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Aminoglycosides can cause inner ear toxicity which can result in sensorineural hearing loss. [19] The incidence of inner ear toxicity varies from 7 to 90%, depending on the types of antibiotics used, susceptibility of the patient to such antibiotics, and the duration of antibiotic administration. [20]
A classic example of this effect is the interaction between β-lactams, which damage the bacteria cell membrane, and aminoglycosides, which inhibit protein synthesis. [1] The damage dealt to the cell wall by β-lactams allows more aminoglycoside molecules to be taken up into the cell than would otherwise be possible, enhancing cell damage. [1]
Macrolides, [8] clindamycin [12] and aminoglycosides [7] (with all these three having other potential mechanisms of action as well), have evidence of inhibition of ribosomal translocation. Fusidic acid prevents the turnover of elongation factor G from the ribosome.
Narrow-spectrum antibiotics have low propensity to induce bacterial resistance and are less likely to disrupt the microbiome (normal microflora). [3] On the other hand, indiscriminate use of broad-spectrum antibiotics may not only induce the development of bacterial resistance and promote the emergency of multidrug-resistant organisms, but also cause off-target effects due to dysbiosis.
G418 (geneticin) is an aminoglycoside antibiotic similar in structure to gentamicin B1.It is produced by Micromonospora rhodorangea. [1] G418 blocks polypeptide synthesis by inhibiting the elongation step in both prokaryotic and eukaryotic cells. [1]
Streptothricins are a group of antibiotics in the aminoglycoside class. [1] The first antibiotic in the group was isolated from Streptomyces lavendulae in 1942. [2] It was later determined to be a mixture of closely-related compounds, and is now known as nourseothricin.
Cross-resistance can take place between compounds that are chemically similar, like antibiotics within similar and different classes. [9] That said, structural similarity is a weak predictor of antibiotic resistance, and does not predict antibiotic resistance at all when aminoglycosides are disregarded in the comparison.
Resistance to aminoglycosides is conferred via numerous mechanisms: aminoglycoside-modifying enzymes and inactivation of the aminoglycosides, which is frequently seen in both gram-positive and gram-negative bacteria and is induced by nucleotidyltransferases, phosphotransferases, or aminoglycoside acetyltransferases. reduced permeability.