Antibiotic Resistance
Antibiotic resistance is the general process in which bacteria - usually infectious - becomes insensitive to a specific drug or a specific class of drugs.
Antibiotic resistance usually appears when a microbe is exposed to sub-lethal concentrations of a specific antibiotic: due to the selective pressure, the surviving microbes might develop resistance mechanisms across several generations through mutations in their DNA.
These resistance mechanisms can be sorted into four categories:
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The modification of the primary target of the antibiotic, such as the transpeptidase for ampicillin resistance
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The inactivation of the antibiotic compound itself, such as the production of B-lactamase enzymes to degrade penicillin G inside the cell.
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Preventing the antibiotic from reaching the target, by reducing the permeability of the membrane or using efflux pumps to keep the drug outside the cell, as observed against ciprofloxacin for example.
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Using alternative metabolic pathways to compensate for the action of the antibiotic and ensure the survival of the organism.
A particular concern is the transmission of these drug resistance across species: a drug-resistant bacterial strain can transfer the resistance gene to other strains of the same species - or to individuals of a different species altogether - that have never been exposed to the drug in the first place. This way, antibiotic resistance can spread widely and compromise whole antibiotic therapies.
The accumulation of antibiotic resistance genes leads to the creation of "superbugs" – bacterial strains that are immune to all but the most drastic treatments.
To overcome antibiotic resistance, the current strategies are to discover new antibiotics with novel modes of actions or to use different antibiotics in "cocktails" – presuming that a bacteria might survive facing one, but not two or three antibiotics simultaneously.
In the laboratory, antibiotic resistance genes are an important tool for genetic engineering to select for transformed cells.