Colonization, competition, and dispersal of pathogens in fluid flow networks.

TitleColonization, competition, and dispersal of pathogens in fluid flow networks.
Publication TypeJournal Article
Year of Publication2015
AuthorsSiryaporn, A, Kim, MKevin, Shen, Y, Stone, HA, Gitai, Z
JournalCurr Biol
Volume25
Issue9
Pagination1201-7
Date Published2015 May 4
ISSN1879-0445
KeywordsBacterial Physiological Phenomena, Hydrodynamics, Plant Diseases, Plant Vascular Bundle, Pseudomonas aeruginosa, Tobacco
Abstract

<p>The colonization of bacteria in complex fluid flow networks, such as those found in host vasculature, remains poorly understood. Recently, it was reported that many bacteria, including Bacillus subtilis [1], Escherichia coli [2], and Pseudomonas aeruginosa [3, 4], can move in the opposite direction of fluid flow. Upstream movement results from the interplay between fluid shear stress and bacterial motility structures, and such rheotactic-like behavior is predicted to occur for a wide range of conditions [1]. Given the potential ubiquity of upstream movement, its impact on population-level behaviors within hosts could be significant. Here, we find that P. aeruginosa communities use a diverse set of motility strategies, including a novel surface-motility mechanism characterized by counter-advection and transverse diffusion, to rapidly disperse throughout vasculature-like flow networks. These motility modalities give P. aeruginosa a selective growth advantage, enabling it to self-segregate from other human pathogens such as Proteus mirabilis and Staphylococcus aureus that outcompete P. aeruginosa in well-mixed non-flow environments. We develop a quantitative model of bacterial colonization in flow networks, confirm our model in vivo in plant vasculature, and validate a key prediction that colonization and dispersal can be inhibited by modifying surface chemistry. Our results show that the interaction between flow mechanics and motility structures shapes the formation of mixed-species communities and suggest a general mechanism by which bacteria could colonize hosts. Furthermore, our results suggest novel strategies for tuning the composition of multi-species bacterial communities in hosts, preventing inappropriate colonization in medical devices, and combatting bacterial infections.</p>

DOI10.1016/j.cub.2015.02.074
Alternate JournalCurr. Biol.
PubMed ID25843031
PubMed Central IDPMC4422760
Grant List1DP2OD004389 / OD / NIH HHS / United States
DP2 OD004389 / OD / NIH HHS / United States
F32 AI095002 / AI / NIAID NIH HHS / United States
F32AI095002 / AI / NIAID NIH HHS / United States