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BIOL 2321_Microbiology for Science Majors - 2321_MW4_4_20_23_Lecture
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00:06 With her. No. All right . Uh welcome. Um come down
00:24 the end here rapidly. So, so um today Tuesday and then next
00:36 , so we will not have much to do on next war one or
00:43 diseases. But I, I don't that class being maybe 30 minutes
00:48 So regardless, um so we need finish up chapter 25 then the usual
00:57 , you know, this weekly quiz tomorrow, uh smart work do on
01:02 and then um and one more round that, I still have a unit
01:07 quiz uh next week in the final work. Um uh a couple of
01:15 thing or if you saw my email this morning. Um So evaluations,
01:22 ? Some of evaluations are part of um extra credit thing. So um
01:28 open today if you have until um of May 2nd to it will be
01:37 during that period. So, but I'll, I'll keep reminding you about
01:42 in my next email. Next My email is next week you'll,
01:46 email you this stuff, so you forget. But uh do fill those
01:51 . You go through, uh, , you wage icon, uh,
01:56 evaluations. So, and you don't to, you don't need to email
02:02 that you've completed it. I'll get list of, you know,
02:07 who's done, who hasn't completed who has, you know, and
02:10 if you've done it, then you the credit. But, uh,
02:12 don't, obviously, I don't know about, you know, in terms
02:16 what you're writing on the evaluation. that's completely anonymous. I just know
02:21 , yes or no. You filled out. So, anyway, that's
02:26 . Uh, let's see. uh, so remember the last exam
02:32 just 23 through 26 right? It's not comprehensive. So, uh,
02:37 what we've been talking about since the week a little bit before then.
02:43 , so let's, um, let's . I think we're going to any
02:49 or anything before we go. So we're gonna start with a,
02:53 gonna have a couple of questions to with the first one. Uh Some
02:57 the stuff we talked about last some we're gonna talk about today.
03:02 , but, uh, let me that. So we're looking at this
03:07 to get some um, context, ? So we are, you've started
03:14 looking at the human body and how fight disease, right? Innate immune
03:19 , defenses, chemical physical barriers, chemicals produced, uh processes cell types
03:28 fight infection, um, then into immune system and the B cells and
03:37 cells and antibodies and what they And uh we just began talking about
03:43 the other side of that equation, to speak microbes that cause disease,
03:49 they go in and around and under over all your various defenses,
03:53 So, of course, it all to um real factors. OK.
04:01 , um so, so last time talked about kind of the, hm
04:10 in which they kind of do their , right? So they're, they're
04:13 in a particular reservoir, right? where their natural habitat is uh for
04:19 diseases. It's humans, right? is a reservoir uh but it can
04:23 different things. And um so to from there to you to cause infection
04:29 different modes of transmission, right, uh contact uh other direct modes,
04:39 vehicle transmission, right? Water, food and others uh a vector
04:45 So uh different ways to uh be . And then we look at kind
04:51 the, the pathway of affection if will, right? Getting into a
04:57 , staying in the host, multiplying uh different ways, enzymes that may
05:04 to kind of penetrate tissues, avoid immune system. Um And I think
05:10 kind of where we're at. So we're kind of getting into uh more
05:14 these factors and we'll wrap that up in a little bit. So it's
05:21 look this one. So, all . Um Yeah, all of all
05:31 these are true. Statements. These all true statements. OK. So
05:37 parental route, remember that's through breaking skin sine usually through a could be
05:44 a cut, a wound of some , it could be a post surgical
05:50 . Um And uh so any kind introduction of a pathogen through the
05:55 typically that's parenteral invasions. We'll talk those today, those um that's,
06:02 so intercellular pathogens, you get to that way. They have these collection
06:06 proteins that enable that. Um respiratory is, is likely to be the
06:12 frequent route. The port of um thinking of multi respiratory illnesses,
06:19 amount of colds and flus and COVID uh because it can be transmitted fairly
06:27 . Ok. Uh through the air endotoxin that's associated with gram negatives.
06:33 course, we'll talk about that. K So we sometimes put these terms
06:40 front uh because there may be specific particular to a particular genus. I
06:46 you have a staph, a Uh But they both all they all
06:51 down blood clots. Uh Foite that's inanimate object, right? Uh door
06:58 , uh Kleenex tissues, I mean touch. So any kind of an
07:02 object that transmits the potential pathogens, the O P A protein. So
07:08 were on the surface of certain these will facilitate the entry into the
07:15 . Uh We talked about that last . OK. So, um so
07:20 look at this. So this question get us into toxins. Ok.
07:25 these are a uh another factor these obviously cause damage to cells. Um
07:34 can, um they can lead to able to avoid the immune system as
07:39 . Um In some cases, uh generally we look at these in different
07:46 , categorized and basic kind of how , their similarity of the kind of
07:52 damage they cause, so to Ok. Um And so the,
07:58 he or one of these groups, , sorry. There we are.
08:04 uh let's count down from here. . So these two are a type
08:21 cell membrane disruptor. OK. So gonna break apart. The leos are
08:28 for a generic uh any kind of blood, white blood cell trophy,
08:34 kinds like hemolysin for red blood OK. So uh we look at
08:42 . We um most of them come the category of what we call an
08:50 B toxin. So there are basically parts. So exotoxin is made by
08:56 cell and then it releases so it into the environment and then it will
09:02 a particular target. OK. So bind that target cell get in the
09:07 . And then the other part of um toxin is what interacts with whatever
09:12 to disrupt the cell. OK. um uh they're also um remember that
09:22 you can't have um of course, can be comprised of any toxins to
09:28 things, right? Like tetanus anti to rather teus shot is just
09:34 uh we'll talk about this vaccine that T A P, which um the
09:43 is for T is for tetanus and is for per and all three of
09:48 uh have various toxins. And so a vaccine that is in an to
09:52 well. So if you can, because they can produce your immune
09:58 antibodies to them and they can bind , and activate them. But
10:02 back to toxins themselves. So the still producing it will secrete it and
10:12 a target cell will buy into And then once in the cell,
10:18 the a or the active part, you will, if it, if
10:21 , if there's a protein synthesis, it usually interacts with a ribosome or
10:26 . Uh just depends on the category toxin. It is OK. So
10:34 the one type, so the, example of the question is these basically
10:41 cells by causing them to leak their . So basically, it looks like
10:47 of this as a, a tunnel proteins that comes together basically like straw
10:55 in the membrane. OK. Contents out lic the cell, um protein
11:01 disruptors. These are, we'll see in bacteria and others. Uh Shiga
11:07 is a produced by uh uh gastrointestinal . Um The killing action of a
11:14 toxin is what produces the worst effects , of uh A G I tract
11:20 . OK. Blood can result as because of this because they're basically killing
11:24 in there. And so, um so you see here a typical uh
11:30 sys disruptor, the active portion interacts a ribosome. And so that of
11:35 , if you block protein synthesis, gonna kill the cell. OK.
11:41 this can be particularly um lethal, second messenger uh types, these interfere
11:50 uh the flow of water of Ok. So by upsetting the balance
11:56 ions, right? So remember water to the sign of that's more
12:02 right? Higher. So concentration. these kinds of toxins interfere with the
12:07 of ions which then allow water to cells to lose water. Ok.
12:12 these are the kind of things you in um uh bacteria that have,
12:18 types of toxins are typically gastrointestinal right? Because we all know that
12:24 symptom of that is diarrhea, there's of water, diarrhea, dehydrated.
12:31 of course, it can get worse that. But these are the kind
12:34 things that cause that the loss of , the color of toxin is one
12:38 those very severe severe loss of water leading to death. Uh Another category
12:47 engines and we're gonna talk in a about endotoxin, ok. Um They
12:52 a similar effect on the body, ? They increase the immune response,
13:00 . So we call the inflammatory right? That is um enabled as
13:11 regional um effect, right? It's to contain the infection at the site
13:18 they enter the body, right? so we went through that you have
13:24 dilation of blood vessels, get the out and so on and so
13:29 Um But when it happens, if in inflammatory response is induced throughout the
13:35 body, and that's a whole different , right? Because now you're gonna
13:39 many more immune system cells, which a lot more cytokines coming out,
13:45 means just a, just a hyped response. And that's something that your
13:50 cannot deal with. Ok. And super engines endotoxin, both those can
13:57 to shock the body going into And I'll give you an example of
14:01 with endotoxin here in a second. But that's what super antigens do.
14:06 ? Um proteases, we talked about type uh those ID A proteases that
14:14 counteract the effect of the I G antibody. Um Other types can cleave
14:19 proteins. So well in tetanus, that organism is a toxin that breaks
14:26 the um messenger, the protein messenger , that talks between your muscles and
14:33 . OK. And in doing it creates a, these kind of
14:37 spasmodic contractions. OK. That can to death, of course.
14:42 uh but other toxins have, have targets, but these are, those
14:46 a couple of examples. OK. The proteas is of course protein.
14:51 , that's what they do. All . Um OK. So those are
14:57 categories of exotoxin made by the cell them and goes to a target
15:03 OK. And causes whatever effect that just saw here. Um endotoxin in
15:12 or uh a part of the self , OK. It's not something they
15:20 in them secret. OK. So theoretically any gram negative um we have
15:31 end endotoxin, right? But it's an issue, right? When that
15:37 becomes released. And so specifically, the lipid a portion, right?
15:41 talked about this back in uh chapter , right? So this could be
15:48 outer membrane, right? Of a negative. And the lipid a material
15:55 in this outer membrane and that's what produce the endotoxin effect. So as
16:01 as the cells intact, no but when it breaks apart, then
16:05 individual components here, these will then the effect. OK. And so
16:12 here you see a macrophage, it engulf a gram negative break acid in
16:18 process of cytosis. And then those can induce cytokines that can then trigger
16:25 like fever, for example. Um but it started with the with
16:31 cytosis of this gram negative inducing this production. OK. That's one that's
16:36 one part of it equation here. . So they can have other
16:42 I remember cytokines have varied effects, , causing inflammation, which is which
16:48 a leaky blood vessels, right? factors. OK? Can cause blood
16:53 Um So a multitude of effects. again, the worst of this occurs
17:00 an infection like this goes, gets in your blood and travels throughout
17:06 body. Because that's, that's how can affect many more of your immune
17:10 cells that way, right? You endotoxin float around your blood, then
17:16 lots more cells of your immune system , can bind it and produce this
17:21 . OK. Whereas if it's just local in it can be contained.
17:26 if it gets systemic, then then that's obviously the danger.
17:31 So here's kind of a a hypothetical here. OK. So again,
17:36 key is really uh sepsis, all . So, so gram negative action
17:44 trying to think of some type of mo is a gram negative that can
17:48 be one of these types. Um Of course, your, your things
17:54 e coli and your intestinal pathogens or negatives um potentially could they could they
18:02 become septic. And so the danger when you begin to counteract the gram
18:08 , right? Because you wanna get of it, right? You have
18:10 treat it. So you give your immune system itself can kind of
18:17 its thing. Uh But the danger when you begin to lice, you
18:22 negatives, that's when the problem OK? Um And so it can
18:27 is something possibly utilize the cells they into these to like receptors,
18:33 That's one thing that can happen and causes the release of cytokines.
18:39 And then that will cause multiple effects . This is a, a um
18:45 that induces fever. Uh This one the blood vessels. Ok. Um
18:52 so if you remember, uh you fluid comes out of the blood blood
19:01 goes down, blood pressure goes Ok, then uh clotting factors.
19:06 remember, I like your vital organs fed nutrients by capillary beds,
19:14 Arteries and veins come together in these capillaries in, in your vital
19:19 That's how they get fed the tissues fed. So if you have clotting
19:23 now occurring as a result of this , they can block up these tiny
19:29 . So now your your tissues aren't fit and they begin to die.
19:33 it can become a whole systemic ok, as a result of this
19:39 . And so collectively, then this all leave. So when something like
19:44 multi effects happen to your body, body says I'm gonna check out for
19:49 while, right? The idea being hopefully some some treatment occurs that makes
19:54 better, right? But your in responses that can really just kind of
19:57 out but that there's a limit to long it can do that,
20:01 Because now you're in shock and that very quickly lead to death.
20:06 So, but if you have a negative infection and it's not contained,
20:12 , maybe has progressed. The person into the hospital and infections are full
20:18 and it's septic, right? What you got to be? You have
20:20 give antibiotics to treat the person. . Uh But then you risk a
20:25 of, ok, I'm killing the , but I'm releasing these, these
20:30 . So what do you do? , carefully monitor, obviously, all
20:35 , antibiotics uh and monitor how much you're giving. But you can
20:40 there's also um you can provide antibiotics don't necessarily lice the cells,
20:47 Um Bactericidal agents can do that bactero agent you can give to grow.
20:54 But there's also um don't quote me this, but there is, I
20:59 it's uh probably Mixon B is a you can give that will actually bind
21:09 lipid material. So you can give in conjunction with antibiotics to kill
21:13 So we can kind of mitigate the of the endotoxin by it being bound
21:19 but not causing any interactions with your immune system. So, so that's
21:23 time to treatment with this. But , it's only really if it's
21:28 in, in on the stage, you, but you can control
21:32 you know, you also be controlled then. But if you have
21:37 there are treatments you can do to of the mice, the effect of
21:42 endotoxin. So, um anyway, that's kind of and so super and
21:48 work similarly in terms of how they boost up cytotoxin levels and create the
21:54 kind of effects. Ok. Um me any questions about that. So
22:03 so intercellular pastors. OK. So that kind of along the way of
22:10 about innate immune system, adaptive immune , we um made a point of
22:17 , OK, you have systems that with intra pathogens and systems to deal
22:22 pathogens, right? So things like work a pathogen Figure six cells can
22:29 that extracellular pathogens, right? But do have things that can deal with
22:33 types like your natural killer cells. T cells can do this right.
22:41 , um so the types of intracellular we're talking about, we're focused mostly
22:47 these types, facultative. OK. they don't do this for the purpose
22:55 replicating themselves. That's what the virus . Uh These types are non viral
23:04 types that go inside the cell for purpose of hiding from the immune system
23:10 or um using the cell as a to transport itself to other parts of
23:16 body. OK. And then once gotten to where it wants to
23:20 then it gets out again. So kind of the transitory facultative intracellular
23:27 OK. There are types bacterial types are, that has to be
23:33 A parasitic basically is a uh cause rocky mountain spotted fever. Um tick
23:42 by a tick and uh but it's for a bacterium. It's pretty primitive
23:47 has lost a lot of its own . So if you get bit by
23:50 tick, you come down and rock mountain and a fever. I think
23:54 things tend to hang out in your , in your lungs, a respiratory
23:57 . And uh they just live kind in your cells. That's what they
24:01 . And so, but those, are obvious. So we're not really
24:05 on those types. We're looking more these types. OK? So um
24:10 do they do? So these invasions talked about, OK, a collection
24:16 about a dozen or so proteins and of these, what they do is
24:23 will take acting molecules that are in cells. OK? And they will
24:29 them and so they will cause them elongate. So I'm trying to think
24:34 when you put up a tent, on camping, put a tent,
24:38 a tent pole, right? So kind of like that right by,
24:43 , except we, we're, we're this to the membrane. And so
24:46 make it kind of give it so to speak, by doing
24:49 And so that's what helps engulf the cell here. So here is the
24:54 that injects here and some of those the acting to make it elongate
25:00 and engulf it. OK? So its way in. So it forms
25:05 vesicle gets inside the cell. Um It can also induce these other
25:11 production of cytokines by the cell, cetera. OK. Um Now,
25:19 so here this term called membrane you know, that has to do
25:24 its ability, you see all these folds occurring here, here's the cell
25:31 . And so that's the, that's manipulation of the actor to kind of
25:36 gobble it up, so to OK. Um So once, once
25:42 inside and sell, OK, various can happen, right? So it
25:47 in as a OK? And so see on the next slide. So
25:53 how it comes in. So there's be some things it's gonna have to
25:58 because you'll have over here, a zone. Yes, over here.
26:08 . And the natural tendency is to the the set, right? So
26:13 comes the Liz fuse with it and it. So it's gotta have a
26:19 to kind of get around that if gonna survive. OK? And this
26:23 actually one strategy is to break just get out, right? And
26:31 the places of them all together, get out of there. OK?
26:35 in this example, and so we're kind of looking at uh this
26:42 uh the intestinal wall and just the or cells making up the intestinal
26:50 OK. So for example, this be this is this would be where
26:55 coming in to give you something orientation , right? There's food,
27:01 right? So these cells could absorb and things, right? So this
27:05 kind of to orient ourselves. Um So uh the those things actually
27:15 Listeria E coli these are all intestinal be food borne pageants. OK.
27:23 so, um so she and Asteria particular are non volatile. OK?
27:30 don't have a OK. But yet can move around and what they can
27:37 is utilize acting filaments, monitors rather the, and the proteins on one
27:46 side. And so that attracts acting to it. And so what happens
27:51 it ends up, it has activity can polymerize the act, right?
27:56 it just lengthens. OK. So kind of like um this is
28:02 it takes acting and then sticks it , on its butt, so to
28:06 . OK. And then begins to . And so at length as it
28:10 , it moves the cell for, ? So it's kind of a weird
28:12 of motion but they've tracked this in micrograph. These swimming around like
28:18 OK. All propelled by these acting on one end that are polymerizing.
28:25 . So it can move into other , it could even move out of
28:30 cells. OK. So it provides way to move around or otherwise
28:36 OK. So this is what we , we call these things act and
28:41 . OK. Um OK. So of back to what we talked about
28:47 , an intracellular pathogens inside a I was gonna avoid getting eaten or
28:53 else. Well, here are the of the three scenarios we just
28:57 One. All right, one is break out of the thing,
29:00 You have proteins that can help them this. Um and, and um
29:06 being eaten. OK. So another is, but salmonella does, it
29:15 prevent. So here's our lyo So we can prevent the fusion of
29:21 with the best in. So you , it doesn't get digested,
29:25 And salmonella actually does its own version trans cytosis. So actually, it's
29:30 from here and out of the Ok. So remember you're intestines are
29:40 vascularized, lots of capillaries, Because that's where, how you're
29:44 that's, that's what feeds your right? So, nutrients from the
29:48 , get into the blood and go your tissues, right? So that's
29:52 a way for pathogens to intestinal pathogens get around in your body. Also
30:01 of lymphatic fluids as uh vessels as . So both of these types and
30:06 where these cells can come in and your eye, get, penetrate your
30:12 and your tissues become septic, become septic infection. Ok. Much more
30:17 . Um A third strategy is to , OK, I'm just gonna sit
30:23 this vesicle. Nothing is gonna hurt . And that's what this organism cola
30:28 . It just kind of sits. , so it'll fuse with the
30:32 OK? And, but it has ability to tolerate the acidic P H
30:39 the and not being digested by these . So it can just tolerate
30:42 It's built, it's built to withstand and it will live in there and
30:46 will multiply inside there. That's how of how it lives its life.
30:51 . So kind of the three strategies these intracellular pathogens. Um OK.
31:01 let's look at any questions about Ok. So again, these,
31:05 types here uh salmonella. So they aren't really using this as a
31:13 to replicate, right? Don't think it. Don't think of these as
31:16 virus. They're not doing it for purpose. They're doing it to hide
31:20 the immune system and to, and in some cases kind of penetrate further
31:26 the body. OK. That's, what they're trying to do here.
31:30 , OK. So let's look at question again, more revance factors
31:34 OK. So we'll conclude this chapter uh strategies that extra soul,
32:17 Sure. All right. Let's count . OK. So protein A is
32:39 here. Looks like this. So it is actually a virulence
32:46 Um It's, well, we'll talk it on the next slide, the
32:51 diagrams on the next slide. So talk about it there. Um So
32:56 outside the host. If so if an extracellular pathogen, right, you
33:01 things you can do and one of is to have a capsule.
33:08 Um A capsule can cover your OK. Um Even better is if
33:15 can make something like this. So acid, if you remember, that's
33:23 chemical that kind of binds your cells . Ok. So if you're making
33:27 capsule of something like that, then body doesn't necessarily see that as something
33:34 , right? Because it thinks, , that's what, you know,
33:37 , the body is made of this . It's not something weird,
33:41 So, uh that means it's, less antigenic that way. But you
33:46 prove a very strong response because your thinks it belongs to you,
33:50 It's made out of your, your . So uh very sneaky to do
33:54 that way. OK? Um The a thick capsule can also kind of
34:02 compliment, activating it uh very Uh they can have like m protein
34:10 , you interfere with complement activation. uh that's possible. Uh in terms
34:15 antibodies, that's the pro from the protein A right? It can have
34:21 on the and bind the F C of the antibody, right? So
34:30 it's these parts here that are antigen . OK. So if it can't
34:38 because so we remember that and body your body that leads to a bunch
34:44 different effects, right? So we do that because it's being grabbed by
34:49 end as you see here, then renders it useless, right? The
34:56 can't do its thing. So now because they're being grabbed by the
35:00 So to speak. OK. So in fact, the strategy to prevent
35:05 from attacking you basically. OK. Nice has that I G A pro
35:12 talked about that before, from I A, a lot of your um
35:18 pathogens. Those that stick on your membranes uh will have this kind of
35:26 because I A can prevent them from . But yet, if they have
35:29 protein, they can break apart the that do this. Um some types
35:36 secrete chemicals that induce apoptosis in your cell. So they basically kills
35:42 OK? And then in chapter we talked about our 10, I
35:47 we talked about this one phase So um the antigens being expressed,
35:54 know, if it comes into your your body in one form,
35:57 well, then your body can switch another form of agen and become invisible
36:03 a while to your body. And that allow it to, to multiply
36:08 spread. So, um so for , pathogens have a number of different
36:14 to counteract their various defenses. So always, it's all a back and
36:19 , right? We evolve, they . Um And, and it's a
36:24 battle. So here I just kind wanted to think you may find it
36:29 for study purposes. It's all kind all the factors organized here, just
36:35 we did with the innate an immune functions. Same thing for the real
36:41 here. OK. Um and these all the things you've, all the
36:45 ones we talked about. Um, , uh, just more summary.
36:52 . Is there, um, any in particular? OK. All
36:59 So let's, um, talk about . So, as you get into
37:05 chapter, if you haven't already, , a we'll cover every disease that's
37:13 about in that chapter. OK. stick to what you're seeing here,
37:19 ? So all, most, all cover this topic by body system.
37:25 . So we, we will go this order, OK. Skin beginning
37:29 skin, soft tissue infections. Um And these are the specific strains
37:35 we'll talk about. OK. So another kind of table listing the strains
37:42 and what to know. OK. um the the obvious thing is
37:48 what's the gram reaction we're applicable, ? Because we have some things that
37:51 viruses. Uh here here, some are protozoans, these this group
38:01 So the point being is that the is not gonna be applicable to
38:05 right? So we should be aware that. Um morphology, rod or
38:10 , what have you disease caused? , distinguishing features. I try to
38:16 infectious diseases that have some unique things them. OK. So you might
38:23 this in something like this fashion You can certainly add on up and
38:31 columns likely to what's listed here. . And I just filled in kind
38:38 some things how you might look at approach this. OK, just to
38:41 of summarize it, I think at is heavily memorization and stuff.
38:47 So this may be one way to it. Um Anyway, obviously it's
38:51 to you. But uh that's one . OK. So um all
38:59 So let's look at this question. we begin with something we talked
39:03 Actually, uh let me move this here if I can, we talked
39:09 earlier, which was the um in vaccine section on um uh her herd
39:19 . OK. Dang it. Here go. OK. So um so
39:27 we didn't mention a particular term, , not communicable, but that,
39:32 all goes hand in hand with um immunity. So we'll touch on that
39:37 for a second here. OK. . Let's see. So um so
40:38 communicable disease is one that is passed person to person um airborne or otherwise
40:50 tetanus is not one of those that that. OK. So it is
40:54 noncommunicable disease. Um So what's the deal about that? Well, it's
41:01 diseases are ones uh that can contribute herd immunity, right? Herd immunity
41:08 result from communicable diseases against which we vaccines for. OK. So vaccinated
41:19 as shown here and we mentioned this , but now we have a picture
41:23 go with it. So here's a sick person, right?
41:29 OK? And we only have in or yellow here. Three vaccinated
41:38 OK. So that sick person is . Um, and is spreading that
41:48 to others, right? Blue ones blue are susceptible, not vaccinated.
41:53 first one read at te, it matter because you can't spread tetanus person
42:01 person. Right? So, herd would have nothing to do with the
42:05 . That's noncommunicable like tetanus. Um The only way that person could
42:11 tetanus to another person is if you tennis and he somehow took the toxin
42:22 injected into somebody else, which is insane scenario. So that would,
42:26 not happen. OK? Not So, with the people that um
42:33 in this scenario on the left, , that's not gonna, you're not
42:39 get hurt immune, either the virus gonna keep spreading, OK? Or
42:43 the agent is over here, we lots of vaccinated people, right?
42:51 yellow. OK? And so they as absorbers of the infectious agent,
42:57 ? And minimize spread to these folks . And so um you don't get
43:06 of the disease, you contain the . OK. So uh we looked
43:11 this before, same data here, ? These are o values think of
43:16 as a love, the reproduction of of the infectious agent. Look,
43:22 how contagious it is, right? mumps, polio infect 4 to 7
43:29 , one person can spread it to to 7, something more contagious
43:34 uh many more more contagious. So , the threshold then goes up,
43:40 can have more people vaccinated, the absorbers of the agent because it spreads
43:47 . So the threshold has to go . OK. So as I mentioned
43:51 , again, COVID is on the end down here. OK. So
43:57 so of course, you don't have , the, these we talk about
44:00 in this section, many of course have um a vaccine to them.
44:08 . Uh The we talk about uh and diphtheria. We have vaccines to
44:15 vaccines to pneumonia. Um but not like staff and strep for these skin
44:22 . We don't have vaccines for Um But for many we do,
44:26 nonetheless, let's uh look at, , don't memorize this slide number
44:32 I just put it in to kind show you with skin infections, a
44:36 variety of different types of rashes that occur and, and um and beyond
44:44 four types, there's like a probably or 10 of these different types,
44:48 varying in kind of how big it get the form of it. So
44:54 macular rash you it's kind of more , kind of scabby in this area
45:02 , crusty if you will. But we can build upon that and it
45:06 have pus, liquid fluid can build uh around or in the sore
45:14 Um You know, if it's like chicken pox or smallpox, the fluid
45:20 contain the virus. Ok. So so rashes come in many forms
45:27 And appearances. Um uh So this be a part of these various skin
45:35 we'll talk about first. OK. uh begin with Staph staph. So
45:42 grampa, both uh five um Staph the grape morphology. Strep in chains
45:55 in pears. OK. So we with strep. Um Most of your
46:01 um infections occur as a result of hair follicles. OK. And things
46:10 a boiled uh are that car bundles kind of a step up. It's
46:17 a, it's like a collection of that have come together to form these
46:22 . Um very often boils will have kind of, it'll appear like a
46:29 uh on your skin or just under skin, very kind of hard.
46:34 it's due to this, this um , they produce it kind of takes
46:39 fibers and makes a clot and kind surrounds them in this little cocoon right
46:45 your immune system to treat a You typically have to uh lancet,
46:50 fluid and et cetera. Um and antibiotics. Um coagulate staph aureus and
47:00 particular, coagulate positive. There's a correlation between staff areas that are pathogens
47:08 being quite a positive. At the time, we do have on on
47:13 , staff that will be quite a and cause disease. But by and
47:18 high correlation between quite a positive staff , being pathogens. Um The uh
47:27 is a strain that's a very common inhabitant staphylococcus epidermitis. But it's,
47:36 , it can't cause disease but you know, pretty mild. It's
47:40 , it's not one that's very prevalent terms of causing disease by far.
47:45 aureus is, is the one. . And so in, in various
47:49 . So again, it can have different types of factors. Um the
47:53 shock syndrome uh that emerged kind of the nineties, I believe um uh
48:02 to uh the manufacture of particular type tampons that created a very it was
48:10 absorbent, but it created an environment proliferated the these types of staff uh
48:17 it produces toxin that proved to be . There were a number of fatalities
48:21 a result of this. Um the of course, methicillin resistant and other
48:29 type of staph aureus. So one the things that occurs. So this
48:34 nosocomial, ok, actually means hospital infections. So there's a category of
48:41 we call that's now called health care A I S health care associated because
48:52 you can because health care is not just in hospitals anymore but in
48:56 kinds of clinics and at home. And so what's common among this is
49:04 you acquire an infection that occurs as result of that health care,
49:12 So you go to a hospital with to get your knee scoped or
49:15 right? Arthroscopic surgery, right? you're there, you can you come
49:18 with a staph infection not because you in there with it, but because
49:22 what happened at the hospital, you the infection. Um, anything like
49:27 is what we call health care And obviously it's a big deal.
49:32 staff accounts for like maybe 10% of kinds of infections. There's other types
49:37 are, that uh are very prevalent these types. Um, you think
49:41 a hospital? Well, lots of people in the hospital, right?
49:45 of elderly people could be in hospitals with various infections and bacteria patterns floating
49:52 , right? So it's a, like the perfect storm. Ok.
49:58 that's why um good hospitals are have to like continue educating their staff,
50:08 and whatnot about doing the right What is, what is the number
50:15 thing these health care quite infections from ? Anybody know the one practice
50:25 right? Washing hands, washing hands number one preventative here. That's why
50:30 see um where you see uh hand on every corner in the hospital,
50:36 ? Constantly nurses go into the They should be doing this as they
50:41 in, right? Gloves and gown whatnot. Ok. So um uh
50:46 that's the number one preventative of transmit and that's how it happens. You
50:51 the nurse. So it's not just but you know people that are going
50:55 between different hospital rooms and patients. how you get transmitted if you're not
51:01 . Um But also a lot of , um, devices you use like
51:07 breathing tube, um, uh, . Right. These all come prepackaged
51:14 . Right. If the person handling doesn't handle it. Right. Or
51:17 on your skin. Staph and other of bacteria, you don't, you
51:21 handle it properly, you put it somebody and you come down with an
51:25 . So it's a, it's, a big deal that, um,
51:30 keep testing, testing this and are top of these things because you don't
51:34 go to the hospital with something and get an infection or with something else
51:38 you're there. That's crazy. So , so if, if it uh
51:45 we talk about staph and strip and infections, think of it as different
51:53 or layers, right? Because you superficial layers of skin, you get
51:56 little bit below that what we call layer. They could even penetrate further
52:01 , right? And so there's depending on the pathogen and the collection
52:06 factors. You can get different layers skin infections, right? So in
52:13 and spell the skin syndrome, that's be at the uppermost layer typically.
52:18 ? And is very common among little , right? Because little kids are
52:21 cleanest things, right? They can a little scratch and that could be
52:26 start of a PETA which is basically a little um crusty sores on the
52:33 and the kid itches it and that it further and to another kid.
52:38 it's not uncommon to have a like a daycare setting or kindergarten, things
52:43 that. Uh You know, you die from it. It means not
52:46 be harmless and you give antibiotics and over it within a few days.
52:50 Skull skin syndrome a little more You can see the little baby
52:55 uh get, it causes a a . It kind of creates a blis
53:00 effect of moving the upper layers of skin. Um Again, these can
53:06 begin with just a mild abrasion, think kind of is not, is
53:10 untreated and then kind of progresses to a little more serious. OK.
53:16 And so again, we've seen these uh various factors before. OK.
53:22 Again, no, no one's training necessarily have all these. But you
53:25 the collection, they do have to of determine the level of skin infection
53:31 will cause. OK. So it's strap. OK. Again, grand
53:37 change or pairs these. Um So , we've categorized strep by using blood
53:49 . What do they, what's their on blood? O? OK.
53:52 has to do with the their, have these homolog, OK. Those
53:58 apart red blood cells. OK. there's different categories of that. And
54:03 alpha beta and gamma homos. So uh alpha homos you see here,
54:10 right, greenish color, both alpha beta have that greenish color.
54:16 That's due to the oxidation of the in the red blood cells. Uh
54:23 hemolysis does that, but they don't a heavy clearing zone like we do
54:28 beta homos. So that's what we it. Partial hemolysis. Beta is
54:33 clearing. You can see the clear around the growth. Um and gamma
54:40 is none. So there's no green here and no clearing. Ok.
54:46 But despite that, it doesn't mean aren't pathogens in the group with pathogens
54:53 all three groups. OK. Um coccus obviously is not the same as
55:00 streptococcus, but they're very closely So they're kind of put in the
55:04 group with the streptococcus. Um So group has characteristic types um uh for
55:12 kind of suspected skin infections or strep . Most are on the lookout for
55:20 one. OK? You get a swab, put it on blood,
55:24 look for a clear result that's presumptive tell you. OK. I'm probably
55:28 with this strain of strep of OK. So we look at all
55:35 groups. OK? We've got different in each, in each type.
55:44 uh you have a group ammonia which the um well, I'm sorry,
56:00 . This group called D I don't too much about it, but the
56:05 a kind of and cost effective caine the biofilm. One of the contributors
56:15 that. Um the, any kind oh root canal. Uh These can
56:27 to in point for uh end up where they end up on a different
56:41 of different kind of uh of the uncommon to have. Um That's why
56:55 gave you the answer like that. The, you have a major actor
57:05 . Um Number one, so viruses motion. Um But I uh
57:20 of the um that is also pretty . Um It's really a um basically
57:37 his path, et cetera. Um if you different from these three is
57:50 is a test. Yeah. So so looking at, OK, um
58:02 get various factors. So the it will have that kind of cashless
58:11 plus a host of other enzymes. And so um you're familiar like with
58:19 throat, strep throat, this will strep throat, um right, right
58:25 there, fla um the, the fighting the streptococcal infection, that response
58:36 sometimes uh backfire and say, so this is an example of a
58:46 . So we your response to the protein uh streptococcus, there's a high
58:53 of similarity between this protein structure and heart muscle protein also with um uh
59:02 , certain connective issues, your joints well. So, antibodies can then
59:09 cross react also with joins from. So uh that's what we, that's
59:20 we call a. So you have that count with dramatic fever,
59:30 That's the, the um I, going back to this degree of skin
59:43 , right So, if we go superficial and called the skin, then
59:50 go the deepest IOS, then uh worst is necro fasciitis. Ok.
59:59 , um both of those are due can, can begin with a simple
60:03 that doesn't get treated with that, depending on the pathogen and the number
60:10 Berlin's factors. So, if it a bunch of toxins and enzymes,
60:15 can uh initially become you um uh but not as deep infection as
60:29 advertising fasciitis over here, you have like um certainly for sure, high
60:36 a collagen ace which is been going . Um And, and then it
60:43 get so throwing out toxins and as does, that inflammation occurs and so
60:49 death occurs and it can get so that you get down to the
60:53 So what has to happen is you to remove that dead tissue. Uh
60:58 could even be as bad where you to amputate. So, uh but
61:02 could happen on fairly quickly to sets . OK. Um So, uh
61:13 . So next, we're gonna go a respiratory and any questions about
61:18 soft tissue with. Um let's look this question, shame and, and
61:29 talk a little bit about um upper tract. So we're gonna divide
61:37 Uh There's a few sections here you in that people. OK. All
62:30 . Let's see. So, all . So our answer here is
62:45 They are viral. In nature, respiratory and gastrointestinal tract, stomach
62:50 think of that. Um usually the versions of both of these are the
62:59 severe forms, both types, both and gastrointestinal viral can can then behind
63:07 can come with secondary infection that are bacteria and that can be much
63:13 But in terms of just sheer prevalence how much is out there, they're
63:17 viral or, or in origin, both G I tract infections and
63:23 Think of, think of common how prevalent that is flu COVID these
63:28 , right? Um In any uh so as I mentioned, we
63:32 at this in terms of upper and respiratory upper being um the uh we
63:39 the nasal phal area. I just , I think as the throat,
63:45 kind of upper lower throat if you uh lower respiratory tract sy involves
63:51 Ok? So um upper respiratory So strep throat actually fits into that
63:58 , upper respiratory tract infection, Which we talked about. Um and
64:04 scarlet fever. So this is one uh is probably looks worse than what
64:13 happen, you think? Oh my , this person looks like a bright
64:16 tomato. Something is not, But um you rarely do you die
64:21 that. It's uh typically over within week or so on antibiotics, but
64:27 does this by production of this toxin causes inflammation and then causes your capillaries
64:35 dilate much more so than normal. that creates that blood rushing to the
64:42 and a really bright red rash occurs a result of that. Um The
64:49 but again, it's not, it's as serious, certainly diphtheria diphtheria.
64:55 is, it was. Although uh , we do still see in certain
65:02 in the US, that cases become more prevalent than they should because the
65:08 works quite well. But some you know, have the same degree
65:12 vaccination and you see cases of this up. But in the thirties,
65:17 was a devastating killer of Children. so that's really a success story of
65:24 is when it was developed for The cases of of of Children dying
65:29 diphtheria went dramatically down within like a . Um So this is an organism
65:36 what we call one of these pleomorphic , right? It doesn't have a
65:41 morphology, OK. It is grand but looks kind of like this and
65:46 kind of club called club shaped and forms. It's just not uniform.
65:51 why we give it that term OK. And so again, the
65:56 uh for this one actually be the D form for diphtheria uh was very
66:03 and it is still very good. So like a lot of these respiratory
66:09 appear like cold flu, similar Uh but then, um and of
66:17 , can be spread like like most illnesses spread by droplet or airborne.
66:22 But then so in that early toxin is is being formed, cells
66:28 growing in your throat. Toxin Um And then in that initial area
66:34 your throat, um inflammation occurs, toxin can kill cells. And so
66:41 body's response is kind of maybe the the clotting fibers begin to form
66:46 . Then you need to. This is that collection of material forms what's
66:51 a pseudomembrane. Ok. So you see that right here, which is
66:58 effect of that toxin killing cells in body's response. And so uh this
67:03 particularly um a disease uh particularly in . It's very serious. And so
67:10 of a chi child with smaller smaller throat. So it won't take
67:14 for that pseudomembrane to interfere with the in the child. So that's one
67:19 here. But beyond that, then , the, the toxin begins to
67:23 throughout the body. And that's where worst effects come in because it,
67:27 inhibits protein synthesis. So it's gonna killing cells. And so when it
67:31 to circulate throughout the body, then the organs and things that become affected
67:37 , and it becomes of course, more serious. Ok. But
67:41 completely treatable with uh antibiotics but uh with, with the vaccine.
67:49 Um I think that's all right. questions, no questions, folks.
67:55 um that is all for today. see next
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