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Updated: Aug 6, 2026

Chronic Salmonella Infected Mouse Model
Published on: May 31, 2010
Salmonella Reading Inoculation Dose Impacts the Host Colonization and Immune Response in Turkey Poults
Davis A Fenster1, Estefania Novoa Rama1, Jasmine Kataria1
1Department of Poultry Science, University of Georgia, Athens, Georgia, USA.
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Salmonella enterica serovar Reading has been associated with foodborne disease outbreaks from contaminated poultry products. This study investigated the effect of S. Reading inoculation dose on Salmonella prevalence and cecal loads, and the mRNA abundance of immune response genes in turkey poults, with higher doses expected to increase colonization and elicit stronger immune responses. Day-old poults (n = 487) were assigned to four groups based on S. Reading inoculation doses of 2, 4, 6, and 8-log CFU/mL per bird, with 28 birds per pen and 4 replicate pens per treatment group. Additional poults (n = 39) were assigned to a single pen as the non-inoculated control group. On d 7, all birds were inoculated with their respective dose of S. Reading. On d 9 and d 21, the ceca, liver, and spleen were collected from 10 birds per group to assess S. Reading colonization. Cecal tonsils and spleens were collected to measure the mRNA abundance of immune response genes. On d 14, ceca were collected from 19 birds per pen (76 birds/group) to measure S. Reading loads using the SalQuant™ procedure of the BAX® PCR System. Higher doses (6 and 8-log) resulted in increased colonization of S. Reading in the ceca on d 9 (p < 0.001) and d 14 (p < 0.001), and increased prevalence of S. Reading-positive cecal samples on d 9 (p = 0.001) and d 14 (p < 0.001) compared to lower doses. The 8-log S. Reading dose resulted in greater mRNA abundance of cytokines IFN-γ (p = 0.007) and IL-10 (p = 0.037), and Toll-like receptors (TLR)-4 (p = 0.017) and TLR-15 (p = 0.002) in the cecal tonsils on d 9 compared to all other groups. Inoculation with higher S. Reading doses resulted in greater prevalence among poults and a heightened local innate immune response.

