Antimicrobial resistance (AMR) is jeopardising the efficacy of current and future antimicrobial agents, with the environment as a reservoir for AMR being notably underrepresented in the One Health framework. However, drinking water has emerged as a potential environmental route of transmission of AMR. Irish private drinking water supplies (PDWS) are particularly vulnerable to AMR contamination due to poorer microbiological quality than public supplies. An absence of guidelines that recognise AMR bacteria (ARB) and genes (ARGs) as contaminants of drinking water has limited our knowledge on the contribution of PDWS in the spread and persistence of AMR. Furthermore, AMR plasmids are particularly concerning within One Health, as they can independently mobilise between and across species, and ecosystems. With the support of citizen science, we investigated the bacterial reservoirs of AMR in Irish PDWS and explored the potential of alkyl α-D-mannopyranosides to reduce the transmission of MDR plasmids via inhibition of biofilms amongst Escherichia coli. Irish PDWS were confirmed reservoirs of both commensal and clinically relevant ARB. Bacteria resistant to last-line antimicrobials were identified as carbapenem-resistant H. alvei and linezolid�resistant Enterococcussp. Opportunistic and potentially pathogenic isolates of E. coli, E. cloacae, Enterococcus casseliflavus, Stenotrophomonas maltophilia, and Serratia rubidaea harboured MDR phenotypes. In E. coli, this was attributed to conjugative plasmids, IncP-1α, IncFIA and IncFIB. Whole genome sequencing of two E. coli isolates harbouring IncFIB revealed virulence factors and clinically relevant ARGs such as phenicol- (floR, catI), aminoglycoside- (apha�variants), and β-lactam- (blaTEM-1) resistance genes. Exogenously captured plasmids also harboured IncF, IncQ and Col-plasmids. In addition to the ARGs identified in E. coli, these plasmids additionally encoded clinically relevant ARGs such as the methyltransferase (cfrA), tetracycline efflux (tetB) and broad-spectrum β-lactamase (blaTEM-116). Investigations into a biofilm-inhibiting, next generation antimicrobial, revealed previously unexplored conjugation inhibitor (COIN) activity against MDR F-plasmids. Heptyl α-D�mannopyranoside inhibited biofilms of a broad range of biofilm-forming E. coli strains at µg/mL concentrations, with only a small impact on bacterial viability. In addition, heptyl α-D�mannopyranoside significantly reduced the transmission of MDR IncF plasmids of both clinical (pEK499) and environmental (pEN154, pEN500) background. However, limitations were identified due to an increase in the conjugation of the R388 (IncW) plasmid. Heptyl α-D-mannopyranoside failed to inhibit conjugation in the absence of FimH, demonstrating the significance of FimH interactions. Further, the COIN potency of heptyl α-D-mannopyranoside was determined – in large – by the plasmid host. We also uncovered COIN potential for the galactose analogue, heptyl β-D-galactopyranoside, which demonstrated comparable COIN activity on pEK499 (IncFIA/IncFII), but this was limited by concentration. Overall, this thesis provides evidence that Irish PDWS are reservoirs of AMR. By accumulating information regarding the movement and persistence of ARB and ARGs, efforts can be made to mitigate the potential risk this poses to the Irish population. Moreover, the novel and promising findings have unveiled a new class of COINs for the control of MDR plasmids amongst E. coli. The work suggests that lectins may be used as an alternative target for COINs, a promising starting point for future COIN studies.