Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

So let me just share this. So can everybody see the presentation at the moment? Yeah, it's working. Ok. So, um as I said, my name's Luke. I'm one of the final years and I'm giving the lecture on with one of the lectures on microbiology for this year's path course. So what we're going to cover today sort of the first half of the microbiology section. So I'm gonna cover microbacteria, lower respiratory tract infections, endocarditis, g eye infections, UTIs, iatrogenic infections, um CNS infections, and then finish with sexually transmitted infections. So just before we start just a little bit of a disclaimer about this whole thing, I'm just one of the final year medical students. I edited the microbiology section. I edited the first half of it. I'm definitely not an expert in infectious disease. And so this is not going to be anything like an exhaustive discussion of it. I'm also not going to bore you with every detail. I'm very conscious that in particular, with, with the microbiology section, there's a lot of stuff that is just rote learning and there's not much point me putting up a big table of what's grand positive and what's gram negative and just sort of parroting at you because you're not really going to gain anything from that. With that said, I've tried to focus on what I think are the things that are more you're supposed to actually sort of talk about and talk through. But at any point, if there are any questions, please just pop them in the chat or you're very welcome to one mute and just interrupt me. I'm gonna ask quite a lot of questions as we're going just to keep things moving again. I got one eye on the chat. So please, if you can just respond in the chat, it just keeps things moving nice and quickly. Um And if you are interested in these two sort of topics anymore, I definitely recommend MSD manuals is a really nice resource online. I don't know many people who know much about it or use it really useful resources like a quick sort of summary. Uh a little bit like up to date would definitely recommend it as Kumar and Clark's is sort of the go to. So we're going to start by talking about micro bacteria. So I'm just gonna bring the mentee back up. Uh There we go. And if you could all just join the mentee, let me get a few more. We're just gonna go through a couple of questions just before we start, just sort of framed the discussion. So just get a couple more and then we'll get going. Okay, Bob. Okay. So we're going to the first question to a 50 year old man with a sort of a half year history of hemoptysis, fevers and weight loss. And TB is being suspected, which of these tests is the gold standard for diagnosing? Okay. So the correct answer here is actually the Sputum culture. We're going to talk about this a little bit more. Like I said, these questions are very much designed to frame what we're gonna talk about. So I've deliberately picked on some of the bits that are a little bit more sort of nuanced. So we'll talk about exactly why the correct answer is actually a Sputum culture here. Okay. And next question. So once diagnosed, the patient is started on anti tuberculous meds and vitamin B six. But what is the purpose of giving vitamin B six in this context? Perfect spot on to protect against the side effects of ice. And I is it? So I'm just gonna go back to the presentation now and we're gonna talk about all of this stuff. Okay. So most of this is going to be focused on tuberculosis because it's the micro bacteria that's going to be most important. And I suspect we've all heard quite a lot about TB at Imperial. So like I said, I'm not going to sort of go over things that you've already know sort of inside an apple. So it's an infection infection by mycobacterium tuberculosis. Now, just in the track, can anybody tell me sort of what are the stages that typically a TB infection goes through? Yeah, pretty much spot on. So we start with our primary infection. So this is when the person is first sort of exposed to the bacteria and in most people would have no idea. This happens, typically happens in childhood, typically know nothing about it. They actually get the, get incubated, the macrophages consume it and it just sits there will be no symptoms. Most of the time, it's just something that happens without anybody knowing. Then it hangs around latent at this point. Again, no symptoms. They've just got the back, my cracks here in there and they normally form a focus. I'm going to talk in a second about what these folks fosse are called again. Still totally a symptomatic. What then happened somewhere down the line and we can be talking 2030 40 years later. If something happens that impairs their immune system, classic classic causes would be patient with HIV. Patient started on monoclonals or some other immunosuppressive medications or patients that are alcoholic or malnourished there. You'll, you'll go to causes for allowing a reactivation and this can be called secondary TV or post primary TV. And this is where you get this sort of the classic symptoms that you're all familiar with constitutional symptoms, hemoptysis, cough, etcetera. And like you said, it disseminates it can go anywhere it wants. Now, just referring to this latent bit is just a little bit of terminology. That's really important. What I've highlighted here in this chest X ray is how the TV might exist during that latent phase. Does anybody know what this is called? Yeah. So a gone focus. So there's a little bit terminology just to be careful with here, we'll talk about tuberculoma in just a second. So if you look on that chest X ray, you see there's two arrows. The thing on the left is a little nodule in the actual lung. That is what we call a gone focus. Okay. Just a little bit of just a little ball of, I guess what's forming is um is the actual macrophages sort of forming that cluster so that there's are gone. Focus what you've got on the right, there is some lymphadenopathy. And when you have the gone focus plus lymphadenopathy, we call that a gone complex. And those two things over a sort of a long period of time can become calcified. And at that point is called a rank E complex. Now, the difference between these things sort of clinically is pretty unimportant, but it can certainly come up as an exam question. The idea of the difference between gone focus, which is just the ball on the left in the lungs are gone complex, which is that plus the lymphadenopathy and then a ranking complex when it becomes calcified. And these are all consistent with just latent TB that's hanging around. Not really doing very much now, like we said, if you suffer the right kind of insult, you can then actually become active, you can have post primary CB that is now doing something. And what sort of presentations can active TB have? There's lots of them, but what are some of the more common ones? Yep. So definitely sort of your classics of pulmonary TB with hemoptysis, weight loss, constitutional symptoms. And the tuberculoma is sort of one possibility is how that might look on chest X ray if your pulmonary TB, what other things can TB do? Yep. So you can have sort of like a lymphadenitis picture where you don't have the pulmonary symptoms, but just sort of a really sort of profound sort of disseminated lymphadenopathy. Anything else? Give me one or two more? Yep. Erythema nodosa is definitely one of the symptoms that you might see. So what you, what they're, you've covered all the most common stuff. Your common TB presentations going to be this sort of constitutional floor, see presentations. Pulmonary TB, which may well be with tuberculoma, especially if there is like a pre existing cavity that it can form in and TB lymphadenitis. Some of the slightly less common ones just sort of worth being aware of are these. So miliary TB is something that we often see is something that you identify on chest X ray, but it is not the same as pulmonary TB So miliary TB is when one of your tuberculous lesion's erodes into a blood vessel and it goes everywhere. It's most obvious on chest X ray because you can see all of these tiny little faux, see where it's spread. But if you've got that in your lungs, you've got that all over the place. The bone marrow will be riddled with it and it can go anywhere because it means you've broken into a blood vessel. Men in Geel TB is one really important to be aware of. It tends to present with like a sub acute meningitis. So we'll talk about this a bit more later. It will present with men in gitic symptoms, but onset over a slower period of time and it won't be quite a septic looking. This is a really important to be aware of because it's probably the most severe presentation of TB. It has a really high morbidity and mortality. And you often see in HIV, patient's and then a couple of others, Pott's disease um is when it sort of invades the the spinal column, you get degeneration of the vertebra and then they'll present with sort of back pain with sort of compression fracture type symptoms and then possibly neurology, genital urinary TV is one of your classic causes of sterile pyuria. We'll talk about this a little bit later again. But this is where if you do a urine dip, your urine dip and sample where you get leukocytes in the urine, but no organisms, it sort of classically associated with the genital urinary TV. And it can do a lot of other things. Um some of these cutaneous causes a very pathognomonic. So just to show you a few examples, this is sort of your classic pulmonary TB. You can see that we've got this sort of uh this Cavite ating lesion up in the right apex. This will be a lymph add knittig TV. And you can see on the CT next to it, you can see sort of how profound that lymphadenopathy becomes. This is a miliary TB. So again, I'll just sort of re emphasize even though you'll see this on a chest X ray, this is not the same as pulmonary TB. This is a very different presentation, much more serious one. And this is an example of how it can present cutaneous lee. Does anybody know what the name of this condition is? This is one of your, of your pathognomonic TV presentations? So this is Lupus vulgaris um like that erythema nodosa is sort of a very common presentation in the skin. This is one worth being aware of because it is pathognomonic for TB. That's Lupus vulgaris. So they're investigating for TB. So a lot of you got this question wrong and it's because you got to be very careful how you read these questions. Okay. So we can split, investigating TB into investigating active TB and investigating for latent TB. Now for active TB, a lot of you said Sputum smear and that is in reality, what you're probably going to use. It is probably the thing that's going to get you the diagnosis. However, it is not the gold standard. Your gold standard investigation to diagnose active TB is a Sputum culture and the medium that your cultural is called is called a love and Stein Jensen media. Just a buzzword worth learning. Cultures take ages and they don't always grow. It depends on how active, especially if you got Pulmonary TV. It's easier to get a sample to culture, but it takes ages. And so it's definitely not most of the time what's used for diagnosis, but it is technically what's the gold standard, like you said, Sputum smear and stain is quicker and in reality, probably what is used more often to make the diagnosis. Um in terms of the stain you use zeal zeal Nielsen is one name for it. Another stain you can use is the aura mean Rodham mean stain again. Just a buzzword worth learning and don't confuse it with the rod anin stain which stains for copper that we use to diagnose Wilson's disease because that's what I did in my path exam. Um So that's the diagnosing active TV, latent TV. You've got two things you can use the man to test, which is the same as the tuberculin skin test or you can use an Interferon gamma release assay. This last one has a bunch of different brand names. You might have heard of the Ellis Spot or the quantiferon test. They're both examples of Interferon gamma release assay. Now, this is a list of the pros and cons of each. Don't bother learning it. It's all very nuanced. I'm sure some of you have done the past med questions about trying to interpret a tuberculin skin test based on the diameter of the lesion. I don't think it's very high yield. I'd say this is the approach to take the big difference between a man to test and an Interferon gamma release assay is that the man to test will test positive if they've had a previous BCG vaccination. So if you've been vaccinated against B C G before and you have a man to test, it will come back positive, irrespective of whether it's because of the B C G or because you have latent TV, where the Interferon gamma release assay is not positive to vaccination. It's only positive. If you have latent TB, the interferon gamma release assay is more expensive, which is why it isn't just what we do all the time. But so if you're choosing between the two, that's how I'd make the choice previously vaccinated. Pick the Interferon gamma release assay. If they've not been vaccinated, you can go for a man to and then treating TBI. So again, if someone just puts it in the chat, I'm sure you all know how we treat TB, what's our standard regimen? Right? Perfect. So, rifapentine, Isoniazid, pyrazinamide and ethambutol and it's four for two and two for four. So you give all four for the first two months and you give the first to the rifAMPin and Ison, is it for the next four months now? Again, not going to bore you with all this. You'll know it inside now, but a couple of the details that possibly aren't so well known is pyridoxine. So pyridoxine is vitamin B six and we give that alongside Isoniazid because what's the, what's the side effect we associate with ice on? Is it peripheral neuropathy and the mechanism for that peripheral neuropathy is vitamin B six deficiency. It does, it does something to affect the metabolism of vitamin B six. So we supplement B six that way you're less likely to develop the peripheral neuropathy and pretty much everybody will get that. Um Some of you have mentioned write ups and I suspect what you're referring to there is Streptomycin. If you have drug resistant TV, there's a whole bunch of other stuff you might be using. Streptomycin is one of the more common ones and a case in is used sometimes and there's a whole bunch of new drugs are basically just used for drug resistant TV. Wouldn't worry about it. You're not going to be asked how to manage that kind of presentation. The final final little added detail. I'll add, I don't think they'd ask it. But just so you're aware if you diagnose somebody with latent TV, they don't need the whole, the whole shebang. They don't need the four for two and two for four. The approach to latent TV. There's a few different regimens, broadly speaking. They just have a brief um person and Ison eyes it or just Ison. Is it? I think last time I checked the guidelines, I think you can either have revamps in and Ison. Is it, I think for three months or just ison? Is it for six? But if they have latent TV, it's a far less intensive regimen. And I think it's everything worth saying about TV, that you won't already know what we'll just talk about now is with the other microbacteria again, compared to TB. These aren't going to come up much. I'd suggest just focusing on buzzwords. So can anybody name any of the other sort of micro bacterial illnesses? So, Patrick, you asked about screening for later TB, I'll just flip back to that quickly. Your options are the man to an eye interferon gamma release assay. And like I was saying, I think your best approach here is if they've ever been vaccinated before you choose the Interferon gamma release assay, if they've never been vaccinated, go for the man to test the reason being that the man to test will test positive if they've been previously vaccinated. Whereas the interferon gamma release assay won't, it's only test positive for um later for TB, it doesn't test positive for B C G. So perfect, you've covered most of them there. So, leprosy is actually the second most common microbacteria. And your approach in terms of the exam should be any patient with skin changes and peripheral nerve disease. Think leprosy um in the context of, you know, an appropriate travel history and exposure, there's loads of different pathological classification. And if you're interested, you can read all about poor service Ilary versus multibacillary. Leprosy. Not worth getting bogged down in the classic sort of signs with leprosy. Are you going to get hypo or hyper pigmented skin patches, peripheral nerve disease and thickening of the nerves, thickening of the nerves in particular, if they give you that it is leprosy, there's a whole bunch of other stuff it can do you get a lot of uh neuropathic ulcers. Um Amyloidosis is quite common. So media like medium nerve palsies in particular, quite common, not worth get involved down in the details. Mac is another one worth being aware of. So mycobacterium avium complex, this looks like pulmonary TB, you only see impatience with sort of severe either pre existing lung disease or patient's with HIV. So patient's with HIV, cystic fibrosis, bronchiectasis are high risk getting mac and it will look like pulmonary TB this slow presentation floors, the symptoms, hemoptysis, cough, etcetera. Now, some of you mentioned or somebody mentioned mycobacteria, mycobacteria, abscess ius. So there are two micro bacteria that cause skin changes. First one is microbacterium Maren, um which causes swimming pool granuloma, which is also called fish tank granuloma. Unsurprisingly, what you're looking for here is skin disease and an exposure to pausal fish tanks. That's all I'd worry about as far as this is concerned. And finally, a Berruti ulcer which is caused by mycobacterium ulcerations. Now you're buzzwords here are going to be a patient in the tropics with a slowly progressive but painless but incredibly destructive ulcer just to show you what a couple of these will look like. So this is a classic leprosy patient. What you can see here is you've got these sort of sort of patchy hypo pigmented skin lesions and you can see the nerve thickening, especially in pictures C and D. You see that you're thinking leprosy. This is your fish tank, granuloma. It looks like it's a relatively benign, relatively superficial ulcer and the patient would have been exposed to a fish tank or an aquarium. They're not normally work somewhere like that. Compare that with your brulee ulcer, which is a very destructive ulcer. So again, it could go slowly, but if you don't treat it, it's incredibly destructive. You can see by the last picture it's eating its way right the way through tendon, through muscle, very, very serious, very difficult to treat. And that's everything that I think is worth saying about mycobacteria. Are there any questions about anything we've talked about that before we go into the next section. Uh So if we go back to the mentee, now we'll go on to the next section. If you actually go back over the questions just to sort of recap. So the reason sputum culture is correct here is because the question specifically ask for the gold standard. So excuse some smear is certainly what you're going to do and we'll probably be what used to make the diagnosis. The culture is the gold standard test. And for this one, the ice allies, it is the vitamin B six which is pyridoxine is to protect against isoniazid side effects. So, if we go on to the next section now, so patient with pneumonia is failing to improve after several days of antibiotics and repeat chest X ray shows this, why are they not improving? Good? So we'll talk about everybody has sort of split between the two options that seems most plausible. And we'll talk a little bit about that chest X ray when we come back and why? That is the correct answer? Okay. And the next question. So 23 year old student presents with a two week history of dry cough, fevers, myalgias on examination. They've got a target shaped rash and they're jaundiced chest X ray shows bilateral patchy consolidation. What's the likely organism? Good mycoplasma? So we're all pretty happy that this is one of our atypicals and we'll talk about what our buzzwords are. For different atypicals in a moment just about the presentation. So we talk about low respiratory tract infections. Now, this first is just a little bit of semantics is again, just to clear up some of the terminology in case it comes up. So lower respiratory tract infection is unsurprisingly an infection of the lower respiratory tract. There's a whole bunch of different words, it's just sensible to make sure we all mean the same things. So, bronchitis is inflammation of the medium sized airways. It's something that you're normally going to see in smokers or very young Children. It's typically viral and it's typically characterized by minimal if any chest X ray findings and you don't expect the patient to be that. And well, for that reason, you don't normally treat this with antibiotics. Strictly. The guidelines says that you can offer doxycycline if they are systemically unwell or they have a CRP greater than 100. I don't think that's a guideline worth learning. I think, I think the approach to bronchitis should be pretty normal chest X ray, treat them supportively. Pneumonia is when you've got an infection of the lung parenchyma and it's causing consolidation on the chest X ray. This is typically gonna be typically going to be bacterial. And in contrast to bronchitis, these patient's are going to look sick, they're not going to look well as well as your bronchitis patient's don't really have any symptoms outside of the pulmonary system. Then an abscess is a plus filled cavett ating lesion within the lung parenchyma. So these patient's have some kind of sort of cavity and collection within the actual lung parenchyma itself. These patients are typically present with sort of constitutional symptoms and it can be a bit more of like an ongoing presentation will be over a few weeks and they'll have flaws. The symptoms, swinging fevers is one of your big red flags for an abscess. Often it's a complication of pneumonia. So, a pneumonia that isn't responding two antibiotics. One possible reason for that is the formation of a lung abscess. And if a patient has an abscessed, you're normally gonna have to drain it antibiotics on their own won't normally clear it. Now, an empyema is very similar. The difference between an empyema and an abscess is an empyema is when there's a Pasfield collection in a space that already exists. So, in the lungs, that's in the pleural space, it's basically an infected pleural effusion. Compare that to the abscess which has carved its own space in the lung. The empyema is filling the pleura. It presents very similar to an abscess. A parapneumonic effusion is a complication of pneumonia, much like an abscess can be. So the difference between the two is one you determine with the chest X, right. And again, you normally have to drain them. We can also classify pneumonias based on um sort of where they happen. So caps are community acquired there in the community. Perhaps this is a definition worth knowing perhaps on pneumonias that develop more than 48 hours after hospital admission, it's in the 1st 48 hours, they probably caught outside the hospital. It's still ahap and perhaps are pneumonias that developing patient's on ventilators. The significance of that latter classification is it affects the organisms that are likely to be present. So again, just to show you the chest x rays, this is a bronchitis. If you, if you squint and take my word for it, you might believe that there's a little bit of thickening of some of the sort of central bronchitis. They just like a little bit more prominent than they should. And that's utmost what you're going to see in a bronchitis compare that to the pneumonias like this where you've got a really clear in this case, right, middle zone sort of consolidation. Now, this is an abscess. What you can hopefully see here is, you've got quite a well circumscribed lesion within the lung parenchyma and sort of like sort of patchy airspace is within. And that's because you've got a cavity here which is walled off and you got fluid in it, which is why you got this intermittent sort of air spacing within it. And then this is your empyema. It looks like a pleural effusion. You're looking for a loss of this um this corner and you're looking for the meniscus on the top in terms of what causes, um, a pneumonia. We split them into typical and atypical. This has nothing to do with how common they are. Some of the atypicals are actually very, very common. It's entirely about how they present. So typical neuro nya presents like a pneumonia. The patient's going to be systemically unwell. They can have all the pneumonia's symptoms. It's gonna be rapid onset over a few days. They're going to get a lot worse on the chest X ray. You're more likely to see sort of a typical consolidated lobe and these organisms respond to your penicillins, compare that to your atypicals. They present a typically, they often have sort of flu like pro pro drones, lots of myalgias and sort of just feeling generally unwell, often a dry cough rather than a productive one. And they often have sort of prominent extrapulmonary manifestations and these organisms in general respond a bit better to macrolides. Now, once we split into typical and atypicals, we're just playing buzzword tennis here. This is just about now having buzzwords you associate with the different organisms. So if we start with the most common course, start with strep pneumonia. Any buzz words, people associate with strep pneumonia. Yep. So all your classic pneumonias symptoms and then just a couple of the specific phrases to associate it's the most common organism. So with no other reason to prefer one go for strep pneumonia, a couple of the other ones, sort of classic things to be aware of is the classic, describe a rusty colored sputum. It's a grand positive diplococcus and you have a positive year, an antigen test for strep pneumonia. There's only one other organism that does that and we'll come to that in a second. So, what about, hm. Awful is, what about h flu? What kind of people get hatefully pneumonia? So, the one I would say to associate is COPD, patients with COPD are particularly prone to getting, um, hum awful is influenza pneumonia. Um, so that's the buzzword I'd associate there and then the final of us or typical Xyz Moraxella. Does anybody have any associations with Moraxella? So, classically smokers are said to get this one out of these three, the only meaningful differentiators I would say our strep pneumonia is the most common hum awful is influenza is the one to go for a patient with COPD. That's how I would sort of distinguishing the exams. But these are your typical pneumonias. Now, the ones that have a bit of a stronger signal with the buzz words are some of our atypicals. So if you move onto these, we'll start with Staph aureus. What's the classic history of a staph aureus pneumonia? What some of the buzzwords you might associate with it? Good abscess and the longer term onset. So, going to the sputum. That's interesting. I'm not, I'm actually not sure about that one is not gonna come across, but that might well be correct. The big ones you mentioned some of the really good ones there. So, classically, you often have a longer term onset and specifically, it's often post influenza. So patient will describe a viral influenza. They'll feel crap for two weeks. They'll have, you know, really myalgic, really unwell, coughing up. So hacking up, sputum of shortness of breath, they'll get better for a day or two and then develop a pneumonia. That's your classic staph aureus history. And you're absolutely right on chest X ray. This is one of your causes of a Cavite ating lesion. So they will have what looks like an abscess, they will have a cavity with their staph aureus rather than a lobar consolidation. Perfect. What about klebsiella? Does anybody have any buzz words for Klebsiella pneumonia? Good alcoholic. So this is, and this is an anaerobic organism. So, your associations here are alcoholics and aspiration. So either an alcoholic patient, alcoholic, homeless patient or patient who's just had a stroke, they'll often present with hemoptysis. And again, it's one of your causes of a cavett ating lung lesion. So you're hearing that you're thinking klebsiella, chlamydia pneumoniae, I've just mentioned because people often ask about it. It's not very important. Um, it tends to present with a very mild pneumonia patient are normally very well and normally just get better by themselves. Asthmatics, I think are slightly higher risk for it, but it's not very important. It's very unlikely to come up. Wouldn't worry about it. The two above really put you have those buzzwords associated and if we keep going, what about legionella? So Legionella legionella has a few things we should be looking for. Perfect you covered pretty much all of them there. So first one is in the patient exposure, some kind of exposure to sort of water units. So air conditioning in hotels, plumbers, hot tubs, anything like that is your classic exposure for legionella. Patient's with legionella are really, really unwell. These patients will often be very, very sick and some of the classic symptoms to associate are a transaminitis. So drained LFTs because it affects the liver. They develop hyponatremia and they develop a lymphopenia. Those are all very classic legionella symptoms and like strep pneumonia. It's the other organism which we have a urine antigen test for. So, if they tell you that this patient has a positive urine antigen test, it can only really be strep pneumonia or legionella. Okay. What about mycoplasma? What associations do we have with? Mycoplasma? So, I think half of you got this question right? So some of you definitely know what we're looking for here. So don't confuse mycoplasma and micro bacteria. So, mycobacteria, you're definitely thinking immunosuppressed patient's mycoplasma is a little bit different. So mycoplasma pneumonia classically something you see you had your outbreaks over every few years. So often you've got a young patient, normally a student living in student halls, something like that and it has loads and loads of extra pulmonary manifestations. The ones they like are these patients develop a cold autoimmune hemolytic anemia. So they can present jaundiced and they develop erythema multiform A. So they can they get this target shaped rash and that can progress into sort of a Stevens Johnson, toxic epidermal equalised, really severe sort of lytic skin lesion. But those are your two big associations to have in terms of extra pulmonary symptoms. And then a couple of the rarer ones which I'd give very little worry too. Chlamydia Siddiqui causes silicosis. This is your only reason to ever ask a patient about whether they have exotic birds. Um It also can cause a culture negative endocarditis if they say exotic birds, it's chlamydia Siddiqui. I don't think they will and Coxiella bernetti likewise, um can cause a culture negative endocarditis. But this is exposure to farm animals. Normally those last two are very low yield. I just know those buzzwords and then in terms of immunosuppressed patient just has just been referred to. What do we worry about impatient with HIV. What do they get in their lungs? We ought to mention TB and mycobacterium and sort of mycobacterium avium. Anything else that we think PCP? So, Pneumocystis pneumonia and what sort of things in the history make us think PCP other than HIV. How do they present good de sac dry cough and desaturate on exertion. So they'll be there that will be fine. You ask them to walk up and down the script stairs. It drops by 10%. Is your classic Pneumocystis history. A couple of other associations worth having splenectomy is what our patient's who've had a splenectomy at risk of. Well, good encapsulated organisms. So, in terms of pneumonia, that some haemophilus and strep does anybody know sort of a nice little memory? Eight. Remember which of your organisms are encapsulated? Oh, that's more comprehensive than the one I always, I always just used NHS. So Nasariyah Demopolis and Strep, I like I go to um for encapsulated organisms, cystic fibrosis. They get pseudomonas and they also get Burkholderia psa patient. Um Pseudomonas is the one you're probably more like to have heard of Burkholderia psa patient is uh it's not very important, I wouldn't have said for this bit more important for your Pedes exam because Burkholderia psa patient is, is a contra indication for lung transplant. It's one of the reasons you don't want patients with cystic fibrosis interacting with each other is if they pass this species on to each other, you can no longer have a lung transplant if you're otherwise eligible. Um Monoclonals really high risk for TB reactivation. Um Yes. Yes. So likewise, bronchiectasis see its cystic fibrosis sort of bronchiectasis describes the dilation of the airways. So, cystic fibrosis causes bronchiectases along with lots of other things. Um Yeah, monoclonals really high risk for TB reactivation. Anybody being started on monoclonals that are prone to, this is tested for TV, for latent TB first because otherwise you can push them into that post primary active TV. And neutropenia is a risk factor. In particular for fungal infections, especially Aspergillus in the lungs. Asthma is also a risk factor for colonization. With a specialist. You can develop slightly complex things like a BPA and Aspergillum as the slides cut off. Are they? Oh, sorry. It's because teams give me a notification. There you go. That better. Perfect. So this is what your Pneumocystis. Um X ray would look like it looks pretty normal on chest X ray. What you might have like you have here is a little bit of battling shadowing. So just this, I think you can see my mouth just this sort of shadowing around here around the Hailo regions. Um Yeah, a little bit of back wind shadow. It looks pretty normal on chest X ray despite the fact that d saturated quite profoundly. And then on see higher SCT you get this honey combing this sort of ground glass shadowing and you get these big cystic spaces. This is your classic Pneumocystis patient. Now, if we've decided the patient has pneumonia, just a normal pneumonia, how do we stratify the risk to the patient? Go of 65 and you'll know what it is. Um The only thing I'd highlight here is notice the restaurant has to be 30 it's not 22 score on a curb 65. You've got to have a really high respirator to score. Um and the thing to know about curb 65 is it's not just a scoring system that tells you severity. We're using this to guide our treatment. So a score of zero or one send them home, they go home with a mocks a score of two services 20. Yes. Yes. So tachypnea is 20 breaths per minute but to score the curb 65 it's got to be 30 which is why I think it confuses people sometimes. Yeah. So curve 6501, send them home with Amox Ifco 652. You're admitting and then on Comex and Clary, empirically, curve 65 of three or more is admit on Comex and Clary and discuss whether this patient needs to go to intensive care. Um, so that's how you're going to use your curb 65. And we've touched upon it there in terms of our empiric treatment. Your standard treatment is some combination of, um, a penicillin and a macrolide, Comex and Clary being most common. Perhaps really the answer here is trust guidelines. The only reason I include this is give you an idea that if you're treating a happy, you're going broad spectrum and you're normally thinking that you're sort of the things you need to make sure you're covering our MRSA and pseudomonas. If you're told you have a pseudomonal infection, you'll go to, um, antibiotics should normally be piped azo piperacillin tazobactam, there's loads of other antipseudomonal, um Ciprofloxacin and gent is used to pine is used. Ceftazidime is used in your exams. Pip Tazo tends to be the antipseudomonal. They want you to know about. If you know they've got specific organism you can treat it. So if you can confirm MRSA, you can deescalate the bank. If you confirm pseudomonas, you can deescalate to um Pip Tazo. Yeah. So perfect. So terazosin is your sort of your combination um antibiotic. And finally, just a quick note on aspiration, pneumonia, aspiration, pneumonia is quite controversial in terms of how it's managed often. What you'll hear people say is patient has aspirated high risk for an aerobed. You've got to offer anaerobic coverage. So that's not true more often than not. Despite all the sort of concern, most aspiration events cause a pneumonitis just chemical damage from the acid. They don't cause pneumonias. So they're normally isn't any organism to treat with an antibiotic. You can cover empirically with an antibiotic, but the guidelines are very, very clear on this that you do not start anaerobic coverage unless you have a reason to know there's an anaerobe. Either you culture it or they develop a cavett ating lesion or an empyema or something. At that point, you can add an antibiotic to cover for anaerobe. You'll go to is for anaerobic coverage or either metroNIDAZOLE or clindamycin. But you do not start those just because they've aspirated. It's only if you've got some kind of objective evidence of an anaerobic organism. Um It's a commentary question. So if we just go back to our men to just go over those questions again, there we go. So if you look at the, I can't pull up the, hopefully you can see the chest X ray. If you look back at that chest X ray later, what you can hopefully see is that you've got airspaces within that cavity. That's why we know it's a um an abscess rather than an empyema. The one person who said organism not sensitive to antibiotics used. I've given you it because if they've got an abscess, they've probably got a strange organism. So we probably the antibiotics we're using probably aren't up to it. But really the reason here is a lung abscess. As for this one, we've got lots of features here that push us toward mycoplasma. There. A youngest student with this sort of longish history, dry cough fever, myalgias. It sounds like an atypical. They've also got a target shaped rash and they're jaundiced. This is sounding like um erythema multiform a and like they got a bit of jaundiced, a little bit of Hamal icis. Um I noticed the chest X ray isn't your typical lobar consolidation? Any questions about that before we go on to the next section. So you can either use metroNIDAZOLE or Clindamycin. There you'll go twos for anaerobic coverage. Um There's a very rough rule of thumb. That says you use um, metroNIDAZOLE for Anna Robes in the abdomen or the pelvis and Clindamycin. If it's in the torso, if it's in the chest or the peripheries, that's a very rough rule of thumb. In reality, it's trust guidelines. Um, but metroNIDAZOLE, Clindamycin would be the ones I'd suggest for Anna Robes. Um, what nursery tractors are charismatics at risk of, they're at risk of all sorts, to be honest. Um Chlamydia pneumonia is the one that they say particularly for asthmatics. But if you're asked to pick the most likely organisms, it's still probably strep pneumonia. It's just that if they have chlamydia pneumonia, they're probably asthmatic. Okay. I'll just go back over to the. So the next section is going to be on what, what you would normally manage aspiration pneumonia then treat it like a normal pneumonia if at all like a pneumonia until you have evidence of Anna Robes. So cover with if the patient's unwell, treat them with Comox and clarity unless the chest X ray is showing a cavett ating lesion, unless the chest X ray is showing sort of a um an empyema or unless you've cultured like klebsiella or something or some of the anaerobe. But to start with treat it like a pneumonia, no worries. So we want to endocarditis now. So in the mentee. So which of the following be a major criteria for diagnosing infective endocarditis? Perfect. And there's a little nuance here. So I'm really happy that all of you got that. So many of you got that right. So, go back to presentation. So, endocarditis, effective endocarditis, it's an infection of the end of cardio. It's normally going to be bacterial. Very rarely you get fungal endocarditis. It's not what you're going to get. And we classified by its onset. So the infective endocarditis that you're also going to describe for me would be a subacute endocarditis. This is your indolent presentation. They're going to present with pyrexia of unknown origin. They're very flaws. E again, they feel sort of a bit of a fever that comes and goes a little bit under the weather for sort of weeks to even a couple of months. That's your classic subacute endocarditis is the one everyone always describes. Endocarditis can present acutely. These patient's are sicker ship, they present really, really septic and they often present in acute heart failure. They present nothing like the classic it is you have in your head. Um But that is also a presentation. It's more specific to um certain organisms. And you also get prosthetic endocarditis, which is just to recognize that in the sort of the month or two following a valve replacement, patient's a very high risk for endocarditis of the prosthesis. We also classified by the valve affected. Normally, you're gonna get endocarditis on the left side because that side is higher pressure. As you get more trauma to the valves, it gives somewhere for the bacteria to sit who gets right sided endocarditis, IV, drug users and classic is going to be a tricuspid endocarditis. Um And like we said, prosthetic prosthetic valves anywhere are going to be higher risk. So presentations, like we said, your classic signs of infective endocarditis in sort of your sub acute presentation, pressure of unknown origin constitutional symptoms. You here a new murmur that will normally be regurgitant. Anybody, can anybody tell me some of my embolic phenomena for infective endocarditis, winter hemorrhages. So, glomerulonephritis can be is not normally embolic. It's normally immunological which will come to in just a second. So, but you're absolutely right to say kidney involvement is a really important one to be aware of splinter hemorrhages and janeway lesions are your classic embolic phenomenon. And you can also get septic emboli to the brain, to the spleen, to the kidneys, big spleen and big kidneys or hematuria are really common ways for an SBA to hint at a infective endocarditis. So, watch out for those because they're not quite as well known as the classic Janeway lesion splintered hemorrhage and then immune phenomena. These are your Roth spots and oz nerves and also your glomerulonephritis. So you can get emboli to the kidney that cause a renal infarct or you can get an immunological glomerulonephritis like you mentioned. And again, you all know what these are your oslo's. How do we? So, yeah, in fact, they put it up in the picture. Oslo nose are classically painful, whereas January lesions are painless. You got Roth spots there on fundoscopy and you got your splint hemorrhages and that there is actually sort of a septic emboli, but to a joint instead, which would be a bit more unusual, but theoretically, you can get a septic MBA litter anywhere and then just a new focus of infection. Now, what organisms cause infective endocarditis? So there are probably two that you will have that spring to mind immediately. What would they be? What your two common causes of infective endocarditis? Good staff warriors and strep viridans. Now, this is going to be controversial and unfortunately, I can't not gonna be very helpful here. I don't know what your exam is going to say. It's classically taught that Strep Viridans is the most common cause of infective endocarditis is associated with poor dentition. And staph aureus is what you see in IV drug users. It's not true anymore in Britain part because we tend to treat strep pretty well. The most common organism full stop is staph aureus. Whereas Strep viridans is the most common in the developing world, this is a relatively recently sort of like established fact. So I can't promise what the exam is going to say. Here, I go off what you've been taught in your lectures. What is true is that Staph aureus is now most common in Britain. Strep Viridans most common worldwide, we will come back in slightly further on about another case where I can't really promise what they're going to offer you because the guidelines have changed and imperial don't seem to necessarily keep up, um, a couple of buzzwords to associate with less common organisms, but just to have a tight association with these risk factors, any person who's had a recent prosthetic valve surgery about that, we mean a valve replacement really in the last month or two, they're high risk for staph epidermis. This um that will be the organism if they've had a recent valve replacement beyond two months, it reverts to your normal typical organism. Patient's with colon tumor. Is this is an interesting, does anybody know what organisms we associate with colon cancer? Very good strep bovis. So what you're probably not going to be asked is a patient with colon cancer gets infective endocarditis. What's the organism? What's more important to be aware of? Is patient with infective endocarditis has strep bovis cultured that patient needs a colonoscopy because that's really high risk for having a colon tumor because it trans locates across the bowel wall. That's a really important association to have. What about if I say culture negative, what broad groups of organisms to be associate with culture, negative endocarditis, fungi and TB can both do it. Um They're both relatively uncommon even in the uncommon situation of culture, negative couple of organisms to specific have in mind. Are your hack hack organisms? You can look this up if you want, you'll have very long Impenetrable names because be aware of the abbreviation I would say. And then a couple of specific associations we've already mentioned them. Anybody with exotic birds has chlamydia Siddiqui silicosis. Anybody exposed to farm animals? You're thinking Coxiella. And what about if I said you've, you've drank unpasteurized milk recently? Does anybody know organism we associate with that? So the one to look out for their is brucella. So, Listeria as well, you're absolutely right. Listeria, you would also associate with unpasteurized dairy doesn't tend to cause um infective endocarditis. More concerning for meningitis. That one um for infective endocarditis, brucella is the one to associate with unpasteurized dairy. And then we come to diagnosing infective endocarditis. Now, the duke criteria, this is sort of a summary of the Duke criteria. Massive long list. Don't bother learning it. What I'd say is no, your major criteria. So your major criteria are evidence of endocardial involvement by which we really mean an ultrasound showing the new regurge and ideally a vegetation and blood cultures that are really, really positive for um infective endocarditis. What we mean by that is you need more than one of them and need to be an organism that is normally associated with endocarditis. So you're thinking your staff's your streps, your typical quote unquote culture, negatives. It has to be at least two of them and it has to be a typical organism there. Your major criteria, your minor criteria are kind of everything else. Patient's with fevers, patient's who are high risk vascular phenomena, immulogic phenomena. When it says micro biologic phenomena, that means a culture that doesn't meet the criteria. So it might be one positive culture for staph aureus or three positive cultures for listeria, an organism that doesn't tend to cause it wants to know really well though, know your major criteria and to make the diagnosis, you need two major criteria, one major in three minor, all five minor. Broadly speaking, I would expect them to ask you a question where you have one major in three minor and see if you catch that as meeting criteria. But don't bother learning all the insights of the details. There's too much, it's not worth it. So then we come to treating infective endocarditis, it's a long course of antibiotics. I wouldn't expect them to ask you to pick between antibiotics because it's very sort of specific to the organism and the trust. But empirically, you're gonna go very, very broad and it tends to include gentamicin. So a typical regimen might be something like ciprofloxacin plus gent plus, maybe amox or something. It'll be very, very broad spectrum and includes gent to cover for um gram negatives. Once you know, an organism, you could often pick, obviously pick a specific um antibiotic. So if I told you, you had a staph endocarditis, you can treat with flu clocks or bank. Likewise, if you know it's strep Vera Dance, you might be expected to pick Ben Pen out of a lineup. But if it's empiric, it's going to be very broad. I wouldn't expect you to have to choose between them. Now, alongside antibiotics, the patient's might need surgery. I don't really know any indications for treating infected Benaco to surgically. So there's loads of them. And if you go on like BMJ, best practice, you'll see a massive long list of very precise criteria. These are the ones that are worth knowing. The patient's just not getting better on their antibiotics. They, they're, they're appropriate antibiotics, but they're not improving. If the patient's presented to this acute heart failure picture, they need repairing of the valve immediately. So they would get surgery, any patient with a prosthetic valve, they need the valve normally taken out, cleaned and replaced. So they tend to get surgery and any patient who developed uh an abscess in the aortic root. So this is if you're an aortic infective endocarditis and develops an abscess. The reason I highlight the abscess is the, is the way you know, that is actually very simple. Patient with pr prolongation is something to look out for pr prolongation, infective endocarditis suggest they've developed an abscess and they're probably going to need surgery. And I'm just gonna mention this very, very briefly. Don't know anything about it. Just be aware it exists. You can get endocarditis with vegetations on the valves without an infection. A few things do it sle or antiphospholipid syndrome can do it. Um That's called Libman sacks, endocarditis. And patient's who have musing, producing adenocarcinomas with pancreatic adenocarcinoma being the one that's sort of especially prone to, it can also cause vegetations to fall on the valves. Don't know any of the deals, just be aware it exists. And that's everything worth saying about endocarditis. I say any questions about any about endocarditis in general, anything we've talked about there? Yeah, we just highlight this question here. So the reason this is the correct answer, I've been a bit tricky here. The one positive culture for staff is not a major criteria cause it's only one culture. The three for staff saprophyticus is not a major criteria cause it's the wrong organism. And Ottawa notes and um sort of high risk patient, both are minor criteria. The only major criteria here is where we have multiple cultures of a typical organism. So if that's, if everyone's happy with that will go on to the next section which is on g eye infections. So which of these organisms is least likely to cause dysentery? Just be clear, dysentery. Buddhist really mean bloody diarrhea. It's a bit of a split here. The actual answer is salmonella typhi. And again, I've been a little bit Trixie here cause I wanted to highlight. So lots of you said your senior and I'm glad you did because I certainly want to highlight that organism which will come too soon. So on to gi infections. So we can broadly split the way they're going to present into three groups. You've got secretary infectious diarrhea that just presents the diarrhea, inflammatory, infectious diarrhea, that's going to present with dysentery. So bloody stool. And then you've got your infections that cause systemic unwellness and often these are non bacterial. You're thinking often protozoal things here. And I'll just say right now, up front for the most part, the answer is not going to be antibiotics. The only times you tend to use antibiotics are specific organisms. And I'm thinking c diff mostly here. Um Yeah, that's the main one. I'm thinking, I'm also some of the protozoa ones or if they're really, really high risk or really unwell but broadly patient with a sort of a typical secretary infectious diarrhea, you're probably just going to manage them supportively. They normally don't need antibiotics if they do need antibiotics, version of the organism. Ciprofloxacin is normally a fairly safe guess. Um, if you're not sure, but you can look up if you want and learn specific antibiotics for different gi infections. I don't think it's worth doing. So if we start with secretary bacteria were again, basically just going to play the buzz word game. So if we start with Bacillus cereus, what buzzwords do we associate with? Bacillus causing a secretary? Um, diarrhea. So the one I would say to be aware of for this reheated rice very recently, reheated rice and now sort of sort of sort of have food poisoning, e G eye infection type of presentation. You're thinking bacillus staph aureus, anybody have any association with staph aureus. So, your classic history here, I would say is they've been to a barbecue recently and the key with suffering is very, very short incubation time. The reason being that the symptoms aren't from bacterial colonization is from preformed toxin. So you don't have to wait for the bacteria to multiply the toxins already there. So it's a very, very rapid turnaround between eating and the onset of the diarrhea. E COLI is your classic travelers diarrhea. So somebody's returned from abroad and they've now got this secretory diarrhea. You're thinking e coli notice E coli is normally nonbloody. It's only the specific I think it's called the heck you're hemorrhagic E coli, but mostly coli is non bloody. And finally, cholera. Anybody have any buzz words for cholera. So the one that the one that you should definitely associate with cholera is rice, water stool. Any views described as having rice water stool, think cholera and those I would say your most calm, they're the highest you want to know. For secretary gi infections. The dysentery are are inflammatory causes. These ones that cause bloody diarrhea. Does anybody know any sort of memory aids? But knowing your your dysenteric g eye infections? So the one you might have come across one people tend to know is chess. So these are the organisms you should associate with dysentery. So, campylobacter your hemorrhagic e coli entamoeba hissed elliptical, which is sort of an amoebic abscess. Um salmonella enteritidis notices entering not salmonella typhi that causes typhoid, um which classically actually present with constipation, not diarrhea, salmonella enteritidis causes dysentery and shigella. These are the five that everybody tends to know about. The one people forget about is yesenia. So yesenia anti politica. It presents with non bloody or more often bloody diarrhea. And the other reason to be aware of it is it often causes um, terminal iliitis. It affects the terminal ileum more than any other bit of the bowel. And of course, um sort of a lymphadenitis in the bowel as well. So it often resembles appendicitis. It comes up a lot in your Pedes exams, patient who has sort of a diarrheal illness and they've got sort of that right, lower quadrant pain and it's actually a senior rather than appendicitis is just want to be aware of. And then we have our protozoal g eye infections. So, entamoeba, histological, like we said, it presents with dysentery. It often presents with a bit more of like a chronic diarrheal illness. And the classic thing to point you this way is right, upper quadrant pain, hepatitis, liver, abscess on ultrasound. Now, the buzz words on histology are apparently they have flask shaped ulcers on histology. And if you aspirate them, the abscess contents look like anchovy paste. I'm going to show you in a second. I'm not sure I buy it but that they're the buzzwords to associate and we treat it with metroNIDAZOLE. This is one of the causes we would treat Giardia is the other major, um, protozoal infection to be aware of. This also presents with chronic diarrhea. It's not normally dysenteric, but they often present with a several week history of sort of malabsorptive symptoms that can almost sound like almost like what you find in like a chronic pancreatitis, celiac kind of patient. These patient's often very sound, very much likely have celiac disease. And the buzz word on histology to look for is they have trapezoid, pear shaped trapezoid or what you should be described as seeing. The only other one I just mentioned briefly is cryptosporidium or micros Pyridium. This is your go to course of diarrheal illness in patients with HIV. They often get colonized with this protozoa. Now, that's Giardia allegedly, that is a pear shaped trapezoid. I'm not convinced it's very pear shaped, but that's what they're looking for. And likewise, that is apparently the flask shaped ulcer of entamoeba Hista Lyrica. Again, I can't say I really see it, but that is what you're looking for. I'd expect them to describe it rather than expect you to recognize it. Finally, we're gonna talk about C diff. Now, how does C diff present, what's your classic history for seed if you definitely know this? No one, I think your chat might not be working because like people have been answering for the last few questions, but have they? Okay. Um I see. Sorry. Thanks for letting me know. Um Let me just refresh this because I've got it open in another device so I can see the chat. Sorry about that. Um uh fab there we go. Ok, thank you. Let me know. Um Yeah, absolutely. Spot on. Um, yeah, so recent history of antibiotic use and they've been in hospital for something else. Do we know which antibiotics are classically associated? So, careful sports are the big one. People often say the three CS. So careful sporting's Clindamycin, Ciprofloxacin. But careful sporin wants to most be um sort of aware of diagnosing it. You can diagnosis like your, your first line test, your thinking is a stool toxin test for C diff and you can also diagnosed by visualizing the pseudomembrane cause we also call C diff pseudomembranous colitis. Um Now this is gonna be, this is gonna be again, this probably the most controversial, but I know we argue to toss about it extensively last year. What would you say is the correct way of treating C diff if you confirm the diagnosis, how do we treat it? Okay. Yeah. So, so Jack has hit the nail on the head. There, there is controversy here. Um I can only teach you what is actually correct. So according to nice guidelines and this has been the case for about a year and a half, two years. Now, you never treat C diff with just um with just metroNIDAZOLE. Nice guidelines are very clear on this. If you look this up on the BMJ, best practice, very, very clear patient who has their first infection, you treat with oral vancomycin patient who has their first recurrence. You treat with fid axum icing if it's been within 12 weeks of the last episode, otherwise you can use bank again. But if it Rikers within the 1st 12 weeks, you use a rather new antibiotic called Pradaxa Mission patient's who have further occurrences, you treat the same way again and these patient should be considered for fecal fecal microbiota transplants and any patient with a formal int infection. So really severe illness and that's indicated by patients who are in shock or patients who develop a toxic megacolon. So a dilated large colon should be treated with oral bank IV metroNIDAZOLE and considered for surgery. A quantum eyes guidelines. There is no place for just treating with metroNIDAZOLE as has been mentioned there. This is, this is not what I believe has. So has Mirren still been teaching this year to go metroNIDAZOLE first line? So I'm going to presume that. So yes. In that case, I honestly, I honestly can't tell you what the right answer would be in the exam. All I can tell you is the guidelines now are very good. We had this conversation with, with in one of the lectures last year and sort of asked straight up what would be the correct answer. And we were given a very sort of hand wavy response about if you lose one mark, it's not that big a deal. So I can't tell you what they're looking for the exam. What I can tell you is, that's what the actual guideline is. Now. Oral bank is first line treatment for C diff And give you an idea of why it's called pseudomembranous colitis, which you also sometimes he described sort of rather than appetizing Lee as wet cornflakes. This is what it looks like. So this is what the pseudomembrane looks like um in patients with C diff which is pretty horrible. Um fab. So that's everything on g eye infection. Sorry, I missed the chat of it. There are there any questions about anything and if we go back to this? So this is why salmonella typhi is the correct um is the correct answer. Salmonella typhi is not what causes salmonellosis. This causes typhoid fever which doesn't even normal present with diarrhea. It normally presents with um constipation amongst other other symptoms. You learn about that in the other micro lecture. Um Yeah, I I don't disagree with you, Patrick. I can't say I thought that was a very satisfying answer, but it was, it was the one we got. So, unfortunately, I really can't tell you what they'd be looking for if that was the question. All I can tell you is that the guideline is very clear. Now, the first line treatment of C diff is oral bank. It's no longer IV metroNIDAZOLE. Okay. So on to U T I S. So we'll go back over to the mentee again. So place up, your old woman has a three day history of dysuria and smelly urine, urine dip shows leukocytes and blood but no nitrites, which is the likely explanation, Bob. So this is again a bit of a trick question one that often catches people out. So I'm really glad to see so many of you get this right. We'll talk about why. That's the right answer soon. So UTIs, so we split UTI S into complicated and uncomplicated. And these are the things that would make a uti complicated. Any patient with a physiological or immunological abnormality, any patient who's pregnant and any patient has received instrumentation. Does anybody know why we distinguish between complicated and uncomplicated? Uti s? Good. It has ramifications for your management and in particular, the duration of antibiotic therapy, we can also split by the severity of an infection and where the infection is actually set up. So your lower uti or your cystitis is only affecting the bladder. They're gonna have sort your typical uti symptoms. Pilo nephritis is what we call it when it's ascended to the kidney, pyelonephritis, patient's gonna look unwell, they're gonna be federal there classically present with rigors, sort of flank slash back pain. Um And there's just systemically very unwell. Pyonephrosis is something that is, a lot of people haven't come across. Does anybody know what a pyonephrosis? Well, actually, that's a daft question when I put the answer there. So, pyonephrosis is pyelonephritis with the obstruction. So, a patient has an infection in their kidney and they've now got obstructive symptoms. They're not producing urine. You do an ultrasound, they've got hydroureter hydro um like an enlarged kidney and you can see all the flow backing up. That's a pyonephrosis iss. How would a pyonephrosis change management compared to a pilot nephritis draining? So, I mean, you're absolutely rather senior involvement. I mean, when in doubt, certainly my patient is concerned, just say senior involvement, but you need to drain that infected fluid. It would be surgical. So these patient's normally get nephrostomy troops put in um to drain away all the, all the pus. And then later on, you can think about there's any sort of more definitive surgical management required. But in the short term, they tend to get nephrostomy troops put in. When we say instrumentation, you might mean a patient who's just had a cystoscopy for instances, they've just had a Turp's procedure that some kind of instrument inserted into the urethra. So in terms of investigating UTI S, it's going to be a lot of the stuff you already know urine dip. Now, that question that was just asked was about nitrites. Does anybody know what nitrates signify on a urine dip good. So night try to do are not specific for uti, they are specific for college form uti. If you want to get bogged down in the detail, it's because it's about whether it expresses an enzyme that I believe reduces nitrates to nitrites. All of the you have nitrate in your urine and it's whether it's reduced to nitrites by specific um enzymes in the that the bacteria express. So, nitrites are specific for color form UTIs. For patient is negative for nitrites, doesn't mean it's not an infection. It just means it's probably not echo like any of leukocytes, nitrates, hematuria are all very common on urine dip. You do not need all of them and you especially you do not need the nitrites to have a uti. If you have the nitrites, you've almost certainly got echo like that. But otherwise, it doesn't rule out a uti. These are your diagnostic criteria. Um These are probably worth being aware of the quite like questions that have the specific number of colony forming units and these are your cutoffs to formally diagnose it. Obviously, this is all in the clinical context. If the patient has all the symptoms of a uti, they probably got a uti irrespective of whether it quite meets these criteria. And if there's any concern for complicated uti S, you're gonna think about getting some renal tract imaging. Um normally ultrasound or CT in the first line um in terms of the M C N s, are there any feature, what features would we look for? That might imply a contaminated sample. So, mixed growth is the big one coag negative staph um is actually is actually one of the organisms that is plausible and we'll talk about in a second. But yeah, so epithelial cells or squamous cells in the sample bacteria that don't make sense of staph aureus, If you see staph aureus, that's not really a uti organism. And any patient with mixed growth classically, the way they might ask this is there'll be a patient with no uti symptoms. I know like an elderly person who's a bit confused, they thought sod, it will test for a uti and they get a mixed growth or they get staph aureus and squamous cells that is not convincing for a UTI which just real straight this importance of the clinical context, especially the elderly people. So, urine dips give you lots of false positives, especially in the elderly and a symptomatic back to urea is normally not an indication for treatment. All people often have E coli in the urine doesn't mean you treat it. Who's the only people that we treat a symptomatic back back to urea in pregnancy? Good. So it does the causes of uti we've already touched on most of this. E coli is the most common staff saprophyticus is one to look out for in young women. Um Oh, ignore what I said. Are you are absolutely right. Take coag negative staph, I'm confusing. Saprophyticus. And epidermal is, you're absolutely right. Coag negative staff will be like epidermal is which we wouldn't expect as a uti sorry about that. Um So the colon staff saprophyticus are your most common causes. What organism might you associate with struvite stones? I mean, if anybody knows this is a really useful association to have this one they like in exams. Good proteus. So, Proteus and Klebsiella are two organisms that are a bit more common in patient's who have abnormalities in their renal track, like um structural abnormalities. Proteus in particular causes alkaline urine which it precipitates struvite out. So they form these struvite stones. That's a very tight association in exams. Um Ureaplasma is a good shout I believe. Is you your testament ureaplasma? I think, I think it can cause a uti um but I wouldn't have it as a very common one and I certainly wouldn't very, very loath to get it in an exam. I can't really think of any tight associations I'd have with it. Um It's definitely a legitimate organism though I, I definitely remember it. And then, as I mentioned before, t genitourinary TB classically causes a sterile pyuria. So leukocytes, but no organisms on culture. It's not the only course S T I S can cause a sterile pyuria. Um tubulointerstitial nephritis can cause a sterile pyuria classically with the eosinophil cells, but TB is the one that if they've got gum, like chronic gum symptoms and a sterile pyuria. Think genital urinary TV in terms of treating UTI S. What antibiotics do we go to? Much fear and toe in trimethoprim and can everybody name one other one? It's slightly behind these two, but it's important to keep in mind you can use Bactrim um Keith Alexin I says you want to have in mind. Um And if it's an uncomplicated uti or if it's a complicated uti or if their mail they get different durations, so typical uncomplicated uti three day course, if it's more complicated, it's a seven day course. Now, what are the nuances between picking between nitrofurantoin trimethoprim Catholics in? So trust guidelines, pregnancy. So how does pregnancy affect our choice of antibiotic here? Mm Interviewing can be given in the first but it can be given in third trauma. That can be uh So that is absolutely correct. You're absolutely right to say. So you can't give trimethoprim in the first because it's a folate antagonists. You can't give nitrofurantoin in the third because it causes hemolytic anemia um in the new in the baby. Now, technically, now that's technically true. A lot of guidelines say don't trimethoprim, it'll even though you've taken, there's no reason really that you couldn't, a lot of them are advise against it all the way through the pregnancy. Um So you'll often see people start Catholics in if they, even if they're like third trimester, but you're absolutely right. Say that really, there's no reason to not use trimethoprim in the third trimester. Um uh Obviously careful election is a uh cephalosporin. So, watch out for penicillin allergies. The other thing to watch out for trimethoprim is what drugs you need to look out for that. They might already be on methotrexate. Do not give trimethoprim if they're already on a folate antagonist. Wow. If they got pollen arthritis, they're going to be sick. Admit the patient normally again, trust guidelines, I wouldn't expect them to you to make you pick the antibiotics comex. And gent is a pretty typical starting regimen gent for the gram negatives, co marks for the ground positives. Um but I wouldn't expect them to make you pick between them and a symptomatic back to area do not treat unless they're pregnant. There is no reason to have any questions about that. Okay. And if we go back to the mentee, so that's why this is staff saprophyticus. There, nitrate negative is pretty unlikely to be e coli. This is still very consistent with the uti kidney stone is a reasonable. It's certainly with the urine dip, kidney stone would be consistent. The history here is what the problem is. You've got three days of dysuria and smelly urine. It doesn't really sound like a kidney stone. So, nitrofurantoin is contraindicated in the third trimester. It causes a hemolytic jaundiced um in the, in the in the baby. Okay. In that case, any questions I have left. Um So we don't have a question for this. Actually, this next section is very brief because there's not really much for me to say here. So the next section, this is something you are just gonna have to really brute force learn is iatrogenic infections. The ones that they sort of asked about, commonly, I'll just move this out of the way. Are these four? They like to ask about surgical site infections, Osteomyelitis, septic arthritis, and prosthetic joint infections. These organisms in terms of their prevalence, this is cannon fodder for the ranking questions you have where you've got to sort of rank from most to least likely. I used to like 54321 absolute cannon follow for those questions. So super high yield go through the guide and learn the organisms in order of abundance. I'm not going to bore you by reading out each one in order. Now, I'm just going to highlight a couple of specific features. So for Osteomyelitis and septic arthritis, patient's with sickle cell are specifically a risk of salmonella. It's because they tend to get sick, ling um of the blood vessels that perfuse the bowel wall. The bowel becomes a bit of edematous and leaky Samil across is through and is really prone to causing osteomyelitis and septic arthritis. There's a specific risk factor there to be aware of. Um otherwise just learn those lists of organisms from most least likely. And the only other specific to add is exactly like the prosthetic valve staph epidermis. This is most common in the first two months, right, in that acute or subacute bit after the joint replacement or the whatever prosthesis, they're high risk for staph epidermis. This once you're several months down the line, it reverts to your typical risk factors or your typical most common organism. So, if you've got a prosthetic hip and two years later, you get septic arthritis, most common is most likely is going to be Staph aureus. It won't be staph epidermis. That's only in that first month or two. Otherwise I'm not gonna dwell here very long. There's no point. This is just something, unfortunately, you have to brute force memorize, but just emphasize getting really high yield in the exams. So we'll move on to CNS infections. So now we will go back to the emergency and 34 year old man presents with a two day history of fever and meninges. Um L P shows clear fluid lymphocytosis, raise protein and glucose at 65% of a matched serum sample. What's the most likely diagnosis? So, you're torn between the two that I thought you would be. Um And again, I've been a little bit cheeky here and so we'll talk about why viral meningitis is the right answer in a second. So CNS infections, there are three things that we can have really where infections in the brain are concerned, you can have meningitis, inflammation of the main injuries and this can be bacterial, viral, fungal TB. It can also rarely be some other things and it presents with meninges. Um What is the difference? What, what, what is meninges? Um What do I mean? When I say LA good, it's your stiff neck, your photophobia, your headache, you're positive. Kernig's sign. Why, why do you, why, why is it important to distinguish what causes meninges? Um But isn't meningitis? Yeah. So the reason I highlight is because subarachnoid is worth bearing in mind. Patient's with meninges. Um it could be meningitis. Subarachnoid can definitely irritate them and injuries and cause the same constellation of symptoms. So just be aware that there is a distinction between those two. You can have an N Katha litis and this is almost always going to be viral. It's an inflammation of the actual brain parenchyma. It can rarely be autoimmune things you have probably heard of like limbic and Katha litis NMDA receptor and Katha litis um Edem or all causes of encephalitis. Very, very rare. It's going to be a viral encapsulitis compared with meningitis. They can often present very similar. They can, they are often really, really unwell and they might well have a bit of meningeal inflammation with their encapsulitis so they can present with meninges. Um The big difference between the two is the altered mental state. Often in the vignette, you'll have some description of strange behavior for a few days with an encapsulitis. They've not been themselves, they've been angrier than normal or more tired than normal. Obviously, that isn't necessarily always too easy to distinguish if it's very acute onset or they're just really, really unwell. It's hard to tell if they're drowsy because they're unwell because they're in Catholic tick. So we will often and we'll talk about this in, we'll recap this a bit later. Often you treat empirically to cover both. And then the third type of infection, the CNS is an abscess. This is an actual collection within the brain, upper income. Er, and this presents like all your other abscesses are gonna present, often presents with, um with sort of swinging fevers over a bit of a longer history and it often presents with symptoms of a space occupying lesion as well. So what things cause meningitis? This is again, a list of organisms and again, I'm not going to bore you by going through them all, just highlight a couple of them. So, in neonate, they're high risk group B strep and listeria. What is group B strep. What organism is that in particular? That's the one you made, the right decision to not try and spell it fully that the Strep Eagle actor something or other. Um, the one we're screening for potential. Well, not screening for, but the ones that we sometimes identify in pregnancy and Listeria, um E coli as well. But those first were the ones to keep in mind for donates in adults. Wide list of organisms you'll, you'll go to are going to be in this area and streptococcus and for elderly people it kind of reverts of it. They get a lot of group B strep and listeria again. Um, and also just strep pneumonia. Um Yes. So the reason I highlight the difference there is what's the relevance of younger, very young and old people getting listeria meningitis? What's the importance of being aware of that? So the immune immune status is probably why, but why, why do we care? Good? It's slightly changes are antibiotic coverage. It's yet perfect. It change that we add an extra antibiotic if we're worried about potential hysteria. So there are bacterial causes and don't forget immunocompromised people. HIV, in particular, you're thinking possible tuberculous meningitis viral causes. Your most common ones are enteroviruses. Um So sort of your advisors, Coxsackie and HSV two. I'm just going to highlight this HSV two is the, is, is a common cause of meningitis. The most common cause of encapsulitis is HSV. One, this is again cause a bit of dispute. Let me take that. Really HSV two for meningitis, HSV, one for encapsulitis and also be aware HIV, Sirivudh conversion can present with meningitis. It's not common, just something to be aware of. Then finally, we have our fungal meningitis. Um Cryptococcal near Foreman's is the one to associate with HIV, cryptococcus Gatti is actually cause a fungal meningitis and immuno competent people. It's very, it's pretty small print. The one to know is cryptococcus near four months for patients with HIV. Okay. So going to diagnosing, we're going to take a history and then we want to do an LP and I'm going to take the sort of a moment here cause this is again, something that people often sort of disagree on or there's a bit of confusion around what are are indications for CT before L P. Let me rephrase it slightly. Yes, you're on the right. Let, let me rephrase slightly. Why do we, why do we sometimes worry about doing an LP? If this, if the patient has raised intracranial pressure, why do we worry about an LP? So we worry about koning but it's not but they don't cone because they have raised intracranial pressure, they cone if they have raised intracranial pressure secondary to a space occupying lesion. Because for instance, hydrocephalus causes raised intracranial pressure, but L P is therapeutic for hydrocephalus. The specific concern is if you've got something in the brain, pushing on the brain and raising the pressure, if you put a hole in the base of the spine, you give somewhere to try and relieve the pressure. So the brain is going to, you're going to try and relieve the pressure in the skull, everything moves down towards the hole and you konw. So it's specifically concerned for a space occupying lesion. So any patient who has a focal neurology, any patient with papilledema patient's with reduced G C S or patient's with seizures. You need to be thinking about CT before LP to rule out a space occupying lesion. If the street CT shows no space occupying lesion raise ICP doesn't matter anymore. It's no longer a contra indication. The concern is specifically if there is a space occupying lesion, so then we can get RLP. Ideally you do the L P for antibiotics, but much like with cultures, we don't delay antibiotics. If we can get the LP immediately, which granted it's pretty unlikely, then do it otherwise, um start antibiotics, get the LP as soon as you can. And then we're gonna analyze the CSF. We're gonna do a biochemical analysis. We're gonna gram stain B PCR for viruses. We zeal Nielsen stain for TV. And remember the India Ink stain really good buzz word for cryptococcus pneumonia. Um That's the same. We used to identify it in terms in terms of interpreting CSF, you can find lots of tables like this. I'm not going to go through every bit of this table with you. Um It's a waste of time. You're very, you can very easily look this up. The things that would highlight that are actually useful are patient's with a bacterial meningitis, have a massive neutrophilia. For the most part, it can be something else. It's normally going to be neutrophils and they're going to be sky high, they're gonna have loads of protein, it's gonna be through the roof as well. Glucose is going to be down because the bacteria are eating it. Compare that with a viral meningitis. The fluid looks normal. You get a lymphocytic predominance a bit more protein, normal sugar because there's nothing to eat the sugar. Fungal TB tend to look pretty similar. The fluid's going to look kind of gross. It's not as bad as like a period lint bacterial meningitis. But it's kind of halfway between the protein is kind of halfway in between. It's up, but more than with a viral meningitis, but not as much as a bacterial. The white cells are kind of in between their up but not as much as a bacterial meningitis. And it tends to be lymphocytes and monocytes that you see and again with fungal and TV, because there's an organism there, there's something to eat the sugar, the sugar goes down. So normal sugar kind of tells you you're dealing with the viral meningitis when it comes to treating it. I'm sure you will know this patient presents to the G P with meningitis. What do you do for the patient? Good. I am Ben Pen and then call the ambulance. What about if they're in the hospital, if they are in the hospital? What are you going to give them when you first make the diagnosis of meningitis identity? We had kept try Axon any advances on any, any other antibiotics or any other medications that we're going to give good. So I was hoping somebody would say this the steroids is so I want to talk about cause again, it something people argue about a lot. I know um certain lecturers have strong views on. So in the hospital you diagnose meningitis, empiric treatment is going to be IV kept reaction or kept a taxi. Um They're both third generation cephalosporins and you can add ampicillin or amoxicillin if they're very young. I believe you all know this better than me because you're doing Pedes. I believe the cut off is three months, I think is that under three months you give ampicillin or amox or if they're over 55 I want to say over 50 or 55 you give ampicillin as well to cover for Listeria. Dex is controversial. So actual, the actual guidelines say you do give DEX. The reason you give DEX is if they have specifically meningitis caused by strep um strep pneumonia or by her marvelous influenza, it reduces the incidence of sensorineural hearing loss if you give five days of decks. So what that means is the guidelines say give decks with the first dose ideally just before the first dose of right as you're doing it. And then once you've got your LP and whatnot, if you confirm the organism is strep or h flu, consider, continue a five day course of steroids if not discontinue, that's what people tend to do. I know some of the lecturers say that like, don't worry about, it's not something that happens. That is what the guidelines says. It says steroids with the first dose. If it's strep pneumonia or h flu continue for five days. Wow. And obviously, you know, if you identify different organism afterwards, if you identify cryptococcus, you're gonna treat with antifungals. Uh be amphotericin B I think off the top of my head. But you treat with antifungal if it's fungal anti tuberculous agents, if it's TV. So encapsulitis as I'm information HSV, one is by far and away, the most common cause in the UK be aware that patient, you know, return, you know, recently returned foreign traveler, lots and lots of different viruses that do it. West Nile is one that's like rapidly growing in a lot of tropical and subtropical areas. So one just to know the name of, but the list would be massive. So I don't think they'll ask you to pick out of them. Um A couple of buzzword, the ones that are rare but worth going for the exams. If I told you our patient's unvaccinated, had measles as a child and now 10 years later had um a careful itis anybody have any idea what I'm referring to? Very good. Yeah, S S P which stands for subacute sclerosing panencephalitis. I know nothing about it other than that buzz word association with measles in childhood. Although if a patient either has HIV or has been started on monoclonal immune suppression JC virus. Perfect. And what does it cause? Did we know the name of the syndrome? It is multifocal it. So it's PML or progressive multifocal leuko encephalopathy. Um I believe that's what it stands for the top of my head. So, yeah, those are just a couple of very rare causes but very easy to have like a buzz worthy thing. So just worth being aware of those. And as I said before, if you've got encapsulitis, you're going to treat it empirically because it's normally going to be herpes. You cover empirically with acyclovir to MRI can help you diagnose as can LP. There's no specific LP findings that help you identify organisms. MRI can help you identify organisms based on like the areas of the brain that are showing the inflammation, especially on things like t to flare imaging, not worth worrying about. And you got a PCR for organisms um empirically just treatment they cycle here. Finally, brain abscesses. So, abscesses in the brain typically are going to be mixed growth of organisms. You normally get something staphylococcal or streptococcal in there and a whole bunch of anaerobe that sort of moving as well. Typically, you're looking for a mixed growth specific cause worth being aware of patient with HIV has a brain abscess. What do they have? Yeah, talk. So talks would be the one that you're thinking. So, so people often confuse these two cryptococcus in HIV, is meningitis, toxoplasmosis in HIV is brain abscess. Um, yeah, but yeah, if in the absence of HIV, it's often Staph or strep with a whole bunch of an Arabs mixed in. We're gonna diagnose with, um, sort of central imaging. We prefer MRI S two C T S for brain abscesses and you're looking for a re enhancing lesion and I'm surprised that you're going to treat it with antibiotics. If you're giving antibiotics, again, I wouldn't expect them to make you pick. But because it tends to be a mixed growth, you're thinking broad spectrum plus anaerobic coverage. So it might be again, something with gent and metroNIDAZOLE and like careful something. Um And you might consider whether you need surgical drainage and because they've got a space occupying lesion, you might consider they might need steroids to bring down the swelling. They might need antiseizure educations prophylactically um to prevent them seizures, they often get loaded on Keppra levetiracetam. But I say antibiotics obviously depends on the cause. If a patient has HIV and you're treating Toxo, you treat with a drug for toxoplasmosis. Um You probably know this better than I do at the moment because of oh MG, I believe pyrimethamine is what they use. Um But somebody correctly in the chat, if I've got that wrong. Um And there's your imaging of, there's your sort of your contrast imaging of the brain and you can see this sort of really nice there, this ring enhancement. So if we go back to the question, if anybody has any questions again, pop them in the chat before we move on. But we go back to the mentee question. So this is a viral meningitis because they got clear fluid. They've got a raised lymphocyte count and the glucose is normal. Let me just highlight there as well. Glucose is never really measured in isolations. It's as a percentage of the serum sample and anything less than 60% is what we normally say is starting to besides think it's been reduced. Anything about 60%. That's a normal serum LP to serum glucose ratio. Okay. In that case, we'll go onto the last section which is on S T I S. So anybody can join for the last question up. So 23 year old male with a history of S T I S presents with fevers, postular rash on the body and red, swollen, left knee and right wrist, which of these organisms is most consistent with the presentation good. Um This is indeed gonorrhea and I tell you how much salt you put chlamydia. Um It's very easy sort of like brick to make between the two and it's we're going to talk about it in just a second. So I guess you guys, I apologize in advance some of the pictures um that we're going to be coming here. Um They certainly help you remember the conditions but they're not very, not very pleasant. So, start with chlamydia. It's caused by chlamydia premises. And if they ask this is the most common ST I, um, it's more common than gonorrhea. Now, people say in the chat some of the ways that chlamydia might present. There's quite a few, I would say this sort of fall worth knowing so it can present with ST I symptoms so it can present with sort of pain, passing urine. Um sort of any changes in your discharge, bloody discharge. So not pneumonia, it's a different chlamydia. Um It's the same, it's the same genus. It's a different species. Chlamydia pneumonia is caused by chlamydia, pneumoniae, not chlamydia trachomatis. Any other ways that somebody with chlamydia who've had chlamydia might present reactive arthritis? Good, good. So we've covered a good couple of them. So these the ones I think are worth knowing worth highlighting. It can often be a symptomatic worth just being aware of that. So then the classic presentation is going to be your typical sci symptoms. If you don't treat it, you get P I D, you can get to below various abscesses. You can get epididymo-orchitis. Your classic ST I presentation reactive arthritis, chlamydia are not gonorrhea causes this, which is gonna classically present with anterior uveitis, pain or passing urine oligo arthritis and also your certain it balanitis and keratoderma, blennorrhagia, calm. Now, the last two are a bit more small print but worth being aware of So a couple of the specific serovar is which I think means the same thing as sort of sub species, I guess. Um if anybody has any insight to say in the chat, but specifically serovar L1 to L3 causes disease called lymphogranuloma venereal, which presents a bit differently. It normally presents first with proctitis and then really, really like obvious, painful, swollen, enlarged inguinal lymph nodes called buba bows. It's particularly common amongst men who have sex with men. Um Worth being aware of that presentation. And then in neonatal, it can present something called ophthalmia neonate orum or a neonatal conductive itis. So can gonorrhea. So it's really important to be aware that chlamydia causing neonatal conjunctivitis presents a week or two after birth, which we will sort of compare to gonorrhea in just a second. You diagnosed it with a nuclear Kassid application test. You cannot culture chlamydia in terms of treating it. Loads of things. You can use guidelines changed a couple of years ago. They now prefer doxy to azithromycin. And yeah, actually, I apologize some of the pictures that are coming. So this these are some of the things that you might find in reactive arthritis. So that rash on the hands. That's your brown rat, Parma plantar rash, that's your keratoderma, blennorrhagia, calm and picture d that rash is certain that balanitis. These are inguinal BUE bows. So this is what you see in lymphogranuloma venereal. Uh probably easy to act in, these are very, very, very painful for the patient. And finally, this is neonatal conjunctive itis. And when it's caused by chlamydia, it's a week or two after the child is born. So you compare that with gonorrhea, it's less common than chlamydia. And the ways that it can present are, again, it can be a symptomatic. I believe it's less likely to be a symptomatic than chlamydia. But it can certainly be a symptomatic. Often presents with, it can often turn with your typical ST I symptoms, progressing to P I D. Again, it goes without the disseminated gonococcal infection, which is sort of characterized by um sort of a dermatitis arthritis pattern. So you're looking for lever migratory oligo arthritis. So it be painful, red, swollen wrist and then a different knee and then uh and then an ankle, it'll move around uh rashes classically like a postular rash and tina synovitis. So painful, sort of enlarged sort of tender tendons and it can also present with a family and you know, tore um again, but as compared to chlamydia presenting the first couple of days, so that's how you're distinguish between gonorrhea and chlamydia um causing conductive itis probably more relevant for your prong exam. Um So much like the TB be careful here in terms of what the question asks you in practice, this is diagnosed with the nuclear nuclear acid amplification test, but the gold standard test is a culture and we treat it with a single dose of I M K F and just the idea again. So this is a disseminated gonococcal infection. You can see the migratory arthritis and these sort of small swell well dispersed postule onto syphilis. Now, so syphilis is a spirochete is affected by treponema pallidum. Can nobody tell me what the stages of syphilis are so pretty much. But on latent comes after secondary though it tends to your primary secondary latent tertiary. So, primary syphilis presents with a painless canker. So sort of an ulcer on the, on the genitals or it can sometimes be um sort of an oral ulcer as well. Um depending on where the incubation occurred, but it's a painless ulcer which is really important to remember. You then sort of 6 to 12 weeks later, can you get your secondary syphilis? You get a well disseminated, maculopapular rash, they feel unwell, they're feverish, they get lymphadenopathy, condyloma. Lotta is a really important pattern ammonic presentation during secondary syphilis to be aware of their, these sort of grayish, painless, almost look like water lesion's either on the genitals or in the mouth. Then you get your latent face and the later phase can last decades and decades and decades. Then you get tertiary syphilis, which is where it, it messes everything up. It can cause all manner of different things. Presentations, I'd say to be aware of a gum Ettus disease, which is where it starts eroding through sort of cartilaginous structures in the mouth and face aortitis. You can get sort of um, inflammation and um the formation of um what's what I'm looking for. Um, sort of dissection almost eventually um, of the aorta, um aneurysms, that's whatever you get aortic aneurysms that can eventually dissect near a syphilis. Um Argo Robertson, pewter pupils are the classic sign of neuros if to be aware of and tabs dorsalis, which is the generation of the spinal cord, but it can do all kinds of stuff. Um So those are our stages of CIF how do we treat Ciff? I am Ben Pen. Um That's pretty much always the case. It's slightly different, I think for neuro syphilis, um not worth worrying about. They get I am Ben Pen, be aware of the Jaros herbs, timer reaction. So this is a reaction where when you start them on antibiotics for the first day or two, they feel worse. They get really feverish. They sometimes be there sometimes very shivering and rigorous. The reason is because as your killing the spirochete, they released lots of preformed toxin and it causes a bit of an inflammatory response. Normally, totally unimportant, just give them some penicillin, not penicillin. Um give them some paracetamol, give them some pain relief that we find in a couple of days. Rarely. They can be a bit more unwell with it and then they might need steroids, but just be aware it exists and then yeah, more unpleasant pictures unfortunately, uh in a, that's what your sort of, your primary canker would look like in B and C just to highlight that the rash of secondary syphilis affects the palms and the soles of the feet, which is quite sort of the distinguishing feature because not many rashes do. A picture is just a picture of the spirochete. And then this is an example of a patient who had gum metis um syphilis. And you can see where it's eroded through um structures of the face. Testing for syphilis is complicated and it depends what stage you're in. So if you're in primary syphilis, if the patient still has their canker, how do we test for it? So the way we test the primary syphilis is dark field microscopy. We take scrapings of the actual ulcer and we look at it under this special microscope lighting and you can see the spirochete. So that's how we diagnosed primary syphilis and we still have the primary can Curtis um to take a sample from. If that's not possible, we've got to use serologies. There are two groups of tests. You've got non trepany evil tests and treponema test. There's lots of specific names. VDRL and RPR are the wants to know if the non trepany, we'll just recognize them. And treponema tests often start with T P something. Now, the reason we have both these tests is non treponema tests are not specific, they react to syphilis but also loads of other stuff. So like HIV um lupus amongst lots of others can cause positive VDRL RPR tests. Treponema tests are specific to syphilis but they stay positive. So even if you treat somebody syphilis, the treponema test will stay positive where the non treponema test will reduce with the non treponema test is reported as a titer. So if they both of these tests are positive, it's probably syphilis if the non treponema test is positive, but the treponema test is negative, they've probably got a positive test because it's cross reacting against something else. It might be lupus or whatever. If they've got a positive treponeme or test and a negative non treponema test, that might mean they've had previously treated syphilis because that stays positive. Let me know if any of that didn't make sense, we'll go over it again. So we interpret them together to try and work out what somebody's simple status is. And this is probably a bit more relevant for O N G. But the way we work out whether we've treated it appropriately is with the non treponema test, we look for a four fold reduction in tighter. So from 1 30 to, we have to go down to one in eight to be convinced that we've treated it appropriately. If it went back up again later, that would be evidence they've been reinfected. And then finally, we're on the home straight now, just some of the other stds and they're buzzwords these are relatively uncommon but have quite tight buzz worthy associations. So, can Kreuger, unlike Canker is caused by her marvelous Ducrey and it causes a painful ulcer with lymph nodes. But the ulcer it cause, it will be painful. And patient's tend to live in tropical regions if they catch it. Donovan osis or granuloma inguinally causes painless red ulcers really large, often scrubs beefy red ulcers and I'll show you a picture in a second. I warn you, it's not a very nice one. Um But these very large um sort of beefy red ulcers. And unless unlike having lots of small discrete ones, it's one big ulcer all kind of stuck together and they'll describe something called Donovan bodies on histology. Trichomoniasis. Your classic buzzwords for this is gonna be a yellow, greeny discharge and what's described as a strawberry cervix. And then finally, your viral causes genital warts are caused by HPV. Um Again, you know, more than enough about this row MG. So I won't dwell on it and HSV, herpes tends to cause painless painful ulcers, but no lymph nodes. So we can sort of distinguish between those three causes of ulcers. Syphilis is painless ulcer. Her piece is painful ulcer, no lymph nodes can Croix is painful, ulcer with lymph nodes. And then just so you, well, just so you sort of know what we're looking for. So this is sort of classically what the ulcers would look like for a Canc Roid these would be very painful ulcers and then probably have lymphadenopathy. This is what donovanosis looks like. You can see it's, it's very widespread hump, sort of homogenous. What's not good is a beefy red ulcer. This is sort of the strawberry cervix that's described of trichomoniasis iss, these are what genital warts look like and compare it with herpes which are vesicles, they are fluid filled. Um, it's a fluid filled rash and that's the end of the lecture. Um Thank you for putting up with me for all this time. Are there any questions about any of anything we've talked about there or anything? I've not mentioned? No worries at all. I hope it was helpful. And if there's no questions, I'll let you all get going before everyone goes. Thank you so much. Look for that lecture. It was really, really useful if everyone before they go, could please fill out the feedback form. So I've just put in the chat and I'm also going to share my screen for the QR code. And while I've got you all, I will just put my email in the chat if you have any questions um that you think of later or when you're going through the presentation, which I think is being shared at some point on the website, but always just drop me an email and I will get back to as fast as I can