During growth of Pseudomonas aeruginosa strain PAO1 with the toxic detergent SDS, a part of the population actively formed macroscopic cell aggregates while the other part grew as freely suspended cells. The physiological function of aggregation for growth with SDS was investigated. Three mutants growing with SDS without aggregation were isolated: the spontaneous mutant strain N and two mutants with transposon insertions in the psl operon for exopolysaccharide synthesis. SDS-induced aggregation in strain N but not in a pslJ mutant was restored by complementation with two genes encoding diguanylate cyclases responsible for synthesis of cyclic-di-guanosine monophosphate (c-di-GMP). By expressing a c-di-GMP-specific phosphodiesterase SDS-induced aggregation of strain PAO1 was reduced. Upon exposure to SDS in the presence of the uncoupler carbonyl cyanide chlorophenylhydrazone, the aggregating strains had ca. 500-fold higher survival rates than the non-aggregating strains. Co-incubation experiments revealed that strain N could integrate into aggregates of strain PAO1 and thereby increase its survival rate more than 1000-fold. These results showed that SDS-induced aggregation involved c-di-GMP signalling with the psl operon as a possible target. Cell aggregation could serve as a pre-adaptive strategy ensuring survival and growth of P. aeruginosa populations in environments with multiple toxic chemicals.

Seeding experiments in flow-through reactors were performed to investigate the incorporation of the opportunistic pathogen Pseudomonas aeruginosa into drinking-water biofilms on ethylene propylene diene monomer (EPDM) rubber as an example of an elastomeric material with a tendency to support biofilm formation. The continuous flow of tap water through the reactor resulted in the formation of biofilms which were in a quasi-stationary state after 14 days with average total cell counts of approximately 1.2 × 109 cells per cm2 and heterotrophic plate counts of about 1.0 × 108 colony-forming units (cfu) per cm2. After introduction of P. aeruginosa, these bacteria persisted in the drinking-water biofilms for at least 7 days and 5 weeks under stagnant and flow conditions, respectively. At the same time, P. aeruginosa was detected in the water phase, indicating detachment of cells from the biofilms. The extracellular polysaccharide alginate and cell-bound lectins LecA and LecB, which are known to be involved in monospecies P. aeruginosa biofilm formation, had no significant influence on the colonisation of established drinking-water biofilms. From a health perspective, drinking-water biofilms can thus act as a reservoir for P. aeruginosa and have to be considered as a source of contamination in water distribution systems.

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