Abstract

Dexamethasone (DEX)-induced immunosuppression facilitates Escherichia coli pathogenesis leading to lesions of air sacculitis and turkey osteomyelitis complex (TOC). The purpose of this study was to determine if early handling could affect resistance to disease in this model. Seven hundred twenty male turkey poults were handled 0, 1 (1x), or 2 (2x) times daily for the first 10 d after hatch. Handling consisted of gently catching each individual poult, holding it for 10 s, and placing it into a basket. Starting on Day 11 after hatch, half of the birds from each handling treatment were treated with three injections of 2 mg DEX/kg BW on alternating days. On the day of the third DEX treatment, duplicate pens of birds were also inoculated in the air sac with 0 or 50 cfu of E. coli. All DEX-treated birds were given a second series of DEX injections at 5 wk of age, and 10 birds per pen were necropsied 3 wk later. Surviving birds were treated with a third series of DEX injections at 10 wk of age. Two weeks later, all surviving turkeys were necropsied. All mortalities and necropsied birds were scored for air sacculitis and examined for TOC lesions. All livers, air sacs, and TOC lesions were cultured for bacteria. There was increased mortality after the first series of DEX treatments of birds handled 2x. After the second series of DEX treatments, birds handled 1x had increased mortality, incidence of air sacculitis, and recovery of E. coli from tissues, whereas 2x handled birds were identical to unhandled controls. After the third series of DEX treatments, handling 1x resulted in decreased air sacculitis scores and decreased incidence of mortality, green liver, TOC lesions, and recovery of E. coli from tissues. The effects of early handling of turkey poults were variable, depending on the number of DEX treatments and the age of the birds. These results suggest that early handling can affect the susceptibility of stressed turkeys to E. coli air sacculitis and TOC and that differences in susceptibility may be influenced by age and individual variability in the stress response.

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