avian encephalomyelitis

Identity

Preferred Scientific Name

• avian encephalomyelitis

International Common Names

• English: avian encephalomyelitis; epidemic tremor in chickens; infectious avian encephalomyelitis

English acronym

• AE

Overview

Avian encephalomyelitis (AE) is most serious in young chicks, pathogenic effects being diminished in birds over two to three weeks of age. Infection of susceptible laying hens can result in temporary decreases in egg production; the birds are subsequently protected for life and lay eggs containing maternally derived antibody that provides protection against disease for the chick. Consequently in regions where AE is prevalent it is most appropriate to vaccinate pullets shortly before they come into lay. Vaccination protects them from drops in egg production caused by AE virus (AEV), prevents AEV being transmitted from hen to chick, results in maternal antibody that protects offspring in the vital first three weeks of life and reduces the load of AEV in the environment. There is only one serotype of AEV, vaccines are effective, and immunity is life-long. 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.

The disease was first described as an encephalitis, in the USA during the 1930s. Affected chicks sometimes exhibited ataxia but mainly a rapid tremor of the head and neck. Due to the tremor and the spread of the disease within a flock, the disease acquired the name ‘epidemic tremor’. Subsequently it was observed that tremor was not always evident. So, given the infectious nature of the disease, it was renamed avian encephalomyelitis. The disease has a worldwide distribution.

Hosts/Species Affected

Neurological avian encephalomyelitis (AE) is manifest in chicks of less than one month of age that do not have maternal immunity. If maternal antibody is present then neurological disease is less likely and less severe. Clinical signs are less in older chicks.

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) and quail (Oladele et al., 2014). 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).

AE has been induced by experimental infection of ducklings, young pigeons 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, pigeons 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).

Distribution

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.

Distribution Table

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.

Pathology

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.

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.

Diagnosis

Clinical diagnosis

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. The chicks in later stages sit on their hocks and some move whilst still on their hocks or shanks. When they move they have poor coordination and may fall on their sides. 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. Chicks older than two to three weeks of age are less unlikely to demonstrate the above clinical signs. Birds in lay do not exhibit neurological signs, though may have a temporary drop in egg production.

Lesions

The gross lesion associated with AE 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 recently 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.

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.

Differential diagnosis

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 (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.

Laboratory diagnosis

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.

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).

Real-time reverse transcriptase polymerase chain reaction (rRT-PCR) assays for rapid detection of AEV have been described (Liu et al., 2014; Xue et al., 2016).

List of Symptoms/Signs

Disease Course

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. Chicks hatched from eggs laid during an outbreak of AE develop neurological disease. In these circumstances the virus induces paralysis, ataxia and muscular dystrophy (Tannock and Shafren, 1994; Calnek, 2003). Older chicks exhibit fewer neurological signs and in more mature birds the infection can be unapparent, though there can be a temporary drop in egg production and hatchability. Chicks and older birds are protected from neurological signs by maternal antibody. The course of the disease in turkeys is similar to that in chickens (Holstein et al., 1970).

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. Infected eggs may exhibit reduced hatchability. 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%.

Surviving birds develop lifelong immunity, attributed to circulating antibody, though some become blind.

Epidemiology

Avian encephalomyelitis (AE) has been most thoroughly studied in the domestic fowl, though the course of the disease in turkeys is similar. In regions where AE virus (AEV) is present, nearly all laying flocks will become infected. If they have been vaccinated, then clinical signs are unlikely to be apparent. Natural field strains are enterotropic. 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. 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.

Impact: Economic

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.

Zoonoses and Food Safety

Avian encephalomyelitis has no public health significance.

Disease Treatment

There is no treatment for affected chicks with avian encephalomyelitis (AE). Affected chicks that do not die are considered unlikely to be profitable (Calnek, 2003). Surviving chicks will be immune to AE for life.

Prevention and Control

Control of avian encephalomyelitis (AE) is best achieved by vaccination of breeders or commercial layers with live embryo-attenuated virus several 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. 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). Calnek (1998) has reviewed the development of AE vaccines.

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. Not withstanding, 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).

References

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Distribution Maps