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The host range of reticuloendotheliosis virus is much broader than that of Marek’s disease or lymphoid leukosis. Chickens, turkeys, ducks, geese, and quail have experienced natural infection and disease, and probably many species of birds can be infected. Mammals appear refractory, although certain mammalian cell cultures are susceptible.
Reticuloendotheliosis virus is not ubiquitous but is more widely distributed than once believed. It appears to be particularly prevalent in Israel, Australia, Japan, and the southern USA in chicken and turkey flocks.
Etiology:Reticuloendotheliosis virus is a retrovirus unrelated to the viruses of the leukosis/sarcoma group. The isolates all belong to a single serotype but differ in pathogenicity. Isolates can be classified as either nondefective or defective. Most field isolates appear to be nondefective for replication in cell cultures and contain no viral oncogene. One unique laboratory strain (strain T) is defective for replication in cell cultures and contains a viral oncogene, v-rel, that is responsible for an acute reticulum cell neoplasia in experimentally inoculated chicks; this neoplasm prompted the name reticuloendotheliosis but does not occur commonly in the field.
Transmission and Epidemiology:Horizontal transmission is probably more important than vertical, although both have been documented in chickens and turkeys. Transmission by mosquitoes and other blood-sucking insects is suspected. The virus has been isolated from litter. A high rate of congenital infection has been demonstrated in naturally infected turkeys, but such flocks are probably rare. The virus has been transmitted accidentally through use of contaminated vaccines. Most commonly, however, flocks seroconvert after 10 wk of age without clinical disease or virus shedding to progeny. Experimentally, contact transmission occurs, but the virus is neither highly contagious nor highly stable in the environment. More work is needed to determine the means by which it is maintained and transmitted.
Pathogenesis:The nondefective subgroups in strains of reticuloendotheliosis virus produce three distinct syndromes: non-neoplastic runting, acute neoplastic disease, and chronic neoplastic disease resulting in B and T lymphomas. Typically, the runting syndrome is seen 4-10 wk after administration of contaminated vaccines to day-old chicks. Chronic neoplastic disease has been induced experimentally in chickens, turkeys, and ducks; one type occurs in chickens after latent periods of >4 mo and appears identical to lymphoid leukosis. As in lymphoid leukosis, these tumors are composed of B cells, are bursal-dependent, and have IgM on their surface. Acute neoplasia, which occurs after a latent period of 6-8 wk, also has been seen in chickens, turkeys, ducks, and quail. This tumor in chickens involves T cells and may be confused with Marek’s disease.
Clinical Findings and Lesions:The runting syndrome is characterized by weight loss, paleness, occasional paralysis, and abnormal feathering. Death from neoplasia is preceded by depression and occasionally by some of the same clinical changes described for the runting syndrome.
Lesions include bursal and thymic atrophy, enlarged nerves, anemia, and abnormal feathering. Of these, the abnormal feathering, in which the barbules are compressed to the shaft over a small part of its length, may be of diagnostic value. The neoplasms typically involve the liver, spleen, intestine, and heart. The bursa is involved in the chronic B-cell lymphomas of chickens in a manner similar to that of lymphoid leukosis. Nonbursal (T-cell) lymphomas with shorter latent periods and lesions superficially resembling those of Marek’s disease also are recognized in chickens. In turkeys, prominent lesions include enlarged livers and nodular lesions on the intestines; the bursa is only rarely tumorous. The tumors, regardless of type or host species, are usually composed of uniform, large, lymphoreticular cells.
Diagnosis:The lesions induced by reticuloendotheliosis virus are so diverse and resemble so closely those of other tumors that diagnosis at necropsy is difficult; virus isolation or antibody detection is useful in confirmation. The nerve lesions are usually less extensive and may contain more plasma cells than in Marek’s disease, but in other cases are difficult to differentiate by histology. The runting syndrome is easily confused with immunosuppressive syndromes caused by a variety of other viral agents. The chronic B-cell lymphomas induced experimentally in chickens cannot easily be distinguished from those of lymphoid leukosis except by virus studies, including polymerase chain reaction assays. The T-cell lymphomas of chickens cannot easily be distinguished from Marek’s disease except by virus studies. However, both B and T lymphomas induced by reticuloendotheliosis virus contain a clonally integrated DNA provirus usually associated with c-myc oncogene, which can be demonstrated by appropriate molecular methods. The chronic lymphomas that occur in turkeys must be differentiated from lymphoproliferative disease of turkeys based on histology, virus isolation, and characterization of the virus-associated reverse transcriptase for activity in the presence of manganese or magnesium ions.
Control:No control measures are currently practiced. An experimental vaccine on a recombinant fowlpox virus has been developed. Eradication of virus infection from primary breeding flocks based on detection and removal of shedder hens is being evaluated in Israel. Some breeder companies desire to avoid seroconversion of their primary breeder stocks to obviate restrictions on export of progeny to certain countries, but reliable techniques to prevent horizontal transmission have not been developed.
See Also:
Neoplasms
Marek’s Disease
Lymphoid Leukosis
Lymphoproliferative Disease in Turkeys
Other Tumors
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