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Antibiotics are derived from living organism but are usually improved by chemical processes.
They can be divided into two groups: Bacteriostatic ( stops bacteria growth) and bactericidal
(kills bacteria)
They affect some aspect of growth or metabolism of the target bacterium by:
- interfering with the synthesis of bacterial cell walls (penicillin, cephalosporin, vancomycin)
Bacterial cell walls are made of peptidoglycans (long molecules containing peptides and
sugars, held together by cross-links between them). Penicillin prevents the cross-links
between them from forming by inhibiting the enzyme that makes cross-links.
So, when the cell walls expand during growth and enzymes called autolysins make holes in
the cell wall to allow for this expansion (stretching) the cell wall becomes progressively
weaker until it bursts due to the osmotic pressure.
Our cells have no cell walls so penicillin does not damage our cells. It also does not affect
viruses (no cells).
- affecting the activity or proteins in the cell surface membrane.
- affecting enzyme action.
- interfering with DNA synthesis (quinolones)
- interfering with protein synthesis (chloramphenicol, erythromycin, tetracycline, streptomycin,
rifampicin (transcription inhibitor))
- Eukaryotic cells have different cell surface proteins than bacteria so they are also not affected
by antibiotics.
Antibiotic resistance:
- Features which help cause resistance include:
Thick cell walls cause the bacterial cell walls to be less permeable.
The bacterium may contain a gene which codes for an enzyme that catalyses the
breakdown of penicillin (above two are reasons why penicillin has no effect on M.
tuberculosis).
Proteins in the membranes of bacteria can inactivate antibiotics so they have no effect.
Bacterial membranes can have proteins that pump out antibiotics if they enter the
cytoplasm.
Antibiotics may simply not be able to bind to the intended site of action.
- Bacteria sensitive to an antibiotic are called susceptible.