Western Equine Encephalomyelitis (WEE), Venezuelan Equine Encephalomyelitis (VEE), Japanese Encephalitis (JE)
Equine encephalomyelitis is an inflammation of the brain and spinal cord in hoofed animals caused by viruses. Horses (including humans) can contract the infection but do not pass on the virus. Infections in horses are often asymptomatic, but occasionally severe disease, sometimes fatal, can occur.
In horses, the infections are usually clinically inconspicuous; in a small percentage, fever, loss of appetite and depression may occur, but usually go unnoticed. In individual animals, non-specific mild to severe neurological symptoms may occur, mostly when the fever has already subsided. Severe courses can lead to death.
The American equine encephalomyelitides (Western, Eastern, Venezuelan equine encephalomyelitis) are caused by so-called arboviruses (insect-borne - arthropod-borne - viruses). All three viruses belong to the family Togaviridae and the genus Alphavirus. They are all enveloped, spherical, single-stranded RNA viruses with positive polarity and a diameter of 70 nm. Eastern Equine Encephalomyelitis (EEE) - EEE virus: originally 4 subtypes, lineages 2-4 have recently been renamed Madariaga virus Western Equine Encephalomyelitis (WEE) - WEE virus: no other subtypes Venezuelan Equine Encephalomyelitis (VEE) - VEE virus: 6 different subtypes, these are divided into enzootic and epizootic strains (the latter arise from mutations) Transmission is predominantly by blood-sucking insects (mosquitoes) with horses, humans and other mammals usually acting as false hosts. Other transmission routes have also been observed through mites, lice, fleas and predatory bugs. However, direct contact can also lead to transmission (e.g. in the case of EEE by birds or in the case of VEE by humans, horses and rodents). Oral routes of transmission are known in birds (e.g., cannibalism, feather pecking) and aerogenic routes of transmission from VEE to humans (e.g., during mucking out of laboratory rodent cages) are also known. The pathogenesis of American encephalomyelitis is similar.
Initial viral replication occurs after the mosquito bite in regional blood and lymph vessels and lymph nodes. After the first viremic phase, a second viral replication occurs in the lymph nodes and muscles, after which the second viremic phase causes hematogenous infection of the CNS. In the CNS, viral replication occurs in neurons, glial cells as well as endothelial cells. The virus triggers immunopathological reactions, whereby the synthesis of inflammatory mediators is stimulated in the astrocytes and programmed cell death (apoptosis) increasingly occurs in the affected neurons.
Accordingly, the CNS is dominated by the pathomorphological picture of a non-pathological encephalomyelitis, characterized by perivascular infiltrates (lymphocytes, histiocytes, in the early stage also neutrophilic granulocytes), neuronal degeneration and neuronophagy.
Japanese encephalitis (JE) is also caused by an arbovirus. The causative agent, Japanese Encephalitis Virus (JEV) belongs to the genus Flavivirus of the family Flaviviridae. JEV is an enveloped, spherical, single-stranded RNA virus with positive polarity and a diameter of 50 nm and belongs to the so-called Japanese Encephalitis-Serocomplex-Group with other known members in this complex, such as the West Nile Virus (WNV), the St. Louis Encephalitis Virus (SLEV) and others. The disease is widespread in the Asian region, but has also recently been detected in western India and the Western Pacific region (Indonesian Islands, Papua New Guinea, Northern Australia).
Transmission is by mosquitoes, with wild birds (waders) and pigs as reservoirs. Humans, horses and dogs are considered false hosts that do not spread the virus. Human cases often correlate with areas of intensive pig farming, irrigation schemes as well as rice fields. The pathogenesis as well as the pathomorphologic findings in horses largely resemble those of American equine encephalomyelitis. The zoonotic potential of all four diseases cannot be neglected.
The clinical symptoms are by no means specific and vary individually. In addition to clinically inapparent forms, fever, anorexia, and depression may occur but usually go unnoticed. In a few animals, various neurological disorders such as hypersensitivity, involuntary muscle movements, running in circles, head pressing, difficulty swallowing, central blindness, ataxias, paresis to paralysis/convulsions, recumbency with paddling movements and occasionally pruritus may occur. Death or euthanasia due to severe progression occurs after 2-4 days. If the animals survive, they usually show mental deficits. Diarrhoea, constipation and weight loss are also occasionally observed.
Sows affected by JE may have abortions or stillbirths, but do not have specific findings. Fetuses may be mummified, and the weak or stillborn piglets may show hydrocephalus (watery head) and encephalitis (inflammation of the brain). In boars, testicular and epididymitis may occasionally be observed.
Fatal progressive encephalomyelitis cases are investigated neuropathologically as well as molecularly. In case of a suspected case, appropriate tissue samples (CNS from dead or euthanized animals as well as CSF and blood from febrile animals with clinical signs according to OIE) are sent to the European Reference Laboratory (ANSES) for confirmation and further characterization. Suitable organs for direct detection are considered to be the brain and, where appropriate, the spinal cord. Ideally, the horse's head and cerebrospinal fluid (CSF), if applicable, should be sent to the National Reference Laboratory.
If JEV is suspected in pigs, aborted material should be sent.
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