The genus Salmonella is diverse. Currently there are three recognized species: S. enterica, S. bongori and S. subterranean, with S. enterica the most important specie affecting human and food animal health. However, even the species S. enterica is diverse. Unlike most bacterial genera, Salmonella is best known by the Kauffman-White system serotypes that are based on cell-surface and flagellar antigens. Currently there are more than 2,000 serotypes or serovars. Some strains of Salmonella are poorly infective to humans but highly infective to other species. For example, Salmonella Pullorum is highly infective to poultry, and USDA’s Animal and Plant Health Inspection Service (APHIS) will take draconian measures to prevent its spread to other flocks. However, according to a review by Oscar, Salmonella Pullorum is poorly infective to humans. Conversely, other strains of Salmonella are harmless to their food animal carriers but highly infective to humans.  Eswarappa, et alia, in 2005 published a study and review of the genes affecting Salmonella pathogenicity for different hosts. As more is discovered about the genetics of bacteria, the diversity of Salmonella becomes more complex. Salmonellae and other bacteria have genomic islands called “pathogenicity islands.” These islands contain genes that confer virulence to a strain. In addition to pathogenicity islands, pathogenic strains also have plasmids that give resistance to antibiotics or other attributes such as virulence. These islands and plasmids are attained through horizontal gene transfer. That is, they come from other bacteria. In a review by Hacker and Kaper, they wrote that the data “argue for the generation of pathogenicity islands by horizontal gene transfer.” According to Frye, et alia, plasmids can be transferred from other bacteria, even other genera. Thus, one Salmonella serotype may contain strains with widely diverse abilities with regard to virulence, multiplication temperatures, heat resistance, or acid tolerance. In a 2005 review, van Asten and van Dijk wrote,”Whether an infection with Salmonella spp. leads to a disease largely depends on the virulence of the strain and the constitution of the host. The virulence of the strain is determined by so-called virulence factors. … These latter virulence factors, e.g., virulence-plasmids, toxins, fimbriae and flagella, are therefore referred to as “classic” virulence factors.” Using microarray analysis Zou, et al., assayed the virulence gene profiles in S. enterica isolates from food or food animal environments. They reported that variability among the tested strains was independent of serotype. They wrote, “In general, genes belonging to inv, pip, prg, sic, sip, spa or ttr families were detected in more than 90% of the isolates, while the iacP, avrA, invH, rhuM, sirA, sopB, sopE or sugR genes were detected in 40 to 80% of the isolates. The gene variability was independent of the Salmonella serotype.” Serotypes are not the only means of identifying strains of Salmonella. Currently the most popular means is pulsed field gel electrophoresis (PFGE). CDC currently uses PFGE for PulseNet to identify outbreak strains, and it has been useful in identifying sporadic and recurring outbreaks. In the near future, Whole Genome Sequencing (WGS) will be used for greater specificity. FDA is beginning to use WGS and one of the 2014 FSIS goals is: “FSIS Lab system will work with public health partners to identify, and by the fourth quarter in FY14 deploy, an agreed upon genotyping platform that generates genomic information uploaded to a central database. Timely WGS and examination of microbial genomes will result in more rapid detection of mutations that confer phenotypic virulence, antimicrobial resistance, and susceptibility to pathogens of interest to FSIS.” Former FSIS staffer Bill James blogged in November 2013, “… For some raw products, the most common Salmonella serotypes reported from FSIS sampling don’t correlate well with the most common serotypes causing foodborne illness. For example, every year since 1998 FSIS has found S. Kentucky is the most common serotype in broilers. But, S. Kentucky never appears in the top 20 serotypes reported by the Centers for Disease Control and Prevention (CDC) as causing human illness. … We need more focus. A possible approach is to target Salmonella serotype/slaughter class pairs. …” In summary, serotyping Salmonella is useful for epidemiology, but the virulence genes are of primary importance in determining virulence and pathogenicity.  One could say it’s not the color of the gang member’s coats but the weapons in their pockets. PFGE and WGS can better identify those virulent strains that are significant to human health. References: Eswarappa SM, Janice J, Nagarajan AG, Balasundaram SV, Karnam G, Dixit NM, Chakravortty D.2008. Differentially evolved genes of Salmonella pathogenicity islands: insights into the mechanism of host specificity in Salmonella. PLoS One. 2008;3(12):e3829. doi: 10.1371/journal.pone.0003829. Frye, Jonathan G.; Rebecca L. Lindsey, Richard J. Meinersmann, Mark E. Berrang, Charlene R. Jackson, Mark D. Englen, Jennifer B. Turpin, and Paula J. Fedorka-Cray. Related antimicrobial resistance genes detected in different bacterial species co-isolated from swine fecal samples. Foodborne Pathogens and Disease. June 2011, 8(6): 663-679. doi:10.1089/fpd.2010.0695. Food Safety and Inspection Service FY 2014 Annual Performance Plan James, William. 2013. The wrong Salmonella standards. Hacker, Jörg and James B. Kaper. 2000. Pathogenicity Islands and the Evolution of Microbes. Annu. Rev. Microbiol..54:641-679 Oscar, Tom. 2004. Dose-response model for 13 strains of Salmonella. Risk Anal. 2004 Feb;24(1):41-9. van Asten AJ, van Dijk JE (2005) Distribution of “classic” virulence factors among Salmonella spp. FEMS Immunol Med Microbiol 44: 251-259. Zou, Wen , Sufian F. Al-Khaldi, William S. Branham, Tao Han, James C. Fuscoe, Jing Han, Steven L. Foley, Joshua Xu, Hong Fang, Carl E. Cerniglia, Rajesh Nayak. 2011. Microarray analysis of virulence gene profiles in Salmonella serovars from food/food animal environment. J Infect Dev Ctries 2011; 5(2):094-105.