sulphonamideresistant

Sulphonamide resistance, also referred to as sulphonamideresistant, describes the ability of bacteria to survive or multiply in the presence of sulphonamide antibiotics, including sulfamethoxazole, sulfadiazine, and sulfisoxazole. It is a common form of antimicrobial resistance that can arise through chromosomal mutations or the acquisition of resistance genes, often carried on plasmids.

The principal mechanism involves changes to the target enzyme dihydropteroate synthase (DHPS) in the bacterial folate synthesis pathway, reducing drug binding. Other mechanisms include increased production of para-aminobenzoic acid (PABA), which competes with sulphonamides, decreased drug uptake, and active efflux of the drug. Resistance genes, such as sul1, sul2, and sul3,encode altered DHPS and are frequently responsible for these phenotypes.

These resistance genes are commonly located on mobile genetic elements like plasmids, transposons, and integrons, enabling rapid horizontal transfer between bacteria. They are often found alongside determinants for resistance to other antibiotic classes, contributing to multidrug resistance in clinical and environmental isolates.

Clinically, sulphonamide resistance reduces the effectiveness of sulphonamide-containing regimens, including the commonly used trimethoprim-sulfamethoxazole combination. Treatment choices rely on susceptibility testing and local resistance patterns. Agricultural and veterinary use of sulphonamides also contributes to the selection and spread of resistant strains through animal reservoirs and environmental routes.

Detection and surveillance typically use standard laboratory methods such as disk diffusion or minimum inhibitory concentration testing, interpreted according to guidelines from bodies like CLSI or EUCAST. Ongoing stewardship and surveillance are essential to monitor resistance trends and guide appropriate antibiotic use.