Eastern equine encephalitis | |
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Specialty | Infectious diseases |
Symptoms | high fever, muscle pain, altered mental status, headache, meningeal irritation, photophobia, and seizures |
Causes | Eastern equine encephalitis virus |
Risk factors | People over the age of 50 or younger than the age of 16 are at greatest risk of developing severe disease.[ medical citation needed ] |
Diagnostic method | Cerebrospinal fluid or brain tissue examination |
Prognosis | ~33% fatality rate in severe cases [1] |
Eastern equine encephalitis (EEE), commonly called Triple E or sleeping sickness (not to be confused with African trypanosomiasis), is a disease caused by a zoonotic mosquito-vectored Togavirus that is 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 of EEE in horses have continued to occur regularly in the United States. It can also be identified in donkeys and zebras. Rarely, it can also infect humans. Due to the rarity of the disease, its occurrence can cause economic impact beyond the cost of horses and poultry. [2] 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 Coast and Gulf Coast states. [1] In Florida, about one to two human cases are reported a year, although over 60 cases of equine encephalitis are reported. In years in which conditions are favorable for the disease, the number of equine cases is over 200. [3] 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 cerebrospinal 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 cerebrospinal fluid is taken, it is sent to a specialized laboratory for testing. [4]
Eastern equine encephalitis virus (EEEV) is closely related to Venezuelan equine encephalitis virus and western equine encephalitis virus.
The incubation period for Eastern equine encephalitis virus (EEEV) disease ranges from 4 to 10 days. The illness can progress either systematically or 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. [1] 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. [1]
Eastern equine encephalitis virus | |
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Colourised TEM micrograph of a mosquito salivary gland: The virus particles (virions) are coloured red. (83,900x magnification) | |
Virus classification | |
(unranked): | Virus |
Realm: | Riboviria |
Kingdom: | Orthornavirae |
Phylum: | Kitrinoviricota |
Class: | Alsuviricetes |
Order: | Martellivirales |
Family: | Togaviridae |
Genus: | Alphavirus |
Species: | Eastern equine encephalitis virus |
The causative agent, later identified as an alphavirus, 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 America and the Caribbean, while the other three lineages, groups IIA, IIB, and III, are typically found in Central and South America, causing equine illness. [1]
These two clades may actually be distinct viruses. [5] 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.[ citation needed ]
EEEV 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 (enzootic) cycle. Two mosquito species are primarily involved in this portion of the cycle; they are Culiseta melanura [6] and Culiseta morsitans .[ citation needed ] These mosquitoes feed on the blood of birds. The frequency of the virus found in nature increases throughout the summer as more birds and more mosquitoes become infected.[ citation needed ]
Transmission of EEEV to mammals (including humans) occurs via other mosquito species, which feed on 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 taeniorhynchus [7] , Aedes vexans , Coquillettidia perturbans , Ochlerotatus canadensis, and Ochlerotatus sollicitans . Ochlerotatus canadensis also frequently bites turtles.[ citation needed ]
Humans, horses, and most other infected mammals do not circulate enough viruses in their blood to infect additional mosquitoes. Some cases of EEE have been contracted through laboratory exposures or from exposure of the eyes, lungs, or skin wounds to brain or spinal cord matter from infected animals.[ citation needed ]
The disease can be prevented in horses with the use of vaccinations, which are usually given with vaccinations for other diseases, most commonly western equine encephalitis virus, Venezuelan equine encephalitis virus, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans, no vaccine for EEE is available; prevention involves reducing the risk of exposure. Using insect repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention. [1]
No cure for EEE has been found. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) [8] such as intravenous fluids, tracheal intubation, and antipyretics.[ citation needed ] About 4% of humans known to be infected develop symptoms, with a total of about six cases per year in the US. [8] A third of these cases die, and many survivors suffer permanent brain damage. [9]
The examples and perspective in this section may not represent a worldwide view of the subject.(September 2019) |
Several states in the Northeast U.S. have had increased virus activity since 2004. Between 2004 and 2006, at least ten human cases of EEE were reported in Massachusetts. In 2006, about 500,000 acres (2,000 km2) in southeastern Massachusetts were treated with mosquito adulticides to reduce the risk of humans contracting EEE. Several human cases were reported in New Hampshire, as well. [10] [11]
In July 2012, the virus was identified in a mosquito of the species Coquillettidia perturbans in Nickerson State Park on Cape Cod, Massachusetts. On 28 July 2012, the virus was found in mosquitos in Pittsfield, Massachusetts. [12]
As of September 2019 [update] , a notable uptick in cases erupted in New England and Michigan, prompting some health departments to declare an outbreak. [13] [14] [15] [16] [17] [18] [19] As of 31 October 2019 [update] , five people died in Michigan, [20] [21] three people died in Connecticut, [22] one person died in Rhode Island, [19] one person died in Alabama, [23] one person died in Indiana, [24] and three people died in Massachusetts. [25] [26] [27] The virus was also found in goats, [28] in turkeys, [29] in deer, [29] and in horses. [30] [21] [31] [19] [29]
As of September 2020, there were five confirmed human cases between Massachusetts and Wisconsin. [32] As of October 9, 2020, one person died in Michigan, [33] and one person died in Wisconsin. [34]
In 2024, a man in New Hampshire died due to the virus. [35] In Plymouth Massachusetts, the town closed parks in the evenings due to new cases being found in August 2024. [36] Spraying for mosquitos is being used to reduce the risk of EEE. [37] [38] [39] [40]
In October 2007, a citizen of Livingston, West Lothian, Scotland became the first European victim of this disease. The man had visited New Hampshire during the summer of 2007, on a fishing vacation, and was diagnosed as having EEE on 13 September 2007. He fell ill with the disease on 31 August 2007, just one day after flying home, and later fell into a coma. [41] He later awoke from the coma with severe brain injuries. [42]
EEEV was one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological-weapons program in 1969, a few years before signing (1972) and then ratifying (1975) the Biological Weapons Convention. [43]
This section needs additional citations for verification .(November 2022) |
From its natural reservoir in birds, EEEV is known to infect reptiles and amphibians as well as both humans and other mammals, including horses. [44]
After inoculation by the vector, the virus travels via lymphatics to lymph nodes, and replicates in macrophages and neutrophils, resulting in lymphopenia, leukopenia, and fever. Subsequent replication occurs in other organs, leading to viremia. Symptoms in horses occur 1–3 weeks after infection, and begin with a fever that may reach as high as 106 °F (41 °C). The fever usually lasts for 24–48 hours.[ medical citation needed ]
Nervous signs appear during the fever that include sensitivity to sound, periods of excitement, and restlessness. Brain lesions appear, causing drowsiness, drooping ears, circling, aimless wandering, head pressing, inability to swallow, and abnormal gait. Paralysis follows, causing the horse to have difficulty raising its head. The horse usually suffers complete paralysis and death 2–4 days after symptoms appear. Mortality rates among horses with the eastern strain range from 70 to 90%.[ medical citation needed ]
West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes. In about 80% of infections people have few or no symptoms. About 20% of people develop a fever, headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent.
Arbovirus is an informal name for any virus that is transmitted by arthropod vectors. The term arbovirus is a portmanteau word. Tibovirus is sometimes used to more specifically describe viruses transmitted by ticks, a superorder within the arthropods. Arboviruses can affect both animals and plants. In humans, symptoms of arbovirus infection generally occur 3–15 days after exposure to the virus and last three or four days. The most common clinical features of infection are fever, headache, and malaise, but encephalitis and viral hemorrhagic fever may also occur.
The West Nile virus quickly spread across the United States after the first reported cases in Queens, New York, in 1999. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence. The disease spread quickly through infected birds. Mosquitoes spread the disease to mammals. It was mainly noted in horses but also appeared in a number of other species. The first human cases usually followed within three months of the first appearance of infected birds in the area except where cold weather interrupted the mosquito vectors. Since the virus has become widely established in the U.S., an average of 130 deaths a year have occurred.
La Crosse encephalitis is an encephalitis caused by an arbovirus which has a mosquito vector.
Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs. In these cases, symptoms may include headache, vomiting, fever, confusion and seizures. This occurs about 5 to 15 days after infection.
Saint Louis encephalitis is a disease caused by the mosquito-borne Saint Louis encephalitis virus. Saint Louis encephalitis virus is related to Japanese encephalitis virus and is a member of the family Flaviviridae. This disease mainly affects the United States, including Hawaii. Occasional cases have been reported from Canada, Mexico and the Caribbean, including the Greater Antilles, Trinidad and Tobago, and Jamaica.
Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system. The disease most often manifests as meningitis, encephalitis or meningoencephalitis. Myelitis and spinal paralysis also occurs. In about one third of cases sequelae, predominantly cognitive dysfunction, persist for a year or more.
Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea. It is the causal agent of Murray Valley encephalitis. In humans, it can cause permanent neurological disease or death. MVEV is related to Kunjin virus, which has a similar ecology, but a lower morbidity rate. Although the arbovirus is endemic to Northern Australia, it has occasionally spread to the southern states during times of heavy rainfall during the summer monsoon season via seasonal flooding of the Murray-Darling River system. These outbreaks can be "...decades apart, with no or very few cases identified in between".
Alphavirus is a genus of RNA viruses, the sole genus in the Togaviridae family. Alphaviruses belong to group IV of the Baltimore classification of viruses, with a positive-sense, single-stranded RNA genome. There are 32 alphavirus species, which infect various vertebrates such as humans, rodents, fish, birds, and larger mammals such as horses, as well as invertebrates. Alphaviruses that can infect both vertebrates and arthropods are referred dual-host alphaviruses, while insect-specific alphaviruses such as Eilat virus and Yada yada virus are restricted to their competent arthropod vector. Transmission between species and their vertebrate hosts occurs mainly via mosquitoes, making the alphaviruses a member of the collection of arboviruses – or arthropod-borne viruses. Alphavirus particles are enveloped, have a 70 nm diameter, tend to be spherical, and have a 40 nm isometric nucleocapsid.
Viral encephalitis is inflammation of the brain parenchyma, called encephalitis, by a virus. The different forms of viral encephalitis are called viral encephalitides. It is the most common type of encephalitis and often occurs with viral meningitis. Encephalitic viruses first cause infection and replicate outside of the central nervous system (CNS), most reaching the CNS through the circulatory system and a minority from nerve endings toward the CNS. Once in the brain, the virus and the host's inflammatory response disrupt neural function, leading to illness and complications, many of which frequently are neurological in nature, such as impaired motor skills and altered behavior.
Venezuelan equine encephalitis virus is a mosquito-borne viral pathogen that causes Venezuelan equine encephalitis or encephalomyelitis (VEE). VEE can affect all equine species, such as horses, donkeys, and zebras. After infection, equines may suddenly die or show progressive central nervous system disorders. Humans also can contract this disease. Healthy adults who become infected by the virus may experience flu-like symptoms, such as high fevers and headaches. People with weakened immune systems and the young and the elderly can become severely ill or die from this disease.
The Western equine encephalomyelitis virus is the causative agent of relatively uncommon viral disease Western equine encephalomyelitis (WEE). An alphavirus of the family Togaviridae, the WEE virus is an arbovirus transmitted by mosquitoes of the genera Culex and Culiseta. WEE is a recombinant virus between two other alphaviruses, an ancestral Sindbis virus-like virus, and an ancestral Eastern equine encephalitis virus-like virus. There have been under 700 confirmed cases in the U.S. since 1964. This virus contains an envelope that is made up of glycoproteins and nucleic acids. The virus is transmitted to people and horses by bites from infected mosquitoes and birds during wet, summer months.
Mosquito-borne diseases or mosquito-borne illnesses are diseases caused by bacteria, viruses or parasites transmitted by mosquitoes. Nearly 700 million people contract mosquito-borne illnesses each year, resulting in more than a million deaths.
Usutu virus (USUV) is a flavivirus belonging to the Japanese encephalitis complex, which is an emerging zoonotic arbovirus of concern because of its pathogenicity to humans and its similarity in ecology with other emerging arboviruses such as West Nile virus. It mainly infects Culex mosquitoes and birds; humans form a dead-end host. First identified in South Africa in 1959, the virus has caused outbreaks in birds across Europe since 1996. Nearly 50 cases in humans have been reported as of 2019, mainly in Europe. These are predominantly asymptomatic, but some people experience neurological symptoms.
Jamestown Canyon encephalitis is an infectious disease caused by the Jamestown Canyon virus, an orthobunyavirus of the California serogroup. It is mainly spread during the summer by different mosquito species in the United States and Canada.
West Nile virus (WNV) is a single-stranded RNA virus that causes West Nile fever. It is a member of the family Flaviviridae, from the genus Flavivirus, which also contains the Zika virus, dengue virus, and yellow fever virus. The virus is primarily transmitted by mosquitoes, mostly species of Culex. The primary hosts of WNV are birds, so that the virus remains within a "bird–mosquito–bird" transmission cycle. The virus is genetically related to the Japanese encephalitis family of viruses. Humans and horses both exhibit disease symptoms from the virus, and symptoms rarely occur in other animals.
Culex nigripalpus is a species of medium-sized, dark, blood-feeding mosquito of the family Culicidae.
Middelburg virus (MIDV) is an alphavirus of the Old World Group that has likely endemic and zoonotic potential. It is of the viral family Togaviridae. It was isolated from mosquitos in 1957 in South Africa, MDIV antigens have now been found in livestock, horses, and humans.
The 1998–1999 Malaysia Nipah virus outbreak occurred from September 1998 to May 1999 in the states of Perak, Negeri Sembilan and Selangor in Malaysia. A total of 265 cases of acute encephalitis with 105 deaths caused by the virus were reported in the three states throughout the outbreak. At first, the Malaysian health authorities thought that Japanese encephalitis (JE) was the cause of the infection. This misunderstanding hampered the deployment of effective measures to prevent the spread, before the disease was identified by a local virologist from the Faculty of Medicine, University of Malaya as a newly discovered agent. It was named Nipah virus (NiV). The disease was as deadly as the Ebola virus disease (EVD), but attacked the brain system instead of the blood vessels. University of Malaya's Faculty of Medicine and the University of Malaya Medical Centre played a major role in serving as a major referral centre for the outbreak, treating majority of the Nipah patients and was instrumental in isolating the novel virus and researched on its features.