Salmonella enterica serovar Infantis (S. Infantis) is one of the prevalent Salmonella serovars worldwide and is often associated with human gastroenteritis and asymptomatic persistence in poultry. Previously, we showed that the emergence of S. Infantis in Israel has involved the acquisition of a unique plasmid designated pESI, which confers multidrug resistance and increased virulence phenotypes. This self-transferred episome is a mosaic megaplasmid (~280 kb), which increases bacterial tolerance to environmental mercury, oxidative stress and provides further resistance to tetracycline, sulfamethoxazole and trimethoprim antibiotics. Moreover, pESI carries the yersiniabactin siderophore system and two novel chaperone-usher fimbriae. Recently, the emergence of S. Infantis clones carrying pESI-like plasmids was also reported in Italy, Spain and the USA, indicating that of pESI acquisition is common to geographically-distinct emergent S. Infantis populations.
I will demonstrate the contribution of pESI to S. Infantis pathogenicity and elucidate the ecology, transmission properties and regulation of pESI, including its ability to disseminate from Salmonella to the microbiota and back. In addition, I will discuss the structure, function and regulation of the two pESI-encoded chaperone-usher fimbriae and demonstrate their distinct expression and role in virulence during mammalian vs. avian infection. Collectively, this study highlights the key role of plasmid conjugation in microbial evolution and suggests an overlooked role of the microbiota as a reservoir of resistance and virulence genes.