ATCvet code: QJ01EW11

Trimethoprim and sulfamethoxazole have a broad spectrum of activity against gram-positive and gram-negative bacteria including Streptococcus spp., Pasteurella multocida, Actinobacillus pleuropneumoniae, Haemophilus parasuis, Avibacterium paragallinarum and E. coli in vitro. Sulphonamides block the conversion of para-aminobenzoic acid to dihydrofolic acid. Its effect is bacteriostatic.

Trimethoprim inhibits dihydrofolic acid reductase, which converts dihydrofolic into tetrahydrofolic acid.

The effect of trimethoprim is bacteriostatic and in combination with sulphonamides it is bactericidal. Sulphonamides and trimethoprim thus cause a successive blockage to two enzymes that play an important role in the metabolism of bacteria and protozoa. Their effect is synergistic.

Bacterial resistance to trimethoprim and to sulphonamides can be mediated via 5 main mechanisms: (1) changes in the permeability barrier and/or efflux pumps, (2) naturally insensitive target enzymes, (3) changes in the target enzymes, (4) mutational or recombinational changes in the target enzymes, and (5) acquired resistance by drug-resistant target enzymes.

Following oral administration, trimethoprim and sulfamethoxazole are rapidly and almost completely absorbed from the gut. The bioavailability of sulfamethoxazole is slightly higher than that of trimethoprim. It is distributed to all tissues except the brain. The highest concentrations can be found in the lungs, the liver and the kidneys. Sulphonamides are metabolised in various ways. The degree of acetylation, hydroxylation and glucuronidation depends, among other things, on the species and age of the animal. Trimethoprim is metabolised to a large extent in the liver. Important metabolic pathways are O-methylation, N-oxidation in the ring structure and alpha hydroxylation. Sulfamethoxazole and trimethoprim are primarily excreted through the kidneys.

Trimethoprim is persistent in soils.