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Do my capstan winch logging capstone title defense the last song book review essay example [Music] I'd like to end up this discussion by talking about antimicrobial compounds that are used to treat bacterial infections and think we have a bacterial infection in us we need to treat them with drugs that will kill the bacteria but will not harm us in other words the antibiotics or antimicrobial compounds have to be selective they have to target things in the bacteria that are not present in our cells fortunately this is relatively easy to do because bacteria are very different from eukaryotic cells I'll give you an example of such selectivity there is a class of antibiotics called the beta-lactam antibiotics and these include the penicillins the cephalosporins and the carbapenems there they're called beta-lactam antibiotics because they have a chemical ring in them called the beta-lactam ring these antibiotics target the synthesis of murine now do you remember from an earlier lecture what marinas and gram-positive bacteria this forms a thick layer on the outside of the bacterium just above the cell membrane and it's composed of sugar molecules joined together and cross linked by amino acids of short lengths on the right of this slide is a diagram of the synthesis of murine murine is exclusive to bacteria it does not occur in eukaryotic cells and on this slide are four different antibiotics fosfomycin cyclo serine vancomycin and penicillin which blocked different steps on the synthesis of murine so these antibiotics work beautifully because murine is only in bacteria and not in ourselves so they have very very little toxicity and you can see we have developed over the years antibiotics that target different steps in the synthesis of murine including penicillin last step which is assembling the cross-linking amino acids between the sugar chains unfortunately as as we develop new antimicrobial compounds resistance to them rapidly emerges and today we have resistance to almost every antimicrobial compound that we have developed and the situation is becoming dire because we have fewer and fewer options with which to treat bacterial infections antimicrobial resistance occurs in nature at its ancient bacteria make antibiotics to compete with each other in nature and many of those we have harnessed to use as antimicrobial treatments of infections of people we know that these genes that confer resistance have been around for thousands and thousands of years we can find them in very old sites on earth and there's plenty of evidence that they existed way before humans developed and a mic antimicrobial compound so we're really taking advantage of something that exists in nature there are a number of mechanisms by which these antimicrobial genes or I should say antimicrobial resistance genes work for example they may direct the synthesis of an enzyme that breaks down the drug a simple way of doing resistance they may chemically modify the drug so it interferes with its function they could inhibit the uptake of the drug into cells and tissues so it can no longer access its target or they could stimulate the export of the drug from the bacterial cell so it's no longer bacteria seidel or they may modify the target side of the drug so there are many different mechanisms of antimicrobial resistance and again these are all encoded on genes that code for proteins that have these various activities let's take an example to illustrate that and we'll use an example the antibiotic vancomycin its target is cell wall modification so vancomycin acts by blocking the assembly of the Marine cell wall now at the top of this slide is the normal incorporation of the precursors of murine so the blue and the green ovals those are sugar molecules that are going to be part of the growing peptidoglycan chain and this smaller ovals below them those are amino acids that will eventually cross link the murine to make it very strong so the way this works is that subunits are added to the growing chain and the second part of this in the second row of this diagram you can see the growing polypeptide chain vancomycin binds to the precursors by binding to the amino acid vancomycin is shown here in purple with the V or maybe that's brown and it's binding the amino acids and blocking the incorporation into the new chain therefore this inhibits marine synthesis and kills the bacteria resistance to vancomycin one mechanism of resistance is simply that the bacterium changes the D al ideale to D Allah D Lac and lactose can be incorporated into this chain it invades vancomycin resistance and the antibiotic no longer works that's one example of the way resistance works going back to our beta-lactam antibiotics which i mentioned before and the arrow points to the beta-lactam ring that's common to all members of this class that's why we call them beta lactams we have so far identified over 300 beta lactam aces these are enzymes that cut that beta-lactam ring and these beta lactam Isis encode resistance to the beta-lactam antibiotics so you can see the extent of the problem beta lactam aces are everywhere further complicating antibiotic resistance is that the genes encoding resistance factors for example the encode beta lactam aces are often a to move from bacterium to bacteria one way to do that is via plasmids and in fact many of these antibiotic resistance genes are encoded on plasmids this diagram which we saw previously and one of our other lectures shows how plasmids can move from one bacterial cell to another and the upper left is the bacterial cell with a chromosome in green and a smaller plasmid in red let's say this plasmid encodes a beta lactamase which confers resistance to beta lactams to that bacterium well in the second set of bacteria the two bacteria now exchanging DNA through a penis that's joining the two cells and the plasmid is moving from one cell to another the result is that that second cell now acquires antibiotic resistance so you know a problem here is that we often fee feed our animals that we eat for food lots of antibiotics so they grow quickly the effect is that we select for antimicrobial resistance in the animals and then when we eat these foods we acquire antibiotic resistance genes in us which are of no consequence initially but then when we go to have surgery and we need antibiotic therapy it doesn't work because we have the resistance already in us so these antibiotic resistance genes can move around bacteria extensively this is why they're a problem not just by plasmid mobility but by also movement by transduction the exchange of pieces of DNA by viruses or simply by naked DNA so gene transfer among bacteria we call this horizontal gene transfer is widespread and is a big problem for antimicrobial resistance and let's end up with a chart showing you some common mechanisms of resistance to antimicrobial agents for example that penicillins and the cephalosporins are hydrolyzed by beta lactam aces which we mentioned these resistance genes are in fact carried on plasmids methicillin resistance is a change in the penicillin penicillin binding protein not in a beta lactamase but in a separate protein this happens not to be I read on a plasmid tetracycline resistance encodes a pump that pushes the drug out of the bacterial cell this is a plasmid born resistance factor so if you look at all these various mechanisms of resistance modification of the drug synthesis of alternate substrates and so forth acetylation change in binding sites look how many are encoded on plasmids and that simply means that they're easy to go from bacterium to bacterium and we have a hard time treating bacterial infections when these resistance genes are so mobile [Music] you best research topics in economics Finger Lakes Community College.

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