Eastern equine encephalomyelitis virus

Eastern equine encephalitis (EEE), commonly called Triple E or, sleeping sickness (not to be confused with trypanosomiasis) is a zoonotic alphavirus and arbovirus present in North, Central, and South America and the Caribbean. EEE was first recognized in Massachusetts, United States, in 1831 when 75 horses died mysteriously of viral encephalitis.Epizootics in horses have continued to occur regularly in the United States. It can also be identified in asses and zebras. Due to the rarity of the disease, its occurrence can cause economic impact in relation to the loss of horses and poultry. EEE is found today in the eastern part of the United States and is often associated with coastal plains. It can most commonly be found in East and Gulf coast states. In Florida, about one to two human cases are reported a year, although over 60 cases of equine encephalitis are reported. Years in which conditions are favorable for the disease, the number of equine cases is over 200. Diagnosing equine encephalitis is challenging because many of the symptoms are shared with other illnesses and patients can be asymptomatic. Confirmations may require a sample of cerebral spinal fluid or brain tissue, although CT scans and MRI scans are used to detect encephalitis. This could be an indication that the need to test for EEE is necessary. If a biopsy of the cerebral spinal fluid is taken, it is sent to a specialized laboratory for testing. Eastern equine encephalitis (EEE), commonly called Triple E or, sleeping sickness (not to be confused with trypanosomiasis) is a zoonotic alphavirus and arbovirus present in North, Central, and South America and the Caribbean. EEE was first recognized in Massachusetts, United States, in 1831 when 75 horses died mysteriously of viral encephalitis.Epizootics in horses have continued to occur regularly in the United States. It can also be identified in asses and zebras. Due to the rarity of the disease, its occurrence can cause economic impact in relation to the loss of horses and poultry. EEE is found today in the eastern part of the United States and is often associated with coastal plains. It can most commonly be found in East and Gulf coast states. In Florida, about one to two human cases are reported a year, although over 60 cases of equine encephalitis are reported. Years in which conditions are favorable for the disease, the number of equine cases is over 200. Diagnosing equine encephalitis is challenging because many of the symptoms are shared with other illnesses and patients can be asymptomatic. Confirmations may require a sample of cerebral spinal fluid or brain tissue, although CT scans and MRI scans are used to detect encephalitis. This could be an indication that the need to test for EEE is necessary. If a biopsy of the cerebral spinal fluid is taken, it is sent to a specialized laboratory for testing. EEEV is closely related to Venezuelan equine encephalitis virus and western equine encephalitis virus. The virus can progress either systematically and encephalitically, depending on the person's age. Encephalitic disease involves swelling of the brain and can be asymptomatic, while the systemic illness occurs very abruptly. Those with the systemic illness usually recover within 1-2 weeks. While the encephalitis is more common among infants, in adults and children it usually manifests after experiencing the systemic illness. Symptoms include high fever, muscle pain, altered mental status, headache, meningeal irritation, photophobia, and seizures, which occur 3-10 days after the bite of an infected mosquito. Due to the virus's effect on the brain, patients who survive can be left with mental and physical impairments, such as personality disorders, paralysis, seizures, and intellectual impairment The causative agent, later identified as a togavirus, was first isolated from infected horse brains in 1933. In 1938, the first confirmed human cases were identified when 30 children died of encephalitis in the Northeastern United States. These cases coincided with outbreaks in horses in the same regions. The fatality rate in humans is 33%, and currently no cure is known for human infections. This virus has four variations in the types in lineage. The most common to the human disease is Group 1, which is considered to be endemic in North American and the Caribbean, while the other three lineages, Groups IIA, IIB, and III, are typically found in Central and South America, causing equine illness. These two clades may actually be distinct viruses. The North American strains appear to be monotypic with a mutation rate of 2.7 × 10−4 substitutions/site/year (s/s/y). It appears to have diverged from the other strains 922 to 4,856 years ago. The other strains are divided into two main clades and a third smaller one. The two main clades diverged between 577 and 2,927 years ago. The mutation rate in the genome has been estimated to be 1.2 × 10−4 s/s/y. EEE is capable of infecting a wide range of animals, including mammals, birds, reptiles, and amphibians. The virus is maintained in nature through a bird—mosquito cycle. Two mosquito species are primarily involved in this portion of the cycle; they are Culiseta melanura and Cs. morsitans. These mosquitoes feed on the blood of birds. The amount of the virus found in nature increase throughout the summer as more birds and more mosquitoes become infected. Transmission of EEEV to mammals (including humans) occurs via other mosquito species, species that feed upon the blood of both birds and mammals. These other mosquitoes are referred to as 'bridge vectors' because they carry the virus from the avian hosts to other types of hosts, particularly mammals. The bridge vectors include Aedes vexans, Coquillettidia perturbans, Ochlerotatus canadensis, and Ochlerotatus sollicitans. Ochlerotatus canadensis also frequently bites turtles.