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It's gonna shine my screen. Um Can anyone say that? How is that fine? OK, cool. Um Just give maybe a minute so for everyone to like take a break and also just if you wanna scan this mentor code um all the numbers at the bottom as well and I'm Irish, I'm a second year medical student as well. Uh and I'll be looking at hospital acquired um infections. So I think the first thing for the meter is just the first question just what areas of the CSI do you struggle with? So it'd be great if you guys can like just maybe if you have any questions just put that in so that we can just see I can just see what kind of um topics to concentrate more on. Um but just give me a minute and then we'll start I don't think this should be taking the full hours as well. Um But yeah. Uh yeah, sorry. Yes. So maybe another 30 seconds and then start. Mm Yeah, let's just start and then um people can join it. Um oh OK. I see stuff. So areas of struggling with antibiotic resistance, uh amoxicillin and P Beal Act. Yeah, definitely uh cover that uh questions to start. Yes, I'll be also talking about how this can be applied er, in scenarios. Er OK. So let's just start. So the overview um I'll be covering these topics. So defining HAIS transmission to six links, the five mos in the hand hygiene, er antibiotic resistance, amoxicillin and called Amoxiclav, Mr Ratu and CD this and Duce of can. So hopefully these are everything terms that you're familiar with have come across before from both the part two of the CS and I think some part of the part three as well. Um OK, so let's start. So what is aha I, so aha I or a hospital well in uh is an infection that patients get whilst receiving treatment for med medical or surgical conditions of which many are preventable and it can be either considered as a healthcare associated infection or a hospital acquired infection. So for your last CSI and exam, you just need to consider the hospital acquired. Uh but just a general difference is the healthcare associated is a more general term whereas the hospital acquired is looking at a specific setting. OK. The hospital uh and looking at infections caught within that environment. So I think the next question I have is where can you uh pick up ha I so if you guys just wanna uh join the mentee, the code is also at the top and just put in a couple of responses. That would be great in 67 days. Ok, great. So um hospital, the office one GP, nursing home care homes. This is all good. So these are basically different places you can get it. Uh nursing home. Yup. Uh So just some examples uh you have acute health care hospitals, GP practices, uh surgical centers, dialysis facilities, outpatient clinic, hospices. So it's basically saying that there's many different places uh where uh a hospital acquired infection can be picked up and on to. The next part is what are some risk factors of ha I so stuff that make you more prone to catch a hospital acquired infection? All right, let's have a look at this. Yeah, great. So the big ones being age, uh antibiotic resistance, uh immunos im immunosuppression is a good one. Bad infection control. Yeah. So it's all good ideas, guys clear on the right line of thought. Um So, so some of the risk factors that I've listed, there's more as well medical procedures. Er, is this an invasive procedure such as surgery which increases the chance of risks? Um or is it a noninvasive procedure such as like say, for example, ABP reading antibiotic use? So that linked on to antibiotic resistance and I'll talk more about it later on patient characteristics. Uh How compliant are they to treatment? What is their hygiene protocol? Um and likewise, as well, the behavior of healthcare staff, er, are they using the proper like infection control measures. Are they wearing PPE? Um Also another factor is healthcare facility. So the resources present in the uh facility also affects um the chance of catching an infection and also the length of hospital stay. So obviously, the longer you stay, the more you're at risk of catching an infection. Um So yeah, that's all good. And so I'm hoping this is a familiar diagram to all of you. So I'm just gonna give a couple maybe a minute or two if you have like a piece of paper or something. Um Yeah, I mean your exams in like two days. So hopefully everyone can remember all the six steps. So it would be great if you can just list off all the six steps. Um Just so you've confirmed to yourself that you can remember it, but I'll just give it a minute or two for that and then we'll go through each stage as well. You say something just maybe 30 more seconds. OK? Let's go through them. So the first point is infectious agent or germ. Second point is reservoir. The third link is port of exit, fourth is mode of transmission. Fifth is portion of entry and then sixth is susceptible host. So I think it's quite important that you guys know the not just what all six are, but the specific orders are because they are as a lot. Ok? So let's focus on it on each one. So the first bit. Um the first start like start the infectious agent on the germ. So this is any sort of pathogen which has the potential to cause harm. So M RSA er C difficile, which you've heard about your CSI H pylori, these also have the potential to cause infections in the body. The next part is reservoir. So, reservoirs themselves usually don't carry signs of infection, but it's rather just a place where a pathogen grows multiplies and lives. And so there's like three types of reservoir. So there's human reservoirs, which is person to person, such as STD S measles and mumps. And usually, I think it's believed that human reservoirs are easily eradicated. So, for example, um the breakout of smallpox um ages ago was eradicated because it was through human contact and uh we could have done something about it. The second one is animal reservoirs. So, pathogens are animals. Er, the most famous one that we all know of is Sarov two and the third one is environmental reservoirs. So plants, soil and water and usually pathogens such as fungus, uh kind of uh choose this method essentially. Ok. Port of exit. So this is basically the path of the pathogen leaves the reservoir of the host and it's usually the er it usually adopts a path that it kind of enters in via. So for example, TB, found in the respiratory tract, but it's possible of exit to infect others would be via body fluids. Coughing and sneezing. So kind of where it enters the reservoir, the host in the first place, usually the point of um exit for it as well, mode of transmission. So again, there should be a familiar er image to all of you guys. Um And it's quite an important one. You can definitely be asked a question about this where it could be like, er for list a bunch of different, like types of transmission and be like how many are like uh direct contact or droplet and so on. So we'll go through each one and there'll definitely be examples. So for example, let's start off with direct transmission. It's transferred from the reservoir to the susceptible host by direct contact, which is skin to skin, you can see intercourse or via droplet spread. So this is spray aerosols, coughing or talking. So this is like the more the simpler one. whereas in direct transmission, there's a few more kind of different variations. So for first one, for indirect transmission is airborne indirect transmission. So this is via suspended air particles such as dust or droplet nuclei. So this might sound kind of familiar er or similar to the droplet, a direct droplet. But the difference is that the direct droplet as I in its name infects the host that er immediately. So it's aimed the droplets are aimed towards the er victims. Whereas for airborne indirect, it's more like it's it's suspended in the air for some time and hasn't directly gone and entered um into the uh susceptible host. The next one is vehicle borne indirect transmission. So this isn't through inanimate objects, which is food, er water. So for example, like the rivers, blood and foam mis. So foam mis are essentially anything like clothes, furniture such as like table desks, door handles. So that all of that encompasses on the f foams and then you have vector borne in out transmission. So this is er animal intermediate and of this, there are two kind of subcategories. So one is mechanical, um a mechanical transmission is where the animal f for example, like for example, the animal carries a pathogen from one host to the other, but it's not infected itself. So this would be like the rats during like the bubonic plague where the rats themselves weren't infected by the fleas, but they transferred it from one host to the other. Whereas the other variant is biological. So mosquitoes and uh uh sorry mosquitoes and ticks. So, biological revers, the pathogen itself is re reproducing and going through life cycles in that um reservoir. So the mosquito, the famous example that I think we all should know would be the plasmodium parasite which er reproduces in the mosquito and then goes on to ca cause malaria in humans. So I think it's quite important that you guys know which kind of transmission it is because it's highly likely that, that I would ask a question about this. So we've got some questions. So which type of transmission? Um if you guys can just put the answers in the chart, that would be great. Um And the first one is this, so which type of transmission and be specific as well? Rather than just like direct or indirect? I want more like specific details. Great. Got some responses. Yeah, great. So direct droplet, I think I saw a question being like if you directly touch a surface, is that still in direct transmission? Yes, but that's still via fite. So that would be considered as indirect vehicle borne. Uh So yeah, a direct droplet is perfectly fine moving on to the next one. Yeah. Right. So all the responses are indirect airborne. So hopefully you can see the difference between how the first one is di droplet and the second one is indirect airborne, but it's still kind of like pathos in the air. Um OK. Next one. Ok, great. Uh So we've got variety of, well, we've got indirect vehicle borne and we've got direct contact. So the correct answer is indirect vehicle borne so well done to everyone. And this is because it's like touching essentially um a fite. So the iron drip back um or even like perhaps fluids, but it would consider uh it would be considered as um indirect vehicle board. Just remember for direct, it can only be via contact. So that's like skin to skin, uh skin to skin or droplet which is like coughing, sneezing, et cetera, et cetera. Uh OK. This one great um some good responses coming in. Uh Yeah. So this one is indirect vector mechanical er because the fly is landing on the infected feces which has a pathogen and it's not reproducing within the pathogens, not reproducing within the flight itself and then it's going on to land to hu on a human. So the pa the fly is doing literally this just the job of carrying a pathogen from one source and infecting it into a host. Uh ok. Great. Now, port entry. So this is basically how the pathogen enters the host. So it's access to the tissues of pathogen to multiply I uh um ie by the skin, the mucous membranes and the blood. So in this diagram, kind of everything in the green on the left er is um portal of entry and anything on the right. So the blue is portal of exit. So by the eye, by the nose, via the mouth bites, skin breaks or the urinary and reproductive tract are all ways that pathogens can enter into the human uh body and a gain access to the systemic circulation and finally least susceptible host. So this depends on a couple of things. So the three factors are like genetic or constitutional factors, specific immunity and nonspecific factors. So, specific immunity can be like, for example, are they immunosuppressed? So you guys said at the start being immunosuppressed is a risk factor for ha I. So, er, do they have sort of, sort of weakened immune system or even for like babies transplacental? What have they got from the mother in terms of the initial couple of months where they rely on the antibodies that have come from the mother. And then nonspecific immunity is like the skin, as we said before, mucous membranes, the cough reflex and so on and acquired circumstances such as like malnutrition, alcoholism disease and like chemotherapy all would reduce your immunity and make you more susceptible to getting like um an infection. Uh So, yeah. OK. Again, another diagram that you guys should be familiar with. Um So we've got the diagram on the left which is just numbered 1234 and five. And then we've got the pre uh the labels that should be going on from A to E. So if you guys could order them from 1 to 5, uh according to what the label should be representing and then put it in the chart. That would be great. I would just give it maybe a minute ish minute or two for that. Just put in whatever you think is right guys, we'll go over it anyway. So don't be afraid of getting it wrong. All right. Getting some responses. OK, great. So we've got a couple of responses. Let's go through it. So the correct order is DB EA and C which I think most of you got. Great. So the first point is before touching a patient. Second point is before cleaning it out. A as se procedure, third is after body fluid exposure risk. Fourth is after touching a patient and fifth is after touching patients surrounding. So just to clarify here, hand hygiene works both ways. So some look for prevention of infection from patient to doctors such as before touching a patient or before doing the clean or aseptic procedure. Whereas others look for infection, er preventing infection transfer from the patient to the doctor such as after body fluid exposure, after touching a patient or the surroundings. So it's important to know which one kind of helps the doctors and which one helps the patients. Um but yeah, ok, I think this was also a slide you guys got uh but this is should be just recapping a level knowledge where you to check kind of what an so initially you would give broad spectrum antibiotics when they first come in to kind of fight for um as many pa er er passengers as possible. So the an the broad spectrum will be good at kind of tackling whatever the pathogen is, but it won't have the best response possible. And then after you do this bacterial culture and then you'll see which antibiotic is the best. So you can give that and then that will lead first of all to the best response and second of all it would try and reduce antibiotic resistance developing, which is a growing issue er in Pharma um like the pharmaceutical industry. So just to recap the process. So you have a nutri m media and you'll grow the bacteria and then you'd basically put this antibiotic discs and after a certain time of incubation, you would look at the kind of radius er cleared. So the rad the discs which have a greater er radius. Um me means that the bacteria is more sensitive to that uh antibiotic. Whereas for example, the one over here, I hope you can see my cursor uh the one on the top, right? There's essentially no er clear radius. So that means that the bacteria is resistant to this antibiotic. Um So yeah, this could be perhaps like a question you guys get which would be like er talking about how the procedure works. So what these, what the interpretations and what does a big radius mean? What does a smaller radius mean? Ok, let's move on to mechanisms of antibiotic resistance, which I understand was a lot a topic that many people wanted to clear. So just list all the four essentially this is the four main ways in which antibiotic resistance is developed. Er So the first one is older target site. So changing in the structure of the site that the antibiotic inhibits such as for example, er this section here, er if say for exa er for a bacteria um encodes a new protein which binds to the receptor. Then that just means that, that might mean that the shape changes, which means that the antibiotic can no longer er bind to the receptor and cause a response. The second part is decreased drug accumulation. So um they have like eex pumps or they decrease the uptake and that essentially reduces the impact that the antibiotic can have. Third one is alter metabolism. So a different enzyme of pathway. So you can see in the middle where um the bacteria chooses another part metabolic pathway which no longer requires the, for example, the initial enzyme that the antibiotic was targeting and then lastly is inactivation of the antibiotic. So, er enzymatic degradation or alteration at this bottom right hip. So I think this kind of diagram of these four points are quite important for you guys to know and hopefully it clears up kind of which ways antibiotic resistance can develop. Um Yeah. Um because I think this is also another kind of examinable point where they could say um oh a bacteria kind of finds a way to change its um er like bind a protein to its receptor. Er What part of what mechanism of antibiotic resistance does this come under? For example, in which case, you would say alter target site because the antibiotic can no longer fit. Um So yeah, hopefully that cleared up again. This should also be a picture that you guys are familiar with. So uh if I just go through each part here, the D allenyl D alanine transpeptidase is a PVP. So a penicillin uh penicillin binding protein. Er and this is basically the target of beta lactase in bacterial cell synthesis. And then you have amoxicillin which is a type of betalactin um of another famous one is penicillin and then you have betalactamase which with the A S and the name you should know breaks down beta Latins. Then obviously, we have two types of bacteria, gram positive and gram negative where gram positive has only an in a cell wall and a thick peptidoglycan um layer. Whereas gram negative has two cell walls in in an outer and a thin peptidoglycan er layer. So these are sent through the components er that we'll see later on for amoxicillin and co amoxiclav. Um oh yeah, this is just to introduce and get familiar with. So beta lactam mechanism and how do these antibiotics work? So I think this diagram on the right is quite useful. So we'll walk through it. So first of all, the overall mechanism of beta lactams is to inhibit cell wall synthesis. So how it works is as you can see these P BPS um are present in the cell wall. Basal lactams target the bacterial penicillin binding proteins and that interferes with transpeptidation and that essentially blocks cell wall synthesis. So, er your cell wall is now unstable er on the outer layer of the bacteria. And essentially that causes cell lysis because it loses its structural integrity and can no longer carry out its function. Um So yeah, the main aim that main thing that I want you to take from this is that beta lactones are responsible for inhibiting cell wall synthesis by targeting pepti current synthesis. OK. But this is where beta lactamase comes in. So as we saw here, beta, the be there's a famous, well there's an important part of beta lactams known as a beta lactam ring. And what bacteria develop as, for example, antibiotic resistance. Er they evolve to express beta lactamase. And what that does is as you can see in the image of the bottom is that it breaks down this beta lactam ring and the antibiotic is therefore er inactivated. And so it can no longer hinder cell wall synthesis. So the bacteria evolving to express beta lactamase falls under the the inactivation of the antibiotic kind of mechanism of resistance. So hopefully you can see how that kind of ties in and er this is just one way in which it works. So what can we do? Er So what comes into play is uh um clavulanic acid. So we have beta lactamase inhibitors which basically inhibit the activity of beta lactamases and allow beta lactam to carry out their action. And the one that's famous and we use most is Coamoxiclav, which is made up of amoxicillin, which is a beta lactam and clavulanic acid, which is a beta lactamase inhibitors. And if you can see in the image on the bottom left, the clavulanic acid basically binds to the beta lactamase and kind of stops it doing its action which allows for amoxicillin um to stop cell wall synthesis and peptidoglycan syntheses and essentially carry out its function. Uh So, one thing to point out here is is if you have like a resistant bacteria, there's no good having just amoxicillin or there's no good just having clavulanic acid, you need both co amoxiclav for it to work because otherwise one's just gonna be broken down by beta lactamase and the other on its own was just gonna inhibit beta lactamase but have no beta lactams to act out and carry out the action. Um So, yeah, hopefully that makes sense. There's just a feedback form here um that I would greatly appreciate if you guys did fill in just before we finish on looking at C um C diff for sale and er duty of can. Um Yeah, it'd be great if you guys could fill in this feedback form because it helps with uh getting uh like teaching for you guys what we can improve on next time. Um But yeah, it would be very helpful and I'll also post the link as well in the chat. Um So yeah, I've just posted the link. So just give me maybe a couple of minutes for people to fill that one out uh for where we, we can access the slide. So we'll upload the slide after um the session is done, it'll be done by the end of tonight, hopefully. Um ok. So someone asked what's the difference between mechanical vector borne and biological me vector borne? So, yeah, so mechanical vector borne um is where the say for example, the vector, er let's take the example of rats and like the plague and the bubonic plague. So the rats just had the fleas on them that were infected. But the the fleas itself, the fleas itself did not like reproduce within the rats or use like the rat system. They were just kind of um a method of transport that the fleas use to infect others. Whereas biological vector is where the um pathogen kind of replicates within the host. So, for example, the plasmodium parasite replicates within the mosquito has life cycles carrying out. Er and then um uh and then infects the humans. Er So hopefully that makes sense. A mechanical is just purely for like transport means. Whereas biological is they have um uh like life cycle processes and uh grow and uh like reproduction and so on and so forth inside. Um OK. Just to see since we got, yeah. All right. Uh Let me just go back to this. So um why does Mr ratchet have ac diff infection? So this is I think the last part of the um uh acsi. So um Mr Batley was treated with coamoxiclav. So that works in kind of killing the bacteria. But what that did is uh it led to the disruption of the gut microbe uh microbiome and that activated toxigenic c difficile. And essentially, if you can see in the image of the bottom where you have the healthy gut microbacter, er microbacter, you've got where it's all normal and fine, you have C difficile, but they can't colonize as soon as you treat with like an antibiotic, you've essentially killed someone like the gut bacteria in your um in that line, your gut, you allow for like a bacter opportunistic bacteria such as C difficile to er colonize and er grow and have negative effects. So being treated with Coamoxiclav led to c difficile, kind of being unopposed growing and meant that they were positive for C difficile and had further er infection and er worse symptoms. So I think you also had a bit on duty of candor. So duty of candor is essentially er two things. So empathy. So there ability to understand and share another person's feelings and perspectives and kind of use that understanding to talk about what to do next. Whereas Kandor is more a duty is kind of like it's a legal right, a duty to be open and honest with patients or their families, if something wrong has happened, that could cause harm. So for example, this would be er in a case where you see a scan and initially you don't recognize the issue, uh such as an x-ray, you don't recognize a fracture and you say you send the patient home, er, but then they come back with a lot of pain and then when reviewed again, you notice a fracture that would require a duty of time though, to be open that something has gone wrong. We are apologizing of what happened. So these are covering topics that we've covered. Um And so we've got a lot of this uh part two, stuff. I think you guys were keen on finding stats questions. Uh Let me just see if I can find any and then I'll be glad to share them in the meantime, if you wanna put any questions, anything you want me to recap on, er, if you don't understand or anything of that sort, um Just let me know and then we can be going through them, uh something wrong. Anything you guys also want me to like, explain again. I'll be happy to do. I realize we have some time as well. Um uh Yeah, someone is also the feedback so you can see that I'm just trying to find some uh yes stats questions that could be useful for you guys. I think the main thing with that questions is you have to read everything, like even like the small bits of the um question um because the answer will usually live through there. So, uh I think these are some of the questions we got last year, um which I will show. Um, let me just stop sharing. I think someone also asked, what do we notice about antibiotic sensitivities? Um I don't think um that much, er, in the sense that you just need to know kind of how, uh if I go back to that slide, uh you just need to know how cultures, er, are read in terms of what does it mean when you have like for example, a bigger radius versus a smaller radius? I don't think you need to know any specifics about which antibiotics will be sensitive to. Not, but I guess in the obvious names like M RSA methi methicillin resistant, you obviously know that methicillin is um disc wouldn't have much uh to show. Um OK, I think, let me see if I can share this. Yes. OK. Um Hopefully you guys can see this. Let me see. I can, yeah, I think you can read that. So if you guys just wanna have a go at this question, um I think there's one more after this and then we can just go through the answers and then just put the answer in the box as well in the chat. Um So yeah, and I think it is hard to practice for data um questions uh like trying to find practices. But I think the main, generally, the main thing is uh like uh how like reading everything carefully understanding what it means. Uh Great, see some answers if a couple more can come in. OK, great. So two. So yeah. Uh so I think the main thing that I wanna show is here, but you've basically been bombarded with a lot of numbers, but you kind of have to see which part you have to say. Take. So for how many sites of infections, the proportion of community odds that higher, you'd have to look at the blue ones, for example, instantly and then you've got E coli on the left staphylcoccus ais on the right and looking at the two differences basically. Um So yeah, everyone did well with saying two um perhaps have a go at this one in case. This is, yeah, someone said this is on in, I think it was on our last year as well. But I think it's just good practice to kind of talk it through and if anyone hasn't done it to also do it as well because you see similar stuff to this on the actual CSI as well. Yeah. OK. Right. Yeah. Discover responses. OK. Great. Let's go through it. So again, so it says for how many bacteria is community acquired pneumonia significantly higher than both healthcare associated and hospital acquired. So look at the labels here. So you've got communities, one healthcare is two hospitals, three and you've got significant difference. So instantly you're looking for the columns which be, it's yes and one versus two and one versus three. So that gives uh the third one in gram positive, the pseudomonas Syringa, er, the first one in Obliger anaerobic bacteria. And then within that, you have to see which one is the higher. So some people might have uh automatically gone and, er, put three without thinking uh without looking at the next part, but you have to see in which is at higher. So in the gram positive one, it isn't in Pseudomonas Eryngo, it isn't whereas it is in the uh Preva premalar SPP. So that gives a as the answer. So hopefully that makes that's some, some of the questions um that could um that's like the style of questions that would come up in CSN, I think they're fairly accurate. So er if I just, if anyone also has questions, please put it in the chat and um I'll just go through like areas where I think you definitely will be tested and need to know. So for example, I think uh the six links in the chain of infection is very important knowing uh what each stage is and kind of uh where it affects it. For example, um if you look at the six wearing PPE would prevent portal of ex the transmission, the link would break the link between, for example, portal of exit and mode of transmission, er because you're not allowing it to er the pathogen to further spread. Another thing that I think is very important and I will stress is this kind of schematic. If you guys can understand the er schematic and see where um see which part um which like for example, which examples come under each category, then that will put you in good standing for the CSI. Er And then also another thing I think car amoxiclav and looking at the uh mechanism of beta lactam, beta lactams um would also be greater if anyone wants, I'm happy to also go through the beta lactam mechanism or antibiotic resistance. Again, if you want that, just put it in the chart or if there's any other point you want me to go through, I'd be happy to do that as well. So host susceptibility just looks at how likely is it for the host to be infected by that pathogen. And so there's just different factors that can affect it. So, in terms of specific immunity, are you immunosuppressed? Um uh or even a nonspecific immunity kind of um are there any factors which have kind of weakened that uh physical first line of barrier? And it also matters on genetics? Um And so these are just some factors which affect post susceptibility in general and how likely it is for them to yeah, infected basically. Uh Can you go through the reason why comma club works? Sure. Ok. So we'll look at first the mechanism of beta lactin. So essentially they bind to penicillin binding proteins. PVP S and they stop cell wall synthesis because they target um pepti peptidoglycan synthesis. So that's the general gist. So beta lactams, they target peptidoglycan synthesis which affects cell wall synthesis. What some bacteria have developed via antibiotic resistance is an enzyme known as betalactamase. Um So what beta lactam is, does, is it essentially breaks down that beta lactam ring, which means that the antibiotics such as amoxicillin, penicillin can't work is essentially taking away the most important part of the er or it's taken away the most important part of the antibiotic that need, that is required for it to work. So it then comes in coamoxiclav. So what coamoxiclav has is it has amoxicillin, which is your beta Latin, but it also has clavulanic acid, which is your beta lactamase inhibitors. And so what beta lactamase inhibitors do is they block be the activity of beta lactamases. So they allow beta lactams to function properly. And that's where coamoxiclav co comes. So you have, what would initially happen is you have clavulanic acid which binds to betalactamase and stops, it stops the betalactamase from breaking down amoxicillin. And then you have amoxicillin which is now free to work would be do would be going and stopping cell wall synthesis and peptidoglycan synthesis. So now what we require is to treat it to essentially treat this type of bacteria is you'd require to prescribe coamoxiclav rather than amoxicillin because you might have some bacteria which are resistant. And so amoxicillin on its own won't do anything but rather coamoxiclav will. So hopefully, that makes sense. Uh Someone said, can you go through the different modes of transmission again? And the examples? Yeah, sure. Uh OK. So there's two main divisions in the branch, direct and indirect. So if you look at direct first, you have direct contact, so that's within direct transmission, you can have two options, direct contact and droplet spread. So direct contact is skin to skin kissing and intercourse. Those are examples of direct contact contact whereas you have droplets spread. So coughing on someone sneezing on someone, any aerosols that come from your like for example, if you're infected any aerosols that come out and infect someone else, er they can as droplet spread or even talking. For example, then you have the other main division, indirect transmission. So indirect transmission basically means there's a third party involved er in transmitting the pathogen of which you have airborne. So this is suspended air particles. So this is not quite like for example, sneezing on someone or coughing on someone. This is more that the virus is in like thrust or Doppler nuclear that are suspended in the air floating in the air and then they go on and then they go on to infect someone. So for example, if someone inhales and there's a virus, there's a drop of nuclear with a virus that will then infect the person then you have vehicle bo borne indirect transmission. So that's anything with just inanimate objects. So food, for example, water. So the common case is like in a river uh blood or foite. So fites are again inanimate objects. So clothes, furniture, er phones, for example. And then lastly you have vector board. So these are a er er intermediates where vector borne can be divided further into mechanical and mechanical vectors essentially just carry the pathogen and then transport it on. So they carry it, transport it on with the pathogen, not influencing any part of the vectors kind of uh biological systems. Whereas you can have biological, where the pathogen would enter into that uh vector reproduce and uh have life cycles and then would then infect it. So the famous example is mosquitoes er for biological vectors, they would plasmodium parasite would enter into mosquitoes, they would have life cycles occurring through and then once the life cycles are complete, they would then infect uh a human. So that is a biological vector rather than a mechanical vector of simply just being transported. Hopefully, that makes sense. And the slides will also be up uploaded onto metal. So you guys can go through it. Um Is there any other questions? Uh I'll also just put my, my email in the chart in case if you have any questions. Um And before your exam, uh hopefully, that's helped and thanks a lot for the feedback as well. Be really used to looking for further teaching. Um, and, yeah, good luck for your CSI. Uh, hope it all goes well, thank you.