Table 2.

Mechanism responsible for MABC antimicrobial resistance.

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)

^aTwelve 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).

^bMutations associated with aminoglycoside resistance (Ananta et al., 2018).

^cThese 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).

^dQuinolone 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).