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Review of epidemic aminoglycoside resistance worldwide
Abstract:
Epidemic aminoglycoside resistance may be caused by the spread of a species with distinctive chromosomal genes (e.g., Pseudomonas aeruginosa), or it may be due to the dissemination of plasmids or transposons between genera. Although strains of P. aeruginosa resistant to aminoglycosides because of impermeability may cause nosocomial outbreaks, most of the acute increases in aminoglycoside resistance are due to the spread of inactivating enzymes by plasmids. The index species for intergeneric outbreaks is usually Klebsiella pneumoniae carrying the ANT(2") or AAC(3) gene; however, the distribution of resistance varies greatly by location and species. The AAC(6')-I gene is most common in Serratia marcescens and in East Asian isolates of other species, whereas the AAC(3) gene is common in Chile. In the United States, the ANT(2") and AAC(3) genes are particularly common among Enterobacteriaceae, except for Proteus and Providencia, which often carry the AAC(2') gene. The most common patterns of epidemic resistance lead to the inactivation of gentamicin and, less frequently, tobramycin, but only rarely affect amikacin.
Insights
Epidemic aminoglycoside resistance often stems from plasmid-borne inactivating enzymes, particularly in Klebsiella pneumoniae. Resistance patterns vary geographically, impacting gentamicin and tobramycin more than amikacin.
Area of Science:
- Microbiology
- Molecular Biology
- Epidemiology
Background:
- Aminoglycoside resistance is a growing public health concern.
- Resistance can arise from chromosomal genes or mobile genetic elements like plasmids and transposons.
- Nosocomial outbreaks can be caused by resistant strains, such as Pseudomonas aeruginosa.
Purpose of the Study:
- To investigate the primary mechanisms and genetic elements driving epidemic aminoglycoside resistance.
- To identify key bacterial species and resistance genes involved in intergeneric outbreaks.
- To map the geographical distribution of specific aminoglycoside resistance genes.
Main Methods:
- Analysis of epidemic aminoglycoside resistance mechanisms.
- Identification of bacterial species and mobile genetic elements (plasmids, transposons).
- Gene analysis focusing on ANT(2"), AAC(3), AAC(6")-I, and AAC(2").
Main Results:
- Plasmids carrying inactivating enzymes are the main cause of acute increases in aminoglycoside resistance.
- Klebsiella pneumoniae is a common index species for intergeneric outbreaks, often carrying ANT(2") or AAC(3) genes.
- Geographical variations in resistance gene distribution were observed, with AAC(6")-I prevalent in East Asia and AAC(3) in Chile. Enterobacteriaceae in the US commonly carry ANT(2") and AAC(3), while Proteus and Providencia carry AAC(2").
- Most epidemic resistance affects gentamicin and tobramycin, rarely amikacin.
Conclusions:
- The spread of plasmid-mediated aminoglycoside-inactivating enzymes is the predominant driver of epidemic resistance.
- Understanding the distribution of specific resistance genes and their hosts is crucial for targeted interventions.
- Geographical and species-specific patterns of aminoglycoside resistance necessitate localized surveillance and treatment strategies.