Several antimicrobials act by inhibiting the synthesis of nucleic acids (rifamycins, sulfamides, diaminopyridines), modifying their conformation (quinolones, coumarins) or causing irreversible lesions (nitroimidazoles, nitrofurans). The resistance mechanisms are: a reduction in intracytoplasmic accumulation, modification of the target or the production of a new low-affinity target and, more rarely, enzyme inactivation. Although the mechanisms affecting the targets are specific to each family and can lead to high-level resistance, the reduced permeability of the membrane and the increased efflux are non-specific and result in low-level cross-resistance between several families. The genetic mediation is usually chromosomal for rifamycins and quinolones, although plasmid-mediated resistant genes have been observed. On the other hand, for sulfamides and trimethoprim, plasmid-borne genes are frequent. Resistance to nitroimidazoles and nitrofurans is still not widely understood.