Ventilator-Associated Pneumonia Caused by Pseudomonas aeruginosa in Intensive Care Unit: Epidemiology and Risk Factors

Raineri, Enrico; Porcella, Laura; Acquarolo, Annamaria; Crema, Luciano; Albertario, F; Andrea, C.; iani,

doi:10.4172/2161-0703.1000149

Cited by 1 publication

(1 citation statement)

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“…It is also a major opportunistic pathogen, being one of the most frequent causes of acute infections in hospitalised patients and in patients with predisposing conditions such as severe burns, catheterisation, or neutropenia, causing septicaemia, urinary tract infections, and bacteraemia [2][3][4][5]. P. aeruginosa is a primary cause of hospital-and ventilator-acquired pneumonia [6][7][8]. It also causes severe eye infections and chronic infections in patients with cystic fibrosis or chronic obstructive pulmonary disease [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

β-lactam Resistance in Pseudomonas aeruginosa: Current Status, Future Prospects

Glen

Lamont

2021

Pathogens

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Pseudomonas aeruginosa is a major opportunistic pathogen, causing a wide range of acute and chronic infections. β-lactam antibiotics including penicillins, carbapenems, monobactams, and cephalosporins play a key role in the treatment of P. aeruginosa infections. However, a significant number of isolates of these bacteria are resistant to β-lactams, complicating treatment of infections and leading to worse outcomes for patients. In this review, we summarize studies demonstrating the health and economic impacts associated with β-lactam-resistant P. aeruginosa. We then describe how β-lactams bind to and inhibit P. aeruginosa penicillin-binding proteins that are required for synthesis and remodelling of peptidoglycan. Resistance to β-lactams is multifactorial and can involve changes to a key target protein, penicillin-binding protein 3, that is essential for cell division; reduced uptake or increased efflux of β-lactams; degradation of β-lactam antibiotics by increased expression or altered substrate specificity of an AmpC β-lactamase, or by the acquisition of β-lactamases through horizontal gene transfer; and changes to biofilm formation and metabolism. The current understanding of these mechanisms is discussed. Lastly, important knowledge gaps are identified, and possible strategies for enhancing the effectiveness of β-lactam antibiotics in treating P. aeruginosa infections are considered.

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