L34: Antibiotics

• selective toxicity

  Early treatments for infectious diseases (like syphilis) involved the use of highly toxic 'medicines' more harmful than the actual disease
• Selective toxicity

  Paul ehrlich notes some dyes stained microbes better than host cells. He came up with the idea of a chemical magic bullet
• In 1928, Alexander Fleming observed that colonies of the bacterium Staphylococcus bacteria could be destroyed by the mold Penicillium notatum
• Penicillium label

  A) normal colony

  B) antibiotic

  C) affected zone

  
• Penicillin interferes with the normal formation of the bacterial cell wall by inhibiting the formation of peptidoglycan cross-links (peptide cross bridge)
• penicillin g

  A) Acyl side-chain

  B) Thiazolidine

  C) B-lactam

  
• bacterial cell components affected by different classes of antibiotics

  1. Inhibition of cell wall synthesis
  2. Inhibition of protein synthesis
  3. Disruption of cytoplasmic membrane
  4. Inhibition of general metabolic pathway
  5. inhibition of DNA or RNA synthesis
  6. inhibition of pathogens attachment or entry into host cell
• Mutations are the most important cause of genetic diversity in microbial populations
• By having a selection of Mutants:

  We have a proportion of bacterial population gains resistance to the Antibiotic by mutation. Some bacteria with the resistance survive. The bacteria with the resistance multiply, passing on the resistant trait. Then the resistant bacterial populations survive subsequent encounters with the Antibiotic
• Beta lactamase is an enzyme produced by bacteria and used to destroy penicillin
• B-lactamase breaks a bond in the B-lactam ring of penicllin to disable the molcule. Bacteria with this enzyme can resist the effects of penicillin and other B-lactam antibiotics
• We can reduce the spread of antibiotic resistance by decreasing the antibiotic utilisation, improve diagnostics, identify new targets and combination therapies