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Yersinia enterocolitica, Yersiniosis & treatment (MECHANISM OF TRIMETHOPRIM-SULFAMETHOXAZOLE)

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Okay so if you’re anything like me you probably woke up this morning thinking what the hell is yessenia enterocolitica and that’s fine a lot of us wake up and have those days the heart wants what it wants so let’s learn well the first thing that comes to my head and i see this isn’t think okay answer oh so that reminds me of the enteric nervous system second brain

Which we know is made of two nerve plexuses found within the gastrointestinal walls so straightaway i am thinking gastrointestinal tract and política sort of reminds me of the colon large intestines so again which one might be gastrointestinal tract and that’s exactly what this bacteria causes it is causing a diarrheal disease maybe like this so you see android

Política is a diarrheal disease and it’s specifically of course acting in a gastrointestinal tract and some other things are pretty key to think about is actually what type of bacteria is it well it’s a gram-negative bacillus so what does that mean to us well of course it’s bacillus so that just means that it’s rod-shaped and it’s gram-negative so that just means

That it has a very thin perhaps two glycan wall but it also has that outer membrane that’s not found with the gram positive bacteria so let’s write that down we have a thin – no viking layer i’m just write pg layer making up the cell wall but they also have that outer membrane which has on the surface of it these endotoxins which we know to be lymphoma polysaccharides

We can also say that you see enterocolitica is an aerobic and anaerobic microorganisms so what’s a better way of saying that then just saying well it’s both aerobic and anaerobic well this move refer to you as a facultative anaerobe it can survive in the presence of oxygen and without all sorry in the absence of oxygen that’s great what else can you think of well

Can it move is it motel yeah it is and it’s also not so again just like it’s aerobic and anaerobic it’s also motile and non motile how could this be the case well it depends on the environment okay what sort of temperatures are we dealing with well when we are dealing with lower temperatures then it is going to be motel if we’re dealing with higher temperatures then

It’s not motile another thing that i’d like stingo does it form spores those are not form spores no he does not form spores so we can call it non sporicidal it’s not forming those four suppose are just these bacterial eggs that form if the environment is very hostile to the survival of the bacteria so it’s great in terms of actually being that bacteria technically

Waiting and alive when the environment becomes more favorable great for them really bad for us but luckily you see nia enterocolitica is non sporicidal so we can talk about virulence factors will aid the bacteria in actually trying to evade the hosts immune system as well as actually causing disease and also cause that initial invasion so virulence factors this

Is a general sense not just specific to you see nia and roberta go but they are going to cause invasion of the host of a host immune system and also to actually cause the disease which is what’s so we’ve gotten this far but we haven’t even mentioned what the disease that you see it causes well the disease caused by yersinia enterocolitica is called uc gnosis

Uc gnosis which we’ve all said is a diarrheal disease so some examples of these types of various factors could be things such as our sitter falls and sitter falls are just molecules that have a much higher affinity for iron than our own molecules that bind to iron so those are known as cedar falls and these are very important in actually helping a bacteria if it

Requires iron to grow sometimes iron is actually toxic to the growth of bacteria but in this case they use such a force to actually end their growth so that’s the one type of variance factor that they can use of course other variance factors are endo and exo toxins but we already said that we were dealing with endotoxins such as our liver polysaccharide which is on

The surface of all gram-negative bacteria but also type of extra toxin so these are just toxins that are acting distally from where the bacteria first adheres to you right and in this case because it is an enteric disease we can think of what what’s actually causing the disease because it’s not it here it’s that any disease it’s actually the burdens factors and so

The variance factors that causes any type of diarrheal disease is going to be an entering toxin and enterotoxins are more specifically is a more specific term to describe a type of accent toxin that’s acting for example on the enterocytes which are just epithelial cells found in the gastrointestinal tract another type of brilliance factor that we can think about

Is our capsules which again will aid with evading the immune system an example sorry of a variance factor that helps adherence specific to this type of bacteria would be yard a and l again these are just helping in here it’s tv enterocytes but also know about the type through secretion system type 3 secretion system so what actually is that you can think about this

As sort of like a syringe which is going to inject the virulence factors to the target site so in the case of pisonia enterocolitica tiger ii secretion system going to inject various factors such as jobs and yaffe’s are just our you senior outer proteins and they are here to sort of help the evasion of the immune system right because they’re going to inhibit so our

Macrophages and they’re also going to inhibit pro-inflammatory cytokines such as interleukin-1 beta tumor necrosis factor-alpha and i don’t know let’s say interleukin 8 those are just a few examples of many probes laboratory cytokines i suppose in that question we can ask as health is aware are they replicating so we said that they were already attacking the entry

Sites so that’s exactly it they’re going through replicating within peyer’s patch so pay is patched or found within the gastrointestinal tract and these are just aggregates of lymphoid tissue found within the gastrointestinal tract they also produce a specific type of exotoxin which we know so produce precede specific type of exotoxin notice why is he gastrointestinal

Tract specifically on those entry sites hence causing the diarrheal disease we can say that more specifically this type of exotoxins yc is known as an enterotoxin because it’s acting on the interest lines so that’s type of intro toxin now how is uc enterocolitica transmitted let’s talk about transmission well most likely through the feces of an infected animal

So even from our pets if you’re feeding them types of meat so the feces of animals as well as contaminated milk and from meat such as beef and pork hence why we can actually get this from our own pets such as dogs because of the food that you feed them if they’ve been infected from the food that they become we’ve cleaned it up then we can be infected that way so

Who is going to experience the waste of this well it’s the same as always those who aren’t you know suppressed immunosuppressed patients as well as people with iron overload and this can be caused for a few reasons potentially things like chronic transfusions or hemochromatosis or even something like be tostão the scene here where there is an actual problem with

Their hemoglobin so there’s something to say about that well they’re really going to face the brunt of this diarrheal disease because it’s not only good cause there’s cramps that fever bloody and mucous diarrhea which can also be seen at this or described as pseudo appendicitis but it can lead to septicemia which is where i’ve course new bacteria that the senior is

Going to enter the bloodstream and this is a sure cause of sepsis so sepsis by definition we’ve already learnt in the lectures is the it is a life-threatening dysregulated host responses to infection which can lead to multi stage organ failure and the end-stage being of course disseminated intravascular coagulation now this is something that i’m sorry about much

Of the pronunciation of but sequere so what is this these are basically parts of the pathogenesis of a pathogen that that a care post-treatment so in this specific case we can see things such as reactive arthritis and also erythema nodosum so whilst reactive arthritis is quite self-explanatory what the hell is erythema nodosum well this is where the bacteria may

Have found its way into the deeper sites or fat cells under the skin and so it causes the inflammation of the adipocytes which will be seen by the discoloration whether that be pink or purple lesions found on these skin and whenever you search a soap you’re most likely to come across it found on the legs how do we treat this well hopefully we’re not dealing with

Someone that’s develop sepsis because that’s a completely different other video but let’s just talk about the diarrheal disease let’s say someone hasn’t developed sepsis and we’ve already done the differential diagnosis we’ve cleared out that it’s not a different type of diarrheal disease and we definitely know that it’s not appendicitis so how do we treat it well

Of course we can use antibiotics which actually shouldn’t be your first go to you but we can use antibiotics if necessary so the time to find products that we that we can be using there are various different types there are so many different types i can i’m only going to name a few different classes but things like second-gen cephalosporins now i would give you

An example except they’re all extremely hard for me to pronounce so i’m not going to you but we have cephalosporin the reason that i’m specifically saying second generation cephalosporin is because first gen or really anything post first gen because first generation centers for ins were really not so efficient against gram-positive bacteria that’s like gram gram

Negative bacteria and we are of course dealing with gram-negative bacteria so remember the first gen most likely to target gram positive bacteria anything beyond that they’re pretty pretty even or at least do or effective on gram-negative bacteria of which using enterocolitica days we also have things like fluoroquinolones as well as tetracyclines what else also

Things like our antimetabolites or our and to metabolize let me just wipe this off now i could have gone into the mechanism of action for all of these but i know not everyone that watches is a pharmacologist but i can’t help myself sometimes i just need to talk about it and what better way to talk about trimethoprim so from the bacchus all that is really a little

Bit of pharmacology which is what we’re talking about in terms of adding tablets when treating bacteria in general because that’s what antibiotics they’re doing right targeting bacteria so i’m two metabolites as a name suggest they are effective or they’re their mechanism is functioning by interfering with some form of metabolites and in this case when we’re talking

About if i just i said that we were dealing with our source on amides and trimethoprim when we put them together we get the most glorious of drug names tri methyl prim sulfur meth oxus all so a full-on amides are going to be acting essentially like analogs of paba so that’s our p amino benzoic acid and that’s something that’s necessary for the production of bacterial

Dna what are they do they’re acting as an analogs so first of all you need to kind of know what papa does in in bacteria anyways well pavatt is going to turn into dihydrofolate acid how is it doing that well don’t hydro fluoric acid and what’s happening is when we have the action of our enzyme the high drop rate synthase then when i say ala i’m talking about bacteria

Is going to convert paba into giant hydrofluoric acid from da hydrofluoric acid we are going to form our tetrahydrofolate acid and how is that happening well into the enzyme is required in this case it’s a t’s dihydrofolate reductase okay so we’ve gone from paba p.m. you will the bacterias pia mia benzoic acid into da hydrofluoric acid into tetra hydro fluoric acid

Then we are going to use this not thus the bacteria to produce purines we already know appearance to be guanine and adenine so hopefully you can see at this stage they need haver to produce dna and they need to produce dna in order to replicate and actually live our demise i already said acting as analogues of pavan so really is going to be competing with palette

Itself okay so we can inhibit the uptake or the conversion of paba into johar hydrofluoric acid so our sultana mites are really acting here now what about our trimethoprim trimethoprim is acting in acting after our sultana – despite it being called trimethoprim sulfamethoxazole when we use them in conjunction because our trimethoprim is actually inhibiting this

Enzyme here trimethoprim is going to be inhibiting our dihydrofolate reductase so we don’t get any tetra hydro fluoric acid otherwise more simply put its bulloch acid or bullet okay so without this we can’t produce our purines and without that the bacteria cannot produce their dna is that’s one way of killing them and that’s pretty much it that’s all i wanted to tell you

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Yersinia enterocolitica, Yersiniosis & treatment (MECHANISM OF TRIMETHOPRIM-SULFAMETHOXAZOLE) By tunerd