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University of Toronto St. George
Cell and Systems Biology
William Navarre

Lecture 32 5 1. at the beginning of WWII, if got infection, would die 2. by the end of WWII, penicillin was in production 3. 1 year after penicillin was made, resistant strains occurred 4. methicillin was made in response to penicillin resistance 5. 2 years later, MRSA 6. vancomycin made – very long shelflife 7. but many VISA now 6 8. a single superbug infection in Canada gets a headline in the news 9. represents the loss of our ability to control something we used to be able to control 10. (technology on the other hand is getting better) 8 11. antibiotics came out at the beginning of the 20 century 12. pre-antibiotics, drugs weren’t used by doctors – doctors killed ppl more often than helped ppl 13. in 1909, discovered salvarsan, was effective in the treatment of syphilis 1. has arsenic in it (highly toxic to ppl) 2. not the real first useful antibiotic 9 14. Prontosil Red, a leather staining agent could cure infections in rats 15. if he did this invitro in cell cultures, it would not have worked 16. this compound is broken down into 2 diff compounds (metabolized by host) to get the active preparation 11 17. folic acid is made by combinding two compounds together… 18. the enzyme dihydropeterosynthetase is not found in vertebrates 19. humans get folic acid from our diet, bc we don have a homologue of this enzyme 20. antibiotics selectively kill the microbe over the host 21. prontosil red had limited efficacy, had some side effects 14 22. penicillin was the miracle drug 23. saved more lives than other drugs 24. studied staph, left petri dishes out too long on bench, mold grew on plates, and noticed staph colonies growing close to mold died, those farther away didn’t 25. Fleming first reported it 15 26. these guys ramped up production of penicillin 27. penicillin was precious that it was recycled in urine 16 28. selective toxicity 1. best way is to target pathways that bacteria have, but we don’t 1. target cell wall synthesis (we don’t make PG) 2. LD50 is the lethal dose to kill the animal – want this measure to be high (want to give a mouse a lot of penicillin before it would die) 3. want the minimal inhibitory/lethal concentration – how effective the drug is against bacteria 1. use only a little 18 29. take a nutrient agar plate w bacterial lawn 30. take discs soaked in antibiotic 31. gets a zone of inhibition as the antibiotic diffuses out of the disk and into the surrounding media 19 32. diagnostic labs have streamlined this assay w other tests 33. E-test 1. when the bacteria touch the strip, you can read a number where you start to get inhibition 34. drugs must have at least this MIC in the tissue 35. there are many drugs that can kill bacteria but not humans in a test tube that are ineffective antibiotics bc they cant accumulate at high levels in the tissue, cant be absorbed in intestine 36. small ring of clearance means more resistant 20 37. target pathways unique to bacteria 38. sometimes target only bacteria but still may have side effects 39. favourable pharmacokinetics: 1. drug must be stable and survive in high conc 21 40. not all antibiotics have the same net result on the bacteria 22 41. a broad spectrum antibiotic has activity against a large number of diff bacteria 1. the broadest spectrum antibiotic kill virtually all bacteria 2. ex. penicillin (kills gm- & gm+) 42. a narrow spectrum antibiotic is more ideal for targeting a single pathogen or a subset of pathogens 24 43. best place to find a drug that would kill bacteria is to look at other bacteria and see what they are producing 44. vast majority of antibiotics used today come from secondary metabolites of only a few diff bacterial species 45. in particular, the species of actinomycetes 1. these are soil microbes that produce compounds that kill other bacteria 46. they found soil from all over the world and culture them and see if find anything 25
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