Limited research exists on the potential for leather to act as a fomite of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or endemic coronaviruses including human coronavirus (HCoV) OC43; this is important for settings such as the shoe manufacturing industry. Antiviral coating of leather hides could limit such risks. This study aimed to investigate the stability and transfer of HCoVOC43 on different leathers, as a surrogate for SARS-CoV-2, and assess the antiviral efficacy of a silver-based leather coating. The stability of HCoV-OC43 (6.6 log10) on patent, full-grain calf, corrected grain finished, and nubuck leathers (silver additive-coated and uncoated) was measured by titration on BHK-21 cells. Transfer from leather to cardboard and stainless steel was determined. HCoV-OC43 was detectable for 6 hours on patent, 24 hours on finished leather and 48 hours on calf leather; no infectious virus was recovered from nubuck. HCoV-OC43 transferred from patent, finished and calf leathers onto cardboard and stainless steel up to 2 hours post-inoculation (≤3.1–5.5 log10), suggesting that leathers could act as fomites. Silver additive-coated calf and finished leathers were antiviral against HCoV-OC43, with no infectious virus recovered after 2 hours and limited transfer to other surfaces. The silver additive could reduce potential indirect transmission of HCoV-OC43 from leather.

Aims To investigate the priming effects of sub‐inhibitory concentrations of biocides on antibiotic resistance in bacteria. Methods and results Escherichia coli, Pseudomonas aeruginosa and Staphylococcus aureus were exposed to sub‐inhibitory concentrations of biocides via a gradient plate method. Minimum inhibitory concentration (MIC) and antibiotic susceptibility were determined, and efflux pump inhibitors (thioridazine and chlorpromazine) were used to investigate antibiotic resistance mechanism(s). Escherichia coli displayed a twofold increase in MIC (32–64 mg l−1) to H2O2 which was stable after 15 passages, but lost after 6 weeks, and P. aeruginosa displayed a twofold increase in MIC (64–128 mg l−1) to BZK which was also stable for 15 passages. There were no other tolerances observed to biocides in E. coli, P. aeruginosa or S. aureus; however, stable cross‐resistance to antibiotics was observed in the absence of a stable increased tolerance to biocides. Sixfold increases in MIC to cephalothin and fourfold to ceftriaxone and ampicillin were observed in hydrogen peroxide primed E. coli. Chlorhexidine primed S. aureus showed a fourfold increase in MIC to oxacillin, and glutaraldehyde‐primed P. aeruginosa showed fourfold (sulphatriad) and eightfold (ciprofloxacin) increases in MIC. Thioridazine increased the susceptibility of E. coli to cephalothin and cefoxitin by fourfold and twofold, respectively, and both thioridazine and chlorpromazine increased the susceptibility S. aureus to oxacillin by eightfold and fourfold, respectively. Conclusions These findings demonstrate that sub‐inhibitory concentrations of biocides can prime bacteria to become resistant to antibiotics even in the absence of stable biocide tolerance and suggests activation of efflux mechanisms may be a contributory factor. Significance and Impact of the Study This study demonstrates the effects of low‐level exposure of biocides (priming) on antibiotic resistance even in the absence of obvious increased biocidal tolerance.