Quinolones -- Nalidixic Acid and Cinoxacin -- These agents are older and typically less effective due to narrow spectrum of activity and increased resistance to their actions.
Fluoroquinolones (FQ) -- Ciprofloxacin, Ofloxacin, Norfloxacin, Lomefloxacin, Enoxacin, Levofloxacin, and (Ala)Trovafloxacin.

Mechanism of Action -- In the process of normal cell division and DNA replication/transcription, DNA must separate to expose the relevant portion of the strand (the portion to be copied).  If this were to occur in stranded DNA, supercoiling or tension would be created within the helix.  This is avoided by the action of an enzyme, DNA gyrase, which cuts the DNA allowing un-coiling for transcription/replication.  The DNA gyrase then also acts to snip portions of the un-coiled DNA, where portions are re-inserted and rejoined, once again by DNA gyrase.  The quinolone and FQ antibiotics inhibit the action of DNA gyrase.  (NOTE that a similar enzyme in mammals, topoisomerase II, is NOT inhibited by these drugs except at extremely high concentrations.)

Spectrum -- These agents are bactericidal against E. coli and some spp. of Salmonella, Shigella, Enterobacter, Campylobacter, Neisseria, Chlamydia, Mycoplasma, Legionella, Mycobacterium, and Brucella (undulant fever and contagious abortion in cattle).

Therapeutic Uses -- The FQ are used in UTI, prostatitis, STDs (sexually transmitted diseases, except syphilis, Treponema spp.), GI infections, RTI, and infections of bone, joints, and soft tissues.

Adverse Effects -- GI upset, headache, dizziness, and rarely -- hallucinations, seizures, delerium.  The FQ may also cause arthropathy in children, characterised by joint swelling and pain.  They may also have teratogenic effects of a similar nature and are therefore contraindicated during pregnancy.  A slight risk of hepatotoxicity associated with the use of trovafloxacin has recently been reported by the FDA.  Subsequently, its use has been limited to initial in-patient prescription with out-patient therapy following, if there is no evidence of elevated liver enzymes.

Nitrofurantoin
Mechanism of Action -- Decreases DNA function, inhibiting bacterial protein synthesis and replication.  Resistance is rare.

Therapeutics -- May be used for the treatment of acute UTI or for the prevention of UTI in patients with recurrant infections.

Adverse Effects -- Nausea, vomiting, diarrhea, renal calculi -- patients should drink copious amounts of water.

Methenamine
Mechanism of Action -- A urinary antiseptic, by the metabolites formaldehyde and ammonia.

Therapeutics -- Primarily used for chronic suppression of UTI in patients with recurrent infections.

Adverse Effects -- May turn the urine blue to blue-green in colour.  May cause crystalluria and stone formation.

Phenazopyridine
Mechanism of Action -- Urinary antiseptic and analgesic (presumably through some action on PG synthesis or function).

Therapeutics -- Primarily used for its analgesic effects in the treatment of acute UTI.

Adverse Effects -- May cause GI upset and discolour the urine a reddish-orange.  Overdose may cause methæmoglobinæmia.

Mechanism of Action -- Many bacteria are unable to take up exogenous folic acid.  Therefore, they are required to synthesise their own supply to folate to contribute to DNA synthesis (refer to section on Anæmias for a discussion of the role folate plays).  Bacterial folate synthesis occurs by the following scheme:

The sulphonamides are analogues of p-aminobenzoic acid, and as such, inhibit the enzyme dihydropteroate synthase.  Trimethoprim inhibits the enzyme dihydrofolate (DHF) reductase.  Both of these actions will result in inhibition of THF (tetrahydrofolate) synthesis, thus decreasing DNA synthesis.  Mammalian cells do not synthesis folate, consequently the sulphonamides have no effect in humans.  Trimethoprim shows selectivity for bacterial DHF reductase at low doses, although some inhibition may occur at high doses.

Spectrum -- These agents are effective against those organisms that must synthesise folic acid, including Streptococcus pyogenes and pneumoniæ, H. flu, Chlamydia, and E. coli.

Therapeutics --

Oral sulphonamides (sulfisoxazole, suphamethoxazole, sulphadiazine, and sulphadoxine) are used in the treatment of UTI, OM,  and infections of Toxoplasma gondii.  Sulphadoxine may also be used in the treatment of malaria.

Topical sulphonamides include silver sulphadiazine (burns) and sulphacetamide (ophthalmic infections).

Trimethoprim is used almost exclusively in combination with a sulphonamide.  The combination results in synergistic activity and is often seen in the treatment of UTI, RTI, OM, and Pneumocystis pneumonia.

Adverse Effects -- Crystalluria (especially if the patient is dehydrated), aplastic anæmia, hæmolytic anæmia, agranulocytosis, other blood dyscrasias, Steven-Johnson Syndrome, and GI upset.  Hypersensitivity and photosenstivity may also be seen with the sulphonamides.  Typically,  patients who are sensitive to the sulphonamides are also sensitive to PABA.  Therefore, they should use PABA-free sunblocks to reduce the risk of photosensitive reactions.