The aim of the present study was to investigate the impact of stress on the progression of Gallibacterium anatis infection in chickens compared with different immunosuppressive treatments. Therefore, 120 specified pathogen free chickens were equally assigned in six different groups. Three groups were treated with Cyclophosphamid, Cyclosporin and 5-Fluorouracil to diminish B cells, T cells and heterophils, respectively, and one group was treated with Corticosterone to induce stress. On day 28 of life, all birds in these groups were intranasally infected together with untreated birds of the positive control group. The remaining group consisted of untreated chickens without infection (negative control). Four birds per group were killed and sampled at 0, 3, 7, 10, 28 days post infection. Different populations of leukocytes (B cells, T cells, heterophils, monocytes/macrophages) were quantified in blood samples applying flow cytometry analysis. Likewise, intensity of local and systemic infections were monitored in trachea and spleen respectively by colony forming unit count and real time PCR. Additionally, pattern of bacterial tissue distribution into the host organs was studied by direct plating. Inoculation with G. anatis resulted in a transient depletion of B and T cells in the blood. Furthermore, local and systemic colonization of the bacteria was observed in all infected groups. Hence, the adaptive immune system of the host might be less crucial for clearance of the local infection. Compared to untreated and infected birds, the immunosuppression did not affect the intensity of local infection but the bacterial load in spleen was acutely increased. Therefore, it can be concluded that corticosterone-induced stress boosts the systemic infection of G. anatis in chickens.