Oral Presentation BacPath 2024

Genomic epidemiology and phenotypic characterisation of Salmonella enterica serovar Panama in Victoria, Australia (#20)

Samriddhi Thakur 1 2 , Sarah L Baines 1 , Cheryll M Sia 3 , Mary Valcanis 3 , Louise M Judd 4 , Benjamin P Howden 1 3 5 , Hayley J Newton 2 , Danielle J Ingle 1
  1. Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Parkville, Melbourne, Victoria 3000, Australia
  2. Infection Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Melbourne, Victoria 3168, Australia
  3. Microbiological Diagnostic Unit Public Health Laboratory, Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Parkville, Melbourne, Victoria 3000, Australia
  4. Doherty Applied Microbial Genomics, Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Parkville, Melbourne, Victoria 3000, Australia
  5. Centre for Pathogen Genomics, The University of Melbourne, Parkville, Melbourne, Victoria 3000, Australia

Australia records one of the highest incidences of non-typhoidal Salmonella (NTS) gastroenteritis among high-income countries. Predominantly self-limiting, NTS infections can disseminate beyond the gastrointestinal barrier leading to systemic illness. Salmonella enterica serovar Panama is notably associated with invasive NTS infections. However, its genomic epidemiology and pathogenesis remain poorly understood. To provide context for the invasive nature of the serovar, we characterised the genomic population structures of 89 S. Panama isolates collected from human cases in Victoria, Australia over a 20-year period. We identified two subpopulations of S. Panama sequence type 48. We examined the characteristics of S. Panama host-pathogen interactions in both epithelial and macrophage cells lines, compared to the S. Typhimurium SL1344 strain. Only 2 among 7 S. Panama isolates entered epithelial cells and replicated to comparable levels as S. Typhimurium SL1344 in 24 hours. Despite reduced entry into THP-1-derived macrophages compared to S. Typhimurium SL1344, S. Panama replicated to equivalent levels over time. From the genomes of S. Panama isolates from this study, we identified in silico known and potential virulence genes conserved in the serovar, particularly those of typhoidal origin. In addition to typhoid toxin encoding genes cdtB, pltA, and pltB, S. Panama harboured taiA, encoding for an invasin, and hlyE, encoding for cytolysin, on Salmonella pathogenicity island (SPI)-18. SPI-18 has previously been shown to modulate host cell infection for human adapted S. Typhi. We also identified a homolog of the S. Typhi specific ubiquitin ligase STY1076/t1865, a putative type III secretion system effector, present in all S. Panama isolates. The varied in vitro infection dynamics of S. Panama compared to S. Typhimurium, and the presence of S. Typhi virulence genes may contribute to S. Panama’s increased capacity to become invasive. Future phenotypic characterisation of S. Panama virulence proteins can provide more insights into its host-pathogen dynamics.