A disease of growing chicks. It occurs most often in meat-type birds and broiler chickens. Common features of the disease are stunted growth and lack of skin pigmentation. In fact, the disease has been identified in all countries with intensive poultry production.
Etiology and transmission: Causative factors include mycotoxins and several viruses, including parvoviruses, astroviruses, calicivirus-like viruses, and reoviruses. Although the cause is considered complex, a single reovirus has been identified as the main pathogen. This group of viruses is widespread among commercial poultry and many other kinds of birds throughout the world. Avian reoviruses appear to be species-specific. Viruses isolated from chickens all share a common, group-specific, soluble antigen, which helps with identification and diagnosis of the disease.
Transmission can occur through both the oral and respiratory routes, with respiratory transmission being the most common. In addition, in persistently infected hens, the virus can be transmitted through eggs over an extended period. The persistence of the virus and increased infectivity are generally associated with increased viral virulence.
Clinical signs: The disease occurs mainly in broiler chickens aged 1 to 6 weeks. It is characterized by stunted growth, lack of skin pigmentation, feather loss in feathered areas, abnormal feather growth, undigested feed in the feces, and reluctance to move due to arthritis, tenosynovitis, and osteoporosis. Diarrhea is uncommon in the early stages of the disease. Mortality is generally higher than in uninfected flocks, but the exact pattern has not been established. Severely affected birds do not respond to changes in feed or management practices and are often condemned during processing. Joint lesions may also occur (see viral arthritis).
Pathologic changes: The severity and type of pathologic changes in naturally and experimentally infected birds vary with the specific reovirus and the age of the birds.
In birds infected with highly pathogenic reovirus during the first few weeks of life, pathologic changes include arthritis, osteoporosis, hepatitis, myocarditis, pancreatitis, and atrophy and necrosis of the intestinal villi. Other digestive tract pathologic changes reported in older commercial production chickens include gizzard atrophy, proventriculitis, and enteritis. In addition, encephalomalacia is occasionally observed, possibly as a result of poor nutrient absorption or utilization.
Diagnosis: Although reoviruses can cause a similar syndrome (see reticuloendotheliosis), a presumptive diagnosis can be made based on clinical signs and pathologic changes. Isolation of the virus in yolk sacs, chicken embryo kidney cells, or primary cultures of liver cells from 5- to 7-day-old chicken embryos can provide definitive evidence. The isolated virus is inoculated intratracheally into 1-day-old chicks to test its pathogenicity. Virus neutralization and agar gel precipitation tests can be used to detect infection in flocks or individual birds.
Control: Some commercial vaccines are available. Use of a live attenuated vaccine at 1 days of age can produce active immunity. Alternatively, immunizing breeder flocks with live and/or inactivated vaccines can provide broilers with passive immunity. There is no effective treatment for severely infected birds.
Source: Tan Ji Lun Dao; translated by Li Wengang, reviewed by Zhao Deming