Deletion of genes encoding anti-inflammatory proteins in Salmonella Pullorum: Impact on persistence and virulence in Gallus gallus domesticus.

Abstract

Pullorum disease is a non-zoonotic disease caused by Salmonella enterica serovar Pullorum (SP), which can be vertically transmitted, causing high poultry mortality. S. Pullorum induces persistent infection in chickens, but its survival and immune evasion mechanisms remain unclear. This study investigated whether anti-inflammatory effector proteins contribute to S. Pullorum persistence and pathogenicity. Four S. Pullorum mutants (SP ΔavrA, SP ΔgtgA, SP ΔpipA, SP ΔsseL) with deletions in genes encoding anti-inflammatory proteins were generated by site-directed mutagenesis. Three hundred chicks were divided into seven groups. Groups A-F were orally challenged at 7 days old with SP ΔavrA, SP ΔgtgA, SP ΔpipA, SP ΔsseL, wild-type S. Pullorum (wt-SP), and S. Gallinarum (SG), respectively, while Group G remained uninfected. Samples of liver and spleen were collected at 7, 14, 21, 35, 49, and 63 days post-infection (dpi). Clinical signs and lesions were evaluated. At 7 dpi, wt-SP was detected in the liver and spleen in higher numbers than all mutant strains, although bacterial loads were similar at later time points. Chicks challenged with SP ΔavrA and SP ΔgtgA had more frequent and marked histological lesions, resembling S. Gallinarum infections. Gross lesions did not differ statistically among groups. Pathogenicity differences were observed only in SP ΔavrA and SP ΔgtgA groups, with no significant differences in persistence comparing the wild-type and mutant strains. These mutant strains seem to cause more severe tissue damage, potentially linked to increased inflammation, highlighting the critical role of these genes in S. Pullorum pathogenesis.