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Mechanistic understanding of bacterial spreading in soil is critical to control pathogenic contamination of groundwater and soil as well as design bioremediation projects. However, our understanding is currently limited by the lack of direct bacterial imaging in soil conditions. Here, we overcome this limitation by directly observing the spread of bacterial solution in a transparent chamber with varying corner angles designed to replicate soil-like conditions. We show that two common soil bacteria, Bacillus subtilis and Pseudomonas fluorescens, generate flows along sharp corners (< 60°) by producing surfactants that turn nonwetting solid surfaces into wetting surfaces. We further show that a surfactant-deficient mutant of B. subtilis cannot generate corner flows along sharp corners, confirming that the bacteria-generated corner flows require the production of bacterial surfactants. The speed of biosurfactant-induced corner flow at the sharp corner is about several millimeters per hour, similar to that of bacterial swarming, the fastest mode of known bacterial surface translocation. We further demonstrate that the bacteria-generated corner flow only occurs when the corner angle is less than a critical value, which can be predicted from the contact angle of the bacterial solution. Furthermore, we show that the corner flow has a maximum height due to the roundness or cutoff of corners. The mechanistic understanding and mathematical theories of bacterial spreading presented in this study will help improve predictions of bacterial spreading in soil, where corners are ubiquitous, and facilitate future designs of soil contamination mitigation and other bioremediation projects.

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Bacterial pathogenicity relies on both firm surface adhesion and cell dissemination. How twitching bacteria resolve the fundamental contradiction between adhesion and migration is unknown. To address this question, we employ live-cell imaging of type-IV pili (T4P) and therewith construct a comprehensive mathematical model of Pseudomonas aeruginosa migration. The data show that only 10% to 50% of T4P bind to substrates and contribute to migration through random extension and retraction. Individual T4P do not display a measurable sensory response to surfaces, but their number increases on cellular surface contact. Attachment to surfaces is mediated, besides T4P, by passive adhesive forces acting on the cell body. Passive adhesions slow down cell migration and result in local random motion on short time scales, which is followed by directionally persistent, superdiffusive motion on longer time scales. Moreover, passive adhesions strongly enhance surface attachment under shear flow. ΔpilA mutants, which produce no T4P, robustly stick to surfaces under shear flow. In contrast, rapidly migrating ΔpilH cells, which produce an excessive number of T4P, are easily detached by shear. Wild-type cells sacrifice migration speed for robust surface attachment by maintaining a low number of active pili. The different cell strains pertain to disjunct regimes in a generic adhesion-migration trait space. Depending on the nature of the adhesion structures, adhesion and migration are either compatible or a trade-off is required for efficient bacterial surface colonization under different conditions.

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