Vaccines, Antibiotics and Bacterial Resistance: Mechanisms of Action
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Vaccines and Immunity
Vaccine: inoculation of a dead virus (fragmented) or an attenuated system. It activates the immune response against dead or weakened pathogens.
Serum: contains specific antibodies, used in emergency cases.
Passive Immunity
Passive immunity is conferred by the inoculation of serum or by transfer of cells.
Active Immunity
Active immunity is produced by contact with a foreign antigen. Small antigen contact activates the immune system.
Antibiotics and Spectrum of Action
Some antibiotics act on only one type of bacteria, such as isoniazid, which acts on Mycobacterium.
Broad spectrum antibiotics act on many varieties of microorganisms, such as chloramphenicol and tetracycline.
Classification of Antibiotics
Antibiotics are classified by their mechanism of action:
- Inhibiting cell wall synthesis: reduces the bacterial population by inhibiting the synthesis of the peptidoglycan cell wall.
- Inhibiting protein synthesis: inhibits the bacterial ribosome.
- Inhibiting nucleic acid function: interferes with the function of DNA and RNA.
Inhibitors of Cell Wall Synthesis in Bacteria
Beta-lactams, including penicillins (natural and synthetic) and cephalosporins, are effective against Gram-positive bacteria. Their mechanism destroys the cell wall structure through the beta-lactam ring found in cephalosporins and penicillins.
Penicillin binds to penicillin-binding proteins (PBPs), which are receptors that inhibit the formation of peptidoglycan. This prevents the cell wall from forming, resulting in bacterial death.
Action of Beta-Lactams
Beta-lactams inactivate bacterial enzymes such as penicillinases. Combining penicillin with a beta-lactamase inhibitor blocks the enzyme, preserving the effect of the antibiotic.
Inhibitors of Protein Synthesis
Macrolides and tetracyclines bind to bacterial ribosomes, inhibiting protein synthesis. As a result, bacteria are unable to multiply. These are broad-spectrum, bacteriostatic drugs.
Inhibitors of Nucleic Acid Function
- Quinolones: inhibit enzymes required to replicate new DNA, preventing bacterial growth.
- Sulfonamides: inhibit enzymes involved in bacterial metabolism, reducing bacterial multiplication.
Antibiotic Resistance
a) Chromosomal mutation: the bacterium undergoes a genetic change in its own DNA. For example, the bacterium becomes impermeable to the antibiotic, or produces an enzyme that destroys the drug, or alters its metabolic target, or creates an efflux mechanism that pumps the antibiotic out.
b) Acquisition of plasmids: bacteria exchange plasmids carrying genetic information that codes for drug-inactivating enzymes, efflux pumps, or uptake-blocking mechanisms that prevent drugs from entering the cell.
Beta-Lactam Resistance
Resistance arises through plasmid acquisition and chromosomal mutation. Bacteria produce beta-lactamase, an enzyme that chemically destroys the antibiotic, rendering it inactive.
Tetracycline Resistance
Resistance arises through plasmid acquisition. Bacteria begin producing efflux enzymes (TET) that pump the antibiotic out of the cell.
Chloramphenicol Resistance
Bacteria produce an enzyme that alters the chemical structure of the drug, reducing its affinity for its target.
Erythromycin Resistance
Resistance arises through chromosomal mutation. The bacteria begin producing altered ribosomes, so the antibiotic no longer recognizes its target and loses its effect.
Quinolone Resistance
Resistance occurs through chromosomal (DNA) mutation. Bacteria begin producing modified enzymes, so the antibiotic no longer recognizes the enzyme it targets.