other types of equine encephalitis. This virus shares a close resemblance with the Eastern Equine encephalitis virus and may even have a genetic connection. Human transmission primarily occurs through the bites of mosquito species such as Culex tarsalis, Culiseta, and Aedes.

The disease typically, outbreaks in mules, horses, pheasants, and other birds coincide with human cases. While birds act as amplifying hosts for the virus, no instances of direct transmission from birds to humans have been documented, indicating they are a reservoir for the virus but not a direct vector. The virus does not spread through the air, but it can cross the placenta, allowing for transmission from mother to foetus. Although the likelihood of transmission through infected blood transfusions is low due to the generally minimal viral loads in most hosts, it remains a potential risk.

Western Equine Encephalitis Diagnosis and Tests


Diagnosing infections with similar presentations can often be delayed or challenging. For patients exhibiting neurological symptoms, neuroimaging studies such as computed tomography (CT) or magnetic resonance imaging (MRI) are typically performed. Inflammatory changes may appear in the thalamus or basal ganglia, but these findings are nonspecific and can occur in encephalitis caused by various factors. A lumbar puncture might reveal elevated opening pressure, protein levels, and cell counts, with a predominance of lymphocytes. However, these findings are also nonspecific and frequently observed in many forms of viral or inflammatory meningitis and encephalitis.

Isolating the virus from serum or cerebrospinal fluid (CSF) is quite challenging. In infected individuals, IgG antibodies usually become detectable within 1 to 3 weeks after infection and peak at 1 to 2 months. The presence of IgG indicates exposure to the virus and, depending on the titer level, may suggest a recent infection. Additionally, the presence of IgM antibodies is associated with acute infection and can be detected within 1 to 3 weeks from the onset of symptoms. It is important to note that the test for Western equine encephalitis can cross-react with the St. Louis encephalitis virus, which complicates the distinction between these two infections.

Western Equine Encephalitis Treatment


There are currently no specific antiviral medications available that effectively target the Western equine encephalitis virus. Therefore, your doctor will focus on providing supportive treatment to manage symptoms such as fever and pain. If there is involvement of the nervous system, more intensive care may be necessary. This can include mechanical ventilation, seizure control, maintaining hydration, and managing increased intracranial pressure, which is a dangerous condition due to high pressure within the skull.

Preventive Measures for Western Equine Encephalitis


While a safe and effective vaccine for WEE is available for horses, human vaccination is finite. A vaccine for humans called TSI-GSD 210, has been developed and tested, but it is not available for general clinical use. Instead, the Department of Defense under the Special Immunizations Program (SIP) produces this and provides it only to laboratory workers who are at risk of WEE exposure.

To reduce the risk of WEE, the most effective personal protection is to prevent mosquito bites. Follow these guidelines to minimise exposure:
Cover as much skin as possible by wearing long-sleeved shirts and trousers.

  • Choose a net long enough to tuck securely under the mattress for full coverage.
  • Use EPA-approved insect repellents on exposed skin. Effective options include DEET, Oil of lemon eucalyptus, Picardin (KBR 3023), 2-undecanone, Para-menthone-diol and IR3535
  • Mosquitoes are most active at dawn and dusk, so limit outdoor activities during these times.
  • Remove any standing water at least once a week. Be sure to empty items such as birdbaths, buckets, planters, flowerpots, trashcans, and tyres, and cover all water containers.
  • Use screens on windows and doors to keep mosquitoes out.
  • For horses, vaccination helps protect them against WEE.
  • Apply 0.5% permethrin to clothes, bed nets, and camping equipment. This insecticide repels and kills mosquitoes.
What are the main hosts for Western equine encephalitis?

The primary reservoir hosts of the Western equine encephalitis (WEE) virus are passerine birds, which generally carry the virus without showing symptoms. However, the WEE virus can sometimes cause illness in other birds, including poultry, game birds, and ratites. Horses and humans are incidental "dead-end" hosts, meaning they do not contribute to further transmission of the virus.

How does Eastern equine encephalitis differ from Western equine encephalitis?
Which mosquitoes transmit Western equine encephalitis?
What biosafety level is required for handling equine encephalitis viruses?
How can Western equine encephalitis be prevented?

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