Mechanisms of bacterial resistance to aminoglycosides


Efflux pumps transport antibiotics from within the cell into the external environment rendering the antibiotic useless. The inducible RND-type pump possessed by P. aeruginosa and AcrD multidrug efflux transporter in E. coli are both capable of ejecting aminoglycosides out of the bacterial cell.1,6

Ribosomal mutations of the ribosomal proteins and 16S rRNA along with enzymatic methylation of the rRNA will interfere with the aminoglycosides ability to bind to the rRNA therefore conferring resistance. The rRNA methyltransferase enzymes (RmtA, RmtB, RmtC, RmtD, RmtE and RmtF) produce broad-spectrum resistance to the aminoglycosides and are being discovered more frequently world-wide on plasmids with broad-spectrum β-lactamases like CTX-M, NDM and KPC (Table 1).3

Table1. Aminoglycoside resistance mechanisms –  Decreased uptake and modification of ribosome

Resistance typeResistance mechanismAminoglycoside inactivatedBacteria affected
Decreased uptakeChanges in outer membrane permeabilityAllPseudomonas aeruginosa
Decreased uptake Efflux systems such as:
• Resistance nodulation cell division (RND)
• Major facilitator superfamily (MFS)
Allwide range
Modification of the ribosome Point mutations in ribosomal protein S12 and in the 16S rRNAStreptomycinMycobacterium tuberculosis
Modification of the ribosome 16S rRNA point mutation AmikacinMycobacterium abscessus and Mycobacterium chelonae
Modification of the ribosome Methylation of the 16S rRNA by the enzyme rRNA methyltransferase (Rmt)AllGram negative bacilli
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