Table 2.

Antimicrobial resistance mechanisms in Campylobacter (Lynch et al. (2020); Liu et al. (2019))

Antibiotic classes in use against Campylobacter	Resistance mechanism of Campylobacter
Aminoglycosides	Modification by aminoglycoside-modifying enzymes (AphA, AadE, Aad9, Sat, Hph, AacA4, Aac3, Aph(2″)-If (formerly designated as AacA4/AphD), Aph(2″)-Ib, -Ic, -Ig, -If, -If1, -If3, -Ih, Aac(6′)Ie/Aph(2″)-Ia, Aac(6´)Ie/Aph(2″)-If2)
β-Lactams	Enzymatic inactivation by β-lactamases (penicillinase, BlaOXA-61) Reduced membrane permeability through the major outer membrane protein (MOMP) Efflux via CmeABC transporter
Fluoroquinolones	Modification of GyrA (T86I, T86K, T86A, T86V, D90N, D90Y, A70T, also in combination e.g.T86I/P104S, T86I/D90N) Efflux via CmeABC transporter
Macrolides	Point mutations in 23S rRNA genes Mutations in the L4/L22 ribosomal proteins Methylation by Erm(B)rRNA methyl transferase Efflux via CmeABC transporter Reduced membrane permeability due to MOMP
Tetracyclines	Ribosomal protection by binding of TetO or TetO mosaic resistance determinants (e.g., TetO/32/O) Efflux via CmeABC and CmeG transporters
Organoarsenicals	Efflux via ArsP (methylarsenite efflux permease)
Fosfomycin	fosXCC
Multiple drug resistance	CmeABC efflux system (significant role in acquired and intrinsic resistance) Re-CmeABC (variant of CmeABC which confers significantly higher levels of resistance) CmeDEF efflux system (moderate role in intrinsic resistance) CfrC (rRNA methyl transferase) Multidrug resistance genomic islands (MDRGIs)