1. The sulfonamides are structurally similar to PABA, a substrate in bacterial folate synthesis.
  1. Competes with PABA for folate production in bacteria and therefore reduces purine and DNA synthesis (see above picture)
  2. Inhibits both Gram+ve and Gram-ve bacteria
    • Active against chlamydia, E.coli, Klebsiella, Shigella and Salmonella.
    • Note that pseudomonas is intrinsically resistant
    • Rickettsial growth is actually enhanced by sulfonamides.
    • Remember that the sulfonamides have synergy with trimethoprim due to the sequential inactivation of folate production. Therefore, indications are as follows:
      1. Bactrim – treat PCP pneumonia
      2. Sulfadiazine/pyrimethamine – Toxoplasmosis
      3. Sulfasalazine alone – Ulcerative colitis, IBD
      4. Topical sulfonamides – bacterial conjunctivitis and burns
  3. Resistance is usually plasmid encoded. It is due to:
    • Increased production of PABA
    • Production of a folic acid enzyme that is low in affinity for sulfonamides
    • Impaired permeability to sulfonamides
  1. PO
  1. Well absorbed from GIT and distributed widely to tissues, including CNS.
  1. Hepatic
  1. Urinary – reduce dose in renal failure.
Adverse events
  1. All sulfur based drugs (diuretics, diazoxide, sulfonoureas, hypoglycaemics and antimicrobials) are cross allergic.
  2. Most serious (but rare) complication is Steven-Johnsons syndrome.
  3. May cause haemolytic anaemic, granulocytosis or leukemoid reactions.
  4. Increased risk of kernicterus
Withdrawal syndrome  
Special notes