The effects of dexamethasone immunosuppression on turkey osteomyelitis complex in an experimental Escherichia coli respiratory infection.

Six hundred male turkeys were maintained in floor pens for 5 wk at which time half of the birds were given three intramuscular injections of 2 mg/kg BW of dexamethasone (DEX) on alternating days. On the day of the third DEX injection, the left thoracic air sac of each bird was injected with sterile tryptose phosphate broth (TPB) or with TPB containing approximately 1 x 10(2), 1 x 10(3), 1 x 10(4), or 1 x 10(5) cfu of Escherichia coli. All mortalities and birds necropsied at 14 and 15 d postchallenge were scored for air sacculitis/pericarditis (AS) and turkey osteomyelitis complex (TOC). Cumulative mortality and AS score were both increased by either DEX treatment or E. coli. Although TOC incidence was significantly increased by the lowest titer of E. coli inoculation, increasing the number of bacteria inoculated did not increase TOC incidence due to increased mortality before TOC lesions developed. The DEX treatment by itself increased TOC incidence and there was a synergistic interaction between DEX treatment and E. coli on TOC incidence. Both DEX treatment and E. coli significantly decreased BW. Relative weights of liver, heart, and spleen were significantly increased by both E. coli and DEX, whereas both treatments significantly decreased relative weight of the bursa of Fabricius. The number of positive bacterial isolations from tissue and the heterophil to lymphocyte ratio were increased by both DEX treatment and E. coli challenge. These results suggest that stress-induced immunosuppression may be involved in the etiology of TOC, and that bacterial respiratory infection can lead to the development of TOC lesions.