Mechanisms of multidrug resistance in Acinetobacter species and Pseudomonas aeruginosa
1Louis Stokes Cleveland Dept. of Veterans Affairs Medical Center, Section of Infectious Diseases, Cleveland, Ohio 44106, USA. robert.bonomo@med.va.gov
Abstract:
Acinetobacter species and Pseudomonas aeruginosa are noted for their intrinsic resistance to antibiotics and for their ability to acquire genes encoding resistance determinants. Foremost among the mechanisms of resistance in both of these pathogens is the production of beta -lactamases and aminoglycoside-modifying enzymes. Additionally, diminished expression of outer membrane proteins, mutations in topoisomerases, and up-regulation of efflux pumps play an important part in antibiotic resistance. Unfortunately, the accumulation of multiple mechanisms of resistance leads to the development of multiply resistant or even "panresistant" strains.
Insights
Acinetobacter and Pseudomonas aeruginosa exhibit significant antibiotic resistance through enzymes like beta-lactamases and aminoglycoside-modifying enzymes. Multiple resistance mechanisms contribute to the rise of panresistant strains, posing a major clinical challenge.
Area of Science:
- Microbiology
- Molecular Biology
- Pharmacology
Background:
- Acinetobacter species and Pseudomonas aeruginosa are critical Gram-negative pathogens.
- These bacteria possess intrinsic antibiotic resistance and readily acquire resistance genes.
- Mechanisms of resistance are diverse and can accumulate, leading to multidrug resistance.
Purpose of the Study:
- To review the primary mechanisms of antibiotic resistance in Acinetobacter species and Pseudomonas aeruginosa.
- To highlight the role of specific enzymes and cellular processes in conferring resistance.
- To underscore the clinical implications of accumulating resistance mechanisms.
Main Methods:
- Literature review of antibiotic resistance mechanisms in Gram-negative bacteria.
- Analysis of genetic and biochemical pathways involved in resistance.
- Examination of clinical data on multidrug-resistant and panresistant strains.
Main Results:
- Key resistance mechanisms include beta-lactamase production and aminoglycoside-modifying enzymes.
- Reduced outer membrane protein expression, topoisomerase mutations, and efflux pump upregulation are significant.
- The combination of these mechanisms results in strains with extensive or complete resistance to antibiotics.
Conclusions:
- Acinetobacter and Pseudomonas aeruginosa employ a variety of mechanisms to resist antibiotics.
- The cumulative effect of these mechanisms leads to the emergence of highly resistant strains.
- Understanding these resistance pathways is crucial for developing effective therapeutic strategies.
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