Effect of Eimeria acervulina infection history on the immune response and transmission in broilers

2010 
Abstract Heterogeneity in exposure to Eimeria spp. of chickens in a flock will result in differences between individual birds in oocyst output and acquired immunity, which subsequently affects transmission of the parasite in the population. The aim of this study was to quantify effects of previous infection of broilers with Eimeria acervulina on immune responses, oocyst output and transmission. A transmission experiment was carried out with pair-wise housed broilers, that differed in infection history. This “infection history” was achieved by establishment of a primary infection by inoculation of birds with 50,000 sporulated E. acervulina oocysts at day 6 of age (“primed”); the other birds did not receive a primary infection (“naive”). The actual transmission experiment started at day 24 of age: one bird ( I ) was inoculated with 50,000 sporulated oocysts and was housed together with a non-inoculated contact bird ( C ). Oocyst excretion and parameters describing transmission, i.e. the number of infected C birds and time passed before start of excretion of C birds, were determined from day 28 to day 50 for six pairs of four different combinations of I and C birds ( I – C ): naive–naive, naive–primed, primed–naive and primed–primed. Immune parameters, CD4 + , CD8 + , αβTCR + and γδTCR + T cells and macrophages in duodenum, were determined in an additional 25 non-primed, non-inoculated control birds, and in the naive–naive and naive–primed groups, each group consisting of 25 pairs. Although the numbers of CD4 + T cells and γδTCR + T cells increased after primary infection, none of the immunological cell types provided an indication of differences in infectivity, susceptibility or transmission between birds. Oocyst output was significantly reduced in primed I and C birds. Transmission was reduced most in the primed–primed group, but nonetheless transmission occurred in all groups. This study also showed that acquired immunity significantly reduced oocyst output after inoculation and contact-infection, but not sufficiently to prevent transmission to contact-exposed birds.
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