Phage predation, typically assumed to reduce microbial proliferation and not contribute to the spread of antibiotic resistance, can actually increase the spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth by reshaping spatial organization. Using *Escherichia coli* strains, the study demonstrates that phage predation slows the spatial segregation of strains, increasing cell-cell contacts and conjugation-mediated plasmid transfer. This is achieved by shifting the location of fastest growth from the biomass periphery to the interior, where cells are more densely packed and aligned parallel, creating straighter interfaces that are less likely to merge during growth. The findings have implications for phage therapy and reveal a mechanism for how deleterious microbial functions can proliferate without positive selection.Phage predation, typically assumed to reduce microbial proliferation and not contribute to the spread of antibiotic resistance, can actually increase the spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth by reshaping spatial organization. Using *Escherichia coli* strains, the study demonstrates that phage predation slows the spatial segregation of strains, increasing cell-cell contacts and conjugation-mediated plasmid transfer. This is achieved by shifting the location of fastest growth from the biomass periphery to the interior, where cells are more densely packed and aligned parallel, creating straighter interfaces that are less likely to merge during growth. The findings have implications for phage therapy and reveal a mechanism for how deleterious microbial functions can proliferate without positive selection.