Pathology of Komarov vaccine in Hitchner B1 vaccinated and unvaccinated broilers.

Newcastle disease (ND) is a major problem of poultry production worldwide. Control is by biosecurity and vaccination. In this project, we studied the pathology of Komarov vaccine which is commonly used in many countries of Africa on the Hitchner B1 (HBI) vaccinated and unvaccinated broilers. Seventy-five Arbor Acres broilers were obtained at 1 day old. Twenty-five of the broilers were given HB1 vaccine at the hatchery and Komarov vaccine at 5 weeks of age (group HK). A second group of 25 broilers were given only Komarov vaccine at 5 weeks of age (group K). The third group remained as unvaccinated (UU). All the groups were observed for clinical signs and lesions. Depression, sneezing, coughing and noisy respiration were observed in group K broilers from day 2 post Komarov vaccination (PKV). Leg paralysis occurred in 6 broilers on day 8 PKV. The clinical signs were milder in the HK broilers. Only one broiler showed leg paralysis in this group on day 18 PKV. No mortality occurred in the three groups. The bursa, spleen and thymus showed mild to moderate enlargement, atrophy and depletion of lymphocytes on days 3, 5, 8 and 14 PKV in HK and K groups. The trachea and lungs were congested. The haemagglutination inhibition (HI) antibody titres in the K group were higher than those of HK and UU groups on days 7, 24 and 21 PKV. The above observations show that Komarov vaccine may cause no mortality in vaccinated and unvaccinated broilers and higher HI antibodies are produced in broilers that have not been vaccinated earlier.

Atrophy of the lymphoid organs and suppression of antibody response caused by velogenic Newcastle disease virus infection in chickens.

This project was undertaken to study the immunosuppressive capabilities of velogenic viscerotropic pathotype of Newcastle disease virus (VVNDV) infection in cockerels. Two hundred six-week-old cockerels were divided into four groups. Groups B/VUC and C/VC were vaccinated with LaSota in drinking water at 6 weeks of age. Groups C/VC and D/UC were challenged with VVNDV at 8 weeks of age. Three days post challenge (PC), the cockerels in group D/UC came down with clinical signs which included depression and greenish diarrhoea. Total mortality was 74.6 %. The C/VC cockerels showed no clinical signs. But both challenged groups showed significant weight loss, significant loss of total serum proteins, globulin and albumen (P < 0.05). These losses were more severe in the D/UC than in the C/VC. There was severe atrophy of the bursa, spleen and thymus in both groups. Histopathology showed severe necrosis and depletion of the lymphocytes in the three lymphoid organs. However, the lesions were more severe in the D/UC than in C/VC cockerels. On day 28, PC groups B/VUC, C/VIC and D/UIC were revaccinated with LaSota. The haemagglutination inhibition antibody response on days 35, 42 and 49 PC was very low in groups C/VIC and D/UIC when compared with B/VUC cockerels. These observations show that VVNDV infection both clinical and subclinical can cause immunosuppression and vaccine failure due to severe destruction of the lymphocytes in the lymphoid organs. This will be a serious problem for poultry production in those countries where the disease is enzootic.