关于 Pseudomonas aeruginosa

Pseudomonas aeruginosa is a motile, nonfermenting, Gram-negative, rod-shaped and blue-green pigmented bacterium belonging to the family Pseudomonadaceae^[1]. It is often isolated from plants, fruits, soil, and water environments, such as rivers, lakes, and swimming pools. P. aeruginosa is also found on the skin of healthy people and has been isolated from the throat (5%) and stools (3%) of nonhospitalized patients. This bacterium predominantly causes nosocomial infections such as pneumonia^[1], infections of the urinary tract, wounds^[2], bones and joints and the bloodstream^[3]. The bacterium thrives when the epithelial barrier is damaged, or when neutrophil production is depleted, mucociliary clearance is altered and in the presence of medical devices. Medical interventions such as mechanical ventilation^[4], surgery, antibiotic therapy, and chemotherapy are major predisposing factors that may further cause serious P. aeruginosa infections in a hospital environment. Additionally, P. aeruginosa causes community-acquired infections such as gastrointestinal, skin, and soft tissue infections and otitis externa; it is also known to be associated with lower respiratory tract infections in patients with cystic fibrosis.

Treatment of P. aeruginosa infections can be challenging due to its natural and acquired resistance to antibiotics^[5]. Multidrug-resistant P. aeruginosa typically arises from the interaction of several complex resistance mechanisms: reduced expression of outer membrane porins, hyperexpression of AmpC enzymes, increased activity of efflux pumps, and mutations in penicillin-binding protein targets^[6]. Virtually all knowledge regarding the biological cost of horizontally acquired resistance in P. aeruginosa deals with the incorporation of β-lactamases from various Ambler’s classes, including extended spectrum β-lactamases and carbapenemases^[7]. In P. aeruginosa these enzymes are usually encoded in class I integrons, which are the predominant platforms for acquisition of resistance markers and ulterior dissemination through transferable elements such as plasmids. Besides β-lactamases, it is usual that different aminoglycoside-modifying enzymes and even other less frequent determinants (e.g., fluoroquinolones and colistin resistance genes) are carried in integrons/plasmids^[8].

The expression of virulence genes in P. aeruginosa is controlled by extremely complex, interweaving regulatory circuits and multiple signalling systems. For an opportunistic pathogen, P. aeruginosa produces an impressive array of particularly secreted virulence factors, utilising its type III secretion system to secrete various exotoxins (ExoS, ExoU, ExoT, and ExoY), and quorum sensing systems (cell-density-dependent regulation) to control numerous important secreted virulence factors, including secreted pyocyanin, elastase, cyanide, and rhamnolipid.

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