respiratory tract, intestinal tract, urinary tract, and skeletal and soft tissues.

Nalidixic acid, which is a quinolone

but not a fluoroquinolone, is much less active and is used only for the treatment of urinary tract infections.
Fluoroquinolones should not be given to pregnant women and children under the age of 18 years because they
damage growing bone and cartilage.
The FDA has issued a warning regarding the possibility of Achilles tendonitis and tendon rupture associated
with fluoroquinolone use, especially in those over 60 years of age and in patients receiving corticosteroids, such
as prednisone. In view of this, the FDA recommends that fluoroquinolones not be used in the treatment of acute
sinusitis and uncomplicated urinary tract infections. Another important adverse effect of fluoroquinolones is
peripheral neuropathy, the symptoms of which include pain, burning, numbness, or tingling in the arms or legs.

3. Inhibition of mRNA Synthesis

Rifampin is used primarily for the treatment of tuberculosis in combination with other drugs and for
prophylaxis in close contacts of patients with meningitis caused by either N. meningitidis or H. influenzae. It is
also used in combination with other drugs in the treatment of prosthetic-valve endocarditis caused by S.
epidermidis. With the exception of the short-term prophylaxis of meningitis, rifampin is given in combination
with other drugs because resistant mutants appear at a high rate when it is used alone.
The selective mode of action of rifampin is based on blocking mRNA synthesis by bacterial RNA polymerase
without affecting the RNA polymerase of human cells. Rifampin is red, and the urine, saliva, and sweat of
patients taking rifampin often turn orange; this is disturbing but harmless. Rifampin is excreted in high
concentration in saliva, which accounts for its success in the prophylaxis of bacterial meningitis since the
organisms are carried in the throat.
Rifabutin, a rifampin derivative with
difference is that PABA has a carboxyl (COOH) group, whereas sulfanilamide has sulfonamide (SO 2NH2) group. B: Structure of
trimethoprim. C: Inhibition of the folic acid pathway by sulfonamide and trimethoprim. Sulfonamides inhibit the synthesis of
dihydrofolic acid (DHF) from its precursor PABA. Trimethoprim inhibits the synthesis of tetrahydrofolic acid (THF) from its
precursor DHF. Loss of THF inhibits DNA synthesis because THF is required to transfer a methyl group onto uracil to produce
thymidine, an essential component of DNA. (Adapted from Corcoran JW, Hahn FE, eds. Mechanism of Action of Antimicrobial Agents. Vol. 3 of
Antibiotics. Springer-Verlag; 1975.)Para-aminobenzoicacid(PABA)
+OthercomponentsCDihydropteroatesynthaseInhibitedbysulfonamideDihydrofolatereductaseInhibitedbytrimethoprimDihydrofolicacid(DHF
)Tetrahydrofolicacid(THF)COOHNH2NH2SO2NH2AH3COH2CNH2H2NNNOCH3OCH3BHNNFNOCOOH