Avian reovirus infections are important for chickens, for the damages caused and the economic losses they cause. Avian reovirus are Orthoreovirus of the Reoviridae family. Reovirus genus includes five species, distributed in three different subgroups: subgroup I with mammalian reovirus; reovirus subgroup II bird; and subgroup III with baboon reovirus. These viruses 70-80 nm, nonenveloped, icosahedral nucleocapsid with structured surface proteins a double layer, double - stranded RNA divided into 10 segments (L1, L2, L3, M1, M2, M3, S1, S2, S3 and S4), replicate in the cytoplasm of cells. Its genome encodes 11 proteins of which 10 are part of the virion (lambda-a, lambda-B, lambda-C, I-A, I-B, I-NS, sigma-C, Sigma-A, sigma-B, sigma-NS). Of all the protein, including two nonstructural and nine structural.
They tolerate a wide pH range (3.0 to 9.0), and the temperature, but are destroyed at 56 ° C in less than 1 hour. They can survive 10 days on galvanized metal, glass, rubber, feathers, and sawdust. In water they can survive up to 10 weeks. Avian Reovirus are resistant to disinfectants.
This virus can be transmitted through vertical or horizontal path. Infection usually occurs in a pen from a newborn infected via through the egg yolk chicken. The transvitelina route is possible even if the transmission rate is very low. From this source, the extension to other poultry birds occurs most often through the faecal-oral route, followed by airway. Infection can also occur through injuries to the feet of the birds, which can be set to the tarsal joint. Once the infection has penetrated the avian reovirus can survive in tissues for several weeks. Resistance to infection is directly related to age. The chicks are infected one day after birth develop a stronger joint injury and title intestinal virus that those who are infected at two weeks old. There are several microorganisms that increase the pathogenicity of Reovirus joint chickens, as Mycoplasma synoviae, Staphylococcus aureus, virus infectious bursal disease virus, chicken anemia.
Experimentally, it has been found in adults inoculated esophageal, nasal, tracheal or chickens, the virus spreads throughout the enteric tract, respiratory, reproductive tarsal joint and tendon. The primary site of replication is the enteric tract, epithelial cells of the small intestine, but also replicates in the bursa Fabricius. The virus, after 24 to 48 hours, rapidly spreading to other organs. The tibiotarsal articulation and tarsometatarsal are where virus replication causes more intense damage which , in severe cases does cause tendon rupture.
The most important manifestations of infection in birds include arthritis, tenosynovitis, blue - winged disease in chickens (blue wing disease), or "Runting-stunting syndrome" related to widespread involvement manifested by decreased growth, pale legs and peak plumage feathered tips of twisted wings (helicopter), liver size reduction, and enlargement of the gallbladder, pancreas reduction, translucent intestines, etc. Blue - winged disease affects young chickens (young broiler chickens), with a mortality of about 10%. Intramuscular and subcutaneous bleeding and atrophy of the spleen, bursa Fabricius, and thymus usually appear. This virus spreads more frequently to the skin and muscles, which are the places where infections are more evident. Arthritis causes avian lameness, especially involvement of the tarsal joint, which in severe cases reaches cause tendon rupture. This virus has also been shown to cause myocarditis, hepatitis, malabsorption, osteoporosis and immunosuppression syndrome.
There is evidence of enzyme immunoassay (ELISA) to detect sigma-C proteins and sigma-B. This virus can be grown in cell cultures of chick embryo, but its development and subsequent identification are very slow, so it is not suitable diagnostic method. For cell culture isolation primary chick (lung, liver, kidney, and chicken embryo fibroblasts), which produce syncytia are required. It can also be isolated by inoculation with chicken embryo manifesting embryo death with hemorrhagic and necrotic liver injury. Currently, the recommended method is the molecular detection by RT-PCR.
Being a relatively resistant to environmental conditions universal infection distribution is very difficult to eradicate. In addition, the inability to detect it in cloacal swabs difficult diagnosis in birds. Transmission through the egg also facilitates its extension to new pens. Therefore, the best thing to control is vaccination. Live and inactivated vaccines exist that can protect from early stages chicks. Vaccination of layers allows the protection of chicks by transfer of antibodies across the yolk sac.