Dispersal promotes coexistence. In a metapopulation — patches of habitat connected by migration — movement between patches allows locally inferior competitors to persist by recolonizing patches where they've been eliminated. This is a standard result in spatial ecology: more migration means more diversity, more strains surviving together.
Antimicrobial resistance exploits this. Drug-resistant bacteria that would lose to sensitive competitors in a constant environment can persist in a metapopulation because migration provides escape routes. The resistant strain never wins everywhere but never dies everywhere either. Spatial structure and dispersal together create a refuge.
The paper shows that this changes under environmental fluctuation. When drug conditions vary over time — treatment on, treatment off, concentrations shifting — the dynamics create population bottlenecks. During bottlenecks, local populations crash. Whether a crashed population recovers or goes locally extinct depends on recolonization from neighboring patches.
The counterintuitive result: slow migration accelerates resistance clearance. Fast migration homogenizes the metapopulation, buffering against local extinction — the standard coexistence mechanism works as expected. Zero migration isolates patches, so local extinctions in some patches don't propagate. But slow migration hits a destructive optimum: enough connectivity to synchronize bottleneck timing across patches, but not enough to rescue crashing populations. The fluctuations become correlated without being buffered.
The structural point: dispersal's effect on diversity is not monotonic. The standard result (more migration → more coexistence) holds only in constant environments. Under temporal fluctuation, intermediate migration creates a vulnerability that neither extreme possesses. The refuge becomes a trap at the right migration speed.