Hi orris. I'm ready for today's patho and micro. I did cell adaption complete chapter and staph and strepto in micro

Wait wasn't we planned I'll explain tou the topic first and then we'll go from question to clinical and everything?

So, our topic for today in Pathways, uh, cell adaptation in response to cell injury. Firstly, what is happening in a normal cell? It is maintaining the homeostasis. But when there is a stressful condition, uh, a cell adapts. What is adaptation? Adaptation is, uh, the changes in the functioning in response to the change in the environment, to adapting and changing the functioning, the structure, and everything to adapt to the changed environment. Now, adaptation is of, uh, different kinds. Firstly is hypertrophy. What do we mean by hypertrophy? Hypertrophy is simply the increase- ... in the size and not the number. So, whenever there is increase in the size of the cell and not the number, it is due to the, uh, increase in the size of the organelle. Now, hypertrophy can be, uh, pathological or physiological. Physiological, we can see in bodybuilder when there is, uh, abundant use of the massive fiber, it leads to increase, uh, because of the increased workload, it leads to increased size of the massive fiber. In, uh, pathological condition, we can see is cardiac hypertrophy in case of increased hemodynamic disturbance caused by hypertension. Now, what is the mechanism? Mechanism is there are certain sensors in that- Mm-hmm ... respective orga- uh, respectable organ where, uh, it senses the, uh, change in the workload, increased workload, and along with the agonist and growth factor, they lead to the activation of certain transcription pathway, which lead to transcription, uh, - Mm-hmm ... and effectors, and that would, uh, lead to... Uh, fetal proteins, increase in fetal proteins, which, uh, increases the mechanical performance and decreases the workload. Along with that, in- increases the contractile protein, which increases the performance, and it also leads to increase in growth factor, which again give in feedback. Second is hyperplasia. Hyperplasia is simply increase in the cell number and not the cell size. Though hypertrophy and hyperplasia, they are two different processes, but they, uh, they occur simultaneously many a time. Hyperplasia occurs in dividing cell. Hyperplasia can be physiological- ... pathological. Physiological hyperplasia we can see in breast tissue during puberty or pregnancy. Hyperplasia in pathological condition is endometrial hyperplasia in response to excessive estrogen or benign prosthetic hyperplasia. Hyperplasia occurs due to increased growth factor. Then third is atrophy. Atrophy is decrease in the cell and size of num- uh, uh, increased size and number of cells leading to shrinkage or decrease of an organ or tissue. Now, atrophy can be physiological, pathological again. Physi - ... ology atrophy we see in normal development, like of notochord and, uh... ... during the development, it leads to the atrophy, or uterine atrophy after delivery. Pathological atrophy can be seen... Uh, can't remember the example right now. Okay, what is the reason for, uh, atrophy? Atrophy is because of decreased protein synthesis and increased degradation. This increased degradation of protein is caused by ubiquitin-proteasome pathway. Fourth, and the last cellular adaptation is, uh, metaplasia. Now, metapla-- what is metaplasia? Metaplasia is change from one differentiated cell type to another. Now, metaplasia examples, they're very common, they're very important. Firstly, we see in chronic smoker in, uh, respiratory tract infect-- uh, respiratory tract. Changes from, uh, ciliated columnar epithelium, mucus secreting, to stratified squamous. Now, why is this change? Because in, uh, chronic smokers, they-- there is in c- uh, continuous stress. So, stratified squamous, it is more, uh, able to adapt or more able to respond to the stress, uh, unlike the fragile columnar. But what is the cause? Uh, but the cause is... The mucus secretion or the cilia which was present in this str- uh, columnar epithelium that has been lost. So, protection from infection is lost. Second change in Barrett's esophagus. Barrett's esophagus, the-- due to gastric reflux acid, the epithelium is changed from the stratified squamous to intestinal type, uh, loc- uh, columnar. Then third is, uh, connective tissue metaplasia. What happen in connective tissue metaplasia? We see bone, cartilage, or muscle in areas where they are normally not found. For example, myositis ossificans, where we found bone- ... in muscle. Now, rest of the cellular injury and, uh, cell death pathways and intracellular accumulation, we'll do in next parts.

I cannot remember the fetal proteins re-expressed, but I know why they are re-expressed, because the fetal proteins, they are more efficient in working than adult, uh, proteins. That's why to overcome the mechanical workload, fetal proteins are being expressed.

I'll go with B because the cases of hypertrophy of heart, and as heart is non-dividing organ, so it doesn't go hyperplasia, but only hypertrophy. And the mechanism of hypertrophy is when there is mechanical stretch, it leads to the activation of certain transcription pathway like the PI3K pathway or AKT pathway, which leads to increased protein synthesis. So my answer would be B.

Answer is option B because he's a chronic smoker and it is a case of metaplasia where the respiratory epithelium is changed. So when the stress factor is persistent, so metaplasia leads to dysplasia, which is a precursor for carcinoma. Firstly, leads to carcinoma in situ, then progresses to invasive carcinoma where it spreads to, or metastases to other organs.

Uh, so it's option C because the case is of endometrial hyperplasia caused by excess estrogen secretion. So it is a reversible change, a reversible cell adaptation. So whenever we remove excess estrogen, it would revert back or reverse back to original state.

Proceed with cell injury now

So firstly, we saw what is-- in a normal cell happening. It is maintaining homeostasis. Whenever there is a stress condition, it adapts to the situation. But when, uh, the stress continues or persist, it leads to cell injury. So whatever is-- what is cell injury? Cell injury is when the cell is not able to recover or adapt, or the adaptation is limited and the stress has persist, that condition is cell injury. Now, cell injury is primarily of two point, reversible and irreversible. By the name suggest, reversible cell injuries, whenever the stress is removed, those change or the injury would revert back to the normal cell. Where irreversible, if there is an irreversible cell injury, it would ultimately lead to cell death, either mitosis or apoptosis, either means of the cell death. So... Now we see what are the causes of cell injury. There are certain variable causes, like it can be hypoxia, it can be physical, uh, trauma, it can be chemical toxins, or it can be certain nutrient deficiency, or, uh... And so on. Now, uh, these are the causes of cell injury, where hypoxia is the most important cause of cell injury. Now, coming to the morphological changes seen in cell injury. Yes. In reversible cell injury, we see, uh, the first grossly. Grossly, we can see is there are two major changes seen in reversible cell injury, which is cellular swelling and fatty changes. These are the primary changes that we see in reversible cell injury. So, whenever we see a grossly, the cellular swelling, which is the first manifestation, it can't be seen clearly in laboratory, but as a whole of an, uh, organism. So, when we see an organ, uh, organ as a whole, then, uh, cellular, uh, swelling is very clear, where we see pallor, increased turgidity, increased- Okay. ... weight. Okay. And now, coming on to the microscopic finding, what we see are, there are swelling, there are swelling, uh, blebs. Then there is mitochondria swelling, uh, along with some amorphous densities. ER is dilated. Phagosomes have been detached. Nuclear chromatin has aggregated. And in case of irreversible cell injury, it's the, the mitochondrial or the membrane dysfunction that has occurred in reversible cell injury cannot be reversed by it. That's the only change. Now comes the mechanism of cell injury. Now, mechanism of cell injury, there are various pathways that lead to cell injury. Mm-hmm. We need to be very concise with it because it's really long. So firstly, there would be mitochondrial dysfunction. Mitochondrial dysfunction, it leads to the formation of mitochondrial transition pore. Now, that pore s- in the mitochondria, it disrupts the oxidative phosphorylation, leading to increased ATP. Increased ATP, what it does? Decreased ATP, sorry. Decreased ATP. Now, what does decreased ATP does? It decrease ATPs, impairs the sodium-potassium ATPase pump. That could lead to influx of sodium water, efflux of potassium, leading to swelling, uh, cellular swelling. Then it also leads to anaerobic glycolysis. Increase- decreasing the pH, lactic acidosis, causing nuclear, uh, clumping. And it also leads to detachment of proteasomes or ribosomes from the ER, leading to decreased protein synthesis. Second fun- uh, co- uh, second... Part three of mitochondrial dysfunction is it-- because of impaired oxidative phosphorylation, it leads to ROS, which is reactive oxygen species. Free radicals are species which contain an unpaired electron, and free radical, which is oxygen species related, is reactive oxygen species. Now, they have been generated because of stress, mitochondrial dysfunction, and that lead to lipid, uh, peroxidation, membrane dysfunction, li- that leads to membrane dysfunction, then DNA damage leading to mutation, protein damage leading to misfolded proteins. Okay? So that was ROS. That was mitochondrial dysfunction. Second is membrane- Mm-hmm ... dysfunction. Membrane dysfunction can be due to lipid peroxidation from ROS, then, uh- Mm-hmm ... decreased ATP leading, uh, phospholipid breakdown, then increased calcium lipid, uh, le- uh, due to phospholipase breakdown, lipid breakdown, and impairment of protein. All this lead to membrane dysfunction. What membrane dysfunction does? Firstly, if there is disruption of plasma membrane, plasma membrane disruption leads to- Papa. ... swelling and, uh... Swelling of cell and also related to disruption of the cell. If mitochondria membrane is impaired, we saw that it would lead to decreased ATP, ROS formation. If lysosomes membrane is being disrupted, it would lead to release of its enzyme into the cytoplasm, eating the cellular components. Third, uh, mechanism is increased cyto- cytosol-

Yeah. So the third mechanism is increased cytosolic calcium. Normally, calcium, uh, in extracellular compartment is more, intracellular compartment is really less. But because of disruption, uh, because of certain toxins, the permeability is lost and intracellular calcium level increases. Nice. What does this do? It leads to activation of variable enzymes like endonucleases, proteases, then, uh, lipolysis, and all. So what does this do? It will lead to lipid breakdown, it will lead to protein breakdown, and it will lead to all-- membrane, uh, mitochondrial disruption. So all these are leading to disruption. Fourth and the foremost is DNA damage and proteins. What is DNA damage? When the DNA is damaged beyond repair, that is DNA damage and protein. Whenever-- normally what happens, there are chaperones. Chaperones leads to folding or normal folding of proteins. Now, whenever there is stressful condition, lead to ER stress. Now, what ER stress is, there is lot more protein needed to be folded than the capacity. Like the demand is more than the capacity. So in that condition, what happens? Either it wouldn't survive, it would lead to apoptosis, or it would survive, there would be decreased ATP, uh, sorry, decreased protein and more chaperones. Then there would be folding. So it leads to misfolded proteins. Misfolded proteins of the repeatable conditions like, it has seen Alzheimer's, it has seen alpha-1 antitrypsin deficiency and so on.

Okay. So, cell death is eventually death of cell. It has lost all the viability, functionality. It is dead. Now, cell death is mainly of two pathways, necrosis and apoptosis. What is firstly we'll proceed with necrosis. Necrosis is accidental or unprogrammed cell death. Whenever there is a liberation of lysosomal enzymes, the ఫెనెపతి రెస్లిపేషన్ ఆఫ్ లైక్స్ ఉంటాయి, ఎంజైమ్స్, అండ్ ఆల్సో దేర్ ఇస్ ఇంక్రీస్డ్ బ్రేక్ డౌన్. సో... ఓ... Just a minute.

I didn't change to a language, but I don't even know which language it was. It was something... misunderstanding. Okay, sorry. Now continuing. So what happening in necrosis is whenever this cell injury is beyond repair, it has come to irreversible. So whenever there is liberation of lysosomal enzyme, there is membrane damage, mitochondrial dysfunction, it leads to necrosis. Necrosis is seen in hypoxia, toxic condition, and all. Now what happening is in nec- necrosis is because the membrane dysfunction has occurred, the, uh, cellular com ponence, it is... It, uh... It gets into the extracellular compartment, leading to inflammation. So what prominently we see in necrosis is inflammation. Okay. So what, uh, morphological changes we see in necrosis in general is cytoplasmic changes and nucleolus changes. Cytoplasmic changes is it becomes more eosinophilic, it's more homogenous. There, uh, there is myelin fiber seen, ER dilation it is seen. And certain microscopically, if we s- elec- on my electron microscope, we can see that the membrane has, uh, degenerated. There is, uh, detachment, uh, there is my- uh, myelin fibers and, uh, lysosomes and riven. All those changes are cytoplasmic changes. In nuclear changes, there are prominently three: pyknotosis, karyolysis, and karyorrhexis. Karyolysis is whenever there is cell shr- uh, Cell-- uh, sorry. The chromatin is breakdown. It leads to DNA breakdown. Pyknotosis is whenever there is chromatin condensation or shrinkage, and karyorrhexis is that shrinked pyknotic, uh, chromatin is... It is broken into fragments. That is known as cerebrocerebral. Now, the type of necrosis. Necrosis are of various kind. Firstly, coagulative necrosis. What is happening in coagulative necrosis that whenever there is cell death, along with the protein, the enzymes responsible for the cell death is also lysed, due to which the takedown is incomplete and leads to foam texture. Now, what happen, there is ischemia in particular in that case because of which... The neutrophils and the lysosomal enzymes around it, which was re- required for its breakdown, didn't reach that point, leading to foam texture or coagulative necrosis. And the area of coagulative necrosis is known as infarct. Second type of necrosis is liquefactive necrosis. Now, where, what happen in liquefactive necrosis, there are mainly bacterial or fungal infection, due to which certain neutrophils, uh, because of which lot of neutrophils along with the lysosomal enzymes, which are there, leads to cell, uh, degeneration, leading to a liquid viscous mass that is known as liquefactive necrosis. Liquefactive necrosis is seen in CNS primarily, whereas coagulative necrosis or infarct can be seen in all organ except for brain. So liquefactive, that was for liquefactive. Then there is gangrene. Gangrene is not a type of necrosis, it's just used clinically. Whenever the gangrene is mainly used for lower limbs, limbs or especially lower limbs, whenever there is coagulative necrosis in them, in typical planes, in different planes, that is coagulative necrosis, if only there, that is dry gang- uh, dry gangrene. But if the coagulative necrosis is accompanied by bacterial or fungal infection, due to which there is- ... lot of neutrophil infiltration over there, leading to liquefactive, uh, necrosis, superimposing the coagulative necrosis that leads to wet gangrene. Fourth type is gaseous necrosis. Gaseous necrosis is an intermediate between coagulative and liquefactive necrosis seen in the foci of tuberculosis. Gaseous means cheese-like. So there is white chalky area of, uh, gaseous necrosis. Okay. So what we see in gaseous necrosis microscopically is granuloma. Granuloma is nothing, it's just amorphous density along with epithelial cell surrounded by lymphoc ytic infiltrate. Then fifth is fagocytosis. Fagocytosis is not actual kind of necrosis. It is simply destruction of fagocytosis. Very prime example is acute pancreatitis, whereas the, it is enzyme lead. Traumatic example is breast. Last is fibrinoid. In fibrinoid necrosis, there are, is, uh, there is fibrin formation, fibrin-like formation because of the destruction in the blood vessels, mainly happening with the blood vessels. So there is fibrins entrapped over here. This was all about necrosis.

Okay. Apoptosis is, äh, programmed cell death, where is still when the cell think it's having destruction, it leads to suicidal instinct. It, it initiates suicidal programs that kills its own cell. It is, äh, genetically programmed, so it is also known as programmed cell death. Apoptosis actually means falling off. Apoptosis, unlike necrosis, can be, äh, pa-- äh, physiological as well, and it's not always pathological, whereas necrosis is always pathological. Now, certain examples of apoptosis, this is logical cases we can see in case of embryogenesis implantation, we can see, or... When a host cell has completed its function or... All right. Yeah, I can call back. Uh, Renova, there is a self-reacting levoce- levoceps, et cetera. Pathological, uh, ap- uh, apoptosis we can see in case of injury. Uh, Renova, there is trauma or carcinoma. Not cancer, sorry. Okay, so what happens in apoptosis, we can finally see morphological changes. Firstly, there is cellular swelling, cellular bloating. Then the bloating leads to formation and also the shrinkage of the cellular, the chromatic material and the cytoplasmic material. Then it leads to apoptotic body formation. Now that body, the, uh, membrane is intact. Now that body is being phagocytized. But in the entire process, the membrane is intact, irrespective of the necrosis. No, what is the mechanism of apoptosis that is really very important. The apoptosis is carried out in two processes, which is the initiation phase and the execution phase. Initiation phase are of two, right? Mitochondrial and cell death domain. Mitochondrial, what is happening is normally there are three proteins, which is anti-apoptotic sensors and apoptotic. Whenever there is a case of toxins or certain injurious stress conditions, sensors like, um, BIM, BID, BAM, they sense the toxin and it leads to the inactivation of anti-apoptotic proteins like the BCL-2, and it leads to activation of pro-apoptotic like BAX, ALK, Like BAX and BAK, and that leads to the, uh... That leads to... "You will, uh, remove, uh, or detach of cytochrome c from the mitochondria that lead to the activation of, uh, caspases. Primarily caspase-9 has been activated in mitochondria pathway. Then there is cell death domain. Cell death domain, what happen is that a certain death domain receptors like the, the NF or FAS. Now, what, uh, in FAS, there is FAS-like or the T cells, which is used to primally detect any self-harming antigen. So, FAS-like, it binds to the FAS-like and it leads, uh, so it, uh, the, uh, four to five FAS-like, uh, FAS receptors then come together. They form a binding site for adapter protein, then that adapter protein attaches, FAD attaches over there. That leads to..." Multiple pro-caspases activi- uh, attachment. Multiple pro-caspases when attached over there, it leads to cleaving of each other and their activation. The caspases activating mainly in the death domain path- uh, pathway is caspase 8 and 10. Now, these activated cas- uh, caspases lead to the activation of execution caspases, which is primarily caspase 3 and 6. Now, what happens is the execution phase. In the execution phase is that it leads to endonuclease changes and, like, the chromatin condensation and all. There is also some cytoplasmic changes, and these, these stages leads to the formation of apoptotic body. Now, it leads to phagocytosis phase. Phagocytosis phase, the apoptotic body is being identified by the macrophages and being phagocytosed. For the identification, there are certain changes that is brought by the apoptotic body. First, primarily is the phosphatidyl, uh, phospholipid flip, in which the phosphatidylserine, which is primarily inside the cell, is, uh, expressed outside. And second is the thrombospondin, which is adhesion molecule, is, uh, expressed on the out- Okay.

Membrane is primarily the feature that will C-O-H-L-E, where the membrane is intact and reversible, but it is disrupted and irreversible. Membrane is very clearly seen in electron microscopy. Uh, let me think. Can't think of the, of an HME feature. Sorry.

Option 3 is the answer because from what we can see, there is massive MI. In fact, the myocardial infarct is obviously seen in case of coagulative necrosis. There is preserved cell outlines. In coagulative necrosis, the cell outer ductus been preserved and, uh, usually fail cytoplasm, nuclear pyknoticosis, and absence of inflammatory fluid is clearly is indicating towards coagulative necrosis. And because in coagulative necrosis, neutrophil do not migrate, there isn't any neutrophil infiltration on inflammatory infiltrate, see.

Option C is the answer because the method of elimination, because when the activation of caspase is by the death receptor, it has to do nothing with the mitochondria. The release of cytochrome c and subsequent caspase-9 activation is seen in apoptosis and death, the mitochondrial transition door is not being opened. And fourth, the activation of ubiquitin proteasome pathway during atrophy is seen in atrophy and has nothing to do with the permeability transition pore, which is seen in case of some injury. So, answer is C.

Option C, microvilli changes in the electro-microscopy showing swelling, blue morphic mitochondria, and fatty changes which is the sign of reversible cell injury, which are mediated by mi-- disrupted mitochondrial oxidative phosphorylation and beta-oxidation.

C is the answer since the cell is viable with large cytoplasmic vacoules and undigested cellular debris it indicates irreversible cell injury caused by increased ros

C is the answer because during ischemia cell adapted to low oxygen supply which on reperfusion gets over whelmed

Okay

I'll take a look at the two, uh, two family central from microquiesis and staphylococci. Microquiesis and staphylococci is differentiated on the basis of catalysts. Microquiesis catalyst positive and staphylococci is catalyst negative. Then at the microquiesis, there are two... Do you know which is microquiesis and staphylococci? They are differentiated based on oxidase test. Staphylococci is oxidase negative. In staphylococci, there is staph aureus and cons. Staph aureus and cons is differentiated on the basis of coagulase tests. So we then look into staph aureus. Staph aureus is a gram-positive cocci arranged in grape-like clusters. They are catalyst positive, oxidase negative, coagulase positive, facultative anaerobe, non-motile, non-spore. Then we talk about the virulence factor. There are certain virulence factor. Firstly, are the cell mem- when we divide the virulence factor, it is cell wall, virulence factor, then there are toxins, and there are certain enzymes. In the cell wall, there are Uh, peptidoglycan, which is for the rigidity, lipoteichoic acid, uh, then there are... They have addition molecules and addition molecules that are bound coagulase. Bound coagulase gives the test tube, uh, te-- uh, tube coagulase test positive. Then there is protein A and also capsules. Then in toxins, there are two tox-- uh, there are, uh, certain... Toxins like hemolysin. Then there are certain preformed toxins. In preformed toxins, there are enterotoxins, which causes food poisoning, and toxic shock syndrome toxins, which to-- uh, which causes toxic shock syndrome, which is... And these two are, uh... Sorry. These two are superantigens. Enterotoxin and toxic shock syndrome, they are superantigens in which the enterotoxin is preformed toxin, which causes food poisoning. There is also then, uh... Pyrogenic toxin, enterotoxin. Enteroto-- exotoxin, pyrogenic exotoxin, staphy-- uh, staphylococcus. This... No. Sorry, sorry, sorry, sorry, sorry, sorry. There is also, uh... Toxin which causes? Staphylococcus clated skin syndrome, 4S. Then, uh, there are certain enzymes like DNase, uh... Staph-- uh, staphylocainase, et cetera. Okay? Now, these are the virulence factor. After virulence factor, there are certain... Then we move on the clinical manifestation. In clinical manifestation of Staphylococcus, there are superficial clin- uh, skin and s- uh, soft tissue. Skin and soft tissue. In skin and soft tissues causes folliculitis, uh, furuncle, carbuncle, impetigo. cellulitis, et cetera. Then in musculoskeletal, it causes osteomy- uh, myelitis. Uh, polyarthritis, myositis. Then in, it causes RTI, pharyngitis. Then in RTI, UTIs. Then, uh, bacteriami, tox- uh, then in, uh, toxins that causes toxic shock syndrome or... Uh, food poisoning. Then it also causes community-acquired MRSA diseases. Then after the clinical manifestation, we move on to the lab diagnosis, which is most important. In lab diagnosis, firstly, we'll collect the sample. Now, sample collection depends upon the type of wound. If it is a s- skin or mucosal, we'll take pus swab or, uh, wound swab. If it is, um, UTI, then we'll take urine sample. RTI, then we'll take throat swab, or, uh, in case of certain bacteremia, we will take blood sample, et cetera. Then after taking the sample, we'll move on to direct microscopy. In direct microscopy, we'll absorb, uh, observe Gram-positive coccoid clusters. Then culture. In culture, when we do nutrient agar, we'll see a golden yellow non-diffusible pigment. In blood agar, it is similar as nutrient agar along with narrow zone of beta hemolysis. In

Hmm. Then, uh, uh, we talked in nutrient agar. In nutrient agar, blood agar, then Mekong ki agar. In Mekong ki agar, there is pink colonies. Then there are certain selective media like minute salt agar and, uh, salt milk agar. Then af-- Uh, then we'll do culture smear microscopy. In culture smear microscopy, we also see, uh, gram-positive cocci in clusters. And along with that, in, uh, hanging drop, there would be non-motility. S-- Then we'll go for... Identification. In identification we'll do firstly: catalyst test, which differentiated from Streptococcus. Then there is, uh... Quagliz test. This Quagliz test is used for differentiation of Staph aureus from the other species of cons. And there are two type of, uh, Quagliz test: tube Quagliz and slide Quagliz. In the tube Quagliz we emulsify the serum, Staphylococcus, in plasma at thir-- and then incubate at 37 degrees Celsius for four hour. And the positive test in, uh, in positive test there would be a clot formation which do not flow with the tilt of tube. Then second is the slide agglutination test. In slide agglutination test... In the staph, or yes, we add, uh, we emulsify in normal saline. Then we'll take plasma and mix it thoroughly. In a positive test, there is... Course, granules formation. Otherwise, in the negative test, there would be the milky white suspension formed. We can detect, uh, protein A using the lactase, uh, titration test. Then there is serology, uh, uh, like, uh, typing. Phenotyping can be done by bacteriophage typing. Serological can be done by PCR-RFLP. Then we move on, uh, for identification automatic system like VITEK or MALDI-TOF. Then there are s- uh, then we move on to antimicrobial susceptibility testing, which can be done either through disk diffusion method on Muller-Hittman agar or direct, uh, direct dick method, uh- Quick method, direct method. Direct method, which includes... Direct MIC method, which include Meltdoff and Vitex and, uh. In that, firstly, uh, there are... Methicillin resistance. Now, this methicillin resi-- uh, beta-lactam antibiotic resistance. This antibiotic resistance can be of two kinds. Firstly, either there is formation of beta-lactamase. In that case, we add beta-lactam along with anti-lactamase enzymes like clavulanic acid or sulbactam. Then second is... अ, through... Impaired PBP, which is pro-- penicillin-binding protein, which is primarily the methicillin-resistant Staphylococcus aureus, Staph aureus. In that it is coded on MAC AG, this resistance is of two kind, uh, community-acquired or hospital-acquired. On the basis of antimicrobial susceptibility, the treatment varies. If it is penicillin, uh, sensitive, we'll give penicillin. If it is methicillin-sensitive, we'll give methicillin. If it is methicillin-resistant, then we'll move for vancomycin. If it is, uh, for empirical treatment and we don't know about the susceptibility, we'll move with vancomycin. Alternate for vancomycin, if it is a skin or superfici aI soft tissue infection, then we move for Tic- Klo- Ticloksilin. Dip- Diplo- Diplo- ...line zolad if it is a s-- uh, line zolad if it is a skin and soft tissue infection and if it is a, uh, systemic infection or severe bacteremia, then we'll go for diplo mycin. Okay. Then we'll talk also about something from the cons, which is Quagliz negative, uh, Staphylococcus species. In which it is Quagliz negative, it is non-hemolytic, it is non-pigmented, and, uh, non-mannitol fermenting. In which there is, uh, epidermi- uh, epidermidis, staph epidermidis. It is the most common, uh, cons. Then second is, um... Hemolyticus, which is beta-hemolytic, and then there is, uh, leudin genesis, which is Bond Quagliz positive. Then the... Sorry, that is novobiocin resistant. Novobiocin resistant. Then there is... Sapro- saprophyticus, which is...

Bound coagulase positive

It is written in book pink colonies on macconkey

Şu an Studquasis, negatif. positive ...değil mi ki? Her 30 gün sonra bir enterokokus, pneumokokus, streptokokus. Now, enterokokus is classified in a different family which is enterococci. In streptokok-- in streptokokus, we divide the streptokokus into streptococci in three top on the basis of amylases. Alpha-amylase, beta-amylase, and gamma-amylase. In alpha-amylase, beta-streptokokus but it is a pneumokokus. In beta-amylase, it's the beta-amylase streptokokus. And in, uh... Come here, we'll take to some of the hemolysis and some of the number 10, 10,000. Then, when we talk about beta-hemolytic streptococcus, we on the basis of C-carbohydrate. To lefeth- ta- uh, lefeth. "Typing in which we divide into 20 zero groups from A to B except for -ing and then the group A, which is Streptococcus biogenes. It is the most common and infectious group. We divide into Griffith typing and divide it into 150 zero types." "150 type apart from Streptococcus biogenes group, a Streptococcus gas in detail. It is." "Katalis, negative gram-positive coccus, pairs or chains." "Facultative, aerobic, non-rotating, non-sporing. Then come the non-fermentative factors. It has got a kill cell wall-mediated, which is decoy acid, then M protein. It is the most, uh..." "Prin-- it is the principal virulence factor, which enables the opsonization from complement factor. Then there is other factors like, uh..." "Then protein associated factor." "There is also microcapsules. Then toxins. There are..." Hemolysins. Hemolysis, there are two type of, uh, hemolysis. Hemolysis, which is streptolysin O and streptolysin S. Streptolysin O is oxygen reactive, labile oxygen labile. They are antigenic and they form anti-streptolysin O antibody, and the titer is used as the diagnostic purposes. Then there is streptococcal pyrogenic enterotoxin, which causes Fever of pyro- pyrogens, for example, scarlet fever. Somatic, acute somatic fever, et cetera. There are other enzymes. In enzymes, there are, uh, streptolysin or fibrinolysin, which break down fibrin. It is used in MI. Then there is... DNase. Then other is NADase or... C5a protein inhibitors. Then we talk about clinical manifestation. The clinical manifestation of the spiro- sporotrophic and non-sporotrophic clinical manifestation. In sporotrophic manifestation, firstly, is RTA, respiratory tract infection, in which it causes pharyngitis. Sore throat is the most common cause in children. Secondly, Superficial skin and soft tissue, in which it causes... Impetigo in children, which is red sores that burst to form honey-colored crust. Second is cellulitis. In cellulitis, one impor- one common form in which there is puffy orange texture. It is erythema. Erythema multiforme. Not very sure about this spelling and pronunciation. Then we talk about deep skin and superficial infection in which it causes vasculitis, necrotizing vasculitis. In which there is acute, uh, it is an acute onset where the skin is separated abnormally, but the tendon is slow. But slowly with progression, it progresses into the necrosis of skin, fascia, and muscle. Therefore, Staphylococcus aureus is also known as flesh-eating bacteria. Then there are bacteremia, et cetera, toxic shock syndrome. Then certain nonsporotophic, um, clinical manifestation include

Mm. So, certain non-spiritative manifestations include, uh, ac- acute rheumatic fever and post-streptococcal glomerulonephritis. Then we move on to the lab diagnosis. In the lab diagnosis, sample collection. Sample collection, again, depends upon the type of infection. It can be pus swab, uh, food swab, blood, throat swab, urine, depending upon the... Disease, then direct microscopy. Direct microscopy, we see gram-positive cocci, aerobes, and spirochetes. Then culture. These bacteria are fastidious bacteria, so they grow only on enriched media like the blood agar, where there is pinpoint and wide zone of beta-hemolysis, and second is selective media like the crystal violet blood agar. Then culture, smear microscopy, we see gram-positive cocci, aerobes, and spirochetes, and hanging-dropper method , they are non-motile. Then cult-- identification. In identification, first we do Catalase, which differentiated from Staphylococcus and Streptococcus are catalase negative. Then second are the peptidase sensitivity, P. Streptococcus pyogenes, Acinetobacter, Pseudomonas aeruginosa, Streptoc Resistant. For the differentiation point between A. collicum and pyogenes, uh... The beta-mollic colonies of pyogenes are pinpoint, whereas in A. collicum they are mucoid. Then identification method continued. Direct identification like the white take or melded off. Then there are typing. Griffith typing can be done. And there are certain serological. And serological can measure two things. Firstly, IgM, IgG, or anti-DNA, B's antibody can be measured. Then treatment of choice, penicillin is the drug of choice. And penicillin-resistant is yet not been adjusted. Then we talk about Streptococcus group B or Streptococcus A collectins. They causes mainly the, uh, 5 to 40% of females in the vagina or rectal, and they're the carriers. They causes neonatal sepsis during pregnancy. They can cause postpartum... Sepsis infection. Or it can even cause UTI. Another one, UTI, pharyngitis, et cetera. Then laboratory, they are camp positive. What happened in camp, uh, then in, in a blood agout, when we strike staph aureus, then perpendicular to the staph aureus strike, we strike this group B streptococcus. What happened the group B lysine phospholipase? This phospholipase are help in the... Molysis of staphylo- oris. So what we see could be shown of... Two type, uh, beta molysis with a narrow pointing at the junction pointing towards staph oris. Okay. And the bladder carter they would be zone of beta hemolysis with big white colonies. Here also the treatment of choice is penicillin.

S. Pneumoniae is a different topic and chapter and therefore i didn't cover it today

Um, I think the answer is B. Because I'm not really sure of the diagnosis, but fever with rash is characteristically caused by pyrogenic exotoxin of staph-- sorry, Streptococcus pyogenes.

It is a case of PSG and which is post-herpetic neuralgia. Post-herpetic neuralgia is normal but NTNA is elevated. So, I guess the answer is D.

The answer is B because the, it is a case of postpartum sepsis caused by group B streptococcus. Group B Streptococcus or Streptococcus A colliculi. It is a carrier 40% of females. So, treatment, prophylactic treatment before screening can lead to other risk or other complications. So, first vaginal or rectal sample screening should be done and then to guide intrapartum prophylaxis.