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How did Ehrlich and Fleming contribute to the development of chemotherapy?
- Ehrlich: the "magic bullet" for syphilis
- -any useful drug must be selectively toxic to harm the MO's cells much more than the host's cells
- *MO must have a target that the host does not
- Fleming: discovered that mold let out a product that did not allow MO to grow
- -discovered penicillin
How did Domagk discover sulfa drugs and why are they not considered an antibiotic?
Domagk: created a red dye called Prontosil which killed bacteria, but no guinea pigs. This became a sulfa drug
* not considered an antibiotic because it is synthetic. instead it is antibmicrobial
- A chemical that kills or interferes with the growth of microorganisms and is produced by microbes
- -antibiotics have been around forever
- -the MOs that produce the antibiotic must have a resistance to it
What are some microorganisms that produce medically-useful antibiotics
- Bacillus (soil bacterium): bacitracin
- Streptomyces (soil bacterium): streptomycin
- Penicillin (mold/fungus): penicillin
What is selective toxicity? Why is this so significant for antibiotics?
- Selective toxicity means that it has a target on the Mo that the host does not have
- -hurts the MO way more than the host
- Fungi, protists, and helminths are eukaryotes so it is harder to be selectively toxic BUT
- -for bacteria, this is great because it has many selectively toxic targets as prokaryotes
(in order to stop a virus, you would have to stop transcription and that harms the host)
What are the advantages and disadvantages of broad spectrum antibiotics?
- Advantage: you don't need to know the specific MO, your're probably going to kill it
- -this can save some time and some $$$
you can kill the good stuff too and cause a super infection
What are the advantages and disadvantages of using a narrow antibiotic?
Advantage: you can kill that specific MO without harming other Flora
Disadvantage: you may pick the wrong one!
What is a superinfection and how does it occur?
- When a pathogenic/resistant MO takes over!
- -Occurs as a consequence of broad spectrum drug use
- -normal flora is killed while other can thrive
- -->normal flora normally out-competes the others
examples: candidiasis and C. difficile colitis
What is a "drug resistant bacterial strain"?
A strain of bacteria that does not respond to certain chemotherapy
What is the difference between innate resistance and acquired resistance?
- Innate Resistance: "expected resistance"
- -humans are innately resistant to antibiotics
- -Gram negative are innately resistant to penicillin
- Acquired resistance: "surprise resistance"
- -Ex: MRSA (Methicillin Resistant Staph Aureus)
- -the concentration of methicillin that kills MRSA is usually too high to put into the patient
What is the mode of the action for β-Lactam antibiotics?
- β-Lactam molecules bind to and inhibit the enzymes that make peptide crosslinks
- -works in vegetative cells
- -bacteria will form weak peptidoglycan resulting in cell lysis
*better known as the "cillins"
What is the mode of the action for tetracylines?
- Tetracycline molecules bind to and inhibit ribosomes
- -translation inhibitors: stops protein synthesis
What is the mode of the action for Quinolones?
- Quinolone molecules bind to and inhibit DNA Gyrase
- -bacterium cannot replicate its DNA
What is the mode of the action for Trimethoprim and sulfa drugs?
PABA (nutrient)-->Enz 1-->intermediate-->Enz 2--> Folic acid (Essential metabolite needed to build aas and nucleotide synthesis)
- -Sulfa molecules bind to and inhibit Enz 1 molecules
- -Trimethoprim molecules bind to and inhibit Enz 2 molecules
- -Bactrim: TMP + Sulfa in low doses
What makes β-Lactams selectively toxic?
Animal cells lack the enzymes that make peptide cross links as they do not have cell walls
What makes Tetracyclines selectively toxic?
Bacterial membranes are tetracyline permeable. Animal cell membranes are tetracycline impermeable
What makes Quinolones selectively toxic?
Bacterial gyrases have a significantly different structure from animal gyrases
What makes Trimethoprim and Sulfa drugs selectively toxic?
- Animal cells lack Enz 1 and Enz 2
- -animals get their folic acid in their food, whereas bacteria make it
What are the 4 common mechanisms of acquired drug resistance in bacteria?
- 1. acquired genes that code for β-lactamases
- -enzymes that destroy β lactam
- 2. acquired genes that code for rapid drug eflux pumps (RDEP)
- -spit the tetracyclines back out of the cell
- 3. acquired genes that code for abnormally tiny porins
- -not permeable to quinolones
- 4. acquired genes that code for mutant Enzyme 1 or 2
- -mutant enzymes work but stop TMP and Sulfa drugs from binding to it
What are some human practices that have caused populations of antibiotic resistance bacteria to increase?
- -unnecessary prescription of antibiotics
- -failure to take full course of antibiotics
- -use of antibiotics in animal feed
**humans are not the cause or creator of resistance, but definitely aide in making it more common
**the emergence of drug resistance is the inevitable consequence of drug use
How are humans trying to slow the spread of drug resistance in bacterial populations?
- -Use less antibiotics (only when necessary)
- -less in food products
- - more specific drug use
*by minimizing drug use, non-resistant strains can out compete the resistant ones once more