diease

Eastern Equine Encephalitis


OVERVIEW OF Eastern Equine Encephalitis :

It is also known as Triple E or sleeping sickness syndrome. It is caused by the virus belonging to Togaviridae.

The alphavirus genus contains 4 viruses which produce encephalitis; EEE, WEE, VEE and Everglades. The Everglades virus is related to EEE but is restricted to the state of Florida in the U.S.A. EEE and WEE plays an important role in the transmission of the diseas between  mosquitoes and birds, similarly VEE between mosquitoes and rodents.

The disease manifestation include flu like symptoms in the earlier stages. The probability of developing encephalitis vary widely between the different viruses; it is highest for the EEE and lowest for the VEE.

No specific therapy is available against these viruses. Although inactivated vaccines have been prepared by the U.S. army against these viruses, they are not available for issue to the public at large and their efficacy had yet to be proven.  Public warnings should be issued when these viruses are prevalent.In cities with highest amount of population vector control is indicated.
Alpha viruses small ,single stranded ,enveloped virus.There are two frames in the genome which are termed as Structural Proteins and Non Structural proteins. The non structure proteins aid the virus in the transcription and replication of the viral DNA.The structural protein helps the virus to build the framework such as Core,nucleocapsid and plays a vital role in the receptor recognization and helps the virus to bind with the host.


STRUCTURE of Eastern Equine Encephalitis :

  1. Morphology
    • Viruses of Togaviridae family are Spherical, Enveloped virus with icosahedral
    • Size: 60 – 70 nm in diameter.
    • Genetic Material :- (+) ssRNA.
  2. Classification
    • Togaviridae contains two Genera: Alphavirus & Rubivirus.
    • Viruses of Togaviridae are transmitted principally by Mosquitoes.
    • Genus Rubivirus contains Rubella virus, is not Arthropod borne.
    • The genus Alphaviruses includes:-
      1. Encephalitis Group
        1. Western equine encephalitis (WEE)
        2. Eastern equine encephalitis (EEE)
        3. Venezuelan equine encephalitis (VEE)
      2. Febrile Illness Group
        1. Chikungunya virus
        2. O’nyong-nyong virus
        3. Sindbis Virus
        4. Ross river virus


CAUSES :

The main spread is by mosquitoes and the people who spend lots of time outdoors.

Children below the age of 15 years of age and older adults above the age of 50.

Patients on cancer treatment such as chemotherapy and targeted therapy.


PATHOPHYSIOLOGY :

Alphaviruses enter cells by receptor-mediated endocytosis and exit by budding from the plasma membrane.

Alphaviruses enter the body via mosquito bites and replicate in various tissues, including Langerhans cells, which then migrate to lymph nodes, causing viremia. Viremia results in invasion of the central nervous system (CNS) by alphaviruses that cause encephalitis or of the joints and internal organs by viruses that cause fever, arthralgia, and rash.

All alphaviruses suppress the innate immune response by inhibiting JAK/STAT signaling, a major early determinant of disease severity.

At later times, recovery is mediated by virus-neutralizing antibodies and cytotoxic T cells.

The viruses are capable of boosting the immune system of the host cell and aids in the formation of interferon.


ROUTES OF TRANSMISSION :

They are zoonotic pathogens and reside in the animals, birds and mosquitoe act as the main vector for the disease.

Lifecycle of the virus:

The virus is maintained in through a bird mosquito lifecycle. Two major mosquito species are involved in this portion of the cycle, those include Culiseta melanura and Culiseta morsitans. These mosquitoes feed on the blood of birds.the frquemcy of thr virus found in nature increases throughout the summer as more birds and more mosquitoes becomes infected. Transmission of estern equitis encephalitis occurs bith by birds and mammals. These mosquitoes are referred to as bridge vectors because they carry the virus from the avian host to other types of host, particularly mammals. The bridge vectors those help the viruses in transmitting the disease includes Aedes taeniorhynchus, Aedes vexana, Coquilletidia perturbans, Ochlerotatus caadensis and Ochlerotatus sollicitans, Ochlerotatus canadensis also frequently bites turtles.

Some virus gets transferred from laboratory exposures or from exposures of the eyes , lungs, skin wound to brain or spinal cord matter from infected animals.

 


COMMON CLINICAL SIGNS AND SYMPTOMS :

The symptoms of the alpha virus include rash, arthralgia and fever. The Incubation period of the virus include 2-10 days. In the early phase, fever, muscle pains, malaise and headache ,meningeal irritation, photophobia, seizures are present. In the long run this can leads to petechiae, purpura, haemetemesis (vomiting of blood),melaena(blood in stools) and  bleeding gums. The joints affected commonly are ankle, wrist and phalanges. The symptoms are similar to other inflammatory joint diseases and it is difficult to differentiate clinically without further investigation


DIAGNOSTIC :

Detection of virus-neutralizing antibodies in combination with recent travel history to an endemic area may be meaningful.

Immunosorbent assay:

 Detect the virus specific IgM or IgG antibodies.

Greater than fourfold rise in titer between acute and convalescent sera  and  cerebo spinal fluid containing virus specific IgG or IgM or both are the diagnostic features.

Real-time polymerase chain reaction (RT-PCR):

 It is valuable in the early confirmation of arbovirus infections. However, the value of RT-PCR is limited to diagnosis in the viraemic phase, with later infection requiring serology.

Direct immunofluorescence assay :

to detect IgM has a high sensitivity and specificity and is used in the latter stages. However, the use of these tests in the tropics may be limited by financial constraints.

A normal erythrocyte sedimentation rate- and a negative rheumatoid factor are useful to differentiate virus arthritis from rheumatoid arthritis. Extensive, symmetrical joint involvement, particularly of the metacarpophalangeal and proximal joints, the presence of rheumatoid nodules or anti-cyclic citrullinated peptide (anti-CCP) antibodies favours rheumatoid arthritis over  with chronic arthropathy. The presence of lower limb asymmetrical joint involvement with axial skeletal affliction favours the diagnosis of spondyloarthropathy

Lumbar puncture:

The spinal fluid is tapped and it is sent to the laboratory for further investigations.

Needle biopsy:

It can be used to collect the brain tissue and examination is done under microscope.

Imaging tests: CT scan, MRI scan SPECTs and  PET scans help doctors locate the tumor and determine if it is cancerous or benign. Your doctor may also look at other parts of the body, such as the lungs, colon or breasts, to identify where the tumor started.

Neurological exam: During a neurological exam, your doctor will look for changes in your balance, coordination, mental status, hearing, vision and reflexes. These changes can point to the part of your brain that may be affected by a tumor.


TREATMENT AND PROGNOSIS :

There is no specific treatment for the eastern equitis encephalitis. Supportive treatment by IV fluids and other electrolytes can be given. If needed breathing problems are given.


PREVENTION :

  • Clean the stagnant area which host for multiplication of virus.
  • Wear clothing that covers the arms, legs, and feet whenever you are outdoors.
  • Use mosquito repellents sparingly on exposed skin. An effective repellent will contain 20% to 30% DEET (N,N-diethyl-meta-toluamide).
  • Spray clothing with repellents containing permethrin or DEET as mosquitoes may bite through thin clothing.
  • Take plenty of fluids
  • Follow healthy life style
  • Minimize outdoor activities at dawn, dusk, and in the early evening when mosquitoes are most active.
  • Inspect window and door screens and repair any holes found.