Preferred Scientific Name
- avian encephalomyelitis
International Common Names
- English: avian encephalomyelitis; epidemic tremor in chickens; infectious avian encephalomyelitis
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Avian encephalomyelitis (AE), caused by avian encephalomyelitis virus (AEV), is considered as an important and widespread neurotropic disease in poultry. AEV can be transmitted vertically or horizontally and causes neurological diseases with clinical signs including paralysis, ataxia and paresis, muscular dystrophy, and subsequently blindness in young chicks (Jones, 1934; Miyamae, 1983; Hauck et al., 2017). Infection of susceptible laying hens is mainly subclinical and can result in a reduction in egg production and hatchability. After recovery from infection, the birds become protected and maternally derived antibodies can provide protection against the disease in both eggs and progeny chicks (Sentíes-Cué et al., 2016; Lin et al., 2018). Consequently, in regions where AE is prevalent it is most appropriate to vaccinate pullets shortly before they come into lay (Butterfield, 1975; Calnek, 1998). Vaccination protects laying hens from AEV-induced drops in egg production, inhibits vertical transmission, and results in induction of maternally derived antibody which can protect offspring in the first three weeks of life. It has also been shown that vaccination reduces viral load and environmental contamination (Burtscher et al., 1967; Dorn and Schindler, 1970; Westbury and Sinkovic, 1976). In addition to chickens, the virus is also known to cause disease in other birds, including turkeys, pheasants and quail, there being serological evidence that other species are susceptible (Toplu and Alcigir, 2004; Welchman Dde et al., 2009). The disease was first described as an encephalitis in the USA during the 1930s. Affected chicks exhibited ataxia and a rapid tremor of the head and neck (Hunton, 1965; Yamagiwa et al., 1969). Due to the tremor and rapid transmission within a flock, the disease acquired the name ‘epidemic tremor’ (Jones, 1934), however, tremor may not be observed in all infected birds, thus the disease was renamed as “avian encephalomyelitis”.
|Animal name||Context||Life stage||System|
|Alectoris rufa (red-legged partridge)||Experimental settings|
|Columba livia (pigeons)||Experimental settings|
|Coturnix coturnix||Domesticated host|
|Gallus gallus domesticus (chickens)||Domesticated host||Poultry: All Stages|
|Meleagris gallopavo (turkey)||Domesticated host||Poultry: All Stages|
|Numida meleagris (guineafowl)||Experimental settings||Poultry: All Stages|
|Perdix perdix (grey partridge)||Experimental settings|
|Phasianus colchicus (common pheasant)||Domesticated host|
Neurological avian encephalomyelitis (AE) is manifest in chicks of less than one month of age that do not have maternal immunity. In the presence of maternal antibody, neurological disease is less likely and less severe (Westbury and Sinkovic, 1978; Hauck et al., 2017). Clinical signs are less in older chicks. Experimental inoculation of young chickens with wild-type and egg adapted- AE virus caused the development of neurological signs in young and chickens of all ages, respectively (Hauck et al., 2017). The disease is also known in other galliform birds such as in turkeys (Deshmukh et al., 1971), pheasant (Welchman et al., 2009), guinea fowl (Vivo et al., 1988), quail (Oladele et al., 2014) and pigeons (Toplu and Alcigir, 2004). Bodin et al. (1981) inoculated three species of game bird, including by the oro-nasal route, with AE virus (AEV). All three species were susceptible, susceptibility being greater in grey partridge (Perdix perdix) than in red-legged partridge (Alectoris rufa) than in pheasant (Phasianus colchicus). Fan et al., 2017 showed tissue trophism and course of infection which lasted for 60 days in experimentally infected quail with AEV isolate XY/Q-1410 and concluded that experimental infection was affected by antibody level and immune maturity of the quail. AE has been induced by experimental infection of ducklings and guinea fowl (Calnek, 2003). Steenis (1971) reported naturally occurring antibodies to AEV in sera from turkeys, pheasants, and quail, but not in sera from doves, ducks, finches, jackdaws, pigeons, rooks, sparrows and starlings. Experimental oral exposure of ducks, jackdaws, and rooks also did not result in AEV antibody production. AE antibodies have been reported in ostrich (Struthio camelus) and rockhopper penguin (Eudyptes chrysocomes) (Karesh et al., 1999). Few cases of AE infection have been also reported in wild turkeys (Ingram et al., 2015).
Avian encephalomyelitis is present in Africa, Asia, Australia, Europe, and North and South America, although there are many countries in these regions for which data is not available.
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Cabo Verde||Absent, No presence record(s)|
|Central African Republic||Absent, No presence record(s)|
|Djibouti||Absent, No presence record(s)|
|Egypt||Absent, No presence record(s)|
|Eritrea||Absent, No presence record(s)|
|Eswatini||Absent, No presence record(s)|
|Ethiopia||Absent, No presence record(s)|
|Guinea||Absent, No presence record(s)|
|Libya||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|Namibia||Absent, No presence record(s)|
|Seychelles||Absent, No presence record(s)|
|Togo||Absent, No presence record(s)|
|Tunisia||Absent, No presence record(s)|
|Zimbabwe||Absent, No presence record(s)|
|Bahrain||Absent, No presence record(s)|
|Bhutan||Absent, No presence record(s)|
|Georgia||Absent, No presence record(s)|
|Hong Kong||Absent, No presence record(s)|
|Jordan||Absent, No presence record(s)|
|Kazakhstan||Absent, No presence record(s)|
|Kuwait||Absent, No presence record(s)|
|Malaysia||Present||Present based on regional distribution.|
|-Peninsular Malaysia||Absent, No presence record(s)|
|-Sabah||Present, Serological evidence and/or isolation of the agent|
|Mongolia||Absent, No presence record(s)|
|North Korea||Absent, No presence record(s)|
|Syria||Absent, No presence record(s)|
|Thailand||Absent, No presence record(s)|
|Uzbekistan||Absent, No presence record(s)|
|Belarus||Absent, No presence record(s)|
|Cyprus||Absent, No presence record(s)|
|Czechia||Absent, No presence record(s)|
|Estonia||Absent, No presence record(s)|
|Iceland||Absent, No presence record(s)|
|Isle of Man||Absent, No presence record(s)|
|Jersey||Absent, No presence record(s)|
|Latvia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Lithuania||Absent, No presence record(s)|
|Luxembourg||Absent, No presence record(s)|
|Malta||Absent, No presence record(s)|
|Moldova||Absent, No presence record(s)|
|North Macedonia||Absent, No presence record(s)|
|Romania||Absent, No presence record(s)|
|Russia||Absent, No presence record(s)|
|Serbia and Montenegro||Absent, No presence record(s)|
|Slovakia||Absent, No presence record(s)|
|Slovenia||Absent, No presence record(s)|
|Spain||Absent, No presence record(s)|
|Ukraine||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Cayman Islands||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|Dominica||Absent, No presence record(s)|
|Haiti||Absent, No presence record(s)|
|Honduras||Absent, No presence record(s)|
|Panama||Absent, No presence record(s)|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|Saint Vincent and the Grenadines||Absent, No presence record(s)|
|Trinidad and Tobago||Absent, No presence record(s)|
|Samoa||Absent, No presence record(s)|
|Vanuatu||Absent, No presence record(s)|
|Colombia||Absent, No presence record(s)|
|Falkland Islands||Absent, No presence record(s)|
|French Guiana||Absent, No presence record(s)|
|Guyana||Absent, No presence record(s)|
|Venezuela||Absent, No presence record(s)|
The gross lesion associated with avian encephalomyelitis virus (AEV) infection is whitish areas in the muscularis of the ventriculus, due to infiltrating lymphocytes (Calnek, 2003). Microscopic lesions have been observed in the central nervous system (CNS) and in some visceral tissues such as the proventriculus and pancreas. Calnek (2003) has summarized microscopic findings. In the CNS there is a disseminated, non-purulent encephalomyelitis and a ganglionitis of the dorsal root ganglia. There is a perivascular infiltrate in all portions of the brain and spinal chord, except in the cerebellum, where it is confined to the nucleus (n) cerebellaris.
It has been shown that experimentally AEV inoculated chick embryos develop focal haemorrhage, malacia, gliosis, focal oedema of brain with degeneration and necrosis of skeletal myofibers, ventriculitis and myocarditis. Calnek (2003) has described a number of lesions that can be considered to be pathognomonic; in the midbrain, two nuclei, rotundus and ovoidalis are, invariably affected with a loose microgliosis; and central chromatolysis (axonal reaction) of the neurons in the nuclei of the brain stem, especially those of the oblongata. The proventriculus exhibits another pathognomonic change, obvious dense nodules in the muscular wall. AE causes the number of lymphocyte follicles in the pancreas to increase several-fold.
Avian encephalomyelitis (AE) is largely a disease of chicks of up to two to three weeks of age. A dullness of the eyes is seen, which becomes more pronounced. There is progressive ataxia, although this is not always observed (Springer and Schmittle, 1968; Lin et al., 2018). At the later stage of the disease, the infected chicks may show difficulty in their movements and could be observed sitting on their hocks and move whilst still on their hocks or shanks. These birds will have poor coordination and may fall on their sides. Mortality in AE infected chicks is between 25 to 50% in severe cases with morbidity as high as 60% (Goto et al., 2019) There may be fine tremors of the head and neck, though these may not be apparent in all birds, and severity is variable. Ataxic signs usually, but not always, appear before tremor. Older birds may not show clinical sigs, with only a temporary drop in egg production and hatchability observed (Itakura and Goto, 1975; Meroz et al., 1990).
The clinical signs of AE are similar to those of some other diseases: Newcastle disease (ND), equine encephalomyelitis infection, nutritional disturbances (rickets, encephalomalacia, riboflavin deficiency), and Marek’s disease (Tannock and Shafren, 1994; Calnek, 2003). Consequently various factors should be taken into account before reaching a diagnosis, including the age of the chicks (typical signs of AE are usually only seen in chicks of up to two to three weeks of age), the AEV immunity status of the parent flocks and histopathological analysis. Although typical AE is associated with very young chicks, ND can affect birds of the same age. The pathognomic lesions described above differentiate AE from ND. Encephalomalacia generally occurs two to three weeks later than AE and the lesions revealed by histopathological analysis are very different from those of AE. Marek’s disease occurs in older chicks and exhibits changes not seen in AE; peripheral nerve involvement and the nature of lymphomatosis of visceral organs is different.
Tannock and Shafren (1994) have reviewed the use of chicks, embryos and various cell cultures for the isolation and propagation of AEV. Chicks and embryos must be from AEV-susceptible flocks. Day-old chicks are inoculated intracerebrally, whilst embryos are inoculated via the yolk-sac at 6 to 7 days of age. Some strains have been adapted to grow in embryos, the most widely used adapted strain being that of Van Roekel. Growth of field strains in various cell cultures usually results in low titres. Chicken embryo brain cells have been used, although these tend to be overgrown by fibroblasts. Chick embryo fibroblasts, chicken embryo kidney cells and chicken pancreatic cells have been used, but with very low yields of AEV. Liu et al. (1999) described the use of the mammalian continuous cell line BGM-70 for the isolation of AEV from the brain of diseased broilers. The authors observed cytopathic effect by the third passage.
Tests like virus neutralization, immunodiffusion, passive haemagglutination, ELISA and fluorescent antibody test, which are based on detection of antibodies, have been developed for detection and diagnosis of AE (Choi and Miura, 1972; Ahmed et al., 1982; Girshick and Crary, 1982). Various agar gel precipitin (AGP) tests have been devised to detect antibody to AEV, summarized by Tannock and Shafren (1994). Extracts of the brain or gastrointestinal tract of experimentally inoculated susceptible embryos have been used as the source of antigen for the AGP test, with conflicting results as to which source is best. Although an inexpensive test, the AGP test has largely been replaced by ELISAs, the results from which have been shown to correlate well with the results of virus neutralization tests. Tannock and Shafren have described the AEV ELISAs as being ‘sensitive, specific, rapid, relatively cheap and amenable to large scale screening.’ Procedures for ELISAs include those of Smart and Grix (1985), Smart et al. (1986), Garrett et al. (1984) and an improved procedure of Shafren et al. (1989). An antigen-capture ELISA, to detect AEV in embryo and chicken tissues, has also been described (Shafren and Tannock, 1988).
A direct fluorescent antibody test was developed to detect AE virions in tissue sections of the cerebellum and pancreas of experimentally and naturally infected birds (Ide, 1974). Real-time reverse transcriptase polymerase chain reaction (rRT-PCR) assays for rapid detection of AEV have been described (Xie et al., 2005; Liu et al., 2014; Xue et al., 2016; Goto et al., 2019). Liu et al. (2014) developed a SYBR green based rRT-PCR test using primers targeting conserved VP1 gene of AE virus genome for rapid and specific detection of AE virus, whereas Xie et al. (2005) developed a RT-PCR kit targeting VP2 gene of AE virus. Goto et al. (2019) found that the RT-PCR test developed by Xie et al. (2005) failed to detect AEV virus in chickens suspected for AE infection based on pathological legions, hence they developed and identified these AE virus infections by RT-PCR test which targeted the 5’-untranslated region of the AE virus.
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Exercise intolerance, tires easily||Poultry:Day-old chick||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Lameness, stiffness, stilted gait in birds||Poultry:Day-old chick||Diagnosis|
|General Signs / Reluctant to move, refusal to move||Poultry:Day-old chick||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness, paresis, paralysis of the legs, limbs in birds||Sign|
|General Signs / Weakness, paresis, paralysis, drooping, of the wings||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Blindness||Poultry:Day-old chick,Poultry:Young poultry||Sign|
|Ophthalmology Signs / Cataract, lens opacity||Sign|
|Reproductive Signs / Decreased hatchability of eggs||Sign|
|Reproductive Signs / Decreased, dropping, egg production||Sign|
|Respiratory Signs / Change in voice, vocal strength||Poultry:Young poultry||Sign|
|Respiratory Signs / Hoarse chirp in birds||Poultry:Day-old chick||Sign|
The manifestation of avian encephalomyelitis (AE) depends on age and immune status. Chicks of less than one month of age from non-immune hens develop neurological disease, which can be fatal (Shafren and Tannock, 1991). Chicks hatched from eggs laid during an outbreak of AE develop neurological disease. In these circumstances, the infection causes paralysis, ataxia and muscular dystrophy (Tannock and Shafren, 1994; Calnek, 2003). Older chicks exhibit fewer neurological signs and in mature birds the infection can be subclinical, while a temporary drop in egg production and hatchability may be observed. Maternal immunity can protect chicks from the disease.
The virus is presumed to replicate first in epithelial cells of the alimentary tract; immunofluorescence revealed infected cells in the epithelium of the tunica mucosa of the duodenum, and in the proventriculus, jejunum and caecum (Miyamae, 1983). Afterwards the virus is believed to enter the bloodstream and spread to other organs and the central nervous system. The oral-faecal is thought to be the main route of infection, virus being detected in faeces within three days of oral administration (Calnek, 1998) Shedding may continue for more than two weeks in very young chicks but those over three weeks of age may shed virus for only about five days (Calnek, 2003). Although this is a major route of spread, the virus also spreads vertically. Following experimental infection of laying hens, infected embryos were laid in the following 5- to 13-day period (Hassan and Abdul-Careem, 2020). Infected eggs may exhibit reduced hatchability (Abdul-Cader et al., 2018). Contact transmission can occur in the incubator as well as in the brooder. Morbidity and mortality within a very young flock will vary depending on the AE history of the laying flocks from which the chicks collectively were derived; if the laying birds were immune to AE virus, their chicks will not develop the typical clinical signs of AE, in contrast to chicks originating from non-immune flocks. Chicks from an infected laying flock may exhibit morbidity of 40 to 60%, with mortality averaging 25% (Goto et al., 2019). Surviving birds develop lifelong immunity, attributed to circulating antibody, though some become blind (Calnek, 1998).
Avian encephalomyelitis (AE) has been mainly studied in the domestic fowl, though the course of the disease in turkeys is similar. In regions where AE virus (AEV) is present in laying flocks, all birds may become infected, however the vaccinated birds may not show clinical signs associated with the disease. Natural field strains of the virus are enterotropic, and thus the virus replicates in the alimentary tract and is shed in faeces during the second week after infection. Shedding ceases as specific antibody is produced. It spreads horizontally, by the faecal-oral route, and also vertically. Birds can also become infected by the oral route, (a route by which live AE vaccines can be applied), though the faecal-oral route is considered to be the main route of natural infection. The nature of the disease depends on age and immune status. Chicks of less than one month of age from non-immune hens develop neurological disease, which can be fatal. Chicks hatched from eggs laid during an outbreak of AEV develop neurological disease.
Older chicks exhibit fewer neurological signs and in more mature birds the infection can be unapparent. Chicks are protected from neurological signs by maternal antibody. Vectors are not known to be involved; presence of virus in faeces is sufficient for transmission. AEV is quite stable, remaining in a contaminated area for long periods (Westbury and Sinkovic, 1976). There is only one serotype and immunity is life-long.
The disease is also known in other galliform birds: turkeys, pheasant and quail. AE has been induced by experimental infection of ducklings, young pigeons and guineafowl (Calnek, 2003). Steenis (1971) reported naturally occurring antibodies to AEV in sera from turkeys, pheasants and quail, but not in sera from doves, ducks, finches, jackdaws, pigeons, rooks, sparrows and starlings. Experimental oral exposure of ducks, jackdaws, pigeons and rooks also did not result in AEV antibody production. AE antibodies have been reported in ostrich and penguin.
Yu et al. (2015) detected AE virus infection by RT-PCR and detected AE specific antibody by ELISA and further ascribed it as a potential reason for drop in egg production from 84% to 71% at 32 weeks of age in a breeder flock. Taunde et al. (2017) showed presence of AE virus infection in free-range indigenous chickens of Mozambique by detecting AE specific antibodies by ELISA in around 60 percent of the samples. Goto et al. (2019) showed presence of AE virus infection in hatched birds exhibiting neurological symptoms such as tremors, ataxia, leg paralysis and ataxia classical to AE infection.
Susceptible layers have a temporary drop in egg production, which can be substantial. Young chicks can be killed. The economic importance of avian encephalomyelitis (AE) was greatly reduced when AE vaccines became available commercially.
Avian encephalomyelitis has no public health significance.
Control of avian encephalomyelitis (AE) is best achieved by vaccination of breeders or commercial layers with live embryo-attenuated virus at least 4 weeks before they come into lay. Calnek (1998) suggests that vaccination should be after eight weeks of age and at least four weeks before egg production. One objective of vaccination is to prevent replication of field virus so that there will be no vertical transmission of the virus to progeny. A second objective is to ensure that there are maternally derived antibodies to protect the chicks; AE virus (AEV) has its greatest effect in chicks of up to three weeks of age. Lastly, vaccination protects against drops in egg production caused by infection of mature layers. Inactivated AE vaccines may be given if previously non-vaccinated flocks that are in lay are believed to be at risk, or if application of live AE vaccine is contraindicated. Vaccination gives life-long immunity, however there are some cases that vaccinated chickens may become infected as early as two weeks post vaccination and the affected birds may show severe clinical signs (Sentíes-Cué et al., 2016). Protection of progeny to infection correlates with the titre of antibody in the layers (Garrett et al., 1985). Anti-AE maternal antibody can be detected in chicks for up to 21 days after hatch (Shafren et al., 1992).
AE vaccines are produced using embryo-propagated AEV virus. Shafren and Tannock (1990) have described an ELISA-based method, involving embryos, for assessing the infectivity of AE vaccines that is much faster than the conventional method that involves chicks. Care must be taken not to adapt the virus to embryos, as one consequence of adaptation is selection of virus that no longer replicates well in the gut when applied by eye-drop or in drinking water, thus resulting in poor stimulation of immunity. Embryo-adapted virus given by wing-web application can result in clinical disease (Glisson and Fletcher, 1987).
Live AE vaccine can be administered in drinking water. Shafren et al. (1992) compared the efficacy of antibody production, measured by ELISA, after vaccination by eye-drop with that achieved by drinking water application. They found that vaccination by eye-drop of only 10% of a flock gave the same results as drinking water application; the vaccinal virus spread to the littermates. However, when only 5% of the birds received the vaccine by eye-drop, the spread of the virus within the flock was not good enough for vaccination purposes.
Smyth et al. (1994) reported instances of clinical AE following live AE vaccination of 14-week-old chickens. Two to five weeks after vaccination, mortality reached 2%. The authors postulated that the birds had earlier been immunosuppressed, in one case probably by Marek’s disease virus, resulting in the vaccinal AE being able to produce severe lesions and mortality. The authors demonstrated by experiment that, contrary to popular opinion, AE vaccine given orally can spread to the central nervous system and produce mild encephalitis. Further, Sentíes-Cué et al. (2016) reported the presence of AE infection in three flocks of AE vaccinated leghorn pullets by clinical signs, histopathological and Rt-PCR diagnosis. Notwithstanding, under good conditions and with proper application live attenuated AE vaccines are very good at controlling AE. AE vaccines can also be used in turkeys (Deshmukh et al., 1974). In spite of routine AE vaccination, the AE outbreaks reported in the vaccinated as well as non-vaccinated flocks of chickens provide scope for further vaccine development.
Lin et al. (2018) reported the use of a low pathogenic GDt29 strain of AE as a live AE vaccine. GDt29 vaccinated birds developed a high-level AE specific antibody which showed high level of protective efficacy against AE challenge. Also, a high level of maternal antibodies in laying hens were developed which protected eggs against decreased hatchability on heterologous AE virus challenge. Sarma et al. (2019) showed that a mixture of AE, fowl pox and pigeon pox vaccines administered to chickens protected them against the respective diseases.
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09/03/2021 Updated by:
Dr Shahriar Behboudi, The Pirbright Institute
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