Salmonella enterica serovar Enteritidis tatB and tatC mutants are impaired in Caco-2 cell invasion in vitro and show reduced systemic spread in chickens.

Salmonella enterica subsp. enterica serovar Enteritidis is a leading causative agent of gastroenteritis in humans. This pathogen also colonizes the intestinal tracts of poultry and can spread systemically in chickens. Transfer to humans usually occurs through undercooked or improperly handled poultry meat or eggs. The bacterial twin-arginine transport (Tat) pathway is responsible for the translocation of folded proteins across the cytoplasmic membrane. In order to study the role of the Tat system in the infection and colonization of chickens by Salmonella Enteritidis, we constructed chromosomal deletion mutants of the tatB and tatC genes, which are essential components of the Tat translocon. We observed that the tat mutations affected bacterial cell morphology, motility, and sensitivity to albomycin, sodium dodecyl sulfate (SDS), and EDTA. In addition, the mutant strains showed reduced invasion of polarized Caco-2 cells. The wild-type phenotype was restored in all our Salmonella Enteritidis tat mutants by introducing episomal copies of the tatABC genes. When tested in chickens by use of a Salmonella Enteritidis Delta tatB strain, the Tat system inactivation did not substantially affect cecal colonization, but it delayed systemic infection. Taken together, our data demonstrated that the Tat system plays a role in Salmonella Enteritidis pathogenesis.

Infectious bursal disease virus-induced immunosuppression exacerbates Campylobacter jejuni colonization and shedding in chickens.

Campylobacter jejuni is the leading cause of food-borne bacterial gastroenteritis in humans in the United States. Infectious bursal disease virus (IBDV) causes an immunosuppressive disease in young chickens. To analyze a possible role of IBDV-induced immunosuppression in colonization and shedding of C. jejuni, two experiments were conducted. In both experiments, group 1 consisted of noninoculated control chickens, groups 2 and 3 were inoculated with varying doses of C. jejuni, and groups 4 and 5 were inoculated initially with IBDV followed by doses of C. jejuni similar to groups 2 and 3. Campylobacter jejuni was recovered from the cloaca and cecum, but not the small intestines, from all chickens in groups 2 and 3. In groups 4 and 5, C. jejuni was recovered from the small intestines, cecum, and cloaca from all chickens. The amount (colony-forming units/sample) of C. jejuni recovered from chickens in groups 4 and 5 was significantly greater (P < 0.05) than the amount recovered from chickens in groups 2 and 3; and C. jejuni was also present sooner in these groups than in groups 2 and 3. Bursa samples from chickens in groups 4 and 5 were significantly smaller (P < 0.05) than in the other groups. Additionally, real-time polymerase chain reaction results for IBDV were positive in groups 4 and 5 and negative in all other groups. This study indicated that IBDV infection exacerbated colonization and shedding of C. jejuni, presumably through the immune suppression this virus causes in chickens. It highlights the need for further investigation into the role of immunosuppression in preharvest control strategies for food-borne disease-causing agents.