Bacterial drug resistance
(This chapter has 4 pages)
© Kenneth Todar, PhD
Bacterial mechanisms of antibiotic resistance
Several mechanisms have evolved in bacteria which confer them with antibiotic resistance. These mechanisms can either chemically modify the antibiotic, render it inactive through physical removal from the cell, or modify target site so that it is not recognized by the antibiotic.
The most common mode is enzymatic inactivation of the antibiotic. An existing cellular enzyme is modified to react with the antibiotic in such a way that it no longer affects the microorganism. An alternative strategy utilized by many bacteria is the alteration of the antibiotic target site. These and other mechanisms are shown in the the figure and accompanying table below.
Three mechanisms of antibiotic resistance in bacteria. Most, but not all, resistance mechanisms are encoded by plasmids, which are potentially transmissible to other bacteria. Clockwise. 12 o'clock: Efflux pumps are high-affinity reverse transport systems located in the membrane that transport the antibiotic out of the cell. This is the mechanism of resistance to tetracycline. 4 o'clock: A specific enzyme modifies the antibiotic in a way that it loses its activity. In the case of streptomycin, the antibiotic is chemically modified so that it will no longer bind to the ribosome to block protein synthesis. 9 o'clock: An enzyme is produced that degrades the antibiotic, thereby inactivating it. For example, the penicillinases are a group of beta-lactamase enzymes that cleave the beta lactam ring of the penicillin molecule.
|Antibiotic||Method of resistance|
|Chloramphenicol||reduced uptake into cell|
|Tetracycline||active efflux from the cell|
|β-lactams, Erythromycin, Lincomycin||eliminates or reduces binding of antibiotic to cell target|
|β-lactams, Aminoglycosides, Chloramphenicol||enzymatic cleavage or modification to inactivate antibiotic molecule
|Sulfonamides, Trimethoprim||metabolic bypass of inhibited reaction|
|overproduction of antibiotic target (titration)|
The acquisition and spread of antibiotic resistance in bacteria
The development of resistance is inevitable following the introduction of a new antibiotic. Initial rates of resistance to new drugs are normally on the order of 1%. However, modern uses of antibiotics have caused a huge increase in the number of resistant bacteria. In fact, within 8-12 years after wide-spread use, strains resistant to multiple drugs become widespread. Multiple drug resistant strains of some bacteria have reached the proportion that virtually no antibiotics are available for treatment.
Antibiotic resistance in bacteria may be an inherent trait of the organism (e.g. a particular type of cell wall structure) that renders it naturally resistant, or it may be acquired by means of mutation in its own DNA or acquisition of resistance-conferring DNA from another source.
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