The transcriptional regulator Np20 is the zinc uptake regulator in Pseudomonas aeruginosa.

Zinc is essential for all bacteria, but excess amounts of the metal can have toxic effects. To address this, bacteria have developed tightly regulated zinc uptake systems, such as the ZnuABC zinc transporter which is regulated by the Fur-like zinc uptake regulator (Zur). In Pseudomonas aeruginosa, a Zur protein has yet to be identified experimentally, however, sequence alignment revealed that the zinc-responsive transcriptional regulator Np20, encoded by np20 (PA5499), shares high sequence identity with Zur found in other bacteria.

A novel plasmid for detection of N-acyl homoserine lactones.

Many bacteria utilize acyl-homoserine lactones as cell to cell signals that can regulate the expression of numerous genes. Structural differences in acyl-homoserine lactones produced by different bacteria, such as acyl side chain length and the presence or absence of an oxy group, make many of the commonly used detection bioassays impractical for broad range detection. Here we present a simple, broad range acyl-homoserine lactone detection bioassay that can be used to detect a wide range of these chemical signals.

PqsE functions independently of PqsR-Pseudomonas quinolone signal and enhances the rhl quorum-sensing system.

Pseudomonas aeruginosa is an opportunistic pathogen that causes both acute and chronic infections in immunocompromised individuals. This gram-negative bacterium produces a battery of virulence factors that allow it to infect and survive in many different hostile environments. The control of many of these virulence factors falls under the influence of one of three P.

Outer membrane permeability for nonpolar antimicrobial agents underlies extreme susceptibility of Pasteurella multocida to the hydrophobic biocide triclosan.

Pasteurella multocida exhibits nonspecific susceptibility to nonpolar antimicrobial agents such as triclosan, despite possessing an ultrastructurally typical gram-negative cell envelope. Capsulated and noncapsulated cell surface variants were examined to investigate the role outer membrane permeability plays in triclosan susceptibility. Test strains were unable to initiate growth in the presence of bile salts and were susceptible to triclosan with minimal inhibitory concentrations (MICs) ranging from 0.

Susceptibility of compound 48/80-sensitized Pseudomonas aeruginosa to the hydrophobic biocide triclosan.

Pseudomonas aeruginosa is intrinsically resistant to the hydrophobic biocide triclosan, and yet it can be sensitized to low concentrations by permeabilization of the outer membrane using compound 48/80. A selective plating assay revealed that compound 48/80-permeabilized YM64, a triclosan-recognizing efflux pump-deficient variant, was unable to initiate growth on a medium containing triclosan. Macrobroth dilution assay data revealed that treatment with compound 48/80 synergistically decreased minimal inhibitory concentrations of the hydrophobic antibacterial agents rifamycin SV and chloramphenicol for all cell envelope variant strains examined.

Effect of outer membrane permeabilisation on intrinsic resistance to low triclosan levels in Pseudomonas aeruginosa.

The present study was undertaken to investigate the possibility that outer cell envelope impermeability might be involved in the intrinsic resistance of Pseudomonas aeruginosa to low levels of the hydrophobic biocide triclosan. Macrobroth dilution and batch cultural turbidimetric assays were employed to assess the ability of compounds that render the Gram-negative outer membrane permeable to non-polar molecules to sensitise cell envelope variants to triclosan. Pseudomonas aeruginosa strains possessing highly refractory (PAO1) and atypically permeable (Z61) outer cell envelopes as well as a PAO1 derivative lacking four multidrug efflux pumps (YM64) were examined.