Abstract

The present study evaluated the changes in leucogram, serum protein parameters and histology of lymphoid organs associated with cyclophosphamide–induced immunosuppression in broiler chickens infected with velogenic Newcastle disease virus. At four-week-old, one hundred broiler chickens were randomly assigned into four groups of 25 each viz: A/CYTI – cyclophosphamide treated and velogenic Newcastle disease virus infected, B/CYTU – cyclophosphamide– treated and uninfected, C/CYNTI – cyclophosphamide non-treated, infected and D/CYNTU– untreated uninfected. Groups A/CYTI and B/CYTU were injected with cyclophosphamide at the dose of 75mg/kg body weight daily for 3 days while groups A/CYTI and C/CYTU were infected with velogenic Newcastle disease virus at six-week-old. Blood samples were collected from randomly selected chickens in each group for leucogram and serum protein assays, while tissue samples were collected for histopathology. Cyclophosphamide induced significantly (P < 0.05) lower levels of circulating total leucocytes, lymphocytes and heterophils on days 7 and 14 post-treatment. On day 14 post-treatment, the total serum protein values of groups A/CYTI and B/CYTU were significantly (P < 0.05) lower than those of groups C/CYNTI and D/CYNTU. Examination of the tissue sections showed severe diffused lymphocytic necrosis and depletion in the bursa, spleen and thymus. Newcastle disease virus infection induced significantly (P < 0.05) higher levels of circulating total leucocytes, lymphocytes and heterophils and significantly (P< 0.05) decreased serum proteins in cyclophosphamide treated chickens on day 3 PC. The results showed that severe decreased leucogram and serum proteins and lymphoid cell depletion in cyclophosphamide treated broiler chickens, which together with the increased leukogram observed following velogenic Newcastle disease virus infection could be used as indicators of exposure to immunosuppressants.Keywords: Broiler chickens, Cyclophosphamide, Leucogram, Serum proteins, Newcastle disease

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