Table 2.
ANTIMICROBIAL | MECHANISMS OF RESISTANCE | ENZYME/GENE | LOCATION |
---|---|---|---|
Aminoglycosides | Target modifying enzymes | Aminoglycoside2- N –acetyltransferase and aminoglycosies phosphotransferasesa | |
Deoxystreptamine Aminoglycosides | Acquired resistance by point gene mutations | rrs gene encoding 16S rRNA protein | Mutations include T1406A, Cl409T, A1408G, and G1491T. b |
Beta Lactams | Antibiotic degrading enzymes | β-lactamase encoding genes. | Class A β-lactamase Bla_Mab (MAB_2875) |
Macrolides | Target modifying enzymes Acquired resistance by point gene mutations |
Functioning erythromycin ribosome methylase erm(41) gene rrl gene encoding 23S rRNA transferase |
Reversion to susceptibility: 274 bp deletion at positions 159- 432 and T28C point mutation.C
Point mutations at positions 2058 and 2059 |
Fluoroquinolones | Polymorphism in target genes | Nucleotide variation at the Quinolone resistance determining region in the DNA gyrase- GyrA – GyrBd | Ala-90 gyrA gene Arg-516 and Asp-533 gyrB gene |
Tetracyclines | Enzymatic inactivation | Flavin- adenine- dinucleotide (FAD)- inactivating monooxygenase (MabTetX) |
Twelve putative aminoglycoside phosphotransferases are encoded within the MABC genome, which could contribute to resistance to this group of antibiotics (Nessar et al., 2012; Luthra et al., 2018).
Mutations associated with aminoglycoside resistance (Ananta et al., 2018).
These mechanisms are associated with reversion to clarithromycin susceptibility (Nie et al., 2014; Zhu et al., 2015). A T28C point mutation (thymidine to cytosine polymorphism at the position 28) results in tryptophan to arginine amino acid change at codon 10, rendering a non-functional erm 41 gene (Pavan et al., 2017), C28 polymorphism is related to susceptibility (Luthra et al., 2018).
Quinolone resistance is associated with gyrA and gyrB mutations, a previous study showed all resistant isolates encoded the same amino acids in the quinolone resistance determining region (Kim et al., 2016).