Different antibiotics have different ways of controlling the growth and spread of bacteria. The penicillins (amoxicillin, ampicillin, azlocillin, and piperacillin, for example) mostly prevent the cell walls of gram-negative bacteria from growing so the expanding intracellular contents cause the cell wall to break apart. Some members of this group also act on gram-positive bacteria.

The cephalosporins (cefaclor, cefazolin) inhibit bacterial cell wall synthesis; aminoglycosides (kanamycin, gentamicin) block bacterial protein synthesis; tetracyclines inhibit bacterial protein synthesis at the ribosomes; and the sulfonamides block the bacterial synthesis of folic acid. (2)

How do bacteria resist these drugs? They may produce enzymes that inactivate the drugs. Or, generations may arise that are able to close down the doorways through which the drugs once gained access. Or, they may even develop the power to pump antibiotics out of the intracellular environment before the drugs can exert their antibacterial effects. (3) These abilities can be passed on to successive generations of bacteria and even between different bacterial species.

Resistance genes commonly are carried on chromosomes and on tiny loops of DNA called plasmids. Plasmids can be transferred from one bacterium to another. Viruses also can transfer resistance genes. (3) Thus, bacteria are constantly evolving and changing. Their short lifespans, combined with their ability to shuffle genetic material back and forth like some microorganismic game of poker, would seem to give them the upper hand.

This ability of bacteria to mutate into antibiotic-resistant forms is causing infection control specialists to reassess how these drugs are used in community and hospital settings.

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