Table 1.

Mode of action, mechanisms of resistance of antibiotics and some antimicrobial resistance genes (ARG) of animal origin.

Family	Mode of action	Mechanism of resistance	Resistant gene	Locationa	Reference
β-lactams	Cell wall synthesis inhibitors. Binds transpeptidase also known as penicillin binding proteins (PBPs) that help form peptidoglycan	Beta-lactamase production primarily-bla genes	mecC (mecALGA251) mecA blaZ	C C	(83, 86, 87)
	Inactivates the enzyme; beta-lactamase	Expression of alternative PBPs		Tn, P, C
β-lactamase inhibitors	Hydrolysis of the beta-lactam ring	Production of extended spectrum beta-lactamases (ESBLs)	blaSHV blaTEM	P, C P, C
Fluoroquinolones	Binds DNA-gyrase or topoisomerase II and topoisomerase IV; enzymes needed for supercoiling, replication and separation of circular bacterial DNA.	Target modification Decreased membrane permeability Efflux pumps	qnrA qnrB qnrS 9, 10	P P P	(85, 88)
Macrolides, Licosamides and Streptogamin (MLS)	Binds the bacterial 50 S ribosomal subunits; inhibit protein synthesis	Target site modification	ermA, (ermB), ermC, ermF, ermT, erm (73) erm (83)	C, Tn, P, (Tn,P) P, C P, P C	(89, 90)
		Active drug efflux	msr (A) except lincosamides	C, P
Aminoglycosides	Bind to the bacterial 30 S ribosomal subunit thus inhibit bacterial protein synthesis	Target site modification [via the action of 16 S rRNA methyltransferases (RMTs)]			(89, 91, 92)
		Enzymatic drug modification (adenylation, acetylation and phosphorylation)	aacA-aphD aadD	Tn, P, C P, C
		Efflux systems	aadE str	Tn, P P
Tetracyclines	Bind reversibly to the 30 S ribosomal subunit as such blocks the binding of the aminoacyl-tRNA to the acceptor site on the mRNA-ribosome complex	Efflux systems Target modification Inactivating enzymes Ribosomal protection	Tet (K), tet (K) Tet (M), tet (O)	P Tn/C, C	(93, 94)
Sulfonamides (Folate pathway inhibitors)	Inhibit the bacterial enzyme dihydropteroate synthetase (DPS) in the folic acid pathway, thereby blocking bacterial nucleic acid synthesis	Excessive bacterial production of dihydrofolate reductase (DHFR) Reduction in the ability of the drug to penetrate the bacterial cell wall Production of altered forms of the dihydropteroate synthetase (DPS) enzyme with a lower affinity for sulfonamides Hyperproduction of PABA, which overcomes the competitive substitution of the sulfonamides	sul1 sul2 sul3	P, C	(95–97)

^aC, chromosomal DNA; P, plasmid; Tn, transposon.