Salmonella enterica

  • Arun K. Bhunia
Part of the Food Science Text Series book series (FSTS)


Salmonella enterica causes gastroenteritis, typhoid fever, and bacteremia. Worldwide there are 16 million annual cases of typhoid fever, 1.3 billion cases of gastroenteritis, and 3 million deaths. Poultry, egg, meat, dairy products, fish, nuts, and fruits and vegetables serve as vehicles of transmission. Non-typhoidal Salmonella (NTS) causes gastroenteritis, and the inflammation is primarily localized in the gastrointestinal tract; however, it can cause invasive disease in immunocompromised host with underlying conditions. To induce gastroenteritis, Salmonella passes through the M cells overlying Peyer’s patches, through dendritic cells, or through the epithelial lining in the lower part of the small intestine or the proximal colon to arrive in the subepithelial location. Salmonella induces apoptosis of macrophages and dendritic cells (DCs), and localized infection is characterized by neutrophil infiltration, tissue injury, fluid accumulation, and diarrhea. During invasive disease, Salmonella is transported to extraintestinal sites such as the liver, spleen, and mesenteric lymph nodes (MLN). Typhoidal Salmonella is an invasive pathogen and disseminates to extraintestinal sites with the aid of DC and infects the liver, spleen, and MLN and resides in the gall bladder for reinfection and to promote fecal–oral transmission.

Salmonella can invade intestinal epithelial lining by induced phagocytosis and survive and multiply inside the Salmonella-containing vacuole (SCV). Invasion of epithelial cells is a complex process involving multiple virulence factors, which orchestrate events that lead to membrane ruffling, actin polymerization, bacterial localization and replication inside SCV, and cell lysis. Salmonella injects virulence proteins directly inside the epithelial cell cytoplasm using the type III secretion system (T3SS), a syringe-like apparatus, to induce its own internalization. Genes encoding the T3SS are located on Salmonella pathogenicity islands SPI-1 and SPI-2. Genes located on other pathogenicity islands are responsible for survival inside the macrophages, enteropathogenicity, iron uptake, and antibiotic resistance. During the intestinal phase of infection, Salmonella has to survive under harsh environmental conditions including stomach acid, bile salts, oxygen limitations, nutrient starvation, antimicrobial peptides, mucus, and the presence of natural microbiota. A global regulator, sigma factor like RpoS is thought to regulate the expression of more than 60 proteins, which possibly promote bacterial survival under these conditions. In addition, the transcriptional regulator, HilA, controls genes required for invasion, and PhoP–PhoQ is required for bacterial survival inside macrophages. Antibiotic therapy is not recommended for self-limiting gastroenteritis, but needed for invasive salmonellosis caused by both NTS and Salmonella Typhi. Proper food handling, avoiding cross-contamination, implementing personal hygiene, and educating the public about safe handling of foods and proper sanitation can help reduce salmonellosis cases.


Salmonella enterica Typhoid fever Gastroenteritis T3SS Molecular syringe 

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Arun K. Bhunia
    • 1
  1. 1.Molecular Food Microbiology Laboratory, Department of Food Science, Department of Comparative PathobiologyPurdue UniversityWest LafayetteUSA

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