Antibiotics
- Treating via annihilation of a pathogen without harming the host – toxic to the pathogen and
non-toxic to the host
- Ehrlich coined the term: maximally parasitotropic and minimally organotropic
- ‘antibiosis’ = ability of one organism to kill another – use bacteria to kill another and the
advantage of these chemicals
- Use antibiotics to describe any antibiotic and includes antimicrobial agents
- Strategy for antimicrobial action
- Exploit biochemical differences between parasite and host cell based on evolutionary
distinction
- Bacteria and Prokaryotes – no nuclei, no single chromosome, no histones
- No mitochondria
- Distinctive cell wall/plasma membrane – no sterol metabolism
- Class 1 reactions: simple reactions for life – same as humans as bacteria no use
- Class 2 reactions – building up further precursors, not many targets
- In the macromolecular synthesis, major differences that could be exploited
- E.g. folate metabolism
- Class 3 reactions: micromolecules e.g. polysaccharides, DNA, RNA
- 5 main exploitable differences; (1) peptidoglycans (2) bacterial membrane (3) DNA replication (4)
Protein Synthesis/ribosomes (5) respiratory e- transport chain
- Bactericidal antibiotics
- Kill the bacteria without killing the host – very good and useful, no immune function
- Bacteriostatic antibiotics
- Slow bacterial proliferation by lowering the ability of the microbes to divide
- At the therapeutic dose, immune system needs to aid, cell-mediated immune responses are
required
- Immunocompromised patients have more difficulty
- (1) Cell Wall Target
, - Cells are not good at controlling osmotic pressure – will continually take up water
- Proteoglycan cell wall to prevent this
- Types
- Gram-positive
- Gram stain violet
- Thick proteoglycan cell wall 5-50nm
- 50% peptidoglycan 45% acidic polymer
- Gram negative bacteria
- Not permeated by gram stain
- Thinner but more complex cell wall than gram
positive bacteria
- Lipopolysaccharide/proteoglycan composition
- Glucosamine and other sugars
- Have pore channels for solutes
- Lots of periplasmic space full of antimicrobial
agents
- Antigenic – cause immune reactions like fevers via the immune system
- Resistant to many antibiotics
- Causes these infections
- Septicaemia, wound infection, pneumonia, endocarditis neonate infection and
meningitis
- Gram Negative infections
- Respiratory tract infections, gonorrhoea, meningitis, typhoid, urinary infections
- Antibiotics that affect all types: known as extended antibiotics
- Cell wall target antibiotics
- Beta-lactams: Penicillin’s, Cephalosporins
- Vancomycin
- Polymyxins
- Anti-mycobacteria’s: leprosy, tuberculosis
- Penicillin: = product of mould from the bacteria genus Penicillium
- Fleming 1928: noticed on his petri dish, no bacteria growing around penicillin
- Cephalosporins work in a similar fashion
- ‘beta lactam chain’ – composed of dense amino acids
- Produce the lactam and thiazolidine ring
- = a penam ring
- Treating via annihilation of a pathogen without harming the host – toxic to the pathogen and
non-toxic to the host
- Ehrlich coined the term: maximally parasitotropic and minimally organotropic
- ‘antibiosis’ = ability of one organism to kill another – use bacteria to kill another and the
advantage of these chemicals
- Use antibiotics to describe any antibiotic and includes antimicrobial agents
- Strategy for antimicrobial action
- Exploit biochemical differences between parasite and host cell based on evolutionary
distinction
- Bacteria and Prokaryotes – no nuclei, no single chromosome, no histones
- No mitochondria
- Distinctive cell wall/plasma membrane – no sterol metabolism
- Class 1 reactions: simple reactions for life – same as humans as bacteria no use
- Class 2 reactions – building up further precursors, not many targets
- In the macromolecular synthesis, major differences that could be exploited
- E.g. folate metabolism
- Class 3 reactions: micromolecules e.g. polysaccharides, DNA, RNA
- 5 main exploitable differences; (1) peptidoglycans (2) bacterial membrane (3) DNA replication (4)
Protein Synthesis/ribosomes (5) respiratory e- transport chain
- Bactericidal antibiotics
- Kill the bacteria without killing the host – very good and useful, no immune function
- Bacteriostatic antibiotics
- Slow bacterial proliferation by lowering the ability of the microbes to divide
- At the therapeutic dose, immune system needs to aid, cell-mediated immune responses are
required
- Immunocompromised patients have more difficulty
- (1) Cell Wall Target
, - Cells are not good at controlling osmotic pressure – will continually take up water
- Proteoglycan cell wall to prevent this
- Types
- Gram-positive
- Gram stain violet
- Thick proteoglycan cell wall 5-50nm
- 50% peptidoglycan 45% acidic polymer
- Gram negative bacteria
- Not permeated by gram stain
- Thinner but more complex cell wall than gram
positive bacteria
- Lipopolysaccharide/proteoglycan composition
- Glucosamine and other sugars
- Have pore channels for solutes
- Lots of periplasmic space full of antimicrobial
agents
- Antigenic – cause immune reactions like fevers via the immune system
- Resistant to many antibiotics
- Causes these infections
- Septicaemia, wound infection, pneumonia, endocarditis neonate infection and
meningitis
- Gram Negative infections
- Respiratory tract infections, gonorrhoea, meningitis, typhoid, urinary infections
- Antibiotics that affect all types: known as extended antibiotics
- Cell wall target antibiotics
- Beta-lactams: Penicillin’s, Cephalosporins
- Vancomycin
- Polymyxins
- Anti-mycobacteria’s: leprosy, tuberculosis
- Penicillin: = product of mould from the bacteria genus Penicillium
- Fleming 1928: noticed on his petri dish, no bacteria growing around penicillin
- Cephalosporins work in a similar fashion
- ‘beta lactam chain’ – composed of dense amino acids
- Produce the lactam and thiazolidine ring
- = a penam ring
