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Salmonella (S.) Infantis strains harbouring multi-drug resistance (MDR) to high-priority critically important antimicrobials have been isolated globally, giving cause for concern. The serovar is highly persistent throughout the poultry industry and is the fourth most reported serovar linked to zoonotic disease. The serovars resistance is attributed to the presence of a megaplasmid termed pESI. Biocides are an important tool to reduce the need to use antimicrobials, including antibiotics. Bacteria can produce a protective exopolysaccharide matrix called biofilm, and biofilm presence can reduce the efficacy of disinfectants. Here, we aimed to assess the role of pESI on disinfectant efficacy and biofilm formation, and as a contributing factor in the serovars persistence. We analysed S. Infantis strains isolated within the United Kingdom (UK) and Austria, using in vitro planktonic and biofilm disinfectant efficacy assays. Commercially available, commonly used Peroxymonosulphate-, Chlorocresol-and Aldehyde-Quaternary Ammonium Compound-based UK poultry disinfectants were assessed. Biofilm formation was evaluated after 72- and 120-hours incubation, and on a variety of surfaces. Comparative genomic analysis was performed between the UK and Austrian isolates, as well as further globally isolated strains. We identified variation in the presence/absence of antimicrobial resistance genes in both the whole genome and plasmid sequences, within and between the UK and Austrian strains. Variation in biofilm formation was observed between strains, and with greater biofilm formation on non-porous surfaces. Despite this, we could not demonstrate an influence of the pESI plasmid on biofilm formation. Additionally, the presence or absence of the plasmid, or variation observed within the plasmid, did not seem to influence planktonic nor biofilm disinfectant tolerance. Further investigation should be undertaken to identify the influence of pESI on the persistence of S. Infantis and to ensure effective prevention and control of the spread of the serovar and the plasmid.