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1 Review on Avian Encephalomyelitis Review on avian encephalomyelitis Tsehaye Neges1 and Haftey Sahle2 1DVM, Area Sales Manager (ASM) at Ethiochicken, Tigray, Ethiopia 2DVM, field Practitioner at Tanqua abergele, Tigray, Ethiopia [email protected] Abstract: Summary: This paper is mainly aimed to review the avian encephalomyelitis. Avian Encephalomyelitis (AE) is an economic concern to poultry industry as it causes economic loss by declining egg production in laying hens as well as egg hatchability . This disease is very common in commercial aviculture which is caused by genus Tremovirus, family of Picornavirridae. It is essentially an enteric infection which can be acquired horizontally between birds by oral ingestion and vertically from infected breeding females through the egg to progeny. It affects mainly young chicken and it is characterized by neurological signs like ataxia and rapid tremors of the head and neck giving rise to the former name of ‘‘Epidemic Tremor ” but no gross lesions are seen in the brain of birds. Both morbidity and mortality can be 50% sometimes reach up to 60% and Its Vertical infection followed by horizontal infection causes a characteristic biphasic mortality pattern. Protection against this virus can be successfully achieved by using the appropriate vaccine strains. Vaccinated birds are life time immune and recovered do not spread the virus. Wild birds are not considered as reservoir of the virus which poses no threat to the human and this disease is not considered as zoonotic disease. Therefore it can be concluded that AE is economically important viral disease which can hinders the poultry production, so it is recommended to control the disease by proper vaccination of parent stock. [Tsehaye N and Haftey S. Review on avian encephalomyelitis. J Am Sci 2020;16(7):1-7]. ISSN 1545-1003 (print); ISSN 2375-7264 (online). http://www.jofamericanscience.org. 1. doi:10.7537/marsjas160720.01. Keywords: avian encephalomyelitis, chicken, vaccination 1. Introduction the chicken. Horizontally infected chicken usually Avian encephalomyelitis virus (AEV) is a show clinical signs at 2–4 weeks of age and vertically widespread infectious diseases with preference of infected chicken commonly show clinical signs of central nervous system and other parenchymatous avian encephalomyelitis during the first week (1-7 organs of birds. This disease is very common in poultry days) after hatching. Both morbidity and mortality industry with significant economic impacts. It’s huge may exceed 50%. Vertical infection followed by economic lost was before introduction of vaccine in the horizontal infection causes a characteristic biphasic 1960s (Cal neck, 2008). Over 200 species of birds are mortality pattern (Freitas and Back, 2015). susceptible to the infection but it mainly affects Protection against this virus can be successfully chicken, turkeys, Japanese quail and pheasants (Sentıes achieved by using the appropriate vaccine strains (i.e. et al., 2015). Turkeys are less susceptible to natural strains that have not been embryo adapted) and infection and generally, develop a milder clinical administration of protocols to the breeders so as to disease than chicken. Duck and pigeon are susceptible transfer maternal immunity to their progeny to experimental infection and wild birds are not (Francisco, 2014). The presence of neutralizing considered as reservoir of the virus which poses no antibodies in the serum of chicken has long been threat to the human (Abdul Aziz, 2013). recognized as a major determinant of resistance to Avian encephalomyelitis virus was first reported infection by avian encephalomyelitis virus (Tannock in New England region of the USA in 1930 in two and Shafren, 1994). It was described that maternal weeks old chicken and this syndrome was termed as antibodies in the chicken yolk sac are fully absorbed "Epidemic Tremor, New England disease and between the second and third week post-hatch (Szabo, Star-gazing Syndrome’’(Jones,1932). OIE classifies 2012). Therefore, the detection of antibodies against this disease as list C disease. It is essentially an enteric AEV in a flock of chicken with 21 days of age or older infection and it is transmitted horizontally between indicates field infection. The best way to prevent and birds by oral ingestion and vertically from infected to control the disease is vaccinating breeder flocks breeding females or parent stock through the egg to during their grow-out period, preventing the infection 1 Journal of American Science 2020;16(7) http://www.jofamericanscience.org JAS of breeders during the egg production period and in tropism and virulence, which can be enterotropic thereby, and virus transmission to the progeny. with horizontal transmission or neurotropic with Moreover, breeder and parent stock vaccination vertical transmission (Martins and Silva, 2009).)The provides good immunization of progeny, ensuring infection by the AEV occurs mainly through the protection against virus infection during the rest weeks fecal-oral route and its replication takes place in the of life, when they are most susceptible to the virus intestinal epithelial cells. Following the oral ingestion (Roy et al, 2009). of virus, it enters the bloodstream via Payer’s patches Hence, this review is under taken with the and lymphatic vessels, reaching other organs, such as following objective: the pancreas, heart, proventriculus, gizzard and the To review avian encephalomyelitis. central nervous system (Tannock and Shafren, 1994) 2. Etiology resulting clinical signs and symptoms in susceptible Avian Encephalomyelitis (AE) is caused by Avian chicken that usually aged between 1 and 30 days encephalomyelitis-like virus 1 (AEV), which is a (Calnek et al., 1997). single-stranded RNA (ssRNA) virus belonging to the 4. Transmission Picornaviridae family. It was formerly classified as an The transmission of the virus is both vertical and Entero-virus. Avian encephalomyelitis-like virus 1 is horizontal. Vertical transmission tends to cause higher not related antigenically to other avian Picoronavirus s losses because day-old chicken are affected. This that is why it has been referred to in the past as an happens when breeders with no immunity are infected Enteroviruses or Enterovirus-like viruses. Recent during the egg production period and transmit the virus characterization of AEV genome or protein homologies to progeny. This virus can also transmitted horizontally indicates that it is more closely related to Hepatitis A by fecal-oral route through ingestion of feed, litter, or virus than to Enteroviruses and it had been contaminated water (Back, 2010). The virus can exist in provisionally classified as a tentative species in the droppings for more than 4 weeks in this case, the genus Hepatovirus (Van regenmortel et al., 2000) in disease is less severe and tends to affect older chickens. the family Picornaviridae. Recently AEV has now Horizontally infected chicks usually show clinical been reclassified as a unique virus and placed as the signs at 2–4 weeks of age; thus, clinical disease sole member of the Tremorvirus genus (King et al., progresses through the flock from the first few weeks, 2012). Recent characterization of AEV genome and the episode is usually over by the time the flock is indicates that it is more closely related to Hepatitis A ~4 weeks old. After oral ingestion the virus can be first virus than to Entero-virus and it had been detected in pancreas, liver and spleen within 3 days and professionally classified as a tentative species in the then CNS and other enteric tissues such as genus Hepatovirus (Van regenmortel et al., 2000) in proventriclus, gizzard, small intestine and caecum the family Picornaviridae. Recently, AEV has now (Tannock, 1994). been reclassified as a unique virus and placed as the Infected eggs laid during the period of viremia, sole member of the Tremorvirus genus (King et al., usually lasts 1–2 week. After 4 weeks of age, chicken 2012). are resistant to disease but not to infection, an The virus has a non-enveloped capsid with exception occurs occasionally in older chicken after icosahedral symmetry and is approximately 26 nm in vaccination with chick-embryo–propagated vaccines diameter and has buoyant density of 1.31 g/ml in in which the vaccine virus inadvertently becomes caesium chloride and it is stable at pH 3.0 and has a embryo-adapted during production of the vaccine. buoyant density of 1.31 to 1.33 g cm-3(ICTV, 2019). Chick-embryo-adapted strains are highly neurotropic This virus is resistant to chloroform, acid media, and can cause clinical disease after parenteral enzyme trypsin and pepsin as well as environmental administration. Affected birds exhibit typical condition. Magnesium cation were shown to stabilize neurologic signs like those seen in younger chicken preparations of the virus against heat effect (56°C, 1 (Calnek, 2008). h), hence, this enables it to be resistant environmental AE is not considered as zoonotic disease (Gough, condition. However, incubation with rib nuclease and R.E. and Mcnulty, M.S. 2007). Recovered birds are treatment at high pH (9.0 to 10.0) reduced its titer by live immune and do not spread the virus, where as in 1007 to 102 EID50/ml (Go sting et al., 1980) and it older birds infection is subclinical, resulting in can be inactivated by single fumigation cycle by declines in egg production in laying chicken, there is a formaldehyde (Francisco, 2014). The laboratory sudden 5%–10% drop in egg production, which protype strain is called Van Roekele strain (Van usually lasts for <2 weeks and hatchability may drop Roekel, 1938). as much as 5% due to late embryonic mortality 3. Pathogenesis followed by a return to normal production and The strains of avian encephalomyelitis virus hatchability (Cheville, 1970). This viral disease can (AEV) are antigenically uniform, but there is variation 2 Journal of American Science 2020;16(7) http://www.jofamericanscience.org JAS produce no deterioration in egg shell quality (Calnek sit on hocks, falling on their backs and laying with one et al., 1960) side to unilateral and bilateral paralysis.
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