Preventing TB transmission | Infectious diseases | NCLEX-RN | Khan Academy

Preventing TB transmission | Infectious diseases | NCLEX-RN | Khan Academy


Narrator: Let’s say you’ve got two people and one person has Tuberculosis,
that’s this person over here, I’ll call him person A and another person
does not, this is person B over here. What are the things that are going
to make person A more infectious? What are the things we
need to think about, in terms of how likely it is that
person B will actually get sick with TB. There are a few things. We know that this person has to actually
cough out some TB particles, right? They’re going to cough them out and that
means that the strength of the cough, let’s say they have a real good cough
like that, versus a really weak, kind of puny cough, something
like that is going to matter. It turns out that the folks that have
the strongest cough are the adults. So, any adults, in general,
adults are going to have a much
stronger cough than children. So, that means that adults are
more infectious than children. Let me actually write that
as my first key point. It turns out that’s exactly right, that
we see that in terms of spreading TB, it’s the adults that spread
it much more than kids and
definitely much more than infants. A second point, is that
you need live bacteria. This seems obvious that of course
you’re not going to get anyone sick if you don’t have live bacteria. The way to know that
someone has live bacteria, you can actually just take
some of there sputum or some
of their mucus from their lungs and look under a microscope
and you would actually see
what we call a positive smear. That literally means you smear
out the mucus under a microscope and you look with a microscope and
you can literally see the TB bacteria. You can also do a culture and see if
you can actually grow the bacteria. If you can see the bacteria
or grow the bacteria, that’s a good indication that
there’s live TB bacteria there and that’s obviously going to make
the person more infectious as well. A third point, is if you look in their
lungs and you see large cavities, some times you call that cavitary disease,
but let me just write cavity here. If you see a cavity there, in
that cavity we know is going to
be full of little TB bacteria. Those cavities are classic for that and so
whenever you see or think about cavities, I want you to remember that the
folks that get cavities are the
secondary progressive disease folks. Remember there’s primary
and there’s secondary, and it’s the secondary progressive
disease that causes these cavities. These are the folks that are
going to be more infectious because they’re loaded
with live TB bacteria. What are the things we can do to
actually prevent the spread of TB? The first one is actually kind
of obvious, it’s medication. We have medications that are really
good for treating Tuberculosis. One classic thing that we’ve done is
what we call directly observe therapy, DOT, directly observe therapy. All that means is sometimes a physician or a nurse will actually watch
a patient take their medications so that they don’t forget or
sometimes people don’t like
to take their medications. This is an easy way to make
sure that someone’s actually
taking their medications. We call it DOT. That’s obviously going to be helpful
for killing off the bacteria, so we don’t have to worry
about live bacteria anymore. Usually that happens in about two
weeks, after two weeks of medications, that usually kills off the bacteria
so you no longer have those positive
smears and positive cultures. It also helps with symptoms,
so if you’re not sick with TB you may not be coughing as much. That’s another important
thing to keep in mind. What else would be important? You could imagine, isolation, making
sure the person is actually isolated. So, isolation is key. And specifically you want to make sure
they’re not around any young people, so definitely don’t want them around
anyone under the age of four years because, of course, children
are really, really susceptible
to getting very sick with TB, so you want to make sure
they’re away from young children and you want to keep
them isolated at night. So, at night when they’re sleeping
– I put a little @ symbol, but at night when they’re sleeping you
want to make sure that they’re isolated and maybe sleeping in their own room. Of course it’s ideal if the
person is completely isolated, but of course that’s not always
practical because they might be
with their family or their children, but you want to make sure that they’re
at least away from children under four and at night that they are sleeping alone. Another thing is a surgical mask. A surgical mask is really good
because it helps prevent too much of the stuff that’s coming out
of your mouth to enter the air. Actually, literally, let
me just draw it for you. It literally catches a lot of
this stuff and prevents it from
entering the space around you. This is a mask, let’s say a
surgical mask, it might hook
up like this, maybe like that, and what it does is it literally catches
the stuff that’s coming out of the mouth and makes it ricochet back in. You can still breath with a surgical mask
on, but it just keeps the large particles, maybe large droplets
from leaving your mouth. Now, what if you’re person B, what’s one
thing you could do if you’re person B? One obvious trick is just
standing further away, you don’t have to stand so close to person
A, you can stand all the way back here. That’s going to make it less likely
that you’re going to get sick with TB. Let me write that here, is
create space, create space. Another key idea is, think about
what happens when someone passes gas, or there’s a horrible smell in a
room, what are you going to do? Usually people are going to find
the door, maybe they’ll open
the door and let some air in. This arrow indicates more air coming in. Maybe there’s a window here,
they’re going to open the window
and let the breeze come in. Basically do whatever you can to
dilute out that horrible smell. If there’s a fan, maybe you’ll try to
turn on the fan and get that spinning. If you can get the fan going that’s
also going to move around the air. You’re just trying to move around the air
to get a dilution of that horrible smell. Let me right it out, dilute. The idea here is that you can
just literally do simple things. You can open up doors and windows,
we call that natural ventilation. You can also turn on a fan to
kind of move the air around and
you’re just trying to dilute out that horrible bacteria so that less
of it is likely to enter your lungs. Another thing you can do is actually
put on an air purifying respirator. An air purifying respirator is
actually a little bit different
then the surgical mask. This one is actually going to keep
out very tiny, tiny particles. Unlike the surgical mask whick gets the
large things, spit and large particles, this one is actually going to
capture very tiny particles and it’s actually not going to allow them
into your breathing area, your airway. It’s actually going to make
things bounce off, essentially, or get caught inside the filter itself. It wont allow TB particles
into your nose or mouth. A common one here, you might have
heard of or seen, is called the N95. There are many other types as
well, but that’s one example
of an air purifying respirator. There are a couple more things
that you might see that are
slightly more expensive, but you might come across them
or at least hear about them. One is called ultraviolet, (writing) ultraviolet germicidal. Let’s see if you can kind of guess
how this works or what it does. (writing) Germicidal, cidal
means killing something. Germicidal irradiation, irradiation. A lot of times people will just
shorten this whole thing to UVGI. They’ll say a UVGI was
installed and what UVGI does, it literally takes ultraviolet
light and shines it out, and actually if there area
couple of TB particles, let’s
say one here and one here, that UVGI, that irradiation kills
that TB particle and X’s it out. So, it’s no longer alive and
the folks in that room are safe. The final thing I want to talk
about is called a HEPA filter. It’s a filter and if I was to draw the
ceiling it would look something like this. Maybe it has some spot on the
ceiling where air is flowing in and some spot where air is flowing out. Just erase these parts right
here and I’ll show you. Let’s say that air is coming in
this way, let’s say three arrows, and you’ve got air coming out
this way, you’ve got three arrows. So in the middle, somewhere in
this area you’ve got a filter. This filter is going to catch TB
particles, so we call it a High
Efficiency Particulate Air Filter. (writing) Particulate Air Filter. No one wants to say all of this because
it’s too long, so just for short, again they say HEPA filter. A HEPA filter is going to then catch some
TB particles that are going to flow in and they’re going to get
stuck in these filters, so coming out on the other
side you have nice clean air because the TB particle will
not get through that filter. You could even take this a step further. You could say well, how about
if we did this and actually, instead of having all of the air returned,
let’s say we return just part of it and actually allow some of the
air to escape outside of our room. Now you have a negative pressure in
this room because you have more air leaving the room then is re-entering
the room, you have negative pressure, almost like a vacuum because all
this air is going up into the filter and not as much is coming back out, so
this room becomes negative pressure. There’s kind of a vacuum in this room
and especially if you do it right. If you close off all these doors
and you close these windows, then you definitely create
a negative pressure. What that means is that now you
can really protect the area around because you close off the
door, you close off the window and now there’s no way that a TB particle
can leave and go into the hallway because if there’s a little bit
of a gap underneath this door, if
that’s the only crack in this room, then the negative pressure is going
to make air flow through that crack into the room instead of air
flowing out into the hallway. That’s actually another key trick that
they use to prevent TB from spreading, is they’ll create a negative
pressure where they pump air out, which is what we showed here, and
then they’ll seal off the whole room, and then the air from the
hallway starts entering the room and you can make sure that no TB particles
are going to get out into the hallway and get people in the hallway sick.

Primary and Secondary TB | Infectious diseases | NCLEX-RN | Khan Academy

Primary and Secondary TB | Infectious diseases | NCLEX-RN | Khan Academy


Let’s say that these are your lungs. This is your right lung. This is your left lung. We’re just going to label them upper and this will be lower. This will be the middle lobe. You’re minding your own business and somebody coughs, and they get TB in your lungs. That TB gets inhaled, you breathe it in, and the location that
the TB likes to go to, it’s actually a pretty interesting thing, is it likes to go along these fissures that I’m drawing out here. These are the fissures; They separate the lobes of the lungs. They are kind of like the boundaries. The TB bacteria like to
go near those fissures. They also actually like to go sub-pleural. Pleural indicates the
outside layer of the lung. So, if it’s sub, it’s right underneath that outside layer. They like to go somewhere
along the fissure and somewhere in the sub-pleural space; right on the edge. They’re going to jump into some alveoli. Let me just draw it out for you here. You know, you’ve got
millions of these guys; I’m going to draw a few more, just to make it really
clear that these things are in packs. What’s going to happen is, of course, you’re going to have an immune response right away to this bacterium that’s in there. You might have a macrophage coming along like that. This macrophage is going to pick up the bacteria that’s now landed inside of that air sac, and it’s going to take a journey through the tissue of the lung. It’s going to go and drain down to a local lymph node. This is a local lymph node; a neighborhood lymph node. Let me label it right here; lymph node. That’s the journey that the macrophage is going to take; not every single one, but some of them are going to go to the lymph node. What they do by doing that is, they actually carry with them the micro bacterium. This little bacterium is now carried along, going for the ride, and now the bacteria is in two spots. It’s in the original spot where it landed in the lungs, but it’s also in the lymph node because it got carried there by the macrophage. I should’ve mentioned this earlier, but let’s assume that this is your primary infection. In other words, this is the first time that this person, or I guess it could be you or me, is breathing in the TB bacteria. What’s going to happen is, there’s going to be a reaction. The micro bacterium and the macrophages are going to start warring. They’re going to fight. You’re going to get this entire area turned into literally a battlefield, with dead micro bacterium and some dead macrophages. Some of your own cells are going to be part of this, but a lot of it is just going to be the bacteria. You’re going to get some of this battlefield going on over here as well, in this lymph node. That’s what it’s going to turn into; a giant battlefield. If you look under a microscope, it actually looks like, well we call it a granuloma. That’s the description that a pathologist might use
for what we are actually describing here. The same thing is true for the lymph node. There’s a little granuloma
in there as well. If you were to peek inside of this granuloma, let’s just actually erase the center out, if you were to peek inside, let’s say I was to cut it open, what you would see is, inside of this granuloma is literally this mess; this goo that somebody at some point, thought looked like cheese. I’m not sure how they came up with that conclusion, but it kind of stuck. So, we call this caseous necrosis. Caseous literally refers to cheese. This is the same kind of cheese that might go on your crackers. Cheese, and you can think of it almost like cheesy death I guess; cheesy death for the necrosis part. I think I added an extra
“e” there by accident. Let me fix that with a little hyphen. So, cheesy death. Because I’m naming things, let me go ahead and give you a couple more names. Ghon Focus; what the heck does that mean? Ghon Focus, actually named after Dr. Ghon. Ghon Focus is what we call this thing. It’s termed a granuloma, and specifically here because it’s a granuloma, which is more a broad term, is in the sub-pleural space, we said, and it’s close to a fissure, and we suspect it’s from TB. We would call it a Ghon Focus; it’s the other name for it. Both of these, if you’re trying to name both of these together, the lymph node that has a granuloma and the Ghon Focus, together make up what we call the Ghon Complex; Ghon complex. That just refers to both of the areas of disease. This is how disease starts, but what happens after time passes? Let me just slide this over a little bit. If we then take a little bit of passage of time. Let’s say there are three options. Time has passed. What are the different possibilities? Well, let me actually go through and talk about micro bacterium; micro bacterium tuberculosis from the standpoint of what is going on. Actually, I just noticed, I have in the past made the mistake of using a capital T, but it should be a lower case t. Micro bacterium
tuberculosis; three options. One option is that the bacterium may be dead. You may have killed it with your macrophages. Another option is that the bacterium is dormant; it’s just lying in wait. The third option is that it’s multiplying like crazy; it’s actually going and dividing and dividing and dividing. The last one, actually, is going to look – if you looked on a chest x-ray, like this, you see lots of disease; this red indicates diseased tissue, not normal tissue. You might even see some large diseased lymph nodes. That’s what it’d look
like on a chest x-ray. These other two, on a chest x-ray, basically would look normal. If you were to look at a chest x-ray, this is what the three options would look like. The first two would look normal, and the third one would look like something is wrong. Actually, this is helpful, because remember, these two together, we call these, both situations we call them latent TB infection. Remember, we can’t really easily distinguish the two because in both situations, you’ve had prior exposure to TB, and in both situations the x-ray looks normal. If you had some super ability to actually zoom in; let’s say you looked under a microscope, you would notice one key difference between these two. This is not something you can see on a chest x-ray, you can see only if you had amazing vision and could look down at the microscopic level at somebody’s lungs. You’d see macrophages, and in the top case where there are dead bacteria, the macrophages would look healthy and happy. In the case where you
have dormant bacteria, you would actually see
some bacteria there; some red, live bacteria. That’s the key difference between these two situations. Again, both of them we call latent TB infection. In this scenario, the bottom one, is going to be called progressive because things are slowly but surely getting worse; you can see more disease
on the chest x-ray. Primary, with a 1 and a
degree sign, infection; this is the name for this, progressive primary infection. It sounds a lot like what we had named that here, with primary infection, but the word progressive tells us that things are actually getting worse. The disease is getting more nasty. Now, let’s actually play
out the rest of this. Let’s think about what will happen with the dormant situation. I wrote out, or drew this out, earlier. Let’s say more time is passing, of course. Maybe years have gone by. This person has had live bacteria in their lungs for years and years; nothing has happened. Now, they have what we call reactivation; maybe it’s because their immune system is
not working properly, or maybe they have another disease. Who knows why, but all of a sudden, now the bacteria, the TB bacteria, are going to come out with a vengeance. There’s going to be a cavity that forms; usually in the upper lobes. A cavity that forms up here. It’s going to be packed full of TB bacteria. This person, you could imagine, if they coughed, they’re
going to be coughing out lots and lots of these little bacteria that i’m drawing. Around that area there’s a lot of disease; a lot of disease in this area and it’s very, very distinct. If you see cavities, and you see lots and lots of disease, you’re really going to be worried that this person might have what we call progressive
secondary infection. The reason I’m saying
secondary is because, again, this is happening separate from that primary infection; this is happening sometimes years later. Another way you can
actually have this happen is through what we call
a secondary infection. Maybe you actually literally get more TB. Maybe you’re on a bus or a boat, and a second person decides to cough and TB gets into your lungs through breathing it in. That’s another way to actually get progressive secondary infection. You can also think that
this is re-infection, because you basically got re-infected with the same bug. The thing that ties
reactivation together with re-infection is that in both situations your immune system has at some point in the past been exposed to TB. We think that’s the main reason why you see these cavities, and you see so much disease. That’s a really horrible infection to get. So, thinking about this a little bit more broadly then, both the progressive primary infection, and the progressive secondary infection, who are the folks that
you’d be most worried getting these diseases? I always worry about HIV patients before any other group because we know that HIV and TB is a really,
really bad combination. They’re at high risk for getting progressive disease; both primary, which is at the time that they got the first infection with TB, or secondary which could be years later.

The Most ICONIC Scandals, Bugs & Broken Updates in Dota 2 History

The Most ICONIC Scandals, Bugs & Broken Updates in Dota 2 History


The history of Dota 2 is one of greatness. LD: Not yet! Sylar to fall, Liquid are doing it! They’re gonna take it! KuroKy: I waited four f***ing years for this day. This time we’re gonna rewrite history. Capitalist: EG might be able to do this! Evil Geniuses, they’re holding! LD: Ravage on everyone! The black hole as well! LighTofHeaveN, turns it around! Ravage as well! Stolen by Dendi, are you kidding me!? TobiWan: TNC have done it! The dream, the reality! But it’s also a history that’s not exempt from the absurd, the embarrassing, and the controversial. From game ruining bugs, to the biggest of professional scandals… TobiWan: I cannot believe it! Let’s look back into the most hilarious balancing blunders, the most shocking news, and the lowest points of Dota 2’s storied past. Match-fixing and intentional throws are a hazard of any competitive game and we’re kicking things off with two of the the most infamous examples in Dota 2 history. On June 14th 2013, RoX.KiS took on zRage in an online match in StarLadder Star Series sixth season. Despite being the favourites, RoX lost the game in suspicious fashion with a number of highly questionable engages and buybacks throughout the game. Sheever: They actually want to try to go in with this, Bzz… He was already very low to begin with… They just run in here to die! What’s up with that? That’s not good… The surprise upset was investigated by StarLadder officials, and two days later it was determined that Alexei “Solo” Berezin had intentionally thrown the match after placing a bet against his own team on egamingbets.com Solo publicly apologized for throwing the match, and admitted to using his girlfriend’s account to place a one-hundred dollar bet against his team. And on June 21st, RoX removed Solo from their roster. StarLadder had initially handed Solo a lifetime ban for his actions, but ended up reducing his ban to one
year following his public apology and cleared up any suspicion against the organization and its other players. Solo’s winnings would have totaled three-hundred and twenty-two dollars and the community wasted no time in making the number three-two-two a popular meme throughout esports, often sarcastically referenced when a player is playing so badly it is borderline suspicious. Maut: Don’t do it Zai, you’re too young! What are you doing?! [laughter] But, a year later, a highly publicized match-fixing scandal took place that ended with much more dire consequences. In October of 2014, in Southeast Asia’s Synergy League, the heavily favoured Arrow Gaming lost to Australian squad Can’t Say Wips, prompting an investigation by Dota 2 Lounge. The examination uncovered several bets placed by individuals associated with the team leading Arrow Gaming to be disqualified from the tournament. Further investigations uncovered that the bets originated from accounts belonging to the girlfriends of ddz and Lance, resulting in the two players receiving lifetime bans from the event. Soon after the investigation, Arrow Gaming protested the players’ innocence providing Synergy League with chat logs and statements regarding the situation in ddz’s name. However, the logs were proven to be doctored and the statements false, and as a result, Synergy League extended the bans to Arrow Gaming’s entire organization. As a result of the whole debacle, Arrow Gaming and all of its players were removed from the line-up for The Summit 2’s SEA qualifiers and are still banned from Synergy League. Shortly after the incident ddz took to Facebook to publicly apologize on behalf of the players. Admitting that they had three-two-two’d and that the statements and chat logs provided to Synergy League were forged by Arrow’s management and not written by the players. A few days later Dota website 2p reported that team manager Jaren Gan had threatened to sue Lance and ddz for eight-thousand dollars each for breach of contract should they not retract their confession. Arrow Gaming would eventually release its entire roster. But that wasn’t the end of it. On March 28th, 2015, Valve stepped in, handing out permanent bans to all former members of Arrow Gaming from Valve sponsored events – including the International. While there are other examples of Dota 2 match-fixing, and still some we might not even know about, Arrow Gaming and Solo’s three-to-two are among the most memorable. Bugs come and bugs go, but some remain in infamy for just how ridiculous they are. Of all the bugs in Dota 2’s history, one stands above the rest for both how broken and straight-up hilarious it was. In patch 6.75 Chen’s abilities received a minor tweak as the ability to send allies back to base was moved off Holy Persuasion and back to Test of Faith. But in this process, something broke in the game. For some reason, Holy Persuasion, the ability used to control creeps, now worked on Roshan. You’d think that having Roshan, with his thousands of health, crushing basic attacks and abilities would be a bit strong to have as a pet… …And you’d be right. The discovery spread like wildfire and pretty soon, level one heroes, towers, and neutral creeps were falling to Roshan’s relentless attack. Basically, whichever team had a Chen would have free reign of the map from minute one. In all but the rarest of times that would lead to a dominant victory. Within hours of the bug’s discovery, Valve issued a hotfix… …Ending Chen’s very brief reign of terror. Now, nearly five-years old this bug remains one of Dota’s most iconic. While it generated plenty of salt at the time of its release, Today, you have to laugh at its absurdity. The International 2014 set records for its 10 million dollar prize pool and with that much money, teams were looking to gain every advantage possible, pouring hours into carefully crafting winning strategies that would make them millionaires. So when a Chinese news crew leaked team strategies during the tournament, you could imagine that some people were pretty pissed. The outrage stemmed from a Weibo post made by a user known as Dr.Kleiber, who posted a passionate open letter explaining the situation. According to the post, the crew of the website Gamefy made their way into Team DK’s off-limits game room and started rolling, despite having no permission from Team DK or Valve to do so. Initially posted to Youku, the video was translated to English and submitted to Gosu Gamers, spreading across the community. While both videos were taken down, after a furious interview by Team DK coach “71”, the video had spawned mirrors and copies all over the internet. According to “71”, the video revealed DK’s core strategy and drafting ideas. For not just the game in question, but the entire tournament. To make matters worse, the Weibo post also indicated that Gamefy had posted a similar video on June 11th, where they recorded Invictus Gaming’s team conversation. Thankfully, Ferrari_430 noticed the camera and left the room meaning not too much of IG’s discussion was leaked. Following the leak, iceiceice joined his coach in expressing his displeasure with Gamefy. A day after the outrage, Gamefy posted an apology to their Weibo, where they begged the community for forgiveness. In compliance with Valve’s rules, the personnel who were involved in the leak did not continue reporting on the event. Although Gamefy still worked for the remainder of the tournament. The community, upon hearing of the leak was understandably furious at the journalist in question. The outrage prompted Gamefy’s producer to post another apology, this time directly defending the “well-intentioned” reporter from whom the leak resulted. The overall impact of the Gamefy leak on TI4’s outcome is hard to extrapolate, But it’s even harder to deny its influence on Team DK, who headed into the tournament as one of the clear favourites. Needless to say, it is one of the largest scale leaks in Dota 2’s history and remains the most memorable scandal to emerge from The International. The term game-breaking can be thrown around loosely… Ayesee: He’s gonna try it again, can he… Got him that time! [crowd cheers] See you in the base, Mu! Welcome home! But in Dota 2, one particular bug stands out for quite literally breaking the game. In patch 6.81, Vengeful Spirit received a change to her aura that would apply a damage debuff to any hero that killed her. Simple right? Unfortunately, a bug caused the game to instantly crash if the aura debuff was applied to any non-player. Essentially a death to creeps or towers would force everyone out of the lobby. The bug was exploited almost instantly, much to the frustration of a large part of the community, as griefers intentionally suicided to prevent themselves from losing, ruining countless games. To no one’s surprise the issue was hot-fixed by Valve within a day of its discovery after massive community outcry. While many bugs have appeared since this rage inducer from 2014, few have had the catastrophic consequences of 6.81’s Venge aura. While Dota has had its fair share of bad tournaments in the past, none have captured the community’s ire quite like the Shanghai Major. KotLGuy: Where to begin? It seemed like every hour saw a new issue arise. As the days rolled on the event went from rage inducing… Draskyl: What? ODPixel: Did they say GG? Draskyl: They definitely didn’t. ..to almost comedic in its ineptitude. [laughter] Between the wealth of production issues, logistical nightmares, and endless delays, nothing seemed to be going right for anyone involved. And that doesn’t even cover all the problems, such as players’ keyboards going missing, talent not receiving food, water or transportation to the venue, the laughable VIP room… LD: So, they’ve added some chairs since I last came in. Not so soundproof booths, and fans and cosplayers being asked to leave the venue. We could go on, but you get the idea. ppd: There’s been so many delays and problems and it really makes our game and what we’re doing here look bad, which is unfortunate for everyone involved. Sheever: Because the production is not great… We’re gonna continue here with one more match today though, Evil Geniuses, MVP Phoenix and we’re gonna go continue with that after a small break, so we’ll see you soon. Soon. [laughter] Eventually Valve fired production company Perfect World and PGL was hired to salvage the rapidly sinking ship. And while PGL saved the show, it was too late. The Shanghai Major was already going to go down in history as one of Dota 2’s most embarrassing events. It really is a shame that the event went so wrong because against the backdrop of disaster, the games were fantastic and the casters and talent poured their all into it. TobiWan: The black hole! The vac is there! There’s a hole! Now they go! Universe force staffs the other way to safety! They can’t do anything to the cleave! In from Arteezy, and that’s the danger zone! In some cases, pulling double or even triple shifts to make sure that the show would go on. But while all that might be enough to put Shanghai on the wrong side of history, it was the firing of James “2GD” Harding that elevated the major to a new level of infamy. On day two, desk host 2GD was unexpectedly replaced on the panel. While the change raised some eyebrows in the community since 2GD was seen as an entertaining if slightly provocative host, there had been little to suggest that his off-brand style of humor would be grounds to have him fired. 2GD: It’s not just me here to talk about the dos and don’ts of Dota 2, and the cans and c***s of the teams. 2GD: The Chinese hotel had disabled pornography. Mr. Wang’s amazing wheelchaired antics were pretty amazing. WinteR: It shouldn’t be “Sir” 2GD, it should be “Old” 2GD. [laughter] 2GD: You can f*** off, WinteR. 2GD: Cons for CDEC… …they’re stubborn and only have one D. [laughter] But it wasn’t just his firing that got the community up in arms, it was the inflammatory response to the situation on Reddit by Valve co-founder and president, Gabe Newell. In that statement, Newell called 2GD “an ass”, while offering little in the way of an explanation for his dismissal. 2GD responded to the post suggesting that he was not just removed from the panel for his raunchy humor, but for a history of conflict with Valve employees and producers. ppd: He came in here trying to be himself and, you know, you can appreciate that but him being himself just isn’t what Valve wanted to be for the face of their Major and that’s their call. Regardless of the reasons or any past history between James and Valve, the manner in which Newell and Valve handled the dismissal and the community fallout it generated has become infamous. To this day, “is an ass” is a high tier meme within the Dota 2 scene. Despite the subsequent Manila, Boston, and Kiev Majors all being praised for their fantastic production values, the aftertaste left by the Shanghai Major will never be forgotten by Dota 2 fans. 2GD: So let’s check out some of the highlights. SyndereN: Your face is a beautiful highlight. Yep. [laughter] Broken hero releases are a pitfall of any MOBA and Dota 2 owns arguably the most outrageous one of all time. The introduction of Centaur Warrunner into Dota 2 in October of 2012 was basically a disaster. He was unkillable levels of tanky, dealt ridiculous damage, and could chain stun into death with ease. His opening day win rate in Dota 2 was staggering, at over sixty-seven percent. The hero was a complete and total nightmare to play against. Part of the reason for this unheard of dominance was that as part of the port from Dota to Dota 2 Centaur was given a new ultimate. Instead of Great Fortitude which gave flat strength, he received Stampede, a global ability on a tiny cooldown that gave all allies maximum movement speed, a ridiculous stun upon contact with an enemy and massive damage. Things were so bad that just four days later, Centaur received nerfs – specifically to Stampede. More nerfs would be dealt to the hero in December, removing the stuns from both Double Edge and Stampede. The hero had finally been brought back into line. Needless to say, the memory of Centaur stomping players into oblivion in 1v3 scenarios is pretty funny in retrospect, but easily makes it one of Dota 2’s most iconic broken updates. [laughs] Hopefully we never see such a busted hero release ever again. CW: Long shall my name be remembered. Since its formation in 2014, Team Secret has been a hotbed of controversy. From public roster disputes to reports of a hostile team environment, it seemed like for a long time Secret couldn’t keep their name out of the news – and not in a good way. Even going back to their inaugural roster, messy break-ups have been all too frequent. From N0tail and Fly’s bitter removal, To w33 and MiSeRy’s very public exits, changing rosters has rarely been smooth sailing for captain, Puppey, and the rest of Team Secret’s management. Redeye: A team of superstars, as they are, but yet to gel properly, perhaps. But if dramatic roster moves were the only thing that they were known for, Secret would not make this list. On February 16th, 2016, Team Secret’s now former manager, Evany Chang, took to Twitlonger and posted a lengthy account of her time with the team, where she alleged that Team Secret had missed making payments to players and staff and neglected to hand out tournament winnings in a timely manner. Later that year, EternalEnvy made similar accusations, alleging that he had yet to be paid for a number of tournaments. Additionally, stating that team director Kemal Sadikoglu and captain Puppey had committed other abuses. EternalEnvy claimed that the organization was secretly removing ten percent of all player winnings without previous consent, that players had never signed contracts and that Puppey had physically bullied w33 – among other accusations. That same day, another former player, MiSeRy, came forward. Stating that the team had failed to pay him for numerous tournaments and claimed that he hadn’t received agreed upon revenue from merchandise. A little more than a week later, Team Secret posted a response on their website simply titled “Update”, which while not acknowledging any accusations directly did admit that the organization had made mistakes attributed to its rapid growth. In March of 2017, Puppey would post his own Twitlonger announcing the departure of Sadikoglu and apologizing to past members of the organization that felt that they had been wronged, further claiming that all obligations to those individuals had now been met. Since then, Team Secret has settled down and kept their name out of negative news, but despite consistently being a strong team that has attracted serious talent over the years, the organization has yet to fully rehabilitate its image in the eyes of many community members. Thanks for watching! If you want to see some more iconic esports moments subscribe to our channel and let us know what you’d like to see next.

Mantoux test (aka. PPD or TST) | Infectious diseases | NCLEX-RN | Khan Academy

Mantoux test (aka. PPD or TST) | Infectious diseases | NCLEX-RN | Khan Academy


Male Voiceover: I wanted to
talk to about the Mantoux test. This is spelled Mantoux, kind
of an interesting spelling. after a French doctor who popularized it. And another way you might hear
this referred to is a PPD or a TST. And what these things stand for is PPD stands for Purified
Protein Derivative, and actually gives us a clue as
to what we’re using in this test, which is that we’re using specifically
TB protein. I’ll put that in parenthesis. and the location of the test
is actually also going to be
kind of a clue here with TST. This is a tuberculin. Again,
referring to tuberculosis. Tuberculin Skin Test. This tells you where we’re
going to put all that protein. We’re going to put it in the skin. You may have seen this, and
this is a picture right here
of someone doing the test. Sometimes it’s referred
to as the bubble test. A lot of people say, “Oh
yeah, my doctor injected “some liquid in my forearm
and it bubbled up.” This is how people usually
think about this test. They remember that because
of a very obvious visual. And so what I wanted to
do was give you an example or a diagram of what’s actually
happening when you get this test done. Let’s imagine this is your skin layer. This is also referred to as the dermis. Below the dermis is some subcutaneous. Below the skin, subcutaneous layer. Usually not layer. One of the
most common things is fat. I’m just going to draw that in here. This is the subcutaneous fat. So the idea here is that you’re basically
putting a little needle in here, which is what you’re seeing in
that picture on the right there. That needle is full of some TB protein. So this Purified Protein
Derivative is in that needle. It’s actually going to be injected in. So you’ve got all these
little TB proteins in here. And the volume you’re
putting in is a small volume. It’s about one-tenth of a milliliter. So 0.1 mL and you’re
putting it intradermally. This is actually an important point. It’s going into that dermis layer. So it’s intradermal injection. What happens is that if you
then let’s say moments later you remove the needle, you throw it away. And now what you’re going
to notice is because you put a little volume
in there, a little 0.1 mL, that is going to bubble
up because that volume is going to make the skin
puff out a little bit. But if I came back over some time,
this protein is diffused over, this liquid has been
absorbed into the skin, and that bubble will disappear. If you come back, you might
see a little bit of redness, because of course poking the skin causes
a little bit of redness and irritation. But the bubble will disappear over time. So what are we hoping to
accomplish with this test exactly? Let me bring up a couple
of more pictures for us. Well this test is going to
help us answer the question of has the person had prior TB exposure? Just remember that. That’s the question
we’re trying to answer. Have they had prior TB
exposure? Yes or no. Let’s think about what would
happen in either scenario. So this would be that they
have not had prior TB exposure. And on this side let’s talk
about what would happen if they
have had prior TB exposure. So two scenarios. Let’s
start on the no side. Let’s draw our skin again. So this is just as before. Let’s draw some TB protein in here. What’s going to happen is you’re
going to have some macrophages. These macrophages are going to come around and they’re always patrolling the area. They’re making sure
that almost like police officers making sure
that there’s no problem. They’re going to come
and they’re going to pick up some of this TB protein. So they’re going to take
it inside of themselves. They’re going to present that
TB protein to another cell. This is our T-cell. They’re going to present this
TB protein to the T-cell. The T-cell is going to
say, “You know, I have had “no prior TB exposure. I don’t
recognize this TB protein. and it’s going to go on its merry way. It’s not going to make a big
deal about what’s going on. So the T-cell kind of meanders away. It leaves the area. It
leaves proteins over time. It starts to get chewed up
and digested by macrophages. Eventually all of it is gone. If you look on the
outside you see flatness. The skin looks nice and flat. This might seem very
obvious from this picture. Of course it looks flat
but that’s essentially what we’re looking at here is flatness. Looking at this picture, you can
see a little bit of redness here. If you were to feel it with
your finger, it would be flat. So it’s red but it’s flat. And that’s the key. In this person we would say
if there is no bulge or bump, we would say this person
has a negative PPD. This person right here has a negative PPD. So that’s basically how we
would read this flat PPD. Now what happens on the yes side. Let’s say the person has
had prior TB exposure. So the same setup as before. Let’s draw the skin. There we’ve got some TB protein. Let me draw that in here. And this TB protein is
going to get picked up as before by the macrophage. The macrophage is going to come by
and pick up some of this TB protein. And just as before it’s
going to find a T-cell. These T-cells are also
kind of moving around. This T-cell this time is going to say, “You know what? I have seen
this TB protein before.” And this T-cell is going to
start getting very excited. And this is the key difference,
right? It’s going to get excited. Before it didn’t get excited. It just left the area unexcited. Now it gets excited and it
starts releasing chemokines,
little chemical messages. You know what that does? That attracts lots and lots
of other cells to the area. Lots of macrophages
start coming to the area. They say, “Aha, interesting.” The T-cell tells us that
we’ve seen this stuff before, and this layer, this intradermal layer, starts to swell up with cells. So it’s getting full
of cells because of all these new macrophages that are
being attracted to the area. So it’s actually going to
start looking like this. Full of cells, right, on both sides. It becomes a nice big bulge
and this is loaded with cells. Macrophages in here. Maybe a few
more T-cells in here as well. You get the idea. Lots and lots of cells. We call this a hypersensitivity reaction. When you see all these
cells coming into this area, this is a classic
hypersensitivity reaction. In fact, there are different types
of hypersensitivity reactions. We would call this a class 4, type 4. The reason that they are
typed out differently is that type 4 in particular
involves lots of cells. So this is a very cellular
reaction meaning lots of your
immune cells are involved. You can see that in the drawing. You can see lots of macrophages
and T-cells in that area. So this is a type 4 hypersensitivity
reaction happening here. And if you were to feel with
your finger from here to here, it would not feel flat, right? This is not flat at all.
This is actually bulging out. We call this indurated.
Meaning it feels very firm. It does not feel flat. This is what you’re seeing
in the picture here. You actually can see from here
to here there is induration. They’re actually
measuring it with a ruler. So this is the induration. You can also see that they’re doing
it perpendicular to the long axis. So in other words, if this
is the long axis this way, they are kind of choosing
a 90 degree angle to that, something like that, to
measure the induration. So that’s how you would
measure induration of a PPD. So this looks like a positive PPD
on this second picture over here. We’ll get into in just a
moment how we actually decide if it’s negative or positive. Now one thing I forgot to mention is
you’re going to be reading these PPDs 48 to 72 hours after you
initially injected the protein. So 48 to 72 hours later. This is when you actually read the PPD. That’s very important because that gives
enough time to either go flat like this or to actually get indurated like that. One key point I want to make
is let’s say you’ve got redness all the way around here. Do you actually
want to measure the redness? No. You want to measure the induration. Just keep that in mind.
Induration not redness. They are very, very easily
confused for one another, but it makes a big
difference. Not redness.

Treatment of Active TB | Infectious diseases | NCLEX-RN | Khan Academy

Treatment of Active TB | Infectious diseases | NCLEX-RN | Khan Academy


Voiceover: This is Charles Proburg. Voiceover: And Morgan Theiss. Voiceover: And we’re going
to talk on this video about the treatment of active
tuberculosis infection. And I’ll state the obvious up front, which is the reason you
want to treat somebody with any infectious disease,
in this case, tuberculosis, is to prevent disability and
death from the infection. Another reason for treating
infectious diseases, especially important with TB is to reduce the spread of infection
to other individuals. The good news about the treatment of active TB infection is that we have a number of drugs which
have been developed over time that are really quite effective at treating the infection. The bad news is that unlike
many infectious diseases, these drugs have to be given for a fairly long period of time. They usually have to be
given in combination, so you need multiple drugs to be effective in treating and the other bad news is that resistance among
strains of tuberculosis is becoming a problem globally and we’re going to talk
about the treatment of resistant organisms on another video because it, in itself,
is quite complicated, but for the purpose of this video, we’re going to talk about the treatment of active TB and we’re
going to make the infection the most common variety. The one that we’re most likely to see and want to treat and that’s an individual with pulmonary tuberculosis. So, the first thing is, of course, we have to diagnose the infection. So, let’s assume that we’ve done that. We know that this person has active TB caused by active TB in their lungs and we want to initiate therapy. For most individuals, the therapy begins with a combination of four drugs. This is assuming we don’t know that this is a resistant organism and the four drugs that we start off with are … There’s an acronym called RIPE. R-I-P-E. Where the R stands for rifampin, the I stands for isoniazid or INH, the P stands for pyrazinamide or PZA, and the E stands for Ethambutol. And we treat the patient
with all four drugs right at the outset,
with the reason for that is anticipate to be for a two month period and the reason for that is we
want to blast the infection and eliminate as many of
the organisms as possible as quickly as possible. So, these are powerful
anti-tuberculosis agents, first line agents that
are aimed to kill the TB as quickly as possible
over that two month period. Voiceover: So, we’re calling
them bactericidal, right? Voiceover: They’re
bactericidal antibiotics that kill the TB. We confirm that by doing
cultures along the way, but those are the antibiotics
that we start with and that’s sort of the
intensive phase of therapy, that two month period. Then, if all goes well, we
back off to just two drugs for the ensuing four
months and the two drugs are refampin and INH. And that’s sort of the consolidation phase of therapy. We can use less drugs because we’ve killed the bulk of the tuberculous
organisms, hopefully, in that first two months
and now we’re giving consolidated therapy. At the end of this therapy, which is a typical six month
period, if all goes well, we do a chest x-ray at the end of therapy. We determine that the
chest x-ray is improved from the first one that
led us to the diagnosis and that is the end of therapy. Voiceover: Okay. Voiceover: However,
there are some patients that actually, we end up
needed to treat longer because they don’t have
the simple pulmonary form of the disease or they have
some underlying problem. Voiceover: So, as if six
months wasn’t long enough, you can actually have a
longer treatment regimen? Voiceover: Exactly. And sometimes the things which are, or the disorders that are often associated with a longer duration of therapy is if you have more severe disease. So, for example, TB meningitis, you would typically treat longer. TB infection of the bones and joint you would typically treat longer. So-called miliary TB,
you would treat longer and even pulmonary TB
where there’s a big cavity in the lung, often will be treated longer. Another circumstance
that yields, makes you treat longer is if the patient is co-infected with HIV or if
the patient is pregnant. Pregnancy creates a certain
degree of immuno-suppression and pregnant women are
treated for longer duration’s. Finally, patients whose
cultures remain positive throughout treatment, or at least, for more than two months into treatment, if they remain positive, they get treated for a longer period of time and patients who have
a resistant organism, which we’ll talk about at another video, get treated for a longer period of time. So, back to the patient
that we’re treating just for the regular period of time, for that six month interval. There are a couple of
very important treatment protocols that you need to be aware of as these patients are being managed. The first is, one has to make sure that they’re taking their drug, so that they’re compliant
with their medication. Voiceover: That seems like it would be pretty hard for a patient
to take all these, four medicines and then two medicines everyday for six months. Voiceover: Exactly. And so, recognizing that this is a challenge for patients to
take multiple medications for multiple months, you need to be aware of that challenge and try to make the taking of the medication
as easy as possible. And make sure that you are observing that they are taking their medication. And let’s talk about that observing first. This has been a huge
benefit in the management of patients with TB. Recognizing the need, the desirability and the benefit for something called directly observed therapy, or DOT. Directly observed therapy means exactly what it sounds like. A healthcare provider is
making sure the patient is taking their medication. The reason that that’s so important, is that it will yield a higher cure rate, if they are taking their
medication consistently and less likely that they will develop a resistant organism. So, DOT, directly observed
therapy, is very important. The other element of assuring compliance is to make it as easy as possible for the patient to take their medication. Well, one strategy is, you can have them take their medication three days a week as opposed to every day and it appears that the treatment is equally effective, so under directly observed therapy, you can have them take it
just three times per week. The patients need to be
encouraged constantly to take their medication, underscoring why it’s important that they do so. There are some logistic
issues that may help assuring compliance. For example, if you have
convenient office hours where the patient can come and see you after their work. Providing incentives
and enablers to patients for taking their medication. For example, providing them meals or giving them travel vouchers to come into the clinic or to
wherever you’re seeing them. And then there are some strategies for simplifying the regimes. I’ve already mentioned the one, which is three times a week therapy. There are also some
combination medications available in some countries
that may be valuable in enhancing compliance. So, while we’re busy assuring compliance when we’re seeing these patients on a regular basis, we’re also monitoring to make sure that the
outcome of their infection is going well. And so what that means is that we’re evaluating them clinically
at regular intervals, often every month or so, examining them. We’re also obtaining cultures from their, if it’s pulmonary TB, from their sputum, at monthly intervals to make sure that they become culture negative in the anticipated two or less months. If cultures aren’t available, you can do smears of their culture, but it’s better to get cultures when they’re available. So, that’s all part of monitoring. Another important part
of monitoring patients who are being treated for tuberculosis is watching for side
effects and we’ll do those for the RIPE again, for the
four key antimicrobial’s used for treating common TB infections. So, R again, is for refampin. And the main side effects to keep in mind about refampin are that
it can cause hepatitis. And so, if a patient
develops clinical symptoms and you think maybe hepatitis, they get jaundice, for example. You have to be recognized that refampin is one possibility. Another side effect of refampin is decreased platelet counts. That is thrombocytopenia and you need to be aware of that. And then a very important
side effect of refampin is drug-to-drug interactions. Because refampin is a potent inducer of certain enzymes in the liver, cytochrome P450 enzymes, there can be interactions with other drugs. As it is side, refampin also may color secretions red, like
red urine and red tears that may interfere with contact lenses, but that’s more of an annoyance than a significant side effect. With regards to INH, or isoniazid, the main side effects to
be familiar with again, are hepatitis. INH can cause hepatitis,
especially in those that already have a reason
for having hepatitis, for example, alcoholics. And isoniazid can also cause
a peripheral neuropathy. Oftentimes, resulting from vitamin B6 or pyridoxine deficiency. So you can take care of that by prescribing pyridoxine
at the same time. That’s especially true if the
patient has poor nutrition, an alcoholic, for example. You can also get neuropathy in patients with chronic renal, who are taking INH, with chronic renal failure and diabetes and so forth, but neuropathy is important to keep in mind. With regards to pyrazinamide,
these individuals may get high uric acid levels
and resulting arthralgias. They can even get overt gout and that would be a reason for
stopping the pyrazinamide. And then finally, with
regards to Ethambutol, patients may develop an optic neuritis which can impair their
vision and that would be a reason to stop Ethambutol therapy. So, being familiar with these side effects as you monitor the response of the patient to therapy and as you
monitor their compliance is also an important part of the treatment of active TB.

Pulmonary TB | Infectious diseases | NCLEX-RN | Khan Academy

Pulmonary TB | Infectious diseases | NCLEX-RN | Khan Academy


Voiceover: I’m Charles Prober. Voiceover: And I’m Morgan Theis. Voiceover: And in this
video, we’re going to talk about pulmonary disease
caused by tuberculosis. The reason we’re dedicating a
full-on video to pulmonary disease is that pulmonary disease is the most
common form of clinical tuberculosis. It represents somewhere between
60 and 80% of all clinical disease attributable to tuberculosis
worldwide, so it’s way important. Voiceover: Okay. Voiceover: With pulmonary disease,
as with any form of tuberculosis, disease may result either
from a primary infection that is the first time the
host is seeing the infection, and that’s called primary,
or it may be secondary, which results from reactivation
of dormant infection or sometimes from infection
from a second source in a person who had a prior infection. It’s their second experience
with tuberculosis. The distinction between these two
is that with primary tuberculosis, pneumonia following primary tuberculosis, or pulmonary disease
following primary tuberculosis is more common amongst
children than adults. Children are more likely to
manifest pulmonary disease with their primary infection. Then the other contrasting element
is that with primary tuberculosis, the part of the lung which is involved is usually the lower
lobes or the middle lobes. That’s contrasted from
secondary tuberculosis, where the part of the lung that’s
involved is usually the upper lobes. it is said that this difference
results from the higher oxygen tension in the upper lobes, which I
think facilitates reactivation, but I’m not sure about the
mechanism, but nonethless, it is an association which
has stood the test of time. From a clinical standpoint, the
disease caused by tuberculosis can be the same whether it’s
resulting from a primary infection or from a secondary infection. The disease can be along
an entire spectrum. At one end of the spectrum is mild disease with a minimal amount of symptoms
attributable to the infection and at the other extreme
it can be very severe with progressive lung damage, severe
disability, even leading to death. Not only is there differences
along that clinical spectrum, but in parallel, there are radiographic
differences along the spectrum. In some occasions, pulmonary
disease is associated with a small infiltrate, a small
abnormality on the chest x-ray, whereas at other times the
disease may be widespread throughout both lungs and may
take on a cavitary appearance, which results from lung
parenchymal destruction, so really across a broad spectrum. Voiceover: Okay, so with either
primary or secondary pulmonary TB, you can be anywhere on this spectrum? Voiceover: Exactly. Voiceover: Okay. Voiceover: The other
thing that I would say about pulmonary tuberculosis
is if it is not recognized and not treated or back in the day where there was no
anti-tuberculous therapy, the clinical course of disease,
a so-called natural history, that is what happens
if you don’t treat it, was divided a third, a third, and a third. One-third of patients went on to die
of their untreated pulmonary disease, and that death could often be
quite rapid and it was called, back in the day, galloping consumption,
consuming the person’s life. That’s about a third. A second third, the patients would
actually spontaneously remit, they would get better. Their signs and symptoms would go
away and they would then be well. Then the final third would have
progressive lung involvement, not galloping, but more slow,
and this was often referred to as consumption without the
word galloping in front of it. That would be the natural
history of tuberculosis. Voiceover: It always seems
like they should just call it the natural course, instead of the
natural history, but there you go. Voiceover: I think that
that’s a good point. Now, when you see somebody who
may be infected with tuberculosis, they often have, in addition to
their pulmonary signs and symptoms, they have other nonspecific
signs and symptoms. So, this person who’s lying
in bed and you can see, first of all, the person
appears to be quite thin. In fact, weight loss is very
common as a nonspecific finding of any chronic illness, but
in this context, tuberculosis. Other common so-called systemic
symptoms associated with tuberculosis are fevers and the fevers may
go on for a long period of time, days to weeks to months. The fevers may be
associated with sweating, and that sweating often is most
prominent at nighttime, I’m not sure why, but that’s so called night sweats,
and this combination, of course, makes somebody just feel generally unwell, they have so-called malaise,
they don’t want to eat, so they’re anorexic and that
contributes to the weight loss. These are the systemic symptoms
that may accompany any kind of tuberculous infection,
including lung disease. Then there are some signs, in
addition to the signs you will get because you have pneumonia, so the clinical signs
associated with pneumonia, or the clinical signs associated with progressive pulmonary symptoms, things like cough, shortness of
breath, inability to breathe well, especially when laying down at nighttime. In addition to those findings, there
are some other nonspecific things that you should keep in mind
when you’re contemplating TB as a diagnosis and they’re
shown in the pictures. One picture, the bottom
picture is of the legs of a young individual who has tuberculosis and it shows these elevated, red nodules. Red, erythema, and nodular, nodosum, and this is referred
to as erythema nodosum. It is not specific to tuberculosis. It can occur in other diseases,
including some fungal infections, like that caused by coccidioidomycosis, and including streptococcal infections, but it also is associated
with tuberculosis and the upper picture,
of course, is an eye and this is showing a particular
form of conjunctivitis, so redness of the eye,
and that is referred to as phlyctenular conjunctivitis
and that is something which is associated with
tuberculosis as well and I wouldn’t worry too
much about spelling it because it’s kind of difficult to spell. Voiceover: All right, well – Voiceover: As Morgan is demonstrating. L-Y-C-T-E-N-U-L-A-R, phlyctenular. Voiceover: Phlyctenular. Voiceover: Conjunctivitis. These are some of the signs and symptoms that may be associated with
tuberculosis in general in pulmonary TB, which is the
predominant form of clinical disease. Voiceover: Okay. Voiceover: The final
thing we’d like to spend a few moments talking
about, because it’s at least in the chest cavity is
pleural tuberculosis. This is little bit distinct
from pulmonary tuberculosis, of course the pleural membrane
is that which surrounds the lung and pleural disease caused by tuberculosis
can result in one of two ways. One is that it may be associated with
the first infection, primary infection and it is said that it can
be due to hypersensitivity, so an immune reaction of
the body to the infection. Then the other way that it can
result, either from primary disease, or I think with secondary
disease, as well, is as a result of contiguous spread. Direct spread of the infection from
the lungs into the pleural space. One of the distinguishing
features of pleural tuberculosis, compared to other forms
of a pleural infection is that the effusions may
really be quite large. The one that you’ve drawn showing it
in the lower part of the left lung, is a modest-sized pleural effusion, but sometimes it can be
even larger than that and extend along the whole
side of the pleural space. A large pleural effusion,
when you see that, you should think of tuberculosis
as sort of one cause. Pleural effusions result in an
extension of the pulmonary symptoms. You can imagine because they’re
squeezing down the lungs that the person is short of breath. If you percuss their chest
on physical examination, it sounds dull, because there’s
not air that you’re percussing, but rather the solid pleural fluid
and when you listen to their chest, they may have decreased breath sounds, because you’re not hearing
the lung as clearly, because the pleural fluid is in
between the stethoscope and the lung. The best way to figure out what’s
causing a pleural effusion in general and for tuberculosis specifically,
is to sample the pleural fluid, to do a pleurocentesis, a pleural tap. When you do that, the typical findings are that the fluid appears straw in
color, so yellowish in color, it typically has a very
high protein concentration, a low to normal glucose concentration, and white cells that number
between 500 and a few thousand. Voiceover: Is that high or low? Voiceover: That’s high, there should
be no white cells in the pleural space. There should be no pleural
fluid, so 500 to a few thousand. With a bacterial effusion, it may be a much higher white count than that,
but with TB it’s in that range. You can try to visualize
the TB in the pleural fluid by doing a TB specific stain, such as
a Ziehl-Neelson stain, or a ZN stain. Voiceover: So it’s
Z-I-E-H-L-N-E-E-L-S-E-N stain and that’s actually looking
for the tuberculosis bacteria. Voiceover: Right. Voiceover: Okay. Voiceover: The Ziehl-Neelsen
stain is positive somewhere between 10 and 25% of the time when TB is actually there,
so it’s not very sensitive. Culturing the fluid is more sensitive. It takes a longer time, it can take
up to four to six weeks to culture and it has a sensitivity
in the range of 25 to 75%. Actually, the best sensitivity
and the test, therefore, that you should do, if you think
that this effusion represents tuberculosis is to
biopsy the pleura itself and a pleural biopsy has
a yield of about 80%. If you think somebody’s got
pleural TB with an effusion, pleural biopsy certainly should be done.

Extrapulmonary TB (part 1) | Infectious diseases | NCLEX-RN | Khan Academy

Extrapulmonary TB (part 1) | Infectious diseases | NCLEX-RN | Khan Academy


Voiceover: This is Charles Prober. Voiceover: And I’m Morgan Theis
and today we’re going to talk about the extrapulmonary disease
associated with tuberculosis, which I find kind of interesting, because I always think of
tuberculosis as a lung disease. Voiceover: In fact, you’re correct, Morgan that the most prominent infection
associated with tuberculosis is pulmonary disease, is lung disease, but extrapulmonary disease
is also very important. In fact, it’s so important that
we’re going to make two videos about extrapulmonary disease. The first one we’re going to focus
on disease involving the lymph nodes and the genitourinary tract
and then the second one, we’re going to talk about
involvement of the bones, the central nervous system, the
gastrointestinal tract, and the heart. The reason that it’s so
important to give this much time to extrapulmonary disease is
that we call tuberculosis, the bug infects one-third
of the world’s population. After that initial infection, some
go on and immediately develop disease and others, as we talked about
before, develop secondary disease and it comes out later and
the infection may present in a myriad number of ways. In fact, that’s one of the reasons
that tuberculosis is referred to as one of the great imitators. It can imitate so many
other kinds of disease. Two videos. Voiceover: Okay, so
TB, the great imitator. Voiceover: Exactly and some
of the other great imitators people talk about these days
are lupus, which is, of course, not an infectious disease, HIV infection, which is an infectious disease,
Epstein-Barr virus infection, which is a viral infection. Those are other great imitators, but
today we’re talking about tuberculosis. Voiceover: Okay and these
are good things to remember because since they can
present in so many ways, we always have to have them
on our differential diagnosis, so we don’t forget about them. Voiceover: Exactly. The first site that I’m
going to talk about, Morgan, is the lymph nodes and I’m
talking about that first because it actually is the most common
place that TB goes, after the lungs. Voiceover: Okay and which lymph
nodes are we talking about? Because they’re everywhere
in the body, right? Voiceover: That is true,
they’re everywhere in the body and the infection of the
lymph nodes can occur anywhere in the body,
but the most common sites are posterior cervical, so the
lymph nodes at the back of the neck, and then another common site
is the supra clavicular area, so that space above the clavicle. Oftentimes, when you feel a
lymph node above the clavicle, you appropriately think of some sort
of malignancy in the abdominal area, because that’s a sentinel node,
the supra clavicular lymph node, but something to remember that can
also cause that is tuberculosis. One of the features of a lymph
node infection with tuberculosis is that the lymph nodes
tend to be painless, so they don’t hurt the
person, and also they tend to be not particular tender,
so when you push on them, they also don’t hurt the person. They often have a lack of
overlying redness or heat, because there really isn’t much
of an acute inflammatory response, it’s more of a chronic, slow process, so these lymph nodes tend to sneak
up on you, gradually enlarging. As they gradually enlarge,
some of them, however, can, because it’s a long-term process,
can actually cause fistulas tracks, that is a connection that
goes from the lymph node all the way up to the skin with drainage. Voiceover: Oh gosh. Voiceover: So if you see a
fistulas track associated with an enlarged lymph node,
tuberculosis should be on your list. The way these are diagnosed is
that a sample of the lymph node may be obtained and when
looked at under the microscope, you may actually see
the tuberculous bacilli, those little red snappers,
as they’re sometimes called, or you may culture them if
you don’t actually see them. Taking a chest x-ray of
patients with suspected TB in the lymph nodes is a good idea. Voiceover: Right. Voiceover: However, half the
time or more than half the time, the chest x-ray is negative,
so don’t be discouraged from the diagnosis if the
chest x-ray is negative, because it oftentimes is negative. Voiceover: Got it. Voiceover: The next site
that I’d like to talk about is the genitourinary site and
I’m talking about this site next because after lymph node
involvement comes the so-called GU, or genitourinary involvement. Thought to represent
maybe 10 or 15% of cases of extrapulmonary TB, as opposed to
lymph nodes, that’s more like 35%. This is about half as common. As is true of any infection that
can involve the genitourinary site, the kidneys and the genital
area, the patients may have very nonspecific complaints,
such as blood in their urine or pain when they urinate or needing
to get up at night to urinate. If you examine their urine
under the microscope, you may actually see white
blood cells, so pyuria, but you don’t see any bacteria,
typically, so that can be a finding. Voiceover: I’m confused about that, because why wouldn’t the bacteria
actually be in the urine? Voiceover: The main reason is that
the amount of tuberculous bacilli that are often present at one
of these extrapulmonary sites is quite small and unless you
either centrifuge the urine or otherwise concentrate it and stain
it with tuberculous specific stains, you will not see bacteria. That’s in contrast to regular bacterial
infections of the urinary tract, where there is typically
hundreds of thousands to even millions of bacteria that show
up in the typical stains that are used. The term that’s used here is when
you see the white cells in urine and you don’t see any bacteria,
and then you culture them for regular bacteria,
and they don’t show up, because TB doesn’t show
up on regular cultures, it’s culture negative pyuria. Culture negative pyuria should
make you think of tuberculosis. Now, if you actually send
those urine samples to the lab and say, “I’m looking for
tuberculosis,” and they’re set up on tuberculosis specific media,
then you often will grow the TB, but if you don’t think about
it, you won’t do the test, and if you don’t do the test,
you won’t make the diagnosis. Voiceover: So you’re
asking for a TB culture? Voiceover: Exactly. I mentioned the chest x-ray in the
context of lymph node involvement and it’s often negative. With genitourinary involvement,
the chest x-ray is often positive. If you see culture negative pyuria
and you’re thinking of tuberculosis, the chest x-ray may have value. The other part of the genitourinary
infection that I’ll mention here is specific to women and it’s that
tuberculosis may actually involve the internal genitalia of women,
that is the fallopian tubes and the endometrium and the
importance of recognizing that is that this is one of
the causes of infertility, especially in the developing world,
where tuberculosis is more common. Men can also get infection of
their internal genital organs, including epididymis and the testicles. They can also have prostate involvement. Again, tuberculosis can cause an -itis,
an inflammation in multiple organs. In this case, in the genitourinary area. Voiceover: And you say endometritis
is one of them, as well? Voiceover: Endometritis in women can occur and I mentioned the fallopian tubes
and when you have inflammation in those areas, that can
result in infertility.

Interpreting the PPD | Infectious diseases | NCLEX-RN | Khan Academy

Interpreting the PPD | Infectious diseases | NCLEX-RN | Khan Academy


Voiceover: Let’s say you plant a
PPD and a person comes back in, and now they want to find out
whether it’s positive or negative. The way I kind of think about it is I break people down into their risk group. I think of 3 risk groups. I think high risk, medium
risk, and low risk. If they’re not high or medium, then they basically by
default become low risk. That’s how it works out. Going to the high risk, there’s
2 ways to think about it. Either I’m really worried that
they are going to have TB, and that could be someone
who I suspect has it, maybe they have a very
abnormal chest x-ray, or maybe they lots of fevers, cough, night sweats, things like
that and I really suspect TB. They would fall in the high risk, right? Because I worry that they have it. In fact, even their family
members, close contacts, let’s say a grandchild
of a person who has TB, or and uncle or an auntie
of somebody who has TB, someone in the household, they are also at high risk of getting TB. These are folks I’m worried
may have tuberculosis, but also in this high risk group I’m going to put a third group, or a third category which is immunocompromised people. This is people that do not have a normal immune system so these folks it’s not that I’m worried that
they have TB necessarily, but it’s that if they did have TB, gosh, that would be really
awful because tuberculosis requires that you have
a good immune system, and if they don’t have
a good immune system then tuberculosis is going to be devasting for these folks especially folks with HIV. In this first group then,
the high risk group, either I’m really worried
that they have it, or I’m worried that if they did get it they would get really sick with it. For these folks, a positive test would be induration, remember in PPD
you’re measuring induration anything above 5 millimeters, anything above this range
would be considered positive. For example, if someone with HIV comes and they have a PPD of,
let’s say, 6 millimeters then they would definitely be positive, but if it was 3, then
they would be negative. This red stuff that
I’m kind of filling in, this is the positive range,
positive anywhere in here. Anything below that, I’m
going to write it in white down here. This would be
negative, anything below 5. If it’s exactly 5, then
that’s still positive. Who’s in the medium range? These folks. One group would be people
coming from an endemic country. Let’s say they recently came across from China or parts of Africa. If they’re coming from a country where tuberculosis is very common or endemic, then they are also in
that medium risk group. Also folks that live or
work in large groups. Think about nursing homes, or let’s say, a jail or an army barracks. Anyone that lives or works in these kinds of places in a large group setting, I’ll say large group setting, is
at risk for getting TB because, of course, it spreads from
person to person very quickly. If you’re around a lot of people,
you’re upping your chances. Similarly, people that are in health care so anyone working in a
hospital setting because, of course, people with TB
often come to health care settings to be take care of. If you’re in a health care setting working as a nurse or a doctor, then
you also are in the medium risk. I, myself, because I’m a physician, am in the medium risk for this reason. I’ll put a few more up here; IV drug use. This also puts you in the medium risk. Then I’m going to actually switch gears, and just as before where
I said I’m also worried, specifically worried about certain groups, here I’m very worried about
children less than 4 years of age. If you’re less than 4 years of age meaning if you’re 3, or 2, or 1, those children they may
not have any other reason for getting TB like the
people I just mentioned like health care setting
or endemic country where it’s around, but if they did get it, it would be particularly
problematic because young kids don’t have
great immune systems. Also, people that are actually
fighting other diseases. We call those comorbidities. Let’s say you have
already gotten a disease like diabetes, or let’s say your
kidneys aren’t working properly, if you already have other diseases then you’re also at risk
because if you did get TB, it would be even tougher to fight it off. For all of these folks, 10 millimeters or above is considered positive. I didn’t make an exhaustive list. There actually are a few other ones, but I tried to highlight some of the most important ones on this list. For example, just to
make sure we understand how to utilize this, let’s
say you have a person who is 3 years old and
that person comes in with a PPD of 12 millimeters. That would be positive here, but
if it was only 8 millimeters, it would be negative so that’s
how you would use this graph. So down here then we have anyone else, anyone that doesn’t fit
into the other categories fits into this final one so
this is the low risk category. For these folks, 15 millimeters
or greater are needed to be considered positive. If you have someone that is very healthy, and doesn’t fit into
any of the other things that we just talked about and
their PPD is 20 millimeters, then they would be considered positive, but if it was only,
let’s say, 13 millimeters somewhere in this other range down here, then they would be considered negative. You basically measure the induration, and then you kind of think
about what risk group a person falls into; high, medium, or low, and then you kind of organize
it using these graphs, very easy, right? So above 5, or above 10, or above 15 tells you which is considered positive versus negative. A couple of questions people
always ask is they think, “What if someone falls into
2 of these categories?” What if they’re, let’s
say, below 4 years old, let’s say we’re talking about a 3 year old so they have this one, but
you’re also really worried that they have TB so they’re in this one. If you ever have someone
that falls into 2 categories, you have to go with the
more conservative approach, and say if they meet
the high risk category, I’m going to use that
one to decide if they’re positive or negative. In this case, a 3 year
old who I suspect has TB automatically I would have
to go with this top one because I suspect TB simple as that. The other question that often
comes up is what about BCG vaccine? This is a vaccine that
some countries offer to their citizens to
help prevent disseminated or spreadout TB especially a
problem among young babies. What if someone has had BCG vaccine? It’s very clear. The
Centers for Disease Control has been very clear on this point. They say, “You do not
need to interpret the PPD “with this in mind. Ignore
the BCG vaccine completely.” In other words, when
you’re trying to figure out whether someone’s PPD
is positive or negative, just rely on the high,
medium, and low risk criteria that we’ve talked about. Do not worry about the BCG vaccine. That should not affect your decision.

Preventing TB using the “4 I’s” | Infectious diseases | NCLEX-RN | Khan Academy

Preventing TB using the “4 I’s” | Infectious diseases | NCLEX-RN | Khan Academy


Charles: This is Charles Prober. Morgan: And I’m Morgan Theis. Charles: And we’re going to talk
about the prevention of tuberculosis. There are I’s, four I’s to consider
in preventing TB infections. One I stands for
“Intensified case finding.” We’ll come back to that,
but finding cases of TB. When we talk about that, we’ll talk
about finding cases of latent TB and what we can do about it and finding cases of active infection
and what we can do about it. Morgan: OK. Charles: The second of the
four I’s is “Isoniazid” or INH, an important anti-tuberculose drug
that, in the context of this video, we’re going to talk about its use
in the treatment of latent TB. Morgan: OK. Charles: The third I is “Isolation,”
and that we’re going to talk about in the context of an
actively infected patient, a patient that may be infectious to others and how we can prevent the spread
of their TB to other people. Morgan: This is a very good
infectious disease principle, right? Charles: Right. you want to isolate the
person from spreading it. Charles: For many, that
is absolutely true. And then the fourth I is “Immunization.” Morgan: OK. Charles: What vaccine we currently
have available for the prevention of TB and perhaps what’s on the horizon. Morgan: OK. Charles: Starting with the first
I, “Intensified case finding,” mentioned at the onset that we’re either
looking for latently infected people, people with a positive TB
skin test, for example, or looking for cases of active TB. First of all, thinking about those
who may be latently infected with TB or actively infected, there are certain high-risk populations
that we always have to keep in mind. For example, persons immigrating, moving
from a country that’s got a high level of infection with TB, such as in many
of the countries in Sub-Saharan Africa, moving to another part of the world
that has a low level of TB infection, such as North America, the
United States or Canada. Another high-risk population, similar, are migrant workers from
highly endemic areas. Another high-risk population
are prisoners, especially
in the United States. The homeless population have
a high risk of tuberculosis. Individuals who abuse drugs intravenously, IVDU, intravenous drug-using individuals, have a high risk of TB. And those co-infected or infected
with HIV have a high risk. These would be individuals
that we would be screening with a tuberculose skin test,
for example, on a regular basis. If we find them to be
positive on that test, that is, to be latently infected with TB, this leads us to the
second I, which is “INH.” Treating these latently infected
individuals with isoniazid
is a very effective way of reducing the likelihood
that the latent infection will become an active infection. INH is about 90% effective
in reducing infection. The prescription of INH is
for a 9-12 month period. Morgan: Whew! Charles: It is a long
time, that’s correct. But with that 9-12 months of treatment, you reduce infection developing. There are some alternatives to INH alone, but the alternatives tend to be a little
bit more toxic, have more side effects. One example of an alternative is to
give INH with rifampin for 4 months or rifampin with pyrazinamide
(PZA) for 2-3 months. These combined therapies seem to
be almost as effective as INH alone for 9-12 months but not quite,
and they also are more toxic. Morgan: OK. Charles: So again, the second I is INH. Morgan: Now, once you start treating
someone who has latent TB with INH, how long before they
stop being infectious? Charles: They’re not
infectious to begin with, so if they have latent TB,
they’re not infectious. The idea of treating them is so
that they don’t develop active TB. Morgan: Which would be infectious. Morgan: OK. Charles: And in fact, let’s stay
with this intensive case finding and go down the active TB pathway. Many persons with active TB are
infectious for other individuals. There are some that are much
more infectious than others. For example, if you’ve got pulmonary TB, the most common site of infection with TB, and that pulmonary TB is cavitary, so there is a big cavity
on the chest X-ray, the likelihood is that that’s
teeming with TB organisms, that is, there is a lot of them, and they may spread to other
individuals quite readily. With those kinds of
infectious individuals, they must be isolated,
which is our third I. Morgan: Right. Charles: They must be isolated so they
cannot spread infection to others. What isolation typically means is
they’re put into a single hospital room with protected airflow, and any visitor to that
hospital room wears a mask
that filters out TB organisms, typically called an N95 mask. And then of course, the person with
active TB is treated for their infection, and usually, in about 2 weeks, 3 weeks,
or 4 weeks, they become non-infectious. That is, their anti-tuberculose therapy reduces the amount of TB
organisms they have present, so
they’re not infectious anymore. So then they can come out of isolation
and go back into their regular home life. Morgan: And is this treatment just
going to be the same, just using INH, or that’s a more intensive regimen? Charles: It’s a more intensive regimen, and we’re going to have a video or
two about different treatment options. The other thing to say
about those with active TB in terms of the intensified case finding is when you find somebody with active TB, you must do contact evaluation as well. You want to look to all the individuals
that they may have been in contact with before they were diagnosed because in doing so, you may discover
other cases of active tuberculosis that also need to be managed with
treatment, isolation, and so forth. Morgan: So you’re looking for
their contacts for evaluating? Charles: Exactly. You’re looking for where they
got the infection potentially or to whom they already
spread the infection. That’s a very important
public health effort to reduce the continued
spread of tuberculosis. The fourth and final I with TB
prevention is “Immunization.” Morgan: OK. That would be great. Why don’t we just immunize everybody
against TB and we won’t have a problem? Charles: And that would be great if
the vaccine were highly effective, which unfortunately, the current
vaccine available worldwide has some effectiveness, but it’s limited. That vaccine is called BCG, all capitals, and it’s a live attenuated vaccine
derived from Mycobacterium bovis, which is another kind of
tuberculose agent, M.bovis. It’s a vaccine which is administered
in many parts of the world that have high rates of tuberculosis
to try and prevent the spread, to try to prevent the individuals from
acquiring TB and then spreading it. The immunization is typically given
around the time of birth, with BCG. The degree of effectiveness of the
vaccine varies widely from study to study, ranging from a low of 0%
to a high of about 80%. Most use the estimated protective
effectiveness of about 50%. It turns out that the vaccine is
especially effective, when it’s effective, when given to children, and
that’s why it’s administered
around the time of birth. Morgan: OK. Charles: And the reduction in TB is
especially evident for severe disease. It seems to reduce the likelihood
of getting very severe disease, including TB meningitis and miliary TB. That’s important because that’s
the worst kind of tuberculosis. But again, its effectiveness
is limited, as I had mentioned. Now, because this vaccine
is live and attenuated, there are also some risks that you can get from vaccinating a large
number of individuals. If you inadvertently vaccinate
somebody who’s got an immunodeficiency, their immune system
isn’t working very well, their vaccine site can
become quite necrotic, and they can even disseminate the BCG. You can have an infection
arising from the vaccination. That’s fortunately not way
common, but it does occur. In just normal individuals, that is, those
who do not have any immunodeficiency, it’s estimated that
somewhere between 1 and 10% will get a little ulcer
at the vaccine site, and you can see this little crater
in their arm over a long term, and that sort of says, “Oh,
this person’s had BCG vaccine.” Less commonly, beyond the ulcer,
you can get some local adenopathy, lymph node swelling around the area
where the vaccine’s been given, for example, in the armpit, and very rarely, maybe
one in a million cases, you can get osteomyelitis, a bone
infection, from the BCG vaccine. These are all quite
uncommon and unbalanced. BCG vaccine is more useful than
not, and that’s why it’s given. Then the final thing I
mention about immunization is there is a lot of interest and work in developing new
vaccines for tuberculosis that would be more effective, of
course, and with less side effects. There are probably about 30
new vaccines under development, but unfortunately, at this point, none of them have been
found to be so beneficial as to be licensed for widespread use. But stay tuned. We hope to have a vaccine against
tuberculosis that’s more effective sometime in the future.

Diagnosing active TB | Infectious diseases | NCLEX-RN | Khan Academy

Diagnosing active TB | Infectious diseases | NCLEX-RN | Khan Academy


Voiceover: This is Charles Proburg. Voiceover: And I’m Morgan Theiss. Voiceover: And we’re
going to be talking about the diagnosis of tuberculosis and the reason that we’re talking about the diagnosis of
tuberculosis is that it’s, as we’ve said before, a
very important infection. It’s estimated that
there are about 9 million new cases of tuberculosis
recognized, RECOGNIZED each year around the world. There’s also estimated
that there’s another 3 million or so cases,
about a third additional, that are not diagnosed. So our goal is to increase our diagnostic abilities around TB. The picture, the x-ray that’s shown, is from the Centers For Disease Control and this was a patient
who had pulmonary TB. You can see the arrows
pointing in the lung to a round lesion, which
appears like a cystic lesion and this is actually a cavity. So this is cavitary TB. So, how would you start
suspecting somebody might have a pulmonary infection with TB? Well, first of all, they
would typically present to the physician with
symptoms, respiratory symptoms; coughing, for example,
shortness of breath, inability to do exercise the
way they used to do it before. When they’re coughing, they might be coughing up sputum,
which is of an odd color, maybe yellow or green or oftentimes the sputum has blood in
it, so-called hemoptysis. So, you would see such a patient. You would think they
have a pulmonary process. You’d do a chest x-ray and this is what you see on chest x-ray and
then you, the astute clinician, would say, “This might be TB.” So the first thing you then would do is a tuberculin skin test, which is shown in the picture of the
skin, also from the CDC and the arrows indicate,
the arrows pointing at the ruler, indicate
that the area of swelling, the area of induration
with this TB skin test is about 10 millimeters and that’s a positive reaction. There’s also surrounding redness, but that doesn’t count in terms of measuring the size of the reaction. So, we now have a person whose got a positive chest x-ray, consistent with tuberculosis and a positive TB skin
test and that suggests that, “Gee, this might really be TB.” But the diagnosis is
not made at that point. One needs to then try to isolate, to find the organism in
the lung of the patient. And what’s done as a first step to that is to obtain a sample
of the patients sputum. So, to induce them to cough
up some of their sputum and then to send that
sputum to the laboratory. And in the laboratory, the
first thing that they will do after you’ve told them
you’re suspecting TB, is they will do a TB specific stain looking for AFB, acid-fast bacilli. There are several TB specific stains. One, for example, is called
the Ziehl–Neelsen stain, which is abbreviated the ZN stain and these are good staining techniques, but they’re not hugely sensitive meaning that even when TB is present the stain may only be positive
about half of the time. So, that’s not good enough. The next thing that the laboratory will do is to take that specimen,
actually whether it’s positive on a TB stain or negative and set it up on culture media
that facilitate the growth of the tuberculous bacilli
and there are some very specific culture media that the laboratory will use for that purpose. The only problem with culture is that it takes a while. So, it takes 4-8 weeks for
a culture to become positive if TB is actually present,
but it’s important to do because culture is much more sensitive, much more reliable in detecting the TB if it’s present, than the stain was. So, instead of 50%, it’s more like 80% and also, you need to grow the
TB to confirm it’s identity and also test whether it’s killed by a variety of different antibiotics, antibiotics directed against the TB and that actually, that’s
called sensitivity testing, meaning determining whether the particular TB isolate is sensitive, is killed by, different kinds of antibiotics. Voiceover: Okay, and so this is often a point of confusing because
we’re using sensitive in two different ways. So, when we say sensitivity testing here, we’re actually talking about how sensitive is my patients tuberculosis
bug to all the antibiotics we have, right? Voiceover: Exactly. Voiceover: Okay and sensitive up here, sensitive … The sensitivity of a test is just of all the people who
actually have this disease, how often are we going
to get a positive test? Voiceover: Exactly and a
very important distinction because it is the same word
with very different meanings. Voiceover: Right. Voiceover: Thank you
for that clarification. Another test that can
be done on the sputum or the specimen from
the patient is actually molecular testing and a molecular test that may be used is something called PCR, Polymerase chain reaction, and this is a laboratory based test
that looks for some DNA and then puts it through a process that augments the amount of DNA present in the laboratory, it does that. So, if there’s even a very small amount of DNA present, this
PCR test may be positive and the advantages of this
test are that it’s quick, results can be present in
hours rather than in weeks, in terms of saying that TB is present, but the disadvantages
are that, first of all, it’s expensive, it doesn’t
allow you to determine the sensitivity, the
antimicrobial sensitivity to that particular organism and you can have false positive reactions. So, you can have a positive PCR and actually TB really isn’t there. So, it’s not routinely used, but under special circumstances, PCR may be used. There’s a test, however, that is used and endorsed by the
World Health Organization as being an important
rapid diagnostic test in the developing world and this test is also based upon molecular techniques in trying to detect the
parts of the tuberculosis and it’s called the expert, meaning it’s an expert kind of test I suppose, MTB, which stands for the
micro-bacteria, tuberculosis. Voiceover: Okay. Voiceover: … /RIF and
RIF stands for rifampin, which is one of the important
drugs to treat tuberculosis. And what this test does is it allows the rapid detection of the presence of TB, for example, in sputum. Concomitantly, it allows one to determine whether that TB that’s
present is rifampin resistant, that’s the RIF part. Very important, again, especially in the developing world. Results may be present. You may get results in, again, a few hours like the PCR test, so
it’s actionable quickly. The downside is that it
really is quite expensive. None the less, because of
the World Health Organization endorsement and it’s wide deployment, this test is now available
in about two-thirds of the countries where TB
is of a very high burden, where there is a lot of disease and about half of the countries worldwide where highly resistant TB is present. So, it’s been a very
important, so-called point of care test under those circumstances. Voiceover: And so the advantage that the Expert MTB/RIF has over
just your regular PCR is that it can actually
figure out if the TB in my patient has rifampin
resistance or not? Voiceover: Exactly. Voiceover: Oh, that’s good. Voiceover: And if it
is rifampin resistance, when we talk about
treatment, there needs to be a modified therapeutic strategy. Voiceover: Got it, so it’s
good to know that quickly. Voiceover: Exactly. So, there may be a circumstance
where, on your table, the chest x-ray is
positive, but the tuberculin skin test is negative
and this may be because the chest x-ray is not representing TB or it may be that the skin
test is falsely negative, either because it’s an
overwhelming infection and then the immune system
may not be kicked in enough to cause a positive
skin test, or it may be that it’s so early in the infection that the skin test is not yet converted. So, if you’re still suspecting TB based upon the clinical presentation, the positive chest
x-ray, but the skin test isn’t positive, you still
may want to go through the diagnostic testing
that we’ve spoken about. Now, in the diagnostic
testing, I’ve talked about sputum all the way along. I’d like to say one thing about children who don’t produce sputum typically. Well, they produce it, but
they immediately swallow it. So, when trying to diagnose
pulmonary infection, lung infection caused by TB in children, instead of using sputum, we
often use gastric aspirates, that is samples from the stomach, typically obtained in the morning after there’s been a chance to collect a lot of what might be coughed up from the lungs and swallowed, so gastric
aspirates are used in place of the sputum. And I also should say, in some patients, you can’t get a good sputum specimen. They just don’t produce it. It may mean the infection is very distant in the lung and for
those patients, sometimes doing a brochoscopy, putting
a tube down into the lungs to sample the fluid,
is used as the specimen to send to the laboratory
to do the testing we’ve spoken about. Voiceover: Okay, and
then just looking back at this table here,
what about the situation where you have a positive skin test, so I’m thinking TB is somewhere, but then you actually have
a negative chest x-ray. What are you thinking there? Voiceover: So, there’s a
couple of possibilities there. The positive skin test will
indicate a prior infection and we know a third of
the world is infected with tuberculosis and
the negative chest x-ray may indicate that the patient
doesn’t have TB at all, or at least doesn’t have pulmonary TB, but the patient may have TB somewhere else other than in the chest. So-called extra pulmonary TB. So, if you have signs of
infection outside of the chest, for example, swollen
lymph node or a problem in the genital urinary tract, or the bones and you’re thinking TB as a possibility then you may see that positive skin test, negative chest x-ray
and then your sampling will not be sputum because
they don’t have anything in their lungs as far as you know. You may be sampling the
lymph node if they have swollen lymph nodes. You may be sampling the
bone if it’s a suspected bone infection. You may be sampling the urine if you think they’ve got infection that might involve the genital urinary
tract or there are other body fluids that might be sampled. They go through the same testing procedure in the laboratory, but
it’s just a different kind of fluid. Voiceover: Okay, and then I guess, just to complete all
the possibilities here, what about someone who, you’re suspicious they may have TB based
on something clinical and then they actually
have a negative chest x-ray and a negative skin test? Voiceover: So, that’s also
an important circumstance to recognize because TB is still possible even though you’ve got
those two negatives. So a negative chest x-ray,
again, may simply be because their TB infection
is not involving the lungs, so it’s a negative chest x-ray and the negative skin test
may be a false negative skin test. They may, in fact, have TB, but either because the infection
is overwhelming them, including their immune
system, or because it’s very early on in the infection
and they haven’t converted, they may not have a positive test. So, you still, you can’t
rule out TB on the basis of both of those being negative and if you have a clinical scenario that still makes you
think of TB and perhaps they’re a very high risk host, such as, an immunodeficient host, for example, somebody infected with
HIV, you still may want to pursue diagnostic testing even under those circumstances. The two terms that I’d like to finish with and we haven’t spoken about
except when we talked about antimicrobial sensitivity
testing, or related to sensitivity testing. So, you check to see if the tuberculosis is killed by the different
drugs you want to use, such as, INH and rifampin and so forth and if the tuberculosis is
sensitive to all of those antibiotics, if it’s
killed by those antibiotics then you’re in good shape
in terms of treatment, but sometimes you will encounter strains and they’re becoming more
common, where the bugs are resistant to INH and rifampin. Voiceover: Oh, dear. Voiceover: And those are called MDR-TB and MDR stands for multiple drug resistant and then TB stands for tuberculosis. And by definition, MDR-TB are resistant, as I mentioned, to INH and rifampin. And then you have to use different drugs other than INH and rifampin to treat them. Another term that is
important to recognize with regards to TB diagnosis
in sensitivity testing is x, little xDR-TB. The x stands for extreme drug resistance, the DR, drug resistance
TB and these are strains that are becoming more common, especially in the
developing world, so they also are resistant to INH and rifampin, like MDR-TB, but they’re also resistant to several other anti-tuberculous agents. And it gets a little complicated, but I’m going to say it
because it’s important for people to know about these xDR-TB. They’re resistant to all
of the fluoroquinolones, which are a whole family of
antibiotics, the quinolones. So these xDR-TB are
resistant to all of those and they are resistant to one of, at least one of, the following three antibiotics that I’m going to mention. One antibiotic is amikacin. Another antibiotic is kanamycin. Both amikacin and kanamycin are so-called aminoglycosides. And then the third one that they may be resistant to is capreomycin. So, again, these xDR-TB
strains are resistant to INH and rifampin. They are resistant also
to the fluoroquinolones and they’re resistant to one of the three other drugs that is written. Voiceover: And that
sounds like a challenge for treatment. (laughing) Voiceover: Indeed it is
and we’ll come to that. Voiceover: Okay.