The resistance to tumor development occurs rapidly in horizontally infected chickens after the first weeks of life. However, environmental and management factors may delay the onset of this resistance. On necropsy of ML-caused mortality, tumors are found in the majority of breeders. Tumors are primarily myelocytomas and myeloblastomas.
ML-related mortality increases, usually beginning at approximately 17 weeks of age. A number of variables affect age of disease onset and mortality pattern. These include genetics of the chicken, age of infection, immunosuppressive diseases, concurrent diseases, strain of ALV-J involved, and management and environmental factors. Marek's disease challenge in susceptible flocks or challenge with highly virulent Marek's disease viruses is associated with immunosupression and an increased incidence of ML.
Improved Marek's vaccination practices coupled with improved sanitation have resulted in reduced losses from myeloid leukosis. Improved control of infectious bursal disease, reovirus infections and chicken anemia agent, and reduced consumption of mycotoxins should also result in a reduced incidence of clinical ML.
These diseases are associated with immunosupression and result in increased susceptibility to ML and greater severity of ML infection. In most cases, horizontal infections with ALV-J in breeders do not result in clinical disease.
That is, in the absence of tumor development, the effects of ALV-J infection in flocks is minimal. However, tumor development will result in progressive disease, resulting in culling or death. The impact of ML on broilers is poorly understood. Broilers from affected breeder flocks typically have reduced performance. It is reported that broiler flocks originating from breeders with high levels of ML virus shed will be poorly uniform and pale in color with poor feathering and increased late mortality.
Whether this loss of broiler performance is due to viral infection and resulting immunosuppression or simply due to the hens being debilitated and producing weak chicks is not clear. ML virus, behaving as an exogenous leukosis virus, is shed both congenitally and horizontally by infected breeders. Horizontal transmission is through close contact with infected chickens or fomites and is very efficient during the first weeks of life.
Subgroup J virus appears to spread more rapidly in chicks than other subgroups of ALV during the initial weeks post hatch. Congenital transmission occurs in hens, which shed ML virus from oviduct secretions to the egg albumen and then chicken embryo. ML-infected breeders have been shown to shed virus to progeny at a high level. BLV positive cattle for the most part will not be clinically affected by disease resultant of their infection.
For beef cattle, we as a research community have not accurately quantified total economic losses from infection. In the dairy industry, BLV losses have been documented in the literature.
This is often called leukemia, although it is a different non-lethal form than what would be seen in human blood cancers. Leukemic cattle do not often have clinical disease, but it could noticed by your veterinarian if the cow were being evaluated for other unrelated disease.
Although most cattle do not develop clinical disease, some do. This typically is a condition of mature cattle 5 years or more , but I have seen animals as young as months develop lymphosarcoma. This disease can lead to carcasses being condemned at slaughter or deaths on the farm.
There is also a juvenile form of the disease as well, but it is relatively uncommon. Tumors usually form in lymph node centers, the heart, the stomach, the uterus, or the spinal cord of infected cows. Where the tumors develop determines the course of disease experienced; tumors in the spinal cord lead to down cows while tumors in the stomach lead to progressive weight loss.
In my experience, tumors hardly ever come alone, therefore the typical cow presents with a variety of symptoms. A subclinical disease syndrome characterized by depressed egg production in the absence of tumor formation is more important economically than are deaths from lymphoid leukosis. Chickens with subclinical disease usually shed virus or viral antigen into the albumen of eggs.
The pathogenic mechanisms are poorly understood. Chickens with lymphoid leukosis have few typical clinical signs. These may include inappetence, weakness, diarrhea, dehydration, and emaciation. Infected chickens become depressed before death.
Palpation often reveals an enlarged bursa and sometimes an enlarged liver. Infected birds may not necessarily develop tumors, but they may lay fewer eggs.
Diffuse or nodular lymphoid tumors are common in the liver, spleen, and bursa and are found occasionally in the kidneys, gonads, and mesentery. Involvement of the bursa has been considered virtually pathognomonic, although bursal lymphomas are also known to be induced by reticuloendotheliosis virus Reticuloendotheliosis in Poultry Reticuloendotheliosis is a neoplastic disease of poultry caused by reticuloendotheliosis virus.
Reticuloendotheliosis bursal lymphomas are virtually identical to lymphoid leukosis B-cell lymphomas Sometimes the bursal tumors are small and seen only after careful examination of the mucosal surface of the organ. Usually, no enlargement of peripheral nerves is apparent, although such lesions have been noted after experimental inoculation of subgroup J virus. Microscopically, the tumor cells are uniform, large lymphoblasts. Mitotic figures are frequent. Outbreaks of neoplasms other than lymphoid leukosis such as myelocytomas, hemangiomas, and renal tumors have also been noted in meat-type chickens infected with subgroup J avian leukosis virus.
Myelocytomatosis and skeletal myelocytomas may cause protuberances on the head, thorax, and shanks. Myelocytomas may occur in the orbit of the eye, causing hemorrhage and blindness. Renal tumors may cause paralysis due to pressure on the sciatic nerve. Microscopically, in cases of myelocytomas induced by subgroup J avian leukosis virus, the liver shows a massive intravascular and extravascular accumulation of myeloblasts characterized by the presence of cytoplasmic eosinophilic granules.
The nature of the tumors and their frequency depend on virus strain, chicken strain, age, dose, and route of infection. Occasional outbreaks of predominantly one type of tumor are seen in the field. The Rous sarcoma virus, a member of this group, has been widely studied in the laboratory. Each strain usually causes a predominantly neoplastic disease and can be distinguished on the basis of pathogenicity.
Some viruses eg, Rous sarcoma and erythroblastosis viruses contain a viral oncogene that enables the virus to induce neoplasms within a short incubation period, but such viruses are rare in the field. Others cannot replicate on their own and require a nondefective helper virus. Advanced criteria: immunohistochemistry, standard and quantitative PCR, virus isolation, serology.
Lymphoid Leukosis appears to be controlled best by reduction and eventual eradication of the causative virus, which are rapidly inactivated at ambient temperature and on exposure to most disinfectants. Prevention is also helped by obtaining chicks from breeder flocks that are free of the virus and rearing birds in isolation with adequate ventilation.
Follow good biosecurity and management procedures to prevent stress and control other diseases, and dispose of dead birds by composting, incineration or deep burial. Some chickens have specific genetic resistance to infection with certain subgroups of avian Leukosis virus, although genetic resistance is unlikely to replace the need for reduction or eradication of the virus. Thus far, vaccination for tumour prevention has not been promising. However, recombinant vaccines have been developed that can induce antibodies in breeders to ensure protective maternal antibodies in chicks and these may be useful to assist with eradication programs.
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