The rise in antibiotic resistance, combined with the shortage in discovery of new classes of these drugs, has led to the pursuit of creative ways to tackle bacterial infections that do not necessarily kill bacteria in conventional ways. Many of these approaches, however, are only partially successful when tested in infection models. We present two such potential treatments in relation to the multi-drug resistant bacterium Pseudomonas aeruginosa: targeting host-cell adhesion and cell-morphology transitions. Through comparison of mathematical models against experimental data, we suggest experimental pathways that could aid in optimising these potential bacterial treatments.