Abstract
Not all Salmonella enterica serovars cause the same disease. S. enterica represents an incredibly diverse species comprising >2,600 unique serovars. While some S. enterica serovars are host-restricted, others infect a wide range of hosts. The diseases that nontyphoidal Salmonella (NTS) serovars cause vary considerably, with some serovars being significantly more likely to cause invasive disease in humans than others. Furthermore, while genomic analyses have advanced our understanding of the genetic diversity of these serovars, they have not been able to fully account for the observed clinical differences. One overarching challenge is that much of what is known about Salmonella’s general biology and virulence strategies is concluded from studies examining a select few serovars, especially serovar Typhimurium. As targeted control strategies have been implemented to control select serovars, an increasing number of foodborne outbreaks involving serovars that are less frequently associated with human clinical illness are being detected. Harnessing what is known about the diversity of NTS serovars represents an important factor in achieving the ultimate goal of reducing salmonellosis-associated morbidity and mortality worldwide. In this review we summarize the current understanding of the differences and similarities among NTS serovars, highlighting the virulence mechanisms, genetic differences, and sources that characterize S. enterica diversity and contribute to its success as a foodborne pathogen.
Highlights
The majority of Salmonella isolates infecting warm-blooded hosts belong to subspecies enterica (I), while subspecies II-VI and S. bongori are primarily isolated from environmental sources or cold-blooded hosts, such as reptiles and amphibians
The complete host-pathogen relationship plays an important role in determining the resulting severity of salmonellosis (Figure 2), some nontyphoidal Salmonella (NTS) serovars excel at causing invasive human clinical infections that are reminiscent of the pathology exhibited by Typhi and paratyphoidal serovars of S. enterica
Typhimurium infections, of which just 5.7% resulted in invasive disease, infections with serovars Choleraesuis (56.4%), Dublin (64.0%), Sandiego (18.9%), and Panama (18.0%) were associated with significantly higher rates of invasive disease among human clinical infections in the US (Jones et al, 2008)
Summary
Yue et al (2012) demonstrated that host adapted/restricted serovars, such as Typhi, Dublin, Paratyphi A, Choleraesuis, and Gallinarum encode multiple non-functional fimbrial genes (Yue et al, 2012). The complete host-pathogen relationship plays an important role in determining the resulting severity of salmonellosis (Figure 2), some NTS serovars excel at causing invasive human clinical infections that are reminiscent of the pathology exhibited by Typhi and paratyphoidal serovars of S. enterica.
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