Module 15 Flashcards
Why do microbes make antibiotics?
Competitive edge with food sources, resources, and space
What two characteristics are essential for an effective antibiotic?
Selective toxicity- harm the microbe nit the host
Target has to be essential
What is selective toxicity?
This means to harm the microbe and not the human host
Which organisms are the easiest to fight, and why? Which organisms are harder to fight, and why? Which organism is the hardest to fight, and why?
Easiest= Gram +=thick cell wall
Gram +
Gram - =outer membrane
Fungi= eukaryote
Intracellular bacteria=inside human cells
Hardest= Viruses=take over and use human cells
What was the first antibiotic discovered? Who discovered it
Penicillin in 1929 by Alexander Fleming.
Specifically, how does the first antibiotic discovered function (what does it stop?).
Active against growing cells only and stops their cell wall synthesis.
Doesn’t hurt humans because of structure differences. Human cells have no peptidoglycan cell wall-the drug specifically targets cell walls
Does this antibiotic (first discovered) work better on Gm+ or Gm-? Why?
Gram + because they have a thick cell wall with no outer membrane while Gm- has an outer membrane lipid layer that it can not penetrate
Within the last 50 years several species of bacteria were not adequately killed by the antibiotic, why? What did scientists do about it? What was the outcome?
The bacteria developed resistance to the antibiotic and so a larger dose was used. We are now to the point where penicillin is not used to treat certain bacteria because the dose is high enough that it would hurt the human host as well.
How does a bacteriostatic antibiotic differ from a bacteriocidal one?
Bacteriostatic stops bacteria from growing and dividing so that the immune system can take over while bactericidal kills the bacteria
How does a broad-spectrum antibiotic differ from a narrow-spectrum one?
Broad spectrum effective against a large number of types of bacteria
Narrow spectrum- effective against a small number of types of bacteria
Why don’t we only use broad-spectrum drugs?
sparks more resistance- better for more focused than more broad-could mess with microbiota
What is the therapeutic dose of an antibiotic?
The drug level required for clinical treatment
Define the toxic dose.
The drug level at which the agent becomes too toxic for the host
Define minimal inhibitory concentration.
The lowest concentration of a drug that prevents growth of the bacteria
Remember some of the antibiotics we went over were the family or category of antibiotic. There are several types in each family.
Cell wall, DNA synthesis, plasma membrane, ribosomes, metabolic pathways
What are the 4 major categories of antibiotics/antibiotics that affect cell wall synthesis?
What are the major characteristics for each of them?
Penicillin-now used to refer to over 50 related antibiotic
Cephalosporins-similar structure to penicillin, resistant to penicillinase, more effective for Gm-, susceptible to other beta-lactamases, mostly injected (some oral), expensive
Bacitracin-mainly effective against Gm+, topical use only, stops synthesis of linear strands of peptidoglycan
Vancomycin (member of glycopeptides class). Effective against penicillinase producers. Stops synthesis of cell wall. Was the last line of antibiotic defense for treating Staphylococcus aureus strains resistant to other antibiotics (MRSA). Problem- they’ve developed resistance-now a different last line.
What are the 4 major categories of antibiotics/antibiotics that inhibit protein synthesis? What are the major characteristics for each of them? What are the toxic side effects for these antibiotics (if listed)?
Aminoglycosides- changes the 30s subunit shape, effective against gram negative bacteria, can cause damage to auditory nerve and kidneys, ex: streptomycin and gentamicin
Tetracyclines- stop tRNA attachment, broad spectrum, long retention in body and penetration, Commonly used in animal feed becoming more of a concern more resistance because of it in the environment, Discolored teeth in children and not given to pregnant women- liver damage
Chloramphenicol- simple structure, Inhibits peptide bond formation, Broad spectrum but toxicity problems, ready diffusion, inexpensive used in low-cost situations, aplastic anemia- individuals stop producing all blood cells-needs bone marrow transplant
Macrolides- Stops MRNA through ribosome, gram positive bacteria- not very effective on gram negative, oral antibiotic for children, ex: erythomycin
What is an antibiotic that causes injury to the plasma membrane? Where is it used and Why?
Polymyxin B
Bacterialcidal- But higher toxicity to patient especially kidneys and nervous cells
We have plasma membrane very similar between eukaryote and prokaryote can carry over toxicity
gram negative bacteria really affects lipopolysaccharides
Often combined with neomycin in tropical ointments
What are the two antibiotics/categories of antibiotics that inhibit nucleic acid synthesis? What are the major differences between the two?
Rifamycin- Inhibits synthesis of mRNA, we have mRNA but ours is different than the enzymes in the bacteria- the antibiotic gets after different enzymes, penetrates tissues, red urine saliva sweat or tears, ex: rifampin
Quinolones- Bacteriocidal, inhibits DNA replication, synthetic drug called nalidixic acid, lead to fluoroquinolones being developed
What are the two antibiotics (natural and synthetic) that are inhibitors of metabolic pathways? What are the major characteristics for each of them?
Sulfonamides- Synthetic antibiotics, inhibit enzyme involved in the production of folic acid, bacteriostatic and broad spectrum, allergic reactions common
Isoniazid- Treat TB, has to penetrate human tissue because that’s where bacteria are hiding, affects enzyme for my colic acid synthesis
How is antibiotic sensitivity measured? What are some problems that can arise when using this test?
Kirby bauer method
Measures
-Sensitivity of microbe to antibiotic
-Can kind of tell if bacteriocidal or bacteriostatic
Problems
-Temperature
-Media
-Disc concentration
-Diffusion
-Human error
E test
-Gradient of antibiotic
-Minima inhibitory concentration
What are some principles why resistance evolves quickly in bacteria?
Microorganisms divide rapidly
Microorganisms are mutating randomly
-Errors in DNA synthesis
Participating in conjugation, transformation, transduction- which accelerate resistance/new strains
Antibiotics used only when needed and as directed usually help the body overwhelm the microorganisms
How does resistance show up? (have mutants, selection for…)
Whenever antibiotics are used on microorganisms a few of them can survive the drug. Random mutation may help protect them against the drug
- Selected for or against
-Too much antibiotic use selects for more resistant mutants
-Misuse of antibiotics allows resistant strains to have a chance t multiply and spread - Environment for selection- our bodies most of the time
-Evolution- genetic change over time with natural selection - Resistant organisms showing up in just a few years
How do patients misuse antibiotics? Overuse?
People don’t take all antibiotics until the bottle is empty or follow directions
Take expired drugs
If you have leftover antibiotic in your medicine chest you are a part of the antibiotic problem
In At least half of the world antibiotics can be sold over the counter
Patients who implore physicians to treat viral diseases like the common cold with antibiotics are not doing themselves any favors
How do physicians misuse antibiotics? Overuse?
Here’s too many broad spectrum drugs
Use exotic drugs first may not need to
Prophylactic use of antibiotics for every surgery
Give in to patients who want them for colds
List some ways the general public can control the antibiotic resistance problem.
The basic rule is to avoid using antibiotics unnecessarily and take properly
List some ways that physicians/hospitals can control the antibiotic resistance problem.
Hospitals and physicians starting to control overuse and look at using most specific antibiotic possible (narrow spectrum)
-Clinic and ear infections
Physicians prescribing the common antibiotics- maybe no need to expose the organisms to more exotic drugs
Improve infection control in hospitals. Kill the organisms before they get inside patients
-UV sterilization, isolation of patients, better sanitation
Consider reducing the widespread use of antibiotics in animal feeds
Invent antibioticsthat have new mechanisms for killing microbes
Use plants and animal antimicrobial peptides/agents
Invent vaccines against common microbial diseases to prevent infection in the first place
Educate general public
