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Antibiotics and Resistance
Antibiotics and Resistance
Selective Toxicity
Early treatments for infections were often more harmful than the disease itself.
Paul Ehrlich introduced the concept of a 'magic bullet' to kill microbial cells without harming the host.
Selective toxicity targets bacterial cells while minimizing harm to host cells.
Penicillin
Alexander Fleming discovered penicillin in 1928, observing its ability to destroy Staphylococcus bacteria.
Penicillin inhibits bacterial cell wall formation by interfering with peptidoglycan cross-links.
Antibiotic Targets
Antibiotics target various bacterial cell components:
Cell wall synthesis (e.g., penicillins)
Protein synthesis (e.g., aminoglycosides)
Cell membrane function (e.g., polymyxins)
Nucleic acid synthesis (e.g., quinolones)
Antibiotic Resistance Mechanisms
Mutations lead to genetic diversity, causing antibiotic resistance.
Bacteria resist antibiotics through:
Enzyme inactivation (e.g., beta-lactamase).
Reduced drug accumulation.
Altered target affinity.
Beta-Lactamase
Beta-lactamase is an enzyme that destroys penicillin by breaking the β-lactam ring.
Gene Transfer
Horizontal gene transfer contributes to antibiotic resistance through:
Transformation
Transduction
Conjugation
Reducing Antibiotic Resistance
Strategies to reduce antibiotic resistance include:
Decreasing antibiotic utilization.
Improving hygiene and infrastructure.
Enhancing diagnostics.
Identifying new drug targets.
Using combination therapies.
Antibiotic Usage Statistics
80% of antibiotics are given to livestock to promote growth and prevent diseases.
50% of antibiotics prescribed to humans are unnecessary or inappropriately used.
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