Hi everyone, welcome back to the YouTube session of the Microbiology Crash Course. For all of those who are new out here, I am Dr. Preeti Soharma and I am an educator for pathology and microbiology. Well, we are continuing with the Microbiology Crash Course for the upcoming NEET, NEXT and FMG exam students and we have already completed 4-5 essential components of this particular crash course.
We finished with two parts of general microbiology. We've finished with a very important section that is fungus or mycology and we've also finished a portion of bacteriology. Today we'll be taking the bacteriology forward and dealing with the other bacteria that come under it.
Soo for all of those who've probably missed out on the previous videos, they are available on the platform. They are available under the video section. There's a separate playlist that is there.
Soo all of you can certainly look at all the microbiology videos from there. Also, as with regard to the PDF of this particular, all these classes that are going on, the PDFs of these will be available on the Telegram group. I've put the link to the Telegram group in the description below. The Telegram channel and the group, the description below has the name.
It goes by the name of Pathology by Dr. Preeti Soharma. Soo you can follow me on the Telegram or Instagram or Facebook groups and you would be able to download the PDF from Telegram and Facebook. Well, having said that, let's begin with the bacteria and the set of bacteria that we have to cover today become the spore forming bacteria.
When I say spore forming bacteria, the ones which make spores, there are two that come under it. One is going to be bacillus. Bacillus having the A immediate to it is an aerob.
It requires oxygen and clostridium is claustrophobic, means claustrophobic means less oxygen. Soo, clostridium happens to be an anaerob. Soo please remember first and foremost bacillus A, so it's an aerob and clostridium reminds us of claustrophobic, so that is an anaerob. Soo let's begin with the very first question and then we'll study accordingly. Question number one out here guys, which of the following is not a virulence factor of bacillus anthracis?
Which of the following is not a virulence factor? Lobyl toxin, edema toxin, lethal toxin or capsular polysaccharide? And the correct answer to this is labile toxin is not a virulence factor. Soo you would obviously ask me what are the virulence factors that are there for Bacillus anthracis. Soo remember Bacillus anthrax that you commonly know it as, it has two things.
Number one, it has a capsule and number two, it has a toxin. Both of them are responsible for its virulence. Now I think when we were studying the first part of general microbiology, we studied that All capsules are made up of polysaccharides.
I think that's a very famous thing that we studied. All capsules are made up of polysaccharides except bacillus anthracis. That is where it comes across as an exception.
Except bacillus anthracis where the capsule is made up of polypeptide. Other than that, all other capsules in the subject with all the bacteria, they are made up of polysaccharides. What about the toxin? The toxin has three parts to it which you call as the EPL. Soo remember many students learn it as the English Premier League.
Soo if you wish to learn it that way. What is EPL? Three parts of the toxin.
Soo remember EPL have to work together. EPL have to work as a combination only then the toxin is going to make its activity. Soo what is EPL? E for edema factor, P for protective factor and L for lethal factor. Soo E for edema factor, edema means how does it cause edema by increasing the cyclic AMP It causes edema, it makes sure that the bacteria is protected, it makes sure that it can cause killing, it can cause destruction that is lethal.
Remember edema, protective, lethal. E, P, L are the three factors. Now when I come back to the question which of the following is not a virulence factor.
Soo is the capsule a virulence factor? Yes. And what is the capsule of bacillus anthracis made up of?
It is made up of polypeptide. It is that exception. Soo it is a virulence factor.
Other than that, E, P, L are virulence factors. Soo E for edema toxin, P for protective toxin and L for lethal toxin. Basically, there is nothing known as a labile toxin.
And that was the question that you had. Now that you've understood everything about anthracis, why don't we study all the other things associated with it? How many types of anthrax are known? Very easy, once you know this, you'll be able to answer a lot of questions. There are three types of anthrax that we have.
The anthrax affecting the skin, so I call it cutaneous. Anthrax affecting the lungs, so I call it pulmonary anthrax. And anthrax affecting the intestine, so we call it intestinal anthrax.
Soimple. cutaneous pulmonary intestine so how do these happen how does the bacteria enter our body how does it cause skin and lung and intestine involvement so for skin remember we call it height poter's disease have you all seen the workers who carry animal skin i'll show you a picture have you seen that whenever the workers carry animal skin they always carry it on their neck on their neck and all their shoulders so as if they are carrying a rug as if they are carrying a bag right Soo whenever we have to carry something, we carry it on our neck and our shoulders. That is the area. Soo imagine if they are carrying animal skin and this is definitely coming from the animals. Soo if they are carrying the hides and the skins of the animals on their bare backs.
Soo can you say that that is why this is referred to as the hide poters disease. It is known as hide poters. What is hide poter? Hide is nothing but animal skin and poters.
Poters are people who carry those heavy things on their back. Soo these are the poters, they are the people who are carrying animal skin and that is why they have this blackish color lesion and this will be a classical history that blackish color lesion will either be on the neck or the shoulder or the upper back because that is the area where they are carrying all of those animal skins, right? Soo please remember cutaneous anthrax known as the Hyde-Poters disease. Coming to the next one, pulmonary anthrax.
Why would someone have pulmonary anthrax? Pulmonary means inhaling. Pulmonary means inhaling right, we would inhale it.
Why would we inhale something? People who work in the wool industry. Soo wool has very thin fibers right, so these fibers are inhaled.
Wool sorters, so all the workers who sort wool, who work in the wool industry, when they inhale these fibers, it reaches the lungs and it causes pulmonary anthrax, it causes pneumonia. Please remember, this is the form of anthrax which is also an agent of bioterrorism because inhalation definitely comes under bioterrorism. Lastly, if someone has uncooked meat, if someone is having consumption of uncooked meat, which kind of anthrax would occur in that case?
Intestinal anthrax will occur. Intestine inflammation will occur. Repeating, if they carry the skin of the animals on their back, cutaneous anthrax, if they inhale it, it is known as pulmonary anthrax. If we eat animal material, it is intestinal anthrax. Which out of these results in the formation of a malignant pustule or also known as ester?
Malignant pustule also known as ester. Soo remember, this is a cutaneous finding. Do you remember I showed you this blackish color lesion on the skin?
Soo this blackish color lesion on the skin is known as a malignant pustule or an ester. You will ask me that why are you calling it malignant? Does it have anything to do with cancer? No. I'm calling it malignant because look at how it's appearing.
The appearance is pretty bad. It is quite invasive. It is quite dirty looking, blackish, eroded.
Only because of the bad looking appearance, I call it a malignant pustule. Otherwise, it has nothing to do with cancer as such. Okay, so the three types of anthrax are pretty much sorted. The cutaneous one, the pulmonary one and the intestinal one. Let's come to the diagnosis.
When you look at it under the microscope, You can very well see that yes, these are kind of bacilli. They are long, they are bacilli. And do you see that if for example, if this is the organism, you will say that in the center, you are seeing a whitish area.
There is an area that is not picking up the stain. What is that area? That area is nothing but the spores. Did we just study that bacillus and clostridium are spore forming organisms? Soo please remember guys, when you are dealing with this, Either look at the appearance, look at the kind of appearance.
Either you can call it the box car appearance or you can also call it the bamboo stick appearance because it looks like this, like cars, box cars. Either you can call it box car appearance or you can call it a bamboo stick appearance and you see it on a gram stain. If you try to grow it on culture media, on agar, you get a medusa head.
What is a medusa head? You won't get a picture. but definitely something that is important to know.
If you grow it on an agar, you get a medusa head appearance. Number three, if you grow it on gelatin, if you tend to put it, if you put bacillus anthracis inside gelatin, it will give you a very important finding. Soee, have a look at it.
This is a test tube. This test tube, what have I filled it with? This test tube has been filled with gelatin.
Do you see what has happened to gelatin? Gelatin is broken over here. It is broken a lot over here. Soo, I can say gelatin has been liquefied.
It has been broken. Where has the gelatin been liquefied more? It's maximum at the surface.
Maximum gelatin is broken at the surface and as you are going down, the amount of gelatin breakage is decreasing. Soo, can I say bacillus anthracis is acting maximally on the surface and least at the bottom. Why?
It is breaking gelatin maximally at the surface and least at the bottom. Why? Because oxygen is present at the surface and oxygen is not present at the bottom and is anthrax aerobic. Yes, that is the first thing we studied.
Anthrax is an aerobic organism. It works in oxygen. On the surface, it's getting oxygen.
It will break the gelatin. On the lower part, it's not getting oxygen. Soo it will not break the gelatin. And what kind of an appearance do I get out here?
We get the inverted fir tree appearance. It's an opposite tree, upside down tree, inverted fir tree appearance. Number four, what does Bacillus anthracis show us? on a penicillin agar, PE for penicillin, PE for pearls.
Remember, on a regular agar, if you guys remember, on a regular agar, it was showing us medusa head appearance. On a penicillin agar, it's showing us a string of pearls appearance. Next, what is the selective media?
Soomething that we'll have to mug up. The selective media is the PET media. And what is the antigen antibody test that we can do, which is hardly done nowadays.
It's more for MCQs. The antigen antibody testing is the Ascoli's thermoprecipitant test. Soo Ascoli's thermoprecipitant test also happens to stand for anthrax. Soo let's do a recap of all six things.
Number one, on gram staining, it looks like boxcar or bamboo stick. On agar, it shows you medusa head appearance. On a penicillin agar, it will show us pearls, string of pearls appearance.
On gelatin, it shows us inverted fir tree appearance. Soelective media is FLET and Ascoli's antigen antibody reaction is also for anthrax. Now that we studied everything, why don't we start doing a few questions.
All of the following are properties characteristic of Bacillus anthracis except motility on wet mount examination, medusa head colonies, poly D glutamic acid capsule, and boxcar appearance all of the following are characteristics so firstly did we see the boxcar appearance yes either you can call it boxcar or you can call it the bamboo stick appearance does it have a polydeglutamic acid capsule anthrax yes it had a polydeglutamic acid is what it's nothing but protein it's nothing but polypeptide and does it have a polypeptide capsule definitely yes does it show you medusa head colonies again yes so what does it not show you i have not told you that it's motile. It's not at all motile. I've not shown you any feature of motility out here.
Soo it is a non-motile organism. This was the first question. Let's practice a few more. Moving on to the next one. Which of the following is not a cultural characteristic of Bacillus anthracis?
Medusa head, string of pearls, inverted fir tree, bamboo stick. You'll say all of these are features of Bacillus anthracis. I asked you which is not a cultural feature of Bacillus anthracis culture. Soo if you see medusa head is on agar, it's on a culture plate.
Sotring of pearls is on what kind of culture plate? It's on a penicillin agar. Soo that is also a culture characteristic. Inverted fir tree appearance is on which agar?
It's on gelatin agar. Soo that is also a culture characteristic. Bamboo stick appearance is not on a culture.
Bamboo stick appearance is on gram staining. Soo that is why they had asked you which of these is not a cultural characteristic. Okay.
Bamboo stick appearance is a characteristic but not a cultural one. It's a gram stain characteristic. Moving on to the next question.
Which disease occurs after eating uncooked meat? I think it's very very obvious over here because of the bias also. With uncooked meat, bacillus anthracis and which type? You had three types of anthrax. Cutaneous, pulmonary, intestinal.
Soo but obvious there's going to be intestinal anthrax. Intestinal anthrax is what is going to be associated. with uncomplete. Okay, having said that, let's move forward.
Soomething that we studied probably in the previous session as well. The organism responsible for toxicity due to Chinese fried rice. The organism responsible for toxicity due to Chinese fried rice is going to be, so I told you a mnemonic that Chinese fried rice and cereus.
We are now moving on to the discussion of bacillus cereus. Please remember. It's the food poisoning one.
Where have I taught you this earlier? Where did we study that there are two organisms, Sotaph aureus and Bacillus cereus. Sotaph aureus also causes food poisoning in less than six hours, whereas Bacillus cereus also causes the same in less than six hours.
Soo, they are both causes of early food poisoning, short incubation food poisoning. When I talk about Bacillus cereus, one thing is certain that there is food poisoning that is involved. And we keep studying it is to do with Chinese food, Chinese fried rice, so cereus for C, C for cereus and C for Chinese.
But actually this food poisoning is of two types. One, in which the patient comes to us with vomitings and the second food poisoning is in which the patient comes to us with diarrhea. Soo there are two kinds of food poisoning.
Remember the vomiting one has a Chinese fried rice and a short incubation period. It's not the diarrheal one. The diarrheal one has a lengthy incubation period of eight to 16 hours and it is by consumption of probably poultry and vegetables so solid food not just chinese food remember easier way of learning it emetic so when we eat food the shorter route of the food coming out is vomiting the longer route of the food coming out are the stools so the shorter incubation period is for the vomiting type and the longer incubation period is for the diarrheal type so remember when i say that staff aureus and bacillus cereus have the same incubation period that is less than 6 hours.
I hope you have understood that which kind of bacillus cereus am I talking about. I am talking about the emetic type. I am talking about the emetic type.
Okay, so yes, that was the question. Chinese fried rice, bacillus cereus. Let's move on to the next. The following are true about bacillus cereus introduced or induced diarrhea.
except. Soo, first and foremost, they are talking about Bacillus cereus and which type of it? They are talking about the diarrheal type of it.
And which of the following are true except? Soo, is it transmitted by parenteral route? Incubation period is longer. It is caused by enterotoxins.
It is usually associated with fried rice or Chinese food which is reheated. Soo, please remember, I know that when I am talking about Bacillus cereus, Be it the emetic type or be it the diarrheal type. Soee, for example, Chinese food can go in both, right? Because emetic type is also Chinese food and diarrheal type is because of meat and veggies. Meat and veggies also ultimately goes in Chinese food only.
Soo, both of them are caused by Chinese food. Soo, is it associated with fried rice or Chinese food which is reheated? Definitely yes.
If it is causing food poisoning, it has to have a toxin which is going to be enterotoxin involving the intestine. Soo, that is also true. For the diarrheal type, is the incubation period longer? Yes. If you remember correctly, for the emetic type, it is less than 6 hours whereas for diarrheal type, it is approximately 8 to 16 hours.
Soo, definitely for the diarrheal type, it is longer. Can it be transmitted by parenteral route means via blood or needles? No, obviously that is not sounding right.
When it is causing food poisoning, it is not something that will go via blood or get transmitted via needles. It's definitely going to be eating so it's going to be definitely a form of eating or oral consumption if you want to know that what is the selective media you don't have to know the full forms that's the good news i've only got to the full form because somewhere for your knowledge you can know but mypa and pemba remember when we are talking about the lab diagnosis of bacillus cereus three words should remain in your mind firstly it is motile it can move around that is how it's causing diarrhea also vomiting also it's moving around and the two selective media are mypa and pemba as i said knowing the full form is not important if you wish to know it's on the screen in front of you but again not important mypa pemba mobile these three motile these three words come to you bacillus cereus is done i hope that's okay with everyone and we can move on forward if you remember all the organisms under bacillus that i was talking about be it anthrax or cereus or all the others that we spoken earlier you They are all aerobic. They need oxygen. Whereas the ones that come under Clostridium are anaerobic and that is exactly what I am starting with next. All that come under Clostridia are anaerobic.
Soo this means they do not need oxygen. They do not need oxygen. Soo what is the classification? I know right now as I said you know sometimes we see some tables in microbiology or even other subjects like biochemistry or pharmacology and it's kind of overwhelming.
because it gives you too much of information in a text manner. Whenever you come across anything like that, the best way is to segregate it into shorter tables, make your mnemonics, visual memory, image-based mnemonics, and that's the only way of cracking such things. Soo let's try and decode this table also.
What have they written about Clostridium? They have said that, what all do you know? Do you know Clostridium is a spore-forming organism?
Yes, we know that. Clostridium will make spores. Where are the spores present?
Let me show you a picture of spores. Can you see that this is an organism and then there's a round spore over here. Soimilarly, this is a bacteria then there is a round spore over here. Soo basically they ask you the location of the spore. Look at these four pictures.
They will tell you the location. Where do you think is the spore located over here? You'll say right at the tip, right at the tip.
Over here also right at the tip. Soo can I say in these two the spore is terminal in location. The spore is terminal. Okay where is the spore over here?
You will say exactly in the center. Soo one more is that the spore can be central. Next you will say ma'am here also it's at the end but not exactly at the tip. A little away from the tip.
Soo can I say this is sub-terminal. What are the three locations guys? Either right at the tip terminal spore. right in the center, central spore, a little away from the tip and that is what you'll call as a subterminal spore. Remember, the most common out of these are going to be subterminal.
The most common of all, so if you say for example, Clostridium perfringens, anything or the most common spore that you can have is subterminal. But for Clostridium tetani and Clostridium tertium, they have TE in them. For Clostridium tetani and Clostridium tertium, we have TE and TE for terminal. Very simple. Tetani and tertium have terminal spores.
Then you will come back and you will say that fine, this is also terminal and this is also terminal. What's the difference? Soo, I will say that one of them, I am very confident that this one is Clostridium tetani and this one is Clostridium tertium. You will say ma'am, both of them are terminal.
How did you get to know? Because please remember when you're writing tertium, you come across T-E-R. Tertium gives us a tennis racket appearance.
Tertium gives us a tennis racket appearance. T-E-R for tertium, tennis racket. Soo tennis racket will always look something like this. A little long spore like a badminton racket or a tennis racket. Whereas when you're talking about Clostridium tetani, it's a tennis racket.
this is going to be a drumstick appearance. Has everyone seen drumsticks? Drumsticks are round. If you look at the organism, the spore will be round like this, like a drumstick. Soo, remember when you see a round spore at the terminal, it's drumstick like tetanus and when you see this oval spore at the terminal, that is tertium tennis racket appearance.
What is common to them? TE for terminal, TE for terminal but I hope you remember TER is the tennis racket appearance. Coming to the next.
When is the spore in the center means when is the spore right in the center. Whenever I put anything in the center, I'm dividing the organism into two parts, bi. I'm creating a bifid.
Remember bi fermentans has a central spore. Soo let's do a recap guys. All the spores in all the organisms are usually subterminal but in Clostridium tetani and in Clostridium tertium, the spores are going to be terminal and terminal. whereas in bifermentans, dividing it into bi, bifid, the spore is central in location. I hope the first part of the table is done because now we move on to the next part.
Clostridium species are unencapsulated and they are motile. What did I learn? Clostridium is not going to have a capsule and has no inhibition. It has no capsule and it's going to move around everywhere.
It has no capsule and it's going to move around everywhere except. exceptions are asked so what do i want to tell you uh when you were when you started off your journey neat ug days get back to neat ug days get back to 11th and 12th class get back to those days where what were your subjects physics chemistry and biology physics chemistry and biology for which exam did you take up pcb as your subjects you took it up for an exam called pre-medical entrance test pmt so that's your mnemonic you took pcb for pm T, right? Soo, what is that?
What am I trying to say? All the Clostridia are unencapsulated, but which are the ones which are capsulated? Which are the ones which have a capsule present in it? You will say Clostridium P for perfringens and Clostridium B for butyricum. Soo, remember P, C, B tells you Clostridium perfringens and Clostridium butyricum, they are capsulated, rest all of them are unencapsulated.
Coming to the next, I told you all of them are motile, all of them can move here and there but PMT which are the ones which are non-motile, which don't have motility, again P for Clostridium perfringens and T for Clostridium tetanitide 6. Repeating, perfringens and tetanitide 6 are non-motile. Soo, I would want to do a very very quick recap. The two mnemonics that I have with me are PCB and why did we take PCB? because what did we want to crack?
We wanted to crack. Soo for crack, I'll write this. We wanted to kill the exam PMT. Soo I took PCB because I wanted to kill PMT. But then there were some of us who were a little overconfident in life.
And I would include myself also in those set of students who apart from PCB also took maths, who also took mathematics, who took math, because they thought that why not even IIT or why not keeping all my options open. Or why not getting a better score? And all of us know that if we were inclined towards PCB, then our math was horrible.
And I really don't know why all of us were so overambitious and still took it up. And also, just in case you were one of those, please type it and let me know so that I know that I was not the only foolish person who decided to do that when I knew that my aptitude was for PCB. And then I burdened myself with mathematics only to keep my options open. Soo in case you're also of the same, you've been through the same, let me know. anyway so we took PCB and we wanted to kill PMT so let's see all the Clostridia species are unencapsulated but which is the one which is going to have a capsule capsule is going to be present in Clostridium perfringens and Clostridium butyricum okay next which of them did not or which of them are all of them motile definitely all of them are motile you But which are the ones which are going to be non-motile?
The non-motile ones are again going to be Clostridium perfringens and Clostridium tetani type 6. That's the final summary. Soo, I hope all of you are okay with the final summary and we can probably attempt a question. Which Clostridium species is capsulated? As soon as you get this, remember capsulated, PCB. Capsulated which all?
Perfringens, yes, capsulated. Butyricum, yes, capsulated. Soo what is the correct answer? The correct answer is both A and B are capsulated.
Soo I hope finally these three tables are making sense. The spores, the capsule, the motility because now we can move on to the next. Gas gangrene is caused by all except. This was a previous year question in the FMG exam. Gas gangrene is caused by all except.
Soo the answer is I think even if you don't know gas gangrene but you know for a fact that tetanus will cause tetanus. tetanus will obviously cause tetanus and not gas gangrene so definitely gas gangrene is caused by all the others so let us start with this what all am i talking about gas gangrene most commonly in 60 percent of the cases is clostridium perfringens remember in the earlier days clostridium perfringens was also known as clostridium welchii clostridium welchii and clostridium perfringens is the same it causes gas gangrene what do i mean by that you gangrene means something is going to die which means the muscle is going to die. There is myonecrosis that is going to happen.
There is myonecrosis that is going to happen. Soo gas gangrene which is going to be seen in 60% of the cases by Clostridium perfringens. Other than that septicum and novi.
Soepticum and Clostridium novi they also cause gas gangrene. Repeating we have perfringens then we have septicum and then we have novi. All of these are responsible for gas gangrene.
Out of these, obviously the question that you will get will be maximally on perfringens. Soo let me come back to the question. Again, like I said, what all causes gas gangrene?
It's caused by perfringens, it is caused by septicum and it is caused by novi. Perfringens, septicum, novi. Soo tetanus does not cause it.
Out of these, they will definitely ask you a question on the lab diagnosis of Clostridium perfringens and I can see a lot of things written in front of me. And yes, that is exactly what is important. Soo one by one, we are going to come down to everything about Clostridium perfringens.
Rather than seeing it like this, I would show you one by one as separate photos. I think that will be a better thing to do, right? Soo first and foremost, whenever I talk about Clostridium and it reminds me of claustrophobic.
clostridium, claustrophobic, the thing that comes to your mind is anaerobic. It does not need oxygen and anything that does not need oxygen will be grown in an anaerobic culture media. What is the anaerobic culture media where there is no oxygen present? Soo anaerobic culture media is RCMB, Robertson's cooked meat broth.
RCMB that is Robertson's cooked meat broth that is not having oxygen that is for all the anaerobic organisms point number one point number two it shows us i'm going to now tell you many many fancy names it's going to show us target hemolysis what is target hemolysis have a look at this target so all of you have played that dartboard game of course you have i'm sure the archery and the dartboard game so you know for a fact that there's a bullseye that you always have to hit i still have one of these in my room because i think it's a game which um you know my childhood went away but this did not and this is still a very famous past time for me and I think many of you also. Soo now we have magnetic ones as well and many others which is a different discussion that we'll have some other time but yes I'm sure everyone's seen a dart board and you've seen those bullseye archery boards so they have a lot of lines around it so that you can hit in different zones right. Soimilarly the kind of blood breakage that is caused by Clostridium perfringens is target hemolysis. which basically tells you that you can see one clearing here and another clearing around it. Soimilarly, one clearing here and another clearing around it.
Soo, there is a double zone of hemolysis also known as the target hemolysis which you see with Clostridium perfringens. That is the next point. Coming to the third one, Nagler's reaction is positive.
What is Nagler's reaction? Let us have a look at this picture out here. We call it a Nagler plate. What is a Nagler plate?
It is basically a culture plate. which is going to have egg yolk in it. It's basically a culture plate which is going to have egg yolk in it.
Why have we added? Why is this whitish? Because of egg yolk.
Egg yolk is something which is very very rich in lecithin. Egg yolk is extremely rich in lecithin. Soo basically there's a lot of lecithin out here.
And from the patient, from the patient I have added clostridium perfringens. I have added clostridium perfringens. Can you see what has happened? All the area around Clostridium perfringens has become white.
Why? Because please remember Clostridium perfringens has something called alpha toxin and do you know what is alpha toxin? Alpha toxin is lecithinase.
Alpha toxin is lecithinase, right? Soo please remember lecithinase will go and break the lecithin. Lecithinase will go and break the lecithin.
And that is why you get an opaque appearance over here. Soo that is the Nagler's reaction. Repeating, Nagler's reaction is due to which toxin of Clostridium perfringens?
It is because of the alpha toxin. And what is the other name for alpha toxin? Alpha toxin is also known as lecithinase.
Coming to the next one, and that's the reverse camp test positive. Before I start off with this, I hope everyone remembers from our basic introduction in the previous session that there was something known as a camp. test And camp test was for an organism known as streptococcus agalecti.
It was for an organism called streptococcus agalecti. Now I am saying reverse camp test which is for clostridium perfringens. And now this is known as reverse camp test. Soo what do I know under reverse camp test?
Vertically I have put clostridium perfringens. Horizontally I have put streptococcus agalecti. Soo please remember. always.
Now I'll tell you the difference. We'll draw two images so that we know the difference between a camp test and we know the difference between a reverse camp test. These two is what we have want to know.
Soo what is camp test versus reverse camp test? Remember in both of them and I'm repeating this again in both of them the vertical line and a horizontal line will be there. There will be a vertical line and there will be a horizontal line. The horizontal line will always be of streptococcus agalecti. The horizontal line will always be of streptococcus agalecti.
It's the vertical line that will vary. If the vertical line is staphylococcus aureus, this means you are dealing with a case of or you are performing a case of camp testing. You are trying to go in for camp testing. On the other hand, if the vertical line has something known as clostridium.
perfringens then you've done a reverse methodology and gone in for reverse camp test. Soo basically you realized that the horizontal line is always going to be agalecti. Agalecti is always going to be horizontal. The vertical line in camp test is to phylococcus aureus whereas in reverse camp test the vertical line is clostridium perfringens and over here the vertical line was clostridium perfringens so this happens to be the reverse camp. test.
Coming to the last one, it shows us stormy fermentation with litmus milk. Although no one will ask you this picture, but can you see that there is a litmus milk and there is some stormy bubbliness that you see at the top? Like I said, no one's going to ask you this, but with litmus milk test, stormy clot reaction is noted.
Let's do a recap. We have to grow it in Robertson's cooked meat broth. Target hemolysis is seen. Nagler's reaction is going to be positive. Reverse camp test is noted and the stormy fermentation with litmus milk is what we see out here.
Soo I hope that's okay. Clostridium perfringens, all fancy names coming up your way. Okay, let's move on to the next one.
Maybe you can answer this question now. Nagler's reaction is predominantly associated with which toxin of Clostridium perfringens? Nagler's reaction is predominantly associated with, so if you remember Nagler's reaction was the one that was utilizing egg yolk.
And if I have egg yolk, how will I break egg yolk? Soo, you had studied that egg yolk has lecithin and if you want to break egg yolk, you will have to use lecithinase. Now, which of these was lecithinase?
Alpha toxin of Clostridium perfringens was lecithinase. Do I have any of these two in the options? Yes, I have lecithinase in the options and that becomes my answer.
Let's move on to the next question. Which of the following is incorrect about the toxin leading to the disease below? which of the following is incorrect about the toxin leading to the disease below. Soo, this is the disease that has been shown. First, we will identify this.
It looks as if the man is smiling. This condition is known as rhesus sardonicus. This condition is referred to as rhesus sardonicus which basically means that it looks as if the patient is actually smiling.
Well, definitely not. This is a classical case of tet. and obviously once if a patient has tetanus he's definitely not smiling but why does it look like as if he's smiling because all the facial muscles all the muscles have basically contracted so there's a contraction there's a spasm that has occurred this results in spasm of the muscles and once all the muscles will undergo spasm all the muscles of the face they undergo spasm it looks as if the patient is grinning or smiling that is known as rhesus sardonicus Soo, if I want to answer this set of questions, I will need a little bit of theory base for myself.
When I am dealing with Clostridium tetani, it has two toxins which are responsible for everything. It has two toxins which are responsible. Number one is known as tetanolizine and the other is known as tetanospasmin. Repeating, tetanolizine, tetanospasmin. If I say that ultimately there has to be...
spasm of the muscles. The muscles have to contract. There's going to be a muscle spasm. Which of them would ideally be the one that will cause it? You will say obviously the spasmin one will have the main role.
The main role in causing the muscle spasm is going to be tetanospasmin and how does it act? At which level does it act? At a neuromuscular junction, at which level does it act?
It acts presynaptically. Does this remind you of some very famous question that you get in forensic? where there's another poisoning that also causes the same kind of muscle spasms but that doesn't act pre-synaptically that acts post-synaptically i hope you all remember the strychnine poisoning strychnine poisoning which is again definitely a question that you can you know anytime get in the exam strychnine poisoning is something that they will tell you for post synaptic attack so that is going to cause post synaptic effect and then it is going to cause spasm of the muscles so please remember for tetanus it is pre-synaptically tetanus is going to be pre-synaptically and who is the main one causing it tetanus spasmin is causing it so how do i differentiate between tetanolizine and tetanus spasmin because both of them are heat both of them are heat labile but their oxygen affinity varies remember tetanolizine versus tetanospasmin. Soo, tetanolizine is oxygen labile and tetanospasmin is oxygen stable. Repeating, tetanolizine is oxygen labile and tetanospasmin is oxygen stable.
Let's come back and let's start reading it. Which of the following is incorrect? Are both of them heat labile? Definitely true.
Okay, is it oxygen stable? Soo, the toxin which is leading to spasm I am talking about tetanospasmin. I am talking about tetanospasmin.
Means is it oxygen stable? Yes, it is oxygen stable. Does it act post-synaptically?
Think again. That is the false statement. I just told you that when we are dealing with a case of tetanus, it does not act post-synaptically. It acts pre-synaptically. And what does it do?
It definitely, I think everyone knows this much of physiology, that it inhibits the release of GABA. It inhibits the release of GABA and it acts presynaptically. That is why there is a spasm of the muscles that is created.
Well, okay, having said that, I suppose we can move forward and go on to the next set of questions. Botulism. Botulism causes what?
Descending flaccid paralysis, descending spastic paralysis, ascending paralysis or ascending spastic paralysis. I think in terms of the answers. botulinum or botulism causes descending flaccid paralysis and which organism am I talking about over here I'm talking about clostridium botulinum in fact I think it's a very very obvious kind of a question that when someone asks you that for botulinum what is the toxin that you have to know the toxin is the botulinum toxin and in fact guys if you've read a little bit of the past literature you would know that the most toxic substance which is the most lethal to mankind you The most lethal and the toxic substance to mankind is Clostridium botulinum or this botulinum toxin. And what does it cause? It causes food poisoning.
It causes food poisoning. Number one, it causes paralysis. Number two, repeating, what does Clostridium botulinum cause? Number one, it causes food poisoning.
Number two, it causes flaccid paralysis. Soo, remember FNF, Clostridium botulinum causes flaccid paralysis and food poisoning. Obviously, if it causes food poisoning, what kind of a toxin does it have?
Intestine, food poisoning, enterotoxin and what kind of food does it grow on? It tends to survive in canned food and all the students who are living in foreign countries and who consume a lot of these canned foods in hostels, always remember that there is a, that's the reason we check for the expiry date and even if it is within the period of consumption even if it has not reached the expiry date but you must have said you must have seen that they've always written on the can that if the can appears damaged or if the can appears very swollen or if it's you know become rounded and there's some gas kind of production or they say if you see any bubbles on the food you should not consume it primarily why because Clostridium botulinum tends to grow on canned food so whenever you open a canned item even if it's not reached the expiry date but the can is looking very swollen or if you see bubbles on the surface of the food as soon as you open it do not consume that okay so enterotoxin on the canned food causes food poisoning similarly it causes flaccid paralysis and obviously if it causes paralysis which toxin is it neurotoxin so finally what are the two toxins of clostridium of clostridium botulinum one of them is going to be neurotoxin one of them is going to be enterotoxin the entero one will cause food poisoning and the neuro one will cause flaccid paralysis and that is the answer to the question it causes descending flaccid paralysis. Soo can I say in other words that tetanus was something that was causing spastic paralysis it was causing spasm and botulinum is something that is going to cause food poisoning and flaccid paralysis FNF. Well having done that let's move on to the next question.
A hospitalized patient developed severe watery diarrhea. and dehydration following a long-term course of antibiotics. The histopathological image is shown below and which of the following toxins are responsible for the production of this condition. Soo firstly you have a case of diarrhea so this means intestine is involved. Soo much of diarrhea has happened that obviously patient has become dehydrated and this is a very important history given next.
This has happened after a very long-term course of antibiotics. Remember you After long-term usage of not just cephalosporins, not just third-generation cephalosporins, but any kind of antibiotics. After a long-term usage of antibiotics, what is the patient at a risk of?
Patient is at a risk of Clostridium difficile infection leading to PMEC, pseudomembranous enterocolitis. Remember, leading to PMEC by Clostridium difficile. Soo they will always give you... a long-term usage of antibiotics or cephalosporins.
That is why the patient will have Clostridium difficile infection. That is when the patient will have pseudomembranous enterocolitis. How does pseudomembranous enterocolitis happen?
First and foremost, the question. This happens because of two toxins called toxin A and toxin B. Soo, remember Clostridium difficile has two toxins.
It has something called toxin A. and it has toxin B and these are the ones responsible for this condition. Further, how does the patient present? The patient is going to present with severe watery diarrhea.
Why is the patient going to present with severe kind of watery diarrhea? Because let's see what has happened to the intestine. This is an intestine.
Normally, you'll always draw the intestine like this closed. What have I done over here? Instead of it being closed, I've opened it. This is the open version of the intestine.
And all of you can appreciate that there is a definitive membrane, dirty, dirty, yellowish, necrotic membrane that is present on the mucosal aspect. That's the next question that you get. It is present on the mucosal aspect.
Soo a necrotic membrane on the mucosal aspect, that is what you know for Clostridium difficile. And when you look at it under the microscope, you will see that there's a lava that has erupted. Everyone's seen a volcano. We all know that in a volcano, a lot of lava is going to come out.
Soo from the intestine, this dirty lava material is coming out. We call it a volcano-like eruption. Soo if you see a dirty membrane on the mucosa and you see a volcano-like eruption, like you saw over here, they gave you the characteristic volcano lava eruption.
You're dealing with a case of Clostridium difficile and toxin A and B are responsible for these. Soo... Coming to the next question, Clostridium difficile, still on the same bacteria, can be spread through all except? Clostridium difficile can be spread through all except orophecal root, direct, hand to hand or needles. Think logically, this is basically a kind of diarrhea, intestine involvement.
It's a kind of diarrhea, it's a kind of an intestine involvement. Soo if I think logically, how do things reach the intestine? I mean definitely by...
hand-to-hand contact, direct contact, orophical contact, reaching the intestine via needles, that is sounding a little weird. And that is what by common sense you have to rule out that Clostridium difficile is not something that is going to spread via the parenteral route. It is not something that is going to go via the needles.
And that is why this is the wrong statement over here. Finally, if you say you want to do the diagnosis, what is the media? Again, two names that you learn, but you don't need to know the full forms per se. CCFA, Ccfa.
Soo remember for Clostridium difficile, Clostridium difficile, CIL has a characteristic, you know, it has a C sound and it has an F sound. Soo remember that when you're talking about difficile, we'll write it in that manner. When you're talking about difficile, we have to talk about CCFA, Ccfa.
Soo difficile has CCFA and Ccfa. If you want to know their full forms in front of you, Most welcome to learn but not required. CCFA, Ccfa, these are the two that you have. Soo, let us do a recap of Clostridium difficile.
Number one, this is always happening after a long-term use of cephalosporins. How does it reach? It reaches by direct contact or orophecal route or hand-to-hand contact, never by needles. This organism has two toxins, toxin A and toxin B. What do they cause?
They cause watery diarrhea in the patient. If I want to look at it under the microscope, I will see there is a pseudomembrane. there is a dirty membrane that is formed on the mucosal aspect. Microscopically, we see a volcano lava-like eruption and in terms of the media, we see that there is CCFA, Ccfa media that are used.
Well, I guess we have done all the clostridia. Why do not we take up a few of the pre-yqs? That'll be good.
All of the following organisms cause gas gangrene except. Soo, quick test. These are PYQs of the FMG exam.
All of the following organisms cause gas gangrene except. Soo, we have studied for gas gangrene, Clostridium perfringens, Clostridium septicum, Clostridium novi, novi is not here, Welchii. Welchii and perfringens is the same thing. Soo, which of them does not cause gas gangrene? Clostridium difficile.
Clostridium difficile causes pseudomembranous. enterocolitis. Next question, necrotizing enteritis, the very, very, very important question, necrotizing enteritis.
Soo, first and foremost, septicum we have not studied only because it is not at all important. Enteritis, when I say enteritis, difficile is sounding right. You will say ma'am it causes pseudomembranous enterocolitis, but they have not written pseudomembranous enterocolitis, they have written necrotizing enterocolitis, so not difficile also. tetani i know causes tetanus that smiling face that tetanus rices sardonicus actually please remember necrotizing enteritis can be caused by clostridium perfringens and that is what that is exactly what i want to add on to your knowledge that clostridium perfringens or clostridium tetani not only causes necrosis of the muscle but it can also cause necrosis in the intestine basically it can also cause necrotizing enteritis that is something that i hope you guys will definitely remember. Soo, answer per Clostridium, per phryngines.
Moving on to the next question. Three-year-old boy fell down and injured his leg while he was playing on the ground. After a few days, there are crepitations felled from the injured area. What could be the probable causative organism? Carini bacterium diphtheria, Peudomonas urogenosa, Clostridium tetani or Clostridium velgii.
Soo please remember a three-year-old boy has fallen down. As soon as I see the history of an injury and a fall, I always start thinking of tetanus. Right now I think of tetanus but when I saw later after a few days there are crepitations felt from the injured area. Now that is something I don't see with tetanus.
When do we see crepitations? What are crepitations? All of those, we consider them as signs of getting old. Do you sometimes move your fingers or move your neck? or your back or your knee or some joint and you get that click kind of a sound there's a click sound that comes maybe from your fingers or your neck or when you're sitting for too long and then you stand up from your back and your knee that those click kind of sounds are known as crepitations but in this three-year-old young boy there are crepitations which are coming from those injured area that is because gas production has happened over here crepitations are an indication of gas and over here after injury they are talking about gas gangrene.
Soo, when they are talking about gas gangrene, the organism that comes to my mind is either Clostridium velchi or it is going to be Clostridium perfringens. Okay. Soo, yes, having said this, I think we can move on to the last question of this family. Drumstick appearance.
carini bacterium diphtheria clostridium tetani nyseria meningitidis and streptococcus pneumonia and by now we've done all so we are going to discuss all when we talk about the drumstick appearance remember the answer to this question clostridium tetani because what kind of a spore does it have te it has a terminal spore so clostridium tetani okay in the previous crash course i had taught you carini bacterium diphtheria has what kind of an appearance It has a very classical Chinese letter or cuneiform appearance. It has a Chinese letter or cuneiform appearance. What about Neisseria meningitidis? The way you write M, the way you write M, we had said that we will call it lanceolate.
We will call it lens-like. Soo, Neisseria meningitidis is lanceolate. And streptococcus pneumoniae also.
This is also going to be a diplococcus with a capsule. This is also going to present in a similar manner. Soo, over here, drumstick appearance.
Clostridium tetanus. Well, having said that, we do wrap up the spore forming organisms and we can definitely move on to the next family and that is Enterobacteraceae family. When we are talking about Enterobacteraceae family, we have certain, I know for a fact that they are all gram negative, we are dealing with all gram negative organisms, but there is a certain kind of, you know, general rule that we follow for the Enterobacteraceae family.
Soo, please remember that. when we are dealing, before I start with questions, when we are dealing with enterobacteraceae family, remember all of them are going to be motile but Ella, Ella are not motile. All of them are motile but Sohigella and Klebsiella, these are immotile, they are non-motile. Repeating, all are motile but Ella, Ella.
they are immotile shigella klebsiella all of them are catalase positive oxidase negative so all the organisms under this they are catalase positive and oxidase negative but shigella ella remember shigella dysentery type one shigella dysentery type one is catalase negative repeating all our catalase positive but shigella ella it is catalase negative so last time repetition All are motile, but Sohigella and Klebsiella are immotile. All are catalase positive, but Sohigella dysentery type 1 is catalase negative. Soo, if I ask you this question, which of the following is a non-motile bacteria? Maybe you have not read all or maybe you have. Soo, if I ask you, is something that we studied?
Soo, you will say, yes, we studied Ella, Ella are immotile, Klebsiella, Sohigella. They are immotile. Soo the answer over here is very obvious and this was a PYQ in the FMG exam.
Sohigella and Klebsiella are immotile. Coming to the next one. Catalyze negative organism of the Enterobacteraceae family.
All of them are catalase positive except one organism and that was Sohigella Dysentery type 1. Sohigella Dysentery type 1 is said to be a catalase negative organism. Soo I think the basic is pretty much clear and we can move forward with the classification. How do we identify this entire enterobacteraceae family? This enterobacteraceae family is identified as lactose fermenter, non-lactose fermenter and late lactose fermenter.
Very simple. Either they ferment lactose or they don't ferment lactose or they ferment lactose slowly, slowly and after a while. Soo late lactose fermentation. L, NL. LL.
That is how we learn it. Lactose fermenter, non-lactose fermenter, late lactose fermenter. Remember, the only two lactose fermenters that you have over here are E coli and Klebsiella. E coli and Klebsiella are lactose fermenters. All the others, Soalmonella, Sohigella, Proteus, Yersinia, everything else of this family then automatically becomes a non-lactose fermenter.
Soo, if you remember, E coli and Klebsiella. Kolai and Klebsiella karenge. Kolai and Klebsiella ferment karenge. That is how we've learnt it. Kolai, Klebsiella karenge.
Everyone else is not going to ferment lactose. And then we have Sohigella Sooni. Sohigella Sooni.
Sooni. Sooni means keep sleeping. Wakes up very very late.
Probably just one of us. Sohigella Sooni keeps on sleeping, wakes up very very late. Soo that is a late lactose fermenter.
Let's repeat. Klebsiella and Kolai karenge ferment. they will be fermenters. Everything else, salmonella, shigella, proteus, yersinia, all shigellas, all others, they are non-lactose fermenter except shigella soni because it keeps sleeping, wakes up late.
That is a late lactose fermenter. Soo how did we identify? On what, you know, what is the way of identifying lactose fermentation?
What are the two media that we use for lactose fermentation? Number one, we have something known as a mekonkyagar. Number one media that we have is a Meconchiagar and the number two media that we have is the Kled media. What are they telling you?
In both of them, we find out lactose fermentation versus non-lactose fermentation. In Kled media also, we find out lactose fermentation versus non-lactose fermentation. But the colors are different.
Over here for lactose fermentation in Meconchiagar, you get a pink color. Whereas when we are talking about clad media for lactose fermentation over here, there is a yellow color. There is a yellow color that is obtained.
Soo repeating that when we are dealing with meconchi agar, lactose fermentation pink color. When we are dealing with clad media, the lactose fermentation is going to give you a yellow color. Soo you can see all this yellow color over here, lactose fermentation. Soo the next question will be that color change is happening.
Color change is happening which means there's going to be a medium, there's going to be an indicator. What is the indicator for Maikonky Agar? Soo firstly, what all does Maikonky Agar contain? It contains plant.
What is plant? P for pepton, L for lactose, A for agar, N for neutral red. T for Torocholate. Let's repeat. P for Pepton and Agar.
Every medium has Pepton and Agar. L for Lactose obviously because you want to find out whether lactose is fermented or not. N for Neutral Red because that is the indicator that will change the color. That will change it to pink or yellow. That's the indicator.
And T for Torocholate because bile salts are needed. Soimilarly in Kled, so if I ask you that what is the indicator, what is the color indicator that you have? for meconchi agar and what is the color indicator that you have for cled.
Soo remember for meconchi agar the color indicator that you will tell me will be neutral red whereas for cled can you see it's all bluish in color because the indicator is bromothymol blue. The indicator is bromothymol blue. These are exactly two questions that I have.
What is the indicator used in meconchi agar? And what is the indicator used in clad? And I think now you can tell me what was the indicator in mekonky agar? Mekonky agar was something by the mnemonic plant, right? Soo, N for neutral red, N for neutral red and for clad, the blue color one.
Soo, for clad, it is bromothymol blue. I hope these two PYQs will also be clear for all of you. Now, there is no problem in solving them. Soo, mekonky also tells me lactose fermentation by a pink color. Kled also tells me lactose fermentation by a yellow color but what is better?
If I ask you, mekonke is better or kled is better and as per the latest guidelines, remember kled is better than mekonke. Kled is going to be better than mekonke. Soo, now my question to you is, why is kled better?
Kled is better and now my question is, why so? Soo, when am I using? If I broadly ask you, what are all these organisms causing?
Ecoli, you will see Ecoli very famously causes urinary tract infection. Klebsiella can also cause urinary tract infection. Proteus can also cause urinary tract infection. Soo basically these are all media that you will use when you are dealing with a patient of UTI. Soo UTI can be caused by gram-negative organisms like all these you studied Ecoli, Klebsiella, Proteus.
Soo you will see all the gram-negatives. Soo will gram negatives grow on meconki? Will they grow on clad?
Yes, they will grow on both. Soo why is clad better? Because sometimes UTI can also be caused by gram positive organisms like Sotaphylococcus aureus can also cause UTI.
Like Candida can also cause UTI. Now the problem is that meconki doesn't grow them. Meconki only gives importance to gram negative organisms.
It gives more importance to gram negative organisms. Clad on the other hand Kled is going to be giving importance to everyone. It will allow the gram-negative and the gram-positive organisms to grow.
It will allow gram-negative and the gram-positive organisms to grow. Soo can I say, Meconki is very very inhibitory. It is not letting the positivity come out only.
It's not letting the gram-positive organisms grow. But Kled is less inhibitory. CLED, remember why did I highlight these two alphabets? CLED is less inhibitory. It allows everyone to flourish.
It allows everyone to grow. And I'll show you two questions of the previous year of Ames and Neat. Very important. Both of them are the same questions, only the language was different.
Let's read. CLED medium is considered better than Meconky Agar for what reason? You know your reason. What does it allow? You will say first option.
it differentiates lactose fermenters from non-lactose fermenters both of them do that clad also differentiates my conky also differentiates but what is why is clad better it allows everyone to grow it allows both gram positive and gram negative organisms to grow means it allows staff and candida what are they staff is gram positive candida is gram positive and clad is better because it allows everyone to grow it is less inhibitory it is less inhibitory it allows everyone to grow Next question, clad medium is considered better than meconkey for the following reason. What is the reason? It will allow everyone to grow. Soo let's read.
It supports gram positive and gram negative. Yes, I found the reason in the first option only. It definitely supports everyone. It supports gram positive as well as gram negative organisms.
Soo remember, what is better? Clad over meconkey. Okay, having said that, coming back on the basis of this, what are the two lactose fermenters?
Kaun karenge? Ferment karenge. Coli and Klebsiella ferment karenge. Soo you will say ma'am, this means that if I try to grow them on a Mekong ki agar, means E coli will also give me a pink color. because it is lactose fermenter.
Any lactose fermenter Ecoli will also give me a pink color, Klebsiella will also give me a pink color. How do I differentiate? Soo for example you get a pink color over here. How will you tell me that whether this is Ecoli or whether this is Klebsiella?
Problem ho gaya, both of them will give a pink color because please remember Klebsiella not only gives a pink color but also gives something called, can you see it's looking very shiny and mucoid? It's pink. Okay. Soo on the basis of pink, you'll say, ma'am, pink could be E coli also.
It could be Klebsiella also. But Klebsiella is having a capsule. Klebsiella is a capsulated organism and anything that's capsulated always gives these shiny mucoid colonies.
Anything that's capsulated will always give shiny mucoid colonies. Soo E coli doesn't have a capsule. E coli doesn't have a capsule. Klebsiella has a capsule. Remember Klebsiella has a capsule and that is why it's going to give these kind of shiny mucoid colonies and mucoid mucoid means if you try to pick it up it will stretch.
If I try to pick it up it's going to stretch like this it's going to be stringy stringy like this so please remember when you are getting mucoid and stringy colonies that is indicative that the organism has a capsule. And over here, out of E coli and Klebsiella, the best answer for a capsule is going to be Klebsiella. I hope the differences are sorted.
Coming back, I've understood how Klebsiella is going to not only give me a pink color, but also a mucoid colony. Now, coming back to E coli. Before I push you into lots of questions, what all does E coli cause, guys? I hope you remember E coli, two main things.
E coli can cause a lot of things. But the two main things that it causes are UTI and diarrhea. These are the questions, UTI and diarrhea.
These are the ones that they're going to ask you in the exam. Soo first and foremost, let's talk about UTI. UTI, urinary tract infection.
What sample will you take from the patient? When you're suspecting urinary tract infection, common sense will take a urine sample from the patient. What kind of a urine sample? We have to take a clean catch.
Which means? The patient will be instructed to clean the genitalia beforehand. Clean catch early morning preferably early morning midstream urine sample. Soo clean catch early morning midstream. What do I mean by midstream?
You will have to instruct the patient that when you go to pass urine early morning, divide the stream of urine into three parts. Soo first pass 10-20 ml of urine. Don't collect that.
Then collect the next 10-20 ml of urine and after that again throw away the remaining 10-20 ml. Soo you don't collect the first part of urine, you don't collect the last part of urine, you are only interested in the midstream sample. That sample is what you collect and what is the culture that you will grow it on, which is better, Meconki or Kled? We've studied Kled is better, Kled is being used nowadays.
Soo you'll find out whether there's E coli, whether there's Klebsiella, you'll find out. what is the criteria for diagnosis of UTI for the diagnosis of UTI we use something known as the CASo criteria what is CASo criteria CASo criteria says that you will give a diagnosis of UTI when the bacteria are more than 10 to the power 5 1 2 3 4 5 when the bacteria are more than 10 to the power 5 that is when you are going to give a diagnosis means one lakh colony forming units per ml when there is more than 10 to the power 5 why have this criteria been kept why not 10 to the power 4 or 10 to the power 3 2 1 because are bacteria only present in case of uti no aren't bacteria normally also present don't we have bacteria in the urinary tract which act as commensals so maybe there is e coli as a commensal 10 to the power 2 rc will you give it as a case of uti no if you want to call it disease if you want to call it pathogenic and disease you must cross 10 to the power 5 colony forming units CFU. However, there are some exceptions to the CASo criteria.
When do we consider a count less than 10 to the power 5 also significant? Remember you will consider it significant in case of a SoPA. What is a SoPA?
So means suprapubic aspiration. Means what? Has the urine come out via the normal route?
Has it come out via the urethra, via the urinary tract? No. You have directly punctured the bladder and taken the urine.
You have directly punctured the bladder. Souprapubic aspiration. Soo if urine would have come from the direct route and urine would have come through the urethra, then the commensals would have been there. Then you would have had to wait for the 10 to the power 5 cutoff to call it pathogenic.
but when you've directly taken the sample from the bladder then the commensals are not there then even one or two bacteria are significant then even a 10 to the power 2 10 to the power 3 is going to be significant so in case of suprapubic aspiration don't consider this cutoff next in gram positive organisms in gram positive organisms like staph and candida they are not commensals of the urinary tract they are not commensals so even if they have a count of 10 to the power 2 3 you consider them as significant Soimilarly, A for antibiotics and diuretics. Many a times in our country, patient will say that, you know, from a local chemist, I took some antibiotics, then I have come to you for the sample. I've been taking antibiotics since five days.
After that, I'm feeling that I'm not showing much of improvement. Soo now I've come to you to give my urine sample. Soo antibiotic will anyway decrease the bacterial load. Soo you won't wait for 10 to the power five.
Below that also, you will give the diagnosis. Soame way patient says diuretic. If the patient is on diuretic, this means the urine is already diluted. The urine is coming to you as a diluted sample. Then again, you don't wait for 10 to the power 5 cutoff.
Soo, repeating what is the significance of finally what is going to be the mnemonic for the CASo criteria exceptions. Firstly, CASo criteria says that you call significant UTI over 10 to the power 5. However, if we have suprapubic aspiration, gram positive organisms like Sotaph aureus and Candida or any antibiotic diuretic therapy, we don't follow the CASo criteria. This is when E coli causes UTI. What about E coli causing diarrhea?
Now that is going to be very, very tough. Obviously, if I've said it's very, very tough, means I'm trying to just scare you because it's very, very tough in the textbooks, means we are going to simplify it. Soo first, let's simplify it and then we'll move ahead with lots of questions, right?
These are all the diarrhea strains that you have for E coli, all the diarrhea strains. And can you see what is the difference? EPEC, so P alphabet, then changes to T, so ETEC, changes to IEIEC, HEEHEC and EAEC. Remember, these are all the different strains of E coli that can cause diarrhea. What do I have to know?
Soo, E will always stand for Entero. Okay. Soo it's going to be Entero something E coli.
For example, I say Entero something E coli. Entero something E coli. Entero something E coli. Soo over here, Entero pathogenic E coli. What does Entero pathogenic E coli cause?
Entero pathogenic E coli causes P for pathogenic, P for pediatric. P for pathogenic, P for pediatric, it causes infantile diarrhea. Enteropathogenic E coli causes P for pathogenic, P for pediatric, infantile diarrhea. E-T-E-C, enterotoxigenic E coli, T for toxigenic, T for traveler's diarrhea.
Easy to learn. Entero E coli causes traveler's diarrhea. Entero E coli, invasion, something that is going in the cells. It's not going only till the intestine. It's going inside the intestine, inside the cells.
Anything that will invade will cause blood, blood to come out. Blood in the stools. What is that condition known as?
Blood in the stools is known as dysentery. Soo because it is invading, it causes bleeding in the stools. That is dysentery.
Enterohemorrhagic E coli. Soo it will cause some bleeding. It will cause some hemorrhage. and it causes HUSo. What is HUSo for those who are unaware?
HUSo stands for Hemolytic Uremic Soyndrome. HUSo stands for Hemolytic Uremic Soyndrome. Hemolytic means blood is going to break. Blood is going to break.
Uremic means kidney is going to get affected. Kidney is going to get affected. For those who don't know, please remember that this Hemolytic Uremic Soyndrome has a very classical triad. It has a very very classical triad that you have to follow in the exam and what is that triad? We call it the rat triad.
We call it the rat triad means when you're dealing with hemolytic uremic syndrome, R stands for renal insufficiency. There is kidney involvement that occurs. A stands for anemia because I think you know hemolytic uremic.
Soo which kind of anemia? Hemolytic anemia. And also there is something that is known as thrombocytopenia.
There is also known as thrombocytopenia. There is also thrombus formation that occurs. clot formation occurs thrombocytopenia can occur so remember rat renal insufficiency anemia and thrombus and thrombocytopenia hemolytic uremic syndrome caused by hemolytic so hemorrhagic Ecoli enterohemorrhagic Ecoli the only one for which you have to learn the strain what strain of EHEC causes hemolytic uremic syndrome O157 H7 O157H7 causes hemolytic uremic syndrome enterohemorrhagic Ecoli.
Lastly enteroaggregative Ecoli. Now guys what kind of diarrhea persistent diarrhea how do I learn that enteroaggregative you and I we are together in this crash course microbiology crash course we really don't like the subject let's be very very honest about it because the subject has a lot of cramming up and too much of mugging up so we don't like it we keep forgetting it it's volatile so what have we decided we've decided we'll do a crash course all of us will sit down together when all of us sit down together united united we stand we mean we are going to make a persistent impact if we decide cumulatively if we decide collectively that we are going to study and we are going to crack this subject we will definitely do that right so when all of us get together we have more impact Soo similarly, when all these aggregate together, when there is enteroaggregative Ecoli, they have a longer time of diarrhea, persistent diarrhea. And one more thing, when you try to grow it on HEP2, what is HEP2?
HEP2 is a kind of a cell line. HEP2 is a kind of a cell line. Soo please remember on HEP2 cell lines, it gives a stacked brick appearance, not any of these, only enteroaggregative Ecoli gives a stacked brick appearance, stacked brick.
means something like bricks. Again, can I learn it like aggregated bricks, bricks which have been kept together, bricks which have been aggregated. Soo everything will make sense now. Enteroaggregative E coli causes aggregated brick appearance or stacked brick appearance and once we aggregate long term means persistent diarrhea.
Let's do a very very rapid revision of all these mnemonics that we've just studied guys. Firstly, Enteropathogenic E coli. P for pathogenic, P for pediatric, infantile diarrhea.
Entero E coli means T for T, traveler's diarrhea. Entero, invasion will cause bleeding in the stools, dysentery. Enterohemorrhagic, hemolytic uremic syndrome, O157H7.
Enteroaggregative, long-term, persistent diarrhea, aggregated breaks, stag break appearance on hep 2 cell lines. These are all the diarrhea strains repeating enteropathogenic, enterotoxigenic, enteroinvasive E coli, enterohemorrhagic E coli and enteroaggregative E coli. All these are important E coli strains which cause diarrhea.
Well, having said that, I think we are ready for some questions. Which organism causes HUSo, hemolytic uremic syndrome? We just studied.
Okay, when I read the options, I think there's no confusion at all. Answer to the question E coli, but which kind of E coli? Hemolytic uremic syndrome, HUSo is caused by enterohemorrhagic E coli. And did I teach you any strain also?
O157H7 strain of enterohemorrhagic E coli causes hemolytic uremic syndrome. Next, again, indirect way of asking you. Hemolytic uremic syndrome short forms given now we know it.
Hemolytic uremic syndrome is caused by EIEC, EPEC, ETEC or EHEC so entero hemorrhagic Ecoli. Coming to question 3. Travelers's diarrhea is caused by? Travelers's diarrhea. IEC, PEC, TEC or HEC.
T for T. Travelers's diarrhea is caused by entero toxigenic Ecoli. Soee how the questions are becoming so smooth and so simple to follow.
Next question. All of these are PYQs of the FMG exam. Antimicrobials are given in which type of diarrhea? Antimicrobials or antibiotics are given in which kind of diarrhea?
Soo, do you give it in diarrhea caused by osmosis or secretory diarrhea or do you give it in something like a viral diarrhea that is rotavirus or you give it in travelers? Travelerss diarrhea is which E coli? Entero E coli basically bacteria. Soo in which of them do you give antimicrobials? Which kind of diarrhea?
Obviously we give antimicrobials and antibiotics when we are dealing with bacterial etiologies, not for viruses, not for osmotic or secretory kind of diarrhea. Antimicrobials are obviously given for bacterial, travellers, ETEC type of diarrhea. Next, which of the following shows the stagged brick appearance on cell lines? Sotagged brick appearance.
I also called it aggregated brick appearance. Soo which of them? Remember Enteroaggregative E coli. Enteroaggregative E coli.
Soo that is going to show you the stagged brick appearance. Let's move forward. Okay, let's take up the next question guys.
Five-year-old girl attended a birthday party at a local fast food restaurant. After 48 hours, she developed cramping abdominal pain and a low-grade fever. and had five episodes of loose bloody stools. Sohe's taken to the emergency room next morning as diarrhea continued and she looked pale. Soo overall right now it looks like a food poisoning.
Fast food restaurant with fever, with pain and loose bloody stools are there. And because her diarrhea is continuing, she started looking very very pale. Sohe's taken to the emergency room. On examination, she is hypotensive with tachycardia.
Soo obviously so much of blood loss has happened, so much of water loss has happened. Soo obviously she is becoming hypotensive with tachycardia and her blood reports have shown hemoglobin 8. Is she coming across as anemic? Is she coming across as anemic? Yes.
Then they found out that there is thrombocytopenia. OK, so they've also found out that her platelet count is low. There is thrombocytopenia and there is evidence of hemolysis. Soo which kind of anemia is there? hemolytic anemia is there.
Is this sounding like some kind of a triad? When I look at the options also, did we study something called RAT? Only this part was missing in the question.
The renal involvement is not mentioned. Other than that, hemolytic anemia is mentioned, thrombocytopenia is mentioned. Are we indirectly targeting a case of hemolytic uremic syndrome? Soee, diarrhea causing organism following which there is hemolytic uremic syndrome, enterohemorrhagic ecolife.
an enterohemorrhagic Ecoli with strain it is O157H7 that is how a question of EHEC will come in the paper. Coming to the next question the blood of a patient is suspected to have pyogenic live abscess was sent for culture so there's a patient who has a pyogenic it would be a liver abscess actually pyogenic liver abscess is sent for culture that makes more sense right so when we are talking about liver abscesses and conditions, two things, either they are dealing with a pyogenic liver abscess or you're dealing with an amoebic liver abscess. Soo, amoebic liver abscess means parasite, entamoeba, parasite. Here, when they say pyogenic liver abscess, bacteria.
The colony morphology shows large mucoid colonies. When I say large, mucoid colonies. Mucoid is something which I have studied is organism that contains a capsule and out of these the organism that contains a capsule is Klebsiella pneumoniae.
The organism with a capsule is going to be Klebsiella pneumoniae. Soo this mucoid word and Klebsiella will always go hand in hand. Coming to the next question.
PPA test is used for the diagnosis of. PPA test is used for the diagnosis of. Soo please remember P for P, PPA test is used for the diagnosis of proteus and that is the next organism that I am going to teach you. Soo first let me teach you and then I'll come back to this.
What is P proteus? Everything about proteus has been written over here. Soo P for there are two P that you have to know.
Soo first it has something known as the PPA test or the PPA reaction positive. You don't have to know the name of the entire reaction but that is P phenyl pyruvic acid. If you wish to know the name, remember protease is phenyl pyruvic acid going to be positive. Another P for Dynes phenomenon. What is Dynes phenomenon?
Let me tell you that. Soo, before I move on, can you see U and So? U for what enzyme does it produce?
It is urease positive. And what motility does it show? It shows the swarming motility. It shows the swarming motility. and urea is positive do you guys know what is swarming this is swarming that if you are dealing with the case of blood agar if you are dealing with the case of blood agar can you see these concentric so bacteria grows then another circle of motility another circle of motility so this is referred to as the swarming motility when you are dealing with microbiology what are all the organisms that show you swarming motility pvcs pvcs show us swarming motility what is all of that Remember, P for Proteus, VP VP means Vibrio Parahemolyticus.
That way, as you will recall, it's not Vibrio Cholera. It's Vibrio Parahemolyticus. C for Clostridium Tetani and So for Soerratia.
Let's do a recap. We have P for Proteus, VP Soo, that is Vibrio Parahemolyticus, Clostridium Tetani and Soerratius. They show you the swarming motility. Soo, I've understood the meaning of swarming motility. I've understood that it produces urease.
I've understood it has a PPA reaction positive. It is something called Dimes Phenomena. What is Dimes Phenomena?
It's the story of you meeting your best friend versus you meeting your enemy before I get on to it. Very interesting. Soo whenever, for example, in the lockdown, you were not able to meet your best friend for two years, for example. Now, after two years, when you meet your best friend, best friend means someone you vibe with, someone you relate to, someone whom you are very fond of. someone who's just like you for that matter.
Soo when you meet your best friend after two years, you're going to just run towards him or her and hug her because you're meeting him or her after a lockdown after two years. Soo if you're same and if you vibe together, you'll hug each other. What if you meet your enemy after two years?
You're going to maintain a distance, right? Because you're not same kind of people. You don't gel together.
You don't vibe together. You don't like each other. Soo you won't hug each other.
You'll stay away. You will maintain a distance. Soame happens with Proteus. Please remember same happens with Proteus.
Soo for example, this is a blood agar that I have over here. Over here, I put one Proteus, strain number one. This is also a Proteus. Soo from patient one also I've taken Proteus. From patient two also I've taken Proteus.
Now, if they are the same, if they are the same strains, if they are the same strains means they are best friends, what will they do? This one will start swarming from here. This one will start swarming from here and ultimately they'll all fuse into each other because best friends are supposed to gel. Best friends are supposed to hug each other, right? However, if from patient 1 and if from patient 2, they are different strains.
If they are different strains, you'll say that is exactly what has happened here. Can you see this has stopped swarming over here? This has stopped swarming over here and this one has stopped swarming over here.
There is a line present. I'll show you one more picture. Soee, very classical. This was Proteus number one. This was Proteus number two.
It started swarming but it stopped over here. This started swarming but it stopped over here. Soo, if you see that there is somewhere a line of demarcation present, means distance has been maintained. Line of demarcation is present and distance has been maintained. Are they same or are they different?
Are they best friends or are they enemies? If there is a distance maintained, you will say they are enemies. They are different strains of proteus that you are dealing with.
They are different strains. Soo let me ask you one question. The phenomenon shown below is indicative of? Soo can you all see the phenomenon shown below is the Dien's phenomenon for sure, right? This is the Dien's phenomenon.
And do we also know that I can see a line in between Soo, they are different strains. Soo, if I ask you what is the answer, are they same strains of protease, different strains of protease, different strains of parahemolyticus or clostridium? I know this is protease and if distance is present, they are enemies, they are different, different people. Soo, what is the answer in that case?
These are different strains of protease. Soo, repeating once again guys, repeating once again, P for protease, P for PPA test positive, P for Dynes phenomena positive. O4 they result in a fishy odor. This organism has a fishy odor.
It is urease enzyme positive and it shows us swarming motility. What are all the other organisms that show us a swarming motility? Sowarming motility is also shown by PVCs which means we have Proteus, Vibrio parahemolyticus, Clostridium tetani and Soerratia.
All of these belong to the PVCs that you have to know right. All of them show. swarming motility. Well, I guess we can take a break on that note and obviously the family that we are dealing with that the enterobacteraceae family still has a really long way to go.
Soo, we will be taking that up in the next part of the microbiology crash course. Soo, we've covered E coli, Klebsiella, we would be covering, we've also covered Proteus, we would be covering Soalmonella, Sohigella, along with that we'll also be taking up Peudomonas, Rickettsia, Chlamydia. and all the tiny tiny bacteria that we are left with.
Soo hope also Vibrio one very important family. Soo these are the bacteria that are left, which we'll be taking up in a slightly lengthy session that we'll have tomorrow. But yes, tomorrow we would be wrapping up or in the next session, we would be wrapping up the final bacteriology portion so that we can move on to virology and parasitology after that. Out of all bacteriology always takes a little more time, it's a little more time consuming because there are so many bacteria. The problem is that I can also teach you all the bacteria in one day in a single session, but then it becomes a big mess in the mind.
Soo it's always better to break it up into smaller portions and study bacteriology for a longer retention. Well, guys, as I said, the PDF of this session, I would also be sharing it over Telegram and other social media platforms. All the links to the social media platforms are already given in the description below. Soo you can definitely join in and download the PDFs from those.
Thank you so much for joining in and I'll sign off for today for this session and I'll be meeting you in the next session with all the other bacteria important as a crash course. Thank you so much, guys. Sotudy well.
All the very best.