How do antibiotics work?
Antibiotics for clinical use are usually divided into object drugs (antibiotics of choices) and relief medications (reserve antibiotics). Antibiotics of choices are drugs that have an optimal benefit-risk profile and from which the treatment is initiated before determining the sensitivity of the microorganisms that caused the disease.
Reserve antibiotics are used in case of resistance of microorganisms to antibiotics of choice or when the patient is intolerant to antibiotics of choices. Reserve antibiotics usually have less activity. They have more pronounced side effects, greater toxicity. Also, resistance to such antibiotics develops rapidly.
Antibiotics by level of efficiency in the anti-bacterial therapy are divided into antibiotics I, II, III, IV generations. Generations of antibiotics differ among themselves in the effectiveness of exposure to bacterial cells. In clinical practice, the interval of appearance of new class of antibiotics is usually every 10 years. First of all, this is due to the fact that during this time resistant microorganism strains are produced for old antibiotics. However, this separation of antibiotics into generations is not always associated with the lead time of new drugs into the treatment practice.
The action of antibiotic at the cellular level can be:
- Bacteriostatic (antibiotic blocks the replication and division of cells and does not cause their death. Cells retain the ability to grow and multiply if the antibiotic is removed);
- Bactericidal (antibiotic kills bacterial cells).
Bactericidal antibiotic has germ-kill effect since it acts on subcellular structures irreversibly disrupting their integrity and/or function. In this case, the antibiotic, because of its high affinity, binds to the enzyme or cellular structures necessary to maintain the viability of the cell, which is practically irreversible. In this case, antibiotic binds to the enzyme or subcellular structures which is necessary to maintain the viability of the cell and almost irreversibly kills them.
Bacteriostatic antibiotics also interact with subcellular structures, but they have less effect on them. Bacterial cells become active again when the patient stops to take these antibiotics.
The cell wall of most bacterial cells is thin, elastic and rigid. It protects the microbial cell from external influences and determines the shape of the microorganism.
Simultaneously, the cell wall maintains the constancy of the internal environment and protects the cell from destruction at high intracellular osmotic pressure.
Through the cell wall there is transport of nutrients into the cell and the release of metabolites. Structures and compositions of cell wall elements are different. This made it possible to differentiate microorganisms into gram-positive and gram-negative microorganisms.
Antibiotics by the mechanism of action are divided into:
- inhibitors of synthesis of microbial wall components or activators of enzymes that destroy cell wall (penicillins, cephalosporins, monobactams, carbapenems);
- drugs which disturbing the structure and function of cytoplasmic membranes of bacterial cells (polymyxins, polyene antibiotics);
- inhibitors of RNA synthesis at the level of RNA polymerase (rifamycins, griseofulvin);
- inhibitors of protein production at the level of ribosomes (bactericidal – aminoglycosides; bacteriostatic – chloramphenicol, tetracycline, fucidin, lincomycin, macrolides).