Coccidiosis in broilers due to infection with parasitic Eimeria remains a significant cause of economic loss. Eimeria have a complex life-cycle beginning when a bird ingests an oocyst (a parasite egg) which contains 8 individual parasites. Once the oocyst is ruptured by digestive acid in the bird, the 8 parasites (termed schizonts) invade the intestinal cells and multiply. Eventually this multiplication ruptures the intestinal cells, releasing many more parasites (known as merozoites) which invade new cells. This (asexual) division causes severe damage to the intestinal cells resulting in poor feed conversion and in some cases death. During this process, new oocysts will be formed which when passed out in bird faeces can infect more chickens if ingested. Therefore, chickens can quickly acquire clinical infection from ingesting relatively few infectious oocysts.

The immune response to Coccidiosis

To prevent disease, the immune system must (1) Attack the parasite inside of the intestinal cells (2) Prevent the large numbers of parasites which emerge from ruptured cells from invading new cells and (3) Prevent infection from establishing the next time the chicken ingests parasite eggs. To do this, different types of immune cell are required (shown in Figure 1).


New findings from PROHEALTH

PROHEALTH researchers at Nottingham University have used gene microarray technologies to study the immune gene profile in the intestines of broiler chickens with clinically diagnosed Coccidiosis. To validate our results these genes were also analysed using a quantitative polymerase chain reaction to measure fold changes in these genes compared to chickens showing no clinical signs in the same flock.

Our results show that many different immune genes are down-regulated in chickens with clinically diagnosed Coccidiosis. These include genes found in lymphocytes which influence recognition of, and reaction to, antigens and genes which influence the activity of antigen presenting cells, such as macrophages and dendritic cells. The function of the immune cells in which some of these genes are down-regulated are shown in Table 3.



The PROHEALTH study shows that in field conditions Coccidiosis may induce significant immune suppression of both the innate and adaptive immune responses. The effect of this may be to increase the duration of Eimeria survival in chickens, thus making clinical disease more likely. However, immune suppression would also provide a less hostile environment for the colonisation of other pathogenic organisms. Thus, initiating poly-infections which could have an even greater pathological effect on these chickens and which would impact more severely on production loss.