Resistance of Pseudomonas aeruginosa and Staphylococcus aureus to the airway epithelium oxidative response assessed by a cell-free in vitro assay.

The antibacterial oxidative response, which relies on the production of hydrogen peroxide (H2O2) and hypothiocyanite (OSCN-), is a major line of defense protecting the human airway epithelium (HAE) from lesions when infected. The in vitro studies of the oxidative responses are performed mainly by one-shot H2O2 exposure that does not recapitulate the complex H2O2/LPO/SCN- system releasing the reactive oxygen species in airway secretions. A cell-free in vitro assay mimicking this system has been described but was not fully characterized.

susceptibility of nonfermenting Gram-negative rods to meropenem-vaborbactam and delafloxacin.

Meropenem-vaborbactam and delafloxacin activities were not assessed against spp. (), complex () and (). A total of 106 , 57  and 100  were tested with gradient diffusion test of meropenem-vaborbactam, delafloxacin and comparators.

An upgraded version of carbapenem inactivation method to detect Bacteroides fragilis carbapenemase.

An increase of carbapenemase-producing Bacteroides fragilis infections is observed. To detect such a resistance in B. fragilis, several tests exist that are expensive or show poor sensitivity and specificity.

A -plasmid allows aminoglycosides to induce SOS in .

The plasmid-mediated quinolone resistance (PMQR) genes have been shown to promote high-level bacterial resistance to fluoroquinolone antibiotics, potentially leading to clinical treatment failures. In , sub-minimum inhibitory concentrations (sub-MICs) of the widely used fluoroquinolones are known to induce the SOS response. Interestingly, the expression of several PMQR genes is controlled by the SOS master regulator, LexA.