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:

  1. Inhibiting cell wall synthesis: reduces the bacterial population by inhibiting the synthesis of the peptidoglycan cell wall.
  2. Inhibiting protein synthesis: inhibits the bacterial ribosome.
  3. 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.

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