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|Year : 2018 | Volume
| Issue : 3 | Page : 301--302
Pseudomonas aeruginosa - Difficult to outmanoeuvre
Payal K Patel1, Twisha S Patel2, Keith S Kaye3,
1 Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan, USA
2 Department of Pharmacy Services, University of Michigan Health System, Ann Arbor, Michigan, USA
3 Division of Infectious Diseases, University of Michigan Medical School, Ann Arbor, Michigan, USA
Payal K Patel
Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan
|How to cite this article:|
Patel PK, Patel TS, Kaye KS. Pseudomonas aeruginosa - Difficult to outmanoeuvre.Indian J Med Microbiol 2018;36:301-302
|How to cite this URL:|
Patel PK, Patel TS, Kaye KS. Pseudomonas aeruginosa - Difficult to outmanoeuvre. Indian J Med Microbiol [serial online] 2018 [cited 2020 Sep 22 ];36:301-302
Available from: http://www.ijmm.org/text.asp?2018/36/3/301/245393
In 1850, as the term the 'Raj' was gaining momentum to describe the British rule in India, a military surgeon in France, Dr. Charles Sédillot, noted that some surgical wounds seemed to share a blue-green discolouration. Eventually, the causative organism was identified as Pseudomonas aeruginosa. Despite learning more each decade about its ability to intrinsically produce and acquire mechanisms of antimicrobial resistance, P. aeruginosa continues to be a major cause of infection in acute-care hospitals worldwide and especially in India.
The ubiquitous nature of P. aeruginosa and its ability to survive with few nutritional requirements make it a dependable pathogen and a common cause of healthcare-associated infections, particularly in the intensive care unit setting. Compounded by this is the fact that P. aeruginosa can have numerous chromosomal and plasmid-mediated mechanisms of antimicrobial resistance. Broadly, these can be classified as target site mutations (ex. mutations in gyrA leading to fluoroquinolone resistance), production of hydrolytic enzymes (ex. production of AmpC beta-lactamases leading to ceftazidime resistance), overexpression of efflux pumps (ex. increased expression of MexAB-OprM leading to resistance to multiple drug classes including fluoroquinolones and beta-lactams) and alterations to outer membrane porins (ex. loss of OprD leading to carbapenem resistance).
Lack of antimicrobial stewardship practices globally has contributed to the loss of fluoroquinolones and beta-lactam antibiotics as viable treatment options due to the development of resistance in many P. aeruginosa isolates. As noted in the manuscript by Pragasam et al., although rates of resistant P. aeruginosa appear to vary by region in India, resistance to individual commonly used beta-lactam antibiotics has been reported to be as high as 80% in larger surveillance databases. P. aeruginosa has been recognised globally as a problematic pathogen and is now included in the National Programme on Containment of Antimicrobial Resistance by the Government of India.
Infections due to multi- and extremely drug resistant strains of P. aeruginosa are associated with particularly poor outcomes, due in part to ineffective antibiotic treatment. Increasing resistance has led to an increase in the practice of 'double-coverage' for serious Gram-negative infections. Combination therapy is commonly used empirically for suspected infection due to P. aeruginosa. This involves combining two anti-pseudomonal antibiotics from different classes to provide broad coverage and increase the likelihood of providing active, effective therapy empirically. It is important to narrow coverage to a single, effective agent once a pathogen has been identified and drug susceptibilities are known. Some clinicians also use antibiotics in combination as definitive therapy for a proven infection due to P. aeruginosa, to take advantage of the synergistic activity of combining agents (for example, a beta-lactam and an aminoglycoside) and also to prevent the emergence of resistance while on therapy. While empiric 'double-coverage' is generally accepted as appropriate in some instances (such as sepsis), there is not good clinical data to support combination therapy for proven P. aeruginosa infection in the setting of susceptible isolates.
In the review article, Pragasam et al. (same IJMM issue) describe several newer antimicrobials that have either recently become available or are in advanced stages of drug development. While these newer agents are welcomed additions to clinicians' therapeutic armamentarium, the authors note that unmet treatment needs persist. As noted in the review, novel agents that are not affected by multidrug efflux pumps would hold particular promise as antipseudomonal therapeutics.
We suggest that in this era of antimicrobial resistance, the importance of antimicrobial stewardship and infection control should not be undervalued in approaching multidrug-resistant Gram-negative infections and outbreaks, including those due to P. aeruginosa. Utilizing rapid diagnostics and optimizing antibiotic use can improve patient outcomes and implementing evidence-based infection control practices can decrease the rates of healthcare-associated infection and spread of antimicrobial resistance. It has been inspiring to witness the surging interest and focus on antimicrobial stewardship in India over the past few years. Along with an increased focus on infection prevention, these efforts provide the best defense to curb the rising incidence of infections due to increasingly resistant strains of P. aeruginosa as well as other types of multidrug-resistant bacteria.
Medicine has come a long way in the last century and a half, yet the war against antimicrobial resistance rages on and P. aeruginosa is a worthy enemy. Given its inherent resistance to multiple drug classes, the ability to gain acquired resistance, and the proclivity of P. aeruginosa to persist in healthcare settings and infect the most vulnerable patients, an ongoing focus on P. aeruginosa from infection control, antimicrobial stewardship and novel drug perspectives is required.
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