Understanding the interactions of pathogenic droplets with surfaces is crucial to biomedical applications. In this study, using E. coli as the model microbe, we investigate the impact of a bacteria-laden droplet on different substrates, both bare and antimicrobial. In doing so, we unveil the significance of kinetic energy and spreading parameters of the impacting droplet in determining the microbes' proliferation capabilities. Our results indicate an inverse relationship between the impact Weber number and the bacterial ability to proliferate. We reveal that the mechanical stress generated during impact impedes the capabilities of microbes present inside the droplet to create their progeny. Following an order analysis of the mechanical stress generated, we argue that the impact does not induce lysis-driven cell death of the bacteria; rather, it promotes a stress-driven transition of viable bacteria to a viable-but-non-culturable (VBNC) state. Furthermore, variations in the concentration of particles on the antimicrobial surfaces revealed the role of the post-impact spreading behaviour in dictating bacterial proliferation capabilities. Contrary to the conventional notion, we demonstrate that during the early stages of interaction, a bare substrate may outperform an antibacterial substrate in the inactivation of the bacterial load. Finally, we present an interaction map illustrating the complex relationship between bacterial colony-forming units, bactericide concentration on the surface, and the impact Weber number. We believe that the inferences of the study, highlighting the effect of mechanical stresses on the soft cell wall of microbes, could be a useful design consideration for the development of antimicrobial surfaces.