Salmonella is a complex pathogen that is represented by over 2,600 different serovars. These serovars are classified based on their unique combination of somatic (O) and flagellar (H) antigens. Underlying this antigenic diversity is remarkable genetic diversity. The genetic plasticity of individual serovars gives rise to a host of unique phenotypes such as serovars that are host restricted and host adapted. For example, serovar Typhi, the causative agent of typhoid, is restricted to humans, while serovar Gallinarum is restricted to poultry, where it causes fowl typhoid. Serovar Dublin is an example of a host-adapted serovar; while it is commonly associated with bovine hosts, it can occasionally cause illness in humans. Conversely, serovar Typhimurium is an example of an unrestricted serovar that can colonize many different hosts. Similarly, some serovars have a greater association with human illness than other serovars: Enteritidis and Typhimurium are collectively responsible for nearly a quarter of salmonellosis cases each year in the U.S.,1 while serovar Kentucky is rarely linked to human illness.2 Highly pathogenic serovars possess an array of virulence factors that allow them to evade host immune responses and to induce pathogenesis.
Each year in the U.S., there are over 1.35 million cases of salmonellosis, 23,000 hospitalizations, and 450 deaths, along with an estimated annual economic burden of $3.7 billion.3,4 According to the Interagency Food Safety Analytics Collaboration (IFSAC), most (> 75 percent) Salmonella outbreaks can be attributed to seven specific food categories, including: