The development of lymphoid leukosis tumours induced by RAV-1, RAV-2, and field lymphoid leukosis viruses was prevented in chickens by feeding a diet containing the androgen analogue mibolerone (17beta-hydroxy-7a, 17-dimethylestr-4-en-3-one) at low levels during the first 7 weeks of life. Chickens fed mibolerone developed neutralising antibodies after inoculation with RAV-1, RAV-2, and after contact exposure to viraemic-tolerant chickens. Mibolerone did not affect the immunological tolerance status of chickens which were viraemic when hatched. Moreover, mibolerone did not seem to change the pattern of shedding of lymphoid leukosis viruses or group specific antigen in unincubated chicken eggs from infected hens. Mibolerone, thus, prevents the development of lymphoid leukosis tumours without interfering with the cycle of infection of lymphoid leukosis viruses.
Duplicate trials with mibolerone at a dose of 1 microng/g of diet for the first 49 days of age reduced the incidence of lymphoid leukosis (LL) significantly (P less than .005) in chickens inoculated as day-old chicks with Rous-associated virus type 1 (RAV-1). The incidence of LL was not reduced in virus-challenged chickens administered mibolerone at 4 microng per gram of diet during days 29 through 49 of age. The bursal lymphocytic follicles atrophied significantly with both the 1- and 4-microng doses; but, on the basis of histologic examination, atrophy was more complete with the 1-microng dose of mibolerone administered during the first 49 days of age. Mibolerone appears to prevent LL development by producing early bursal atrophy of key target cells. These data suggest that mibolerone orally administered at 1 microng/g of diet during the first 49 days of age appears to be useful for LL prophylaxis. Field trials are under way to assess the effectiveness of mibolerone under natural conditions.
Mibolerone, an androgen analog (17 beta-hydroxy-7-alpha, 17-dimethylestr-4-en-3-one), induces a slow but progressive involution of the bursa of Fabricius when fed to chickens at microng levels during the first 7 weeks of life. Chickens receiving mibolerone remained immunologically competent, evidenced by: 1) their antibody response to nonreplicating antigens and infectious antigens; 2) the number of antibody-producing cells in their spleens; 3) the stimulation of their peripheral leukocytes with the plant mitogen phytohemagglutinin; and 4) their capacity to resist challenge with Marek's disease virus and Newcastle disease virus after vaccinations with turkey herpes-virus and the B-1 LaSota strain. This, coupled with the fact that it prevents experimental lymphoid leukosis, makes mibolerone a potential agent to be used under field conditions for the control of lymphoid leukosis.
Chickens fed the androgen analog mibolerone during the first 7 weeks of life regress their bursa of Fabricius but can be properly immunized by vaccination against avian pathogens of major economic importance such as Newcastle disease virus, infectious laryngotracheitis virus, avian encephalomyelitis virus, infectious bronchitis virus, fowl pox virus, Marek's disease virus, and Pasteurella multocida, the pathogen causing fowl cholera. These findings on immunocompetence to infectious agents are important because we have previously shown that the administration of mibolerone prevents the development of lymphoid leukosis tumors.
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