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We get folic acid through diet but bacteria make their own supply
This folate pathway is very important in cell metabolism
This is the ‘selective toxicity’ target
They are competitive inhibitors, binding to intermediat intermediate e molecules in the folate pathway, preventing it from progressing further Sulphonamides and trimethoprim block different processes and so can be used together from increased efficacy (a sequential blockage) blockage)
Class: Aminoglycosides Examples: streptomyci streptomycin, n, gentamycin Why they work:
Form ionic bonds to the cell surface
Penetrate the membrane and diffuse into the cytoplasm
Bind to the ribosomes
Distorts the shape of the ribosome by binding between the 30s and 50s subunits, causing the misreading of the mRNA
The wrong tRNA comes in, resulting in a non-functional protein being synthesised
Must be injected, are kept for bad injections
Class: Tetracyclines Examples: tetracycline Why they work:
Prevent the attachment of the tRNA to the ribosome-mRNA complex
Prevents the addition of amino-acids to the peptide chain
They bind to calcium, and so aren’t used in children as they can build up in the
bones and teeth, causing a fault line
Example: Chloramphenicol Why they work:
Binds to the bacterial ribosome (blocking peptidyl transferase)
This prevents amino-acids from being added
Example: Erythromycin Why they work:
Stops the peptide bond from forming and prevents the translocation of the ribosome along the mRNA Often used for people who are allergic to penicillins
Example: Clindamycin Why they work:
Similar mechanism of action to erythromycin, binding to the 50s subunit and preventing the ribosomal translocation
Inhibit bacterial DNA gyrase enzyme This enzyme catalyses the introduction of the negative supercoil into the DNA, allowing transcription and translation Synthetic antibiotics recently introduced into clinical practice, the first products of rational drug design