P. aeruginosa is the bacteria most commonly responsible for hospital-acquired and
ventilator-associated pneumonia. Numerous factors are encoded in its genome, and they explain its high virulence. P. aeruginosa also develops a quorum sensing (QS), which coordinates the expression of these factors. The
type III secretion system, a needle-complex, allows
exotoxin injections into eukaryotic cells and is involved in the pathogenesis of acute
pneumonia. This pathogen develops a high level of resistance to all
antibiotics, which leads to a shortage of treatment options for many patients. Thus, new preventive or therapeutic approaches are in development.
Immunotherapy that uses
monoclonal antibodies has been successfully tested in blocking the
type III secretion system (anti-PcrV) or helping immune cells phagocytose P. aeruginosa. Inhibiting the quorum sensing has also been efficacious in vitro and in vivo. New antibacterial
peptides may enlarge the panel of treatments in the near future. However, current treatment for patients still relies on
antibiotics. The development of resistance to all classes of available
antibiotics leads to
colistin revival with good clinical results. Topical delivery through
aerosol could allow for the increase in the
antibiotic concentration inside the
infection site while limiting its systemic toxicity. Finally, Candida airway colonization has been found to be associated with P. aeruginosa-associated
pneumonia in ventilated patients. In addition to targeting the bacteria, reducing Candida airway colonization may also decrease the incidence of such
infections.