wilsbach's version from 2016-02-22 18:22

So tired

Question Answer
pic that sums up the diff factors to consider when picking your antimicrobial agent
you must consider interaction between the abx we're giving and the other microbes in the body. Explainbact/microorganisms releases all sorts of chemoattractant substances, making sure WBCs come in and phagocytose the bact. But the drugs we use have influence on all these processes (chemotaxis, phagocytosis, intracellular killing, digestion).. the little B and C arrows are saying microbes themselves have an influence on phagocytes, and phagocytes have an influence on microbes.
which drug inhibits chemotaxis at sub-MC concs?tetracyclines
which 2 drugs enhance chemotaxis?ceftazidime and ampicillin (betalactams)
which 3 drugs depress chemotaxis?gentamycin, erythromycin, minocycline
which 2 drugs at sub-MIC conc inc phagocytosis?clindamycin, lincomycin
which 2 drugs dec phagocytosis?tetracyclines and bacitracin
which 2 drugs interfere with intracellular killing, and how?sulfonamides and trimethoprim (interfere with H2O2 production)
what is quorum sensing? why does this happen?(wiki says: Quorum sensing is a system of stimuli and response correlated to population density. Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population.) (said in class:) It is basically a type of Intra- and interspecies communications. Can emit luminescence from doing this. They only glow bc they are with a certain number of bact- once they reach a number high enough. More cells=mor signaling molecules=bigger response. G+ AND G- do this. There is evidence this is triggered by abx too. It has to do with virulence factors, can determine formation of biofilms, and creates a favorable environment. Diff signaling molecules produced at diff stages of cell growth. Based on cell growth, they either produce products that tell them they dont need to prolif too fast/dont have to produce virulence factors yet until they are ready
4 things quorum sensing determinesvirulence, formation of biofilms, creation of favorable environments, survival
quorum sensing is cell density related, which means they areautoinducers
when are quorums produced?at diff stages of cell growth
what is a biofilm?group of bact which adhere to a surface, then there is some sort of environmental stress, or there is a substrate which allows the bact to start forming biofilms to protect themselves, against the environmental stress (heat, cold, chemical, drug, etc). Then within this biofilm community you see the development of resistant bact as well-- vast majority of abx dont go through biofilm.
explain the arr genes and the ndvB genes and how they relate to biofilmsarr: important in formation of biofilm. ndvB: important in the formation of resistant bact in the biofilm
what are the clinical applications of knowing about biofilms?sometimes there are bact you just can't kill bc they are in a biofilm, or are very difficult to kill. and in that biofilm are a proportion of bact that are resistant already, so even if they get out of their biofilm, they will be very difficult to tx. (so we are trying to find drugs that break down biofilms- there are a few). Biofilms are def sthing to worry about with sthing like plates etc.
DO NOT USE which 4 abx in an ANAEROBIC ENVIRONMENT?Aminoglycosides, Aminocyclitols, Fluoroquinolones, Sulfonamides
DO NOT USE which type of abx in an AEROBIC ENVIRONMENT?Nitroimidazoles (metronidazole)
which two types of abx DO YOU NOT USE IN PUS/DEBRIS?Sulphonamides, Aminoglycosides
which 2 groups of abx DO YOU NOT USE IF THERE ARE CATIONS (Ca, Al, Mg)Fluoroquinolones, Tetracyclines
4 groups of drugs which would be DRUGS OF CHOICE FOR PRIVILEGED SITES?Fluoroquinolones, Macrolides, Chloramfenicol, Florfenicol
what is a wild-type breakpoint?the MIC for any given antibacterial that distinguishes wild-type populations of bacteria from those with acquired or selected resistance mechanisms.
what is a clinical breakpoint?those concentrations (MIC) that separate strains where there is a high likelihood of treatment success from strains where there is a high likelihood of failure (how much do I need to kill all the clinical isolates?)
This apparently has to do with breakpoints. explain. human example looking at pneumococcal infections. pharmacodynamic (effect of drugs on body/target) target is set at 34, represented by red dotted line. If set at 34, the MIC is 1mg/L. So to be able to kill the vast majority of the pneumococcal strains, need to reach a conc of 1mg/L levoflox. in the brain. If you then look at the wild type, and the distribution of MIC-- there is a big column of MIC 1, but then there is a bunch of them with a MIC of 2. And you want to kill ALL of them. So initially looking at in vitro findings, and then looking at the wild type, they can adjust the conc to a reasonable dose which will kill all of the bacteria. That also means the breakpoint was not set at 1mg/L, but at 2mg/L, to cover all of the strains. So based on initial in vitro research, and then based on wild-type susceptibility data, they come to a clinical breakpoint where we know that we are going to kill all of the clinical isolates. So they determine a phamacokinetic and pharmacodynamic breakpoint, and the breakpoint here is at 34 and hence 1mg/L. Now, if you look at 34 for ciprofloxacin, we are at LESS than one, and comparing to the bar graph, there is a large variety of wild types that we dont kill (most of wild types are above the derived breakpoint) So you could argue cipro might not be the right drug to use to tx pneumococcal dz.
CLSI Breakpoints specifically derived for veterinary medicine---> Bovine respiratory disease (6 drugs they have breakpoints for- no idea if he'd actually make us memorize this, didn't seem to emphasize it, but it's here to read at least)ceftiofur - tilmicosin - florfenicol - enrofloxacin - spectinomycin - danofloxacin
CLSI Breakpoints specifically derived for veterinary medicine---> Swine respiratory disease (3 drugs they have breakpoints for- no idea if he'd actually make us memorize this, didn't seem to emphasize it, but it's here to read at least)ceftiofur - tilmicosin - tiamulin
CLSI Breakpoints specifically derived for veterinary medicine---> Bovine mastitis (4 drugs they have breakpoints for- no idea if he'd actually make us memorize this, didn't seem to emphasize it, but it's here to read at least)pirlimycin - penicillin/novobiocin - ceftiofur

Recap + odds and ends from the cases he went through

Question Answer
Know how to determine the right abx for a specific dz (which factors need to be taken into consideration)yep
know what are the therapeutic consequences of implementing antimicrobial therapy according to the mutant prevention concentration
know what are the risk factors for the development of bacterial biofilms and how we can conquer them
when considering IV versus IM in food animals/production setting...keep in mind that IV is impractical, prolly better to IM in cheap meat
big benefit of short acting abx?less side effects
hes gonna give this graph and ask us to pick the best abx. know how to do it you want to pick the drug which has the LOWEST MIC (more effective/effecient at killing the baddies) AND you want the LOWEST resistance (the "R" at the far right) bc resistance is bad, mmkay?
look over the graphs in the cases. I honestly couldnt take notes bc he didnt post itits applying this other crap
4 things you should consider when deciding if you want to do in water or in feed medicationlag time, practicality, reliability, appetite (also consider diff withdrawal times with diff abx and diff Routes)
note: if you are given MC chart and two are the same, you need to know the kinetics-- and the kinetics are even more important than the resistance factor, always go for kinetics apparently.
Question Answer
drug left out of notes on what cant be given to FA additional not allowed drug was Dipyrone

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