The strongest resistance of Staphylococcus aureus to erythromycin is caused by decreasing uptake of the antibiotic into the cells

Abstract

The consequence of excessive use of macrolides is a high occurrence of mechanisms responsible for resistance to these drugs. Of 97 erythromycinresistant bacterial strains gathered in the Wrocław area in Poland, 60% exhibited very high resistance, and those with the inducible MLS B (macrolidelincosamide-streptogramin B) resistance phenotype predominated. Direct genetic investigation revealed that the erm genes coding for ribosomal methylases are the most frequently occurring erythromycin resistance-determining genes. No genetic resistance determinant was detected in 13% of the erythromycin-resistant strains. The efflux mechanism occurs in strains isolated from the nasopharyngeal cavity twice as often as in those isolated from other material, where the mechanism connected with target site modification predominates. Measurements of radiolabelled antibiotic accumulation inside bacterial cells revealed that in highly resistant strains (MIC > 1024 g/ml), an important factor responsible for the resistance is the permeability barrier at the cell wall level. This would be a hitherto unknown mechanism of resistance to erythromycin in Staphylococcus aureus.

Effects of Chlorophyll-Derived Efflux Pump Inhibitor Pheophorbideaand Pyropheophorbideaon Growth and Macrolide Antibiotic Resistance of Indicator and Anaerobic Swine Manure Bacteria

“…High-level resistance to erythromycin can be predominant among S. aureus strains in individual studies (approx. 60% of strains with MIC > 1024 g mL −1 [89]), but, generally it is rare (approx. 3% of strains with MICs ≥ 512 g mL −1 according to EUCAST [78]).…”

ErmF and ereD Are Responsible for Erythromycin Resistance in Riemerella anatipestifer

“…Erythromycin susceptibility tests for each strain were performed in 96-well microtitre plates (Corning Incorporated, Corning, NY, USA) by determination of the minimum inhibitory concentration (MIC) value of erythromycin, as described previously [ 5 ]. E .…”

“…Three major mechanisms of erythromycin resistance have been identified in Gram-negative and-positive bacteria [ 5 , 6 ]. The most well-known mechanism is the target-site modification of the 50S ribosomal subunit, which is mainly mediated by methylases encoded by the erythromycin ribosomal methylase (erm) gene and this methylation also causes resistance to lincosamides and streptogramin B antibiotics (MLS) [ 7 ].…”

“…The second described mechanism is the synthesis and activity of erythromycin inactivating enzymes, such as erythromycin esterase [ 8 , 9 ]. The third known cause of erythromycin resistance is the active removal of the antibiotic by efflux systems, which maintains the intracellular antibiotic concentration at a subtoxic level that does not affect bacterial cell growth [ 5 , 10 ].…”

Clindamycin Resistance among Methicillin Resistant <i>Staphylococcus aureus</i> Isolated from Human and Respective Household Swine in Greater Kabale Region—South Western Uganda

“…The expression of clindamycin resistance in Staphylococcus species can be constitutive or inducible [9] [10] through erm genes which codes for ribosomal methylases [11]. In addition, the resistance to the lincosamides (clindamycin), macrolides (erythromycin), and streptogramins (quinupristin/dalfopristin) is facilitated by three related genes, ermA, ermB, and ermC, that encode for erythromycin resistance methylases [12]. Methylase enzymes binds on to the ribosome resulting in a conformational change or modification in the ribosomal target and consequently, decreasing the ability of these drugs to bind to the ribosome [5] [13].…”