Antibiotic resistance
Resistance is the resistance of microorganisms to the action of antibiotics.
Primary resistance[edit | edit source]
It corresponds to the genetically determined insensitivity of bacteria to a given antibiotic , regardless of previous contact ( aminoglycosides in monotherapy do not affect anaerobic infections).
Secondary resistance[edit | edit source]
It occurs during therapy or as a result of previous antibiotic administration . In the presence of an antibiotic, resistant strains are found that are found in every large bacterial population. The rate at which secondary resistance develops depends on the frequency of mutations and the number of bacteria with a certain degree of resistance.
Secondary resistances also include those that are mediated by plasmids . We encounter them more often in G−bacteria. Genetic material can be transferred either from one microorganism to another by conjugation , bacteriophage transduction , or transformation , where genetic information is transferred by transposomes between plasmids or between plasmid and chromosome.
Resistance can then be divided into two basic types. Penicillin type (multiple step mutation) arises after long-term administration of some antibiotics - eg penicillin , chloramphenicol , bacitracin . Streptomycin type (one step mutation) with rapid emergence of highly resistant strains is known for streptomycin, erythromycin , lincomycin , rifampicin .
General mechanisms of resistance[edit | edit source]
- Limited penetration of the antibiotic into the bacterial cell.
- Alteration of the target structure - receptor (eg chromosomally mediated resistance of Haemophilus influenzae , which conditions the change of PBP protein).
- Metabolic changes in the bacterial cell that prevent the antibiotic from acting on the target structures.
- Enzymatic inhibition or inactivation of antibiotics such as beta-lactamase .
- Efflux pumps - substrate-specific transport mechanisms, arise from increased expression of outer membrane proteins. They actively eliminate xenobiotics from the bacterial cell. Some are responsible for cross-resistance (beta-lactams and fluoroquinolones).
| Antibiotic | Mechanisms of resistance |
|---|---|
| Beta-lactam |
beta-lactamase production reduction of cell wall permeability alteration of penicillin-binding proteins |
| Aminoglycosides and macrolides |
reduced ribosome binding reduction of cell wall permeability production of inactivating enzymes |
| Chloramphenicol |
reduction of binding to target ribosomes reduction of cell wall permeability increase in chloramphenicol acetyltransferase activity |
| Tetracyclines |
reduced transport to ribosomes active cellular efflux (excretion of antibiotic from the cell) |
| Quinolones |
DNA gyrase resistance reduction of cell wall permeability active cell efflux |
| Sulfonamides, Trimetoprim |
folic acid synthetase resistance dihydrofolic acid reductase resistance reduction of cell wall permeability |
Cross-resistance[edit | edit source]
Current insensitivity of microorganisms to antibiotics that have a similar chemical structure and the same mechanism of action.
Bilateral cross-type resistance means that resistance to one antibiotic also means resistance to the other antibiotic (penicillin G and V or tetracyclines to each other). A one-sided cross-type of resistance means that susceptibility to one type can be maintained (penicillin G-resistant staphylococci may not be resistant to methycilin, but MRSA are certainly penicillin-G resistant).
Links[edit | edit source]
[edit | edit source]
- Antibiotics
- Resistance of clinically important bacteria to ATB of choice
- Antibiotics in neonatology
- Bacterial resistance caused by the production of inactivating enzymes: beta lactam antibiotics, hyperproduction of beta lactamases, chromosomal, plasmid beta lactamases
- Resistance to macrolides and lincosamides (main causes of resistance, efflux)
- Beta-lactamase inhibitors
Source[edit | edit source]
- MARTÍNKOVÁ, J, S MIČUDA a J CERMANOVÁ. Antibiotika [online]. [cit. 2010-02-18]. <https://www.lfhk.cuni.cz/farmakol/predn/bak/kapitoly/atb-bak.doc/>.
Reference[edit | edit source]
- VOTAVA, Miroslav, et al. Lékařská mikrobiologie obecná. 2. vydání. Brno : Neptun, 2005. ISBN 80-86850-00-5.
- LINCOVÁ, Dagmar, et al. Základní a aplikovaná farmakologie. 1. vydání. GALÉN, 2002. ISBN 80-7262-168-8.
- MARTÍNKOVÁ, Jiřina, et al. Farmakologie pro studenty zdravotnických oborů. 2. vydání. Praha : Grada, 2018. ISBN 978-80-271-0929-6.
- ŠVIHOVEC, Jan, et al. Farmakologie. 1. vydání. Praha : Grada, 2018. ISBN 978-80-271-2150-2.
