Title of article :
Pseudomonas aeruginosa: Burn Infection, Treatment and Antibacterial Resistance
Author/Authors :
Japoni, A Alborzi Clinical Microbiology Research Center - Nemazee Hospital - Shiraz University of Medical Sciences, Shiraz , Farshad, S Alborzi Clinical Microbiology Research Center - Nemazee Hospital - Shiraz University of Medical Sciences, Shiraz , Alborzi, A Alborzi Clinical Microbiology Research Center - Nemazee Hospital - Shiraz University of Medical Sciences, Shiraz
Pages :
10
From page :
244
To page :
253
Abstract :
Pseudomonas aeruginosa is an opportunistic pathogen causing severe, acute and chronic nosocomial infections in immunocompromised, catheterized or burn patients. Various types of virulent factors have been identified in P. aeruginosa, suggesting their contribution to the pathogenesis of the disease. The organism is generally resistant to numerous antimicrobial agents due to natural resistance in particular impermeability or mutations and acquisition of resistant determinants. Plasmid and integron have a crucial role in acquisition of mobile elements. Most treatment failures are related to inappropriate initial antibiotic therapy with insufficient coverage of multidrug resistant (MDR) pathogens, the rationale for using combinations of antibiotics to cover MDR gram-negatives. However, clinical data supporting this strategy are limited. In fact, systematic combination therapy may have contributed to the overuse of antibiotics and to the emergence of MDR microorganisms. Nevertheless, combination therapy is the best strategy to treat severe infections due to suspected MDR Pseudomonas. Optimally, therapeutic strategies should be sufficiently broad to cover relevant pathogens while minimizing the risk for emergence of antimicrobial resistance. Polymyxin E (colistin) and carbapenems are the most effective antibiotics against MDR isolates.
Keywords :
Integron , plasmid , Multidrug-resistance , Pseudomonas aeruginosa
Journal title :
Astroparticle Physics
Serial Year :
2009
Record number :
2431203
Link To Document :
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