Sulfadimethoxine has been demonstrated clinically or in the laboratory to be effective against a variety of organisms, such as streptococci, klebsiella, proteus, shigella, staphylococci, escherichia, and salmonella.1,2 These organisms have been demonstrated in respiratory, genitourinary, enteric, and soft tissue infections of dogs and cats.
The systemic sulfonamides which include sulfadimethoxine are bacteriostatic agents. Sulfonamides competitively inhibit bacterial synthesis of folic acid (pteroylglutamic acid) from para-aminobenzoic acid. Mammalian cells are capable of utilizing folic acid in the presence of sulfonamides.
The tissue distribution of sulfadimethoxine, as with all sulfonamides, is a function of plasma levels, degree of plasma protein binding, and subsequent passive distribution in the tissues of the lipid-soluble un-ionized form. The relative amounts are determined by both its pKa and by the pH of each tissue. Therefore, levels tend to be higher in less acid tissue and body fluids or those diseased tissues having high concentrations of leucocytes.2
In the dog, sulfadimethoxine is not acetylated as in most other animals, and it is excreted predominantly as the unchanged drug.3 Sulfadimethoxine has a relatively high solubility at the pH normally occurring in the kidney, precluding the possibility of precipitation and crystalluria. Slow renal excretion results from a high degree of tubular reabsorption,4 and plasma protein binding is very high, providing a blood reservoir of the drug. Thus, sulfadimethoxine maintains higher blood levels than most other long-acting sulfonamides. Single, comparatively low doses of Albon give rapid and sustained therapeutic blood levels.1
To assure successful sulfonamide therapy (1) the drug must be given early in the course of the disease, and it must produce a high sulfonamide level in the body rapidly after administration, (2) therapeutically effective sulfonamide levels must be maintained in the body throughout the treatment period, (3) treatment should continue for a short period of time after the clinical signs have disappeared, and (4) the causative organisms must be sensitive to this class of drugs.