this lecture is chapter 20 and it's on antimicrobial drugs so this chapter is going to cover a lot of medications antibiotics that Target different parts of the bacterial cell um and kind of weighing the risks of different medications how medications work together or they might work against each other and kind of where these medications come from so a lot of this is going to be memorization all right all right so first let's talk about the history of chemotherapy so a few terms that we have to be able to Define one is called selective toxicity so selective toxicity basically means being toxic to the pathogen whether that pathogen is a bacterial cell or a viral particle or parasite being toxic to that pathogen but not toxic to us so we always want selective toxicity when we talk about antimicrobial drugs because we want it to destroy for example the bacteria that's infecting our cells but we don't want it to hurt us and our cells so selective toxicity is selectively finding and destroying pathogens without damaging the host so for example the hosts can be us or whatever it's infecting chemotherapy is the use of chemicals to treat a disease so chemotherapy is treating diseases by the use of chemicals like medications what are antibiotics antibiotics are substances produced by microbes that are used in small amounts to inhibit another microbe so if you recall penicillium fungus actually was the source of the penicillin antibiotic because that microbe was able to inhibit the growth of bacteria so that's an antibiotic it's a drug used against bacteria though so remember that we'll talk more about how to use how to properly use antibiotics at the end of this lecture antimicrobial drugs are synthetic substances that interfere with the growth of microbes so they are either going to kill micro microbial growth or they're going to inhibit it and not let it go any further so like I mentioned in the previous slide Fleming Alexander Fleming discovered penicillin right and it was produced by penicillium um and then by 1940 they had the first clinical trials of the new first ever antibiotic penicillin but today there's this problem this ongoing problem of antibiotic resistance if you've ever heard of MRSA this is a specific staphylococcus aureus that keeps growing resistant to multiple medications so antibiotic resistance is always something that kind of research is always trying to battle okay so the next few slides I think it's about six slides if I'm not mistaken is really just a summary of antibiotics and what they target there are antibiotics that Target gram-negative bacteria there are antibiotics that Target gram-positive bacteria so we're going to compare um kind of the range of different antibiotics but the these next few tables that I'm going to kind of skim through are just for your own curiosity you're not responsible for these the ones that you are responsible I'll go over in their individual slides so for example gram-positive rods meaning they're gram-positive bacteria rod-shaped cells so what antibiotic is used against these specific species or if you're if the microbe is a fungal growth what do you use against fungi so depending on what the infection is what the pathogen is there are different types of antimicrobial drugs so we have to compare narrow spectrum and broad spectrum antibiotics narrow Spectrum antibiotics are drugs that affect a narrow range of microbial types maybe they're specific only to gram-negative bacteria only gram-positive or maybe they're specific only to staphylococcus species broad spectrum antibiotics affect a broad range of gram-positive or gram-negative bacteria they are used for a higher number a higher diversity of bacterium what is a super infection a super infection is an overgrowth usually an overgrowth of normal microbiota that's resistant to antibiotics so that can happen a lot if an individual a patient has an overgrowth of a microbe that's normally found in maybe their gut or somewhere else and on their skin but it can actually cause an overgrowth and that is a super infection so this table is really cool because it shows you narrow Spectrum versus broad spectrum so obviously if you look at isoniazid this is specifically to treat mycobacteria for example tuberculosis is caused by mycobacterium tuberculosis and so this drug is narrow spectrum because it's only used to treat mycobacterial infections but if you look at down here we have tetracycline tetracycline is a broad spectrum antibiotic it's used to treat both gram-negative and gram-positive bacteria even chlamydia so this kind of gives you a visual representation of narrow versus broad spectrum make sure you're able to define those terms all right so a couple of other terms that we have to Define are bactericidal and bacteriostatic bacteriocidal describes a drug that kills microbes directly so it'll kill all of living organisms or whatever microbes it's against bacteriostatic is a little a little bit more lenient that is just going to inhibit the microbes from growing anymore so it'll prevent the growth of microbes but it won't directly necessarily kill them but it'll kind of stop them from spreading even more so make sure you know the difference between bactericidal which means it'll kill the microbes directly completely bacteriostatic it'll just stop it from growing any further okay so now we're gonna get into some specific antimicrobial drugs um and anti antibacterial drugs sorry antibacterial drugs depending on the drug all have different mechanisms so for example there are drugs that inhibit cell wall synthesis remember the bacterial cell wall is made up of peptidoglycan so maybe they will interfere with the formation or production of that peptidoglycan that includes penicillin cephalosporins basitracin and Vancomycin or antibacterial drugs can inhibit protein synthesis so that those bacterial cells can't make all those proteins and enzymes that they need for example tetracycline or erythromycin chloramphenical streptomycin these are antibacterial drugs that inhibit protein production and bacterial cells and that's how they kind of Target the bacterium there are also medications that injure the plasma membrane so the cell membrane of bacterial cells can also become injured for example with polymyxin B antibacterial drugs can also inhibit nucleic acid replication for example DNA replication RNA production and transcription so they can cause all this damage to transcription prevent transcription from happening and in that way they can fight off that bacterial cell and lastly they can also inhibit essential metabolite synthesis we're going to talk about how something called folic acid is really important for a cell to be able to carry out reactions and function really well so blocking the production of folic acid is another mechanism that specific antibacterial drugs perform so we're going to get into inhibiting cell wall synthesis the main example of an antimicrobial drugs that inhibits the synthesis of the cell wall in other words it blocks the formation of that peptidoglycan cell wall is penicillin so there are different penicillin drugs and penicillins prevent the synthesis of that peptidoglycan we also have inhibition of protein synthesis so those examples are chloramphenicol erythromycin streptomycin and tetracycline these can actually Target the ribosomes of bacterial cells and not allow any proteins to be made so how do they do this so if we're looking at streptomycin streptomycin can change the shape of the 30s subunit of the bacterial chromosome so here's the bacterial chromosome there is a 50s subunit and there's a 30s subunit in other words there's a 50s part and there's a 30s part streptomycin targets the 30s part chloramphenical actually targets the 50s subunit tetracycline interferes with that TRNA coming and attaching to that mRNA bringing in that amino acid to build a protein so that's what tetracycline does you do need to know the functions that I'm going over so you do need to know that streptomycin affects the 30s portion of the bacterial ribosome you have to know chloramphenical affects the 50s subunit of the bacterial ribosome and you also have to know the function of tetracycline as well foreign so antimicrobial drugs that can injure the plasma membrane maybe they can cause it to break open all the cell contents can spill out basically killing that bacterial cell if the cytoplasmic contents leak out that bacterial cell is gone so there are polypeptide antibiotics that can change the permeability of the membrane polypeptide means protein so it means a big protein so there are protein-based antibiotics that can actually mess with the structure the permeability of the plasma membrane there are also anti-fungal drugs that can combine with sterols with lipids or cholesterol components of that plasma membrane of the bacterial cell and basically cause it to lyse okay what about nucleic acid synthesis so there are antimicrobial drugs that block nucleic acid synthesis and if you think back what is nucleic acid the nucleic acids of a cell are the DNA or the RNA so there are drugs that can mess with or interfere with DNA replication transcription which is DNA going from DNA making an RNA copy of it so they can block this entire processes they can also inhibit the synthesis of essential metabolites so I mentioned folic acid so folic acid synthesis or in other words making folic acid is a really important part of the metabolism of bacterial cells and so blocking the synthesis of folic acid is going to be detrimental to bacterial cells so one drug which is called sulfonylamide also called sulfonamides These are drugs that are anti-metabolites so basically there is a normal molecule that's used to make folic acid and that normal molecule is called paba para Amino benzoic acid and so what sulfonamides do they actually compete with this and kind of block it so that they can stop the synthesis of folic acid and with that folic acid the normal metabolism just won't work in the bacterial cell so that's what they specifically Target okay so there's an animation going through all of this for you guys to watch if you'd like and here is another table of antibacterial drugs so like I mentioned there are different types of penicillins there are natural penicillins there are some that are given orally there are some that are injected they're also semi-synthetic penicillins if you've ever heard of amoxicillin it's a common antibiotic that's given for example like after surgeries and such so that's a semi-synthetic penicillin there are a lot of antibacterial drugs here so again you're not responsible for this table or this table or this table but it's really cool to kind of look at all these drugs and what they target whether they target mRNA synthesis whether they target um what else can I talk a gram-positive bacteria all that stuff okay there are also anti-fungal meaning drugs that are against fungal infection anti-viral drugs that are against viruses even though we don't have too many of those because a lot of them have really risky side effects antiprotozoan which are antibacter antimicrobial drugs against protozoan infections anti-helmintic infections from tapeworm for example from roundworm drugs help against that so again just examples here okay so we're going to talk a little bit more about penicillin so penicillin's structure is actually kind of unique um this is what it looks like all the way here at this purple shaded area so this is the molecule of penicillin and if you notice this highlighted ring right here that's highlighted in yellow this is known as the beta lactam ring this is a key component of penicillin that helps it basically block cell wall synthesis so penicillins contain this beta lactam ring okay this symbol stands for beta and it basically prevents the cross-linking of the peptidoglycans it doesn't let those glycan chains form into chains doesn't let them be bound together with those peptide links peptide Bridges so it basically interferes with the whole construction of the cell wall specifically not specifically especially in gram positive it affects gram-positive cell walls way more so there are natural penicillins again there are semi-synthetic penicillins natural penicillins are the penicillins that are extracted from that penicillium fungi that we've learned about before penicillin G is injected penicillin V is administered orally okay and natural penicillins have a narrow spectrum of activity what did that mean to have a narrow Spectrum that means they are a little bit more specific in what bacteria they affect they don't they're not used for all bacteria just a few um but natural penicillins are susceptible to penicillin Aces or in other words beta lactamases beta lactamases or penicillinases they're inter they're interchangeable they're basically this enzyme that bacteria has evolved to have as kind of an antibiotic resistance Gene and this enzyme breaks up that this beta-lactam ring and basically destroys penicillin and now penicillin can't do its job so again penicillin has this beta-lactin ring it allows it to Target the cell wall of bacteria and not allow the cell wall to be made but bacteria have evolved to express this enzyme called penicillinase or in other words beta lactamase and that breaks down this beta-lactin ring making penicillin get converted into something else and again it can't do its job okay um semi-synthetic penicillins the good thing about them is that they have added side chains so they're semi-synthetic so they're kind of genetically engineered they have side chains added to them and that makes them resistant to penicillinases meaning semi-synthetic penicillins can kind of go against those antibiotic resistant bacteria all right moving on to cephalosporin so cephalosporin was another example of an inhibitor of cell wall synthesis in other words of cell wall formation it works similar to penicillins but they have a beta-lactam ring but it's a little bit different from the penicillin beta-lactam ring there are also polypeptide antibiotics protein-based antibiotics that is base citracin and Vancomycin basic tracin is applied topically and it works against gram-positive bacteria Vancomycin is a glycopeptide what is a glycopeptide glycol refers to sugar or carbohydrate peptide refers to protein so it's a protein attached to a carbohydrate and Vancomycin is the last line against antibiotic resistant MRSA so it is used when when nothing else is working it's kind of like that last resort drug used against MRSA all right anti-microbacterial antibiotics so what does anti-microbacterial mean well remember mycobacterium remember mycobacterium are special they're unique they're acid fast organisms because they include they consist of mycolic acid in their cell wall and so anti-microbacterial antibiotics or antibiotics that specifically Target mycobacteria species for example tuberculosis tuberculosis is an mycobacterium tuberculosis that's its name that's its official name and so it causes that tuberculosis so two drugs we have to know that work against mycobacteria are isaniazid and ethan-butyl isonize it inhibits mycolic acid synthesis in mycobacteria ethan-butyl inhibits the incorporation of mycolic acid into the cell wall so isoniazid will not allow mycolic acid to even be made in the cells of mycobacteria Ethan butyl will not allow mycolic acid to be stored in the cell wall and be part of the cell wall all right so moving on to Inhibitors of protein synthesis so the one that we have to know here is nitrofurantoin nitrofurantoin gets converted into a different form once it enters the cell and it actually attacks the proteins of the ribosome in bacterial cells so once nitrofurantoin is has entered the bacterial cell it'll immediately convert to a different form and it'll attack the ribosomal proteins of the bacterial cell and this is commonly used to treat urinary bladder infections chloramphenegal inhibits peptide bond formation so remember it's targeting the 50s subunit of the bacterial ribosome and therefore not allowing peptide bonds to be formed between amino acids so in that way it's inhibiting and blocking protein production chloramphenical is a broad spectrum drug what does that mean if I say it's broad spectrum that means it can be used against a wide range of different bacteria um chloramphenegal however can suppress bone marrow and it can affect blood cell formation because our blood cells are made in our red bone marrow inside our bones but one of its side effects is that it can suppress the bone marrow and it can affect the formation of blood cells all right aminoglycosides aminoglycosides are Amino sugars linked by glycoside bonds and they affect the 30s subunit of the bacterial ribosome however they can cause auditory damage so damage in the sense of hearing and examples of aminoglycosides are streptomycin neomycin and Gentamicin and yes you do need to know these all right tetracyclines really commonly used they're actually produced by streptomyces species which is a type of bacteria so a bacteria being used to make an antibiotic that's pretty cool and what tetracyclines do is they interfere with the TRNA attachment to the ribosome so if you recall when you're studying translation we saw how the TRNA brings in amino acids it attaches to the ribosome and the MRNA to start building the protein product at the end of translation so that's the part where tetracycline interferes with tetracycline is broad spectrum it penetrates our tissues and that's really helpful in infections by chlamydias which are type of bacteria and rickettsias and yes chlamydias one example is trichomonas which we'll talk about later on okay it can however suppress normal intestinal microbiota so your normal microbiome levels the normal microbiota in our bodies in our intestine can kind of go off balance using tetracyclines all right we also have macrolides macrolides are narrow spectrum they only are used against gram-positive bacteria and the most commonly known example of this is erythromycin erythromycin is used a lot in the clinical field um it's also used against acne as well so that's an example of a macrolide and it's used against gram-positive okay oxazola knowns which I can never pronounce it actually binds to the interface of the 50 and 30s subunits of the bacterial ribosome and it's used against MRSA okay so there is also lipopeptides which the example that we need to know is polymyxin there are different polymyxins or polymyxin drugs and these affect the synthesis of the plasma membrane that surrounds bacterial cells so polymyxin is a type of lipopeptides they cause injury to the membranes of the bacterial cell and polymyxin is administered topically it's bacteriocidal meaning it kills bacteria directly and it's effective against gram negatives all right moving on to the nucleic acid synthesis Inhibitors we have rifamycin which inhibits the synthesis of mRNA and it also penetrates the tissues we have quinolone and fluorocrinolones and those examples are norfloxacin and ciprofloxacin these are broad spectrum medications and they're relatively non-toxic to us going back to that folic acid and blocking folic acid synthesis let's talk about those sulfonamides again sulfonamides inhibit the synthesis of folic acid and folic acid is used and is really required by bacterial cells to build nucleic acids to build proteins so it's a really really um good Target it competitively binds to the enzyme for paba production like we mentioned earlier and again blocks blocks folic acid synthesis okay combining sulfonamides with trimethoprim is an example of what we call drug synergism so we're going to talk about synergy in a second I believe it's coming up but we'll talk about what drug synergism is in a minute okay anti-fungal drugs so agents that affect fungal sterols Okay so there are drugs that interrupt the synthesis of ergosterol ergosterol is this cholesterol based lipid and it makes and interrupting this makes the membrane more permeable and if the membrane becomes too permeable then anything can go in and out of the cell which is really dangerous that cell membrane kind of loses its ability to protect the inside of the bacterial cell so there are anti-fungal drugs that affect the synthesis of ergosterol which is found in the membrane making the membrane too permeable to be protective so there are poly polyenes for example amphotericin B that's also produced by streptomyces bacteria and it's toxic to our kidneys so it is not commonly used and also azles um two examples of azoles are imidazole and triazole and the amidosoles are given topically and they're there to treat cutaneous mycoses for example something on a fungal infection on the skin triazole is used to treat systemic fungal infections so fungal infections that are systemic maybe they're in the bloodstream maybe they're spreading inside your body foreign moving on to anti-viral drugs drugs that affect viruses so um viruses in order to infect our host cells in fact the cells of our body they have to be able to enter if they have an envelope surrounding them they fuse their envelope with the cell membrane of our cells and so there are Inhibitors to that inhibit the entry of viral particles into our host cells and the fusion of the virus and the host cells they can block these two actions there are also antiviral drugs that inhibit nucleic acid synthesis of the viral genetic material so it won't allow viral particles to make their own DNA and RNA inside the host cell they won't be they'll they won't be able to integrate their genetic material with the host cell genetic material and they also won't be able to uncoat and kind of insert their genetic material into our nuclei of our cells so a lot of antiviral drugs with a lot of Targets in the process of a viral infection so they can prevent viral uncoding there are drugs that inhibit integration of the viral DNA into our DNA and of course there are drugs that inhibit RNA and DNA synthesis of the viral genetic material one commonly used antiviral drug is acycloviron and that you can see right here we don't need to know the function of acyclovir but if you want to you can look into these slides all right there are also protease Inhibitors so these can block the cleavage of protein precursors there are Inhibitors that don't allow viral particles to exit the infected host cell that they use so they can't leave and move on and infect more and more host cells and there are drugs that specifically inhibit an enzyme called neuraminidase neuraminidase is an enzyme that some viral particles use some virus is used to be able to Bud out from the host cell and leave and move on and infect the other Hotel so inhibiting this enzyme is really good because it is specific to the virus and we don't have that enzyme in our cells so it would be non-toxic to us and lastly there are also antiretrovirals so for example the major exam the major example of a retrovirus is HIV so HIV is a virus and it causes the disease AIDS eventually so HIV is an RNA virus so there are antiretroviral drugs that are drugs used against retroviruses and usually they're used in combination with each other so maybe three two to three drugs at a time to treat HIV infections and they actually commonly have to be swapped out with different drug combinations because HIV can build resistance so fast all right there are also antiprotozoan drugs so quinine and chloroquine they are actually antiprotozone drugs that treat malaria artemisinin kills plasmodium plasmodium is the thing that causes malaria we'll learn about that more later on metronidazole is a common medication that's used and that interferes with anaerobic bacteria which can also be pathogenic it can treat trichomano trichomonas giardasis and amoebic dysentery so these are all diseases that are from protozoan infections okay so how to kind of see if an antimicrobial drug is effective or if it's not effective how do I know that it is works really well against staphylococcus species or gram-negative bacteria how do we know that so there's one method called the Kirby Bauer test it's also known as the disc diffusion method and it basically tests how effective chemotherapeutic agents are it can test how effective different antibiotics are so you have an auger plate that contains the test organism so let's say you have an auger plate that is just covered in staphylococcus aureus and you have these little paper filter papers kind of these little paper discs look like this and you place them all around and you see which of these plates actually inhibits the growth or kills the bacteria around them and it creates this Zone you can see the Zone created and there are different ones there are ones that that have no Zone meaning that it didn't it didn't was not effective against that bacteria at all you have some like the one up here where the zone is really really big meaning that this is super effective against that specific bacteria and that zone is called the zone of inhibition so the zone of inhibition is this clearance around those discs that you placed and it shows the sensitivity of the organism to the antibiotic in other words how sensitive that organism is to the antibiotic and in other words how effective that antibiotic is so if you look at this disc right here there's basically no Zone that means that this bacteria is resistant to this antibiotic this one has a big zone so it is sensitive against this antibiotic there's another test called the e-test and that this determines something called the mic this is the minimal inhibitory concentration it's basically the lowest concentration of the drug that you need to prevent bacterial growth the mic is important because you don't just want to give a random dosage of a drug so what the e-test looks for is how little of a drug do I need to give that's effective enough to fight off this bacterial growth and so that's called the e-test the E stands for epsilometer we don't have to know um the specific steps of this but basically looks like this and you can see the mic is all the way down here so what's the minimum concentration of a drug I need in order to stop bacterial growth because you never want to give too much of a drug that's not necessary and this also brings us to another concentration which is the minimal bactericidal concentration and that is the MBC so that's basically how little of a drug you need to completely kill directly that bacteria that you're fighting against so in a broth dilution test you can test for the mic you can also test for the MBC of a certain antimicrobial drug so you put the test organism into little Wells of a tray that contain dilutions of a drug so kind it'll kind of range where the lowest concentration of the drug is on one end and then there's this little and then the highest concentration is in the other end so each of these little Wells is diluted more and more and you kind of get to see what's the lowest concentration to kill the bacterial growth and what's the lowest concentration to inhibit that bacterial growth so in other words the MBC and the mic okay there's also resistance right antibiotic resistance so there are cells called persister cells these are microbes with genetic characteristics that allow for their survival when exposed to an antibiotic in other words their antibiotic resistant microbes so they persist they're persister cells there are also bacteria that are called super bugs that are resistant to large numbers of antibiotics so for example MRSA is resistant to a lot of antibiotics so that is considered a superbug okay there are also resistant genes that often spread horizontally among bacteria so that brings us that reminds us about horizontal Gene transfer right horizontal Gene transfer among bacteria among different species of bacteria they can transfer plasmids transposons they can do conjugation transduction and kind of spread these resistance genes to other species of bacteria which is bad for us here's an animation that you can watch about antibiotic resistance but let's talk a little bit about the mechanisms of resistance so what are some mechanisms that for example bacteria have that allows them to be resistant to certain drugs so they can actually inactivate the drug by enzymes they can express enzymes that can destroy the drug if the drug enters into their cell they can prevent penetration to the Target site with the microbe so they won't allow um that antibiotic or that antimicrobial drug to go to whatever it's trying to Target inside the cell they can alter the drugs Target site so once the drug enters into the bacterial cell they can actually convert it to another form that doesn't hurt them they can also eject or efflux that drug out so once an antibiotic enters into the bacterial cell they can actually just shoot it out of the cell for example E coli some strains of E coli are able to do that rapid efflux of the antibiotic and then there are also variations of mechanisms of resistance they can also have multiple mechanisms of resistance at a time maybe they can have an enzyme and they can efflux the drug out so it really depends on the specific species so this um diagram kind of puts that all together so they can inactivate the antibiotic they can break down the antibiotic destroy it um kind of convert it into a form that really doesn't do anything it loses its function they can completely block the entry of the antibiotic so it can't even enter into the bacterial cell they can alter the target molecule so that the antibiotic can't even match it and find it and bind to it anymore and again they can efflux or shoot out that antibiotic here's another animation okay so let's talk about how to battle antibiotic resistance and a lot of that comes with antibiotic misuse so misusing antibiotics using them incorrectly can allow for mutants to come up come up mutated bacteria that is actually resistant to that antibiotic so what are some ways that antibiotics are misused so what shouldn't we do we should not be using weakened antibiotics outdated expired antibiotics antibiotics should not be used for the common cold because the common cold is caused by a virus and antibiotics are against bacteria so that's going to get all the bacteria in your body used to that antibiotic so next time you want to use it it's not really going to be helpful um using antibiotics in animal feed okay failing to complete your course of antibiotics so if the antibiotics that was that were prescribed to you were for 10 days and you feel better after three days not continuing it until the 10 days is over is also misuse using someone else's prescription that they didn't finish or they have extra of that's also antibiotic misuse and it could only hurt you in the end all right um we're also going to talk about antibiotic safety so there's something called the therapeutic index which basically weighs the risk versus the benefit of an antibiotic antibiotics that are not safe that have too many side effects that they're really toxic to us they're not we don't want to use them right we don't want to cause any harm to our body we just want to cause harm to whatever's infecting us whatever that foreign pathogen is so the therapeutic index is this ratio between how beneficial a bacteria an antibiotic is versus how risky it is and antibiotics that are super risky that have really extreme side effects they're only used as kind of like a last resort when nothing else is working okay and it obviously depends on this condition of the patient um it's also important to know how antibiotics react with other drugs there are antibiotics that when used together they actually end up harming you or maybe when they're used together the result is even better when they're used alone that brings us to Synergy which I'll again I'll Define in a minute we have to talk about we have to think about antibiotic damage to organs so does this antibiotic cause damage to the patient to the patient's organs how big are the risks and also risk to the fetus right so it's everyone so it's important to be very careful during pregnancy as to what antibiotics can be taken how antibiotics affect the fetus so this is all important stuff all right so talking about combinations of drugs so synergism versus antagonism so Synergy is the effect of when two drugs are used together their effect together is greater than either of them alone so for example this image on the right you have one drug up here and you have another drug if they're used together then they cause even a greater more bigger benefit than used alone so maybe one used alone is pretty good the other one's pretty good but when used together they are amazing antagonism is the opposite that's when two drugs used together are less effective than either of them alone so maybe if you put two drugs together um actually the effect is not good they're not really effective they're not really good together they're not a good team that's antagonism okay so let's talk a little bit about the future of chemotherapeutic Agents so a lot of times we talk about okay why do we care why do I care how bacteria replicates its DNA or the translation in bacterial cells why do I care about all the steps that a virus has to take to infect a host cell well this gives us a lot of new targets it gives us enzymes that are found in only the pathogenic cell only in viruses only in bacteria that we can Target with new medications with new drugs it gives us a lot of information to do our research and to kind of also fight against antibiotic resistance so targeting virulence factors such as capsules such as certain tox endotoxins or enzymes sequestering iron so kind of storing iron not letting pathogenic cells have iron because they use that for their metabolism or using antimicrobial peptides produced by very this organisms like the one we mentioned earlier which is streptomyces bacterio sins these are antimicrobial peptides used by uh produced by bacteria so this is all really helpful and there's a lot of research that's ongoing to develop more chemotherapeutic agents and more um kind of researching on more targets and also phage therapy so phages are used a lot in biotechnology they can do a lot you can genetically modify cells you can chemically modify different drugs so phage therapy is also part of the future of chemotherapeutic therapy okay that concludes chapter 20. so I'm just gonna go through all the drugs that I want you to know just to kind of focus okay you do need to know how to what the definition of these terms are so be able to Define these terms on this slide again you're not responsible for those tables you do need to know the definition of narrow Spectrum versus broad spectrum what does that mean what does that look like what is a super infection again you don't have to memorize the table you do need to know bacteriocidal versus bacteriostatic you do need to know the different modes of antibacterial drugs so inhibiting the cell wall inhibiting protein synthesis Etc we have to know all about penicillins what they do okay you have to know these examples chloramphenical erythromycin streptomycin tetracycline and what they do so this again you have to know about streptomycin chloramphenegal tetracyclines from this slide um know this slide as well know this slide again don't need to know these tables you do need to know again all about penicillin natural versus semi-synthetic um you have to know about beta lactam betalactamase you have to know cephalosporins you have to know these polypeptides polypeptide antibiotics and what they do so that's basic tracin and Vancomycin you have to know the anti-microbacterial antibiotics which are isoniazide and ethan-butyl you do need to know nitrofurantoin chloramphenical aminoglycosides and their examples so streptomycin neomycin and Gentamicin are examples of aminoglycosides what do they do again tetracycline you have to know all about it macrolides you have to know um you have to know erythromycin is an example of that because that's something that you commonly see this drug in the clinical setting um you have to know the oxazolidinins you have to know polymyxin erythromycin quinolone fluoroquinolones norfloxacin ciprofloxacin you have to again no sulfonamides which were in a previous slide for anti-fungal drugs I want you to know that um they can interrupt the synthesis of ergosterol they can make the membrane excessively permeable so you have to know this one and then I want you to know the azoles so the two azoles I want you to know those don't worry about amphotericine and polyamines for antiviral drugs you have to know what kinds of things these drugs can inhibit you have to know that acyclovir is an example of an antiviral drug acyc liver is something else that's commonly seen in the clinical field again protease Inhibitors exit Inhibitors you have to know what an antiretroviral means what is it used against um for antiprotozoan drugs I only want you to know quinine and chloroquine that's treat that treat malaria and metronidazole know about that too and how it's used to treat anaerobic bacteria as well you have to know the disc diffusion method zone of inhibition know the e-test what does it determine what is the mic what is the MBC and how do we test for that so A broth dilution tests know the definition of persister cells super bugs and how resistance genes can get spread so basically know this slide mechanisms of resistance make sure you know all the mechanisms of resistance so how can a bacterial cell resist antibiotics what are those mechanisms what can it do no antibiotic misuse so in what ways are antibiotic misused what shouldn't you do basically antibiotic safety know about this as well know the difference between synergism and antagonism I might have a short answer question on this um don't worry about this slide okay so the things I just reviewed those are the things I want you to know that concludes this lecture