Abstract
Pseudomonas aeruginosa is a Gram-negative bacterium which is capable of developing a high level of antibiotic resistance. It has been placed on the WHO’s critical priority pathogen list and it is commonly found in ventilator-associated pneumonia infections, blood stream infections and other largely hospital-acquired illnesses. These infections are difficult to effectively treat due to their increasing antibiotic resistance and as such patients are often treated with antibiotic combination regimens. Methods: We conducted a systematic search with screening criteria using the Ovid search engine and the Embase, Ovid Medline, and APA PsycInfo databases. Results: It was found that in many cases the combination therapies were able to match or outperform the monotherapies and none performed noticeably worse than the monotherapies. However, the clinical studies were mostly small, only a few were prospective randomized clinical trials and statistical significance was lacking. Conclusions: It was concluded that combination therapies have a place in the treatment of these highly resistant bacteria and, in some cases, there is some evidence to suggest that they provide a more effective treatment than monotherapies.
Highlights
Pseudomonas aeruginosa is a Gram-negative bacterium in the family of Pseudomonadaceae [1]
In a 104-patient study (Tables 2 and 3), Crusio et al [28] investigated the clinical success of a polymyxin B combination therapy for the treatment of carbapenem-resistant Gram-negative bacteria
All of the P. aeruginosa infections that were included in the study were resistant to penicillins, cephalosporins, quinolones, macrolides, tetracyclines, aminoglycosides, and carbapenems
Summary
Pseudomonas aeruginosa is a Gram-negative bacterium in the family of Pseudomonadaceae [1]. P. aeruginosa currently represents about 10% of all hospital-acquired infections worldwide and, as a result of its aforementioned adaptability, it has become a therapeutic challenge due to its high levels of resistance to most of the known monotherapy antibiotics [3,4]. The mechanisms of resistance to carbapenems include the production of β-lactamases, efflux pumps, and mutations that alter the expression or function of the porins and penicillin-binding proteins [5]. It is the combination of many of these mechanisms together with resistance to other antibiotics that leads to the high levels of resistance which are seen in some strains of P. aeruginosa
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