Inquiry Basket
Loading ......
Avian Encephalomyelitis (AE) is a major infectious disease that affects young chickens caused by the chicken infectious encephalomyelitis virus (AEV). It is characterized by ataxia, head tremors, and can be transmitted vertically through hatching eggs. This virus belongs to the small RNA virus family and enterovirus genus, with a single stranded RNA genome and strong environmental tolerance. After infection, the incidence rate of chicks reached 40% -60%, and the mortality rate was 10% -25%. Most adult chickens showed recessive infection, but the egg production declined in a short time. The pathological changes are mainly characterized by degeneration of central nervous system neurons and proliferation of glial cells, with typical features of cerebral spinal cord congestion and edema. Diagnosis needs to be combined with virus isolation, fluorescent antibody technology, and pathological examination. The focus of prevention and control includes immunization (such as administering inactivated vaccines 18-20 weeks before the start of production) and optimization of aquaculture management.
Figure 1. Structure of Avian Encephalomyelitis Virus. (Elhassan, Fatima Khalid,et al, 2021)
The chicken infectious encephalomyelitis virus (AEV) belongs to the enterovirus genus of the small RNA virus family. The virus particles have a hexagonal outline, no capsule, a diameter of about 26 ± 0.4nm, and are symmetrical in a icosahedron. Their capsid (or virus particle) consists of 32 or 42 shell particles, and the floating density of the virus in cesium chloride is 1.31-1.33g/ml. The virus is resistant to chloroform, ether, acid, trypsin, pepsin, and DNAse. All different isolates of AEV belong to the same serotype, but their pathogenicity and tissue affinity are different. Most field isolates are enterophilic and can be easily transmitted to chickens by mouth and detoxified through feces and feces. They can cause disease in susceptible chicks through vertical transmission or early horizontal transmission after hatching. In these cases, neurological symptoms are generally present. Wild isolates can also produce neurological symptoms through intracerebral inoculation of susceptible chicks.
Natural infections are found in chickens, pheasants, quails, and turkeys, but only in young birds do they show obvious clinical symptoms. Ducklings, guinea pigs, and other chickens are the most susceptible to this disease. Chickens of all ages can be infected artificially, but mice, guinea pigs, rabbits, and monkeys have resistance to brain inoculation of the virus. It is easy to replicate AE in chicks through brain inoculation, and this disease can be transmitted vertically or horizontally. The main transmission mode of AE is through the digestive tract. Infected chickens excrete the virus through feces, and the detoxification time is about 5-14 days. The younger the chicken age at the time of infection, the longer the detoxification time. Viruses have strong resistance in the environment and can survive for more than 4 weeks in bedding. Infected chickens are susceptible to infection when exposed to contaminated feed, water, utensils, etc. Vertical transmission is the main mode of transmission for this disease, and eggs laid by laying hens within 3 weeks of infection carry the virus. Some severely infected embryos die in the later stages of hatching.
Chickens infected through vertical transmission have a latent period of 1-7 days, while those infected through horizontal transmission have a latent period of 11 days or more (12-30 days). This disease mainly occurs in chicks under 3 weeks old, and the author has also confirmed multiple cases of AE in Shiqi chickens over 6-7 weeks old. In cases of natural outbreaks, chicks gradually develop symptoms after hatching. The sick chicks initially exhibit sluggishness, depression, and are unwilling to walk or squat down after taking a few steps. They often land on their tarsal joints, leading to ataxia. Some surviving chickens may have cloudy or faded light blue lenses on one or both eyeballs, enlarged eyeballs, and blindness.
| Pathological Changes | Details |
| Changes in autopsy | Generally, there are no characteristic macroscopic lesions in internal organs, and in some cases, meningeal vascular congestion and bleeding can be seen. If observed carefully, scattered gray white areas can occasionally be seen in the muscular layer of the stomach of sick chicks. Adult chickens do not have the above-mentioned lesions. |
| Histological lesions | The main lesions are concentrated in the central nervous system and some internal organs such as the muscular stomach, glandular stomach, pancreas, myocardium, and kidneys, while the peripheral nerves are not affected, which is an important diagnostic criterion. The central nervous system mainly displays lesions of viral encephalitis, such as neuronal degeneration, glial cell proliferation, and vascular sheath phenomenon. |
Avian encephalomyelitis virus is a highly contagious small ribonucleic acid virus with a unique dual affinity for the gut and central nervous system. The pathogenesis depends on the neural invasion after viremia, which leads to direct neuronal damage and inflammatory host response of the central nervous system. The age-related susceptibility emphasizes the crucial role of immune maturation. Effective diagnosis utilizes the combination of histopathology and serology with specific viral antigens. The successful control of the poultry industry almost entirely depends on strategic vaccination of breeding flocks, which utilizes maternal immunity to protect vulnerable offspring, highlighting the successful application of preventive veterinary medicine.
Reference
| Target | Cat. No. | Product Name | Host | |
| AEV | DAGC527 | Avian Encephalomyelitis Virus (van Roekel) Brain Homogenate | N/A | Inquiry |
| AEV | DAGC528 | Avian Encephalomyelitis Virus (van Roekel) Antigen | N/A | Inquiry |
Loading ......
