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Video transcript

hi I'm Charles prober and I'm Morgan theis and today we're going to talk about the pathophysiology of tuberculosis that is how tuberculosis makes people sick great so in this cartoon there is an infected individual shown on the left and that person is coughing or sneezing and all those little small white dots are particles coming out of the person's mouth and if this person and the person on the right is a non non suspecting individual who is susceptible to infection with TB now the person on the left when they cough if they have tuberculosis in their system then some of those bacilli will COFF out and enter the person they're coming into close contact with enter in the droplets and some portion of those infected droplets estimated to be about 10% go all the way down the susceptible individuals airway and land in the lung they have to be very very small to get to the most distal portion of the lung called the alveoli so they have to be around five or ten microns in diameter once those Vasili have entered the person's lung the host the person's immune system kicks in at the local level and the first part of the immune system to greet these bacilli are macrophages that line the lung Airways these macrophages take up the bacilli and within the macrophages the bacilli may reproduce that is increase in numbers the macrophage may then release the bacilli other macrophages will pick them up and eventually one has a number of cells in this distal part of the lung that are infected when these macrophages then come together and lung destruction occurs in the mixture of this they end up forming up particular kind of lesion in the lung called a granuloma so a granuloma which is often used in the context of TB infections it's also called a tuberculoma are a group of macrophages and other inflammatory cells that are the reaction to this TB infection once that granuloma becomes large enough for one to see so if a pathologist is looking at the lung that is called a Gaon focus G o HN of course named after somebody doctor going after the local infection in the macrophages occurs the granuloma has been formed if the infection is not controlled in that local site there is spillover of the infection to the regional lymph nodes so that the lymph nodes in the lung then those regional lymph nodes have an immune reaction and the regional lymph nodes plus the infected granuloma is referred to as a going complex' and this may be evident on a chest x-ray that a person has done either for routine basis or for whatever reason and a radiologist seen this will say oh this looks like a previous infection with tuberculosis and we'll show later an example both of a granuloma and a gong complex on radiographs so all of this infection the person who's now infected this is referred to as a primary infection the individual is infected with tuberculosis and for many individuals that's the end of the story the tuberculosis remains in what is referred to as a latent state and remains latent for the person's entire life without causing any problem and they actually get rid of the bacteria entirely so it's not clear if the bacteria are ever completely killed or not there is some evidence that in fact some do clear the bacteria but from a clinical standpoint one has to assume that once you've been infected with tuberculosis it's with you forever and may cause subsequent problems which speak about in a moment okay so so for 90% of people it's sort of the story ends there however that leaves 10% about half of that 10% so 5% their primary infection is progressive so they go on and they develop a problem shortly after they've been infected with tuberculosis that problem may be represented as local progression of the infection so that lung gone focus actually becomes larger and larger and end up with tuberculosis pneumonia so pulmonary disease caused by tuberculosis or they may go on even beyond that the infection may disseminate widely go to many organs in the body most especially the liver other parts of the lung or even into the brain and other organs so that's about 5% of the patients that go on to have local progression or dissemination one pattern that's been associated with this dissemination and it's not the only pattern is when the infection seeds multiple organs of the body with tiny little spots that are called millets because they're so tiny and this is referred to as miliary tuberculosis and that's most often recognized in the lungs where you see these little tiny spots all over the lungs so that's one form of disseminated infection so that's primary infection and that's 5% now an additional five to ten percent of patients emerge from the latent state of the infection and they developed so called secondary disease and so that represents a reactivation of a prior latent infection or a prior dormant infection and again it's estimated that about 5% of the total population who've been infected go on and have this reactivation disease now cannot have an any point during your life it can happen absolutely any point during your life either within several months of the infection or many many years later and that reactivation is referred to as as you've written secondary tuberculosis in contrast to primary infection this is secondary infection now the likelihood that somebody may reactivate is actually influenced by many factors including the immune state of the host that is if the host the person who's got latent TB has depressed immunity especially depressed cell-mediated immunity their likelihood of reactivating can be quite high relatively speaking and some of the immune factors that are most recognized as causing an increased chance of reactivation are co-infection with human immunodeficiency virus so that's a big one worldwide HIV another is if the individual has received a transplant or is receiving chemotherapy for some other reason for example cancer so the transplant we're actually giving them immunosuppressant medicine so they don't reject the transplant exactly that's in that risk of that knocks down their t-cells and then they have an increased risk and then patients who abuse drugs intravenously also are at an increased risk quite a substantial increased risk these groups together each of them are more than tenfold risk over the general population of reactivation there other host factors that also influence reactivation to a lesser extent they may have a 2 or 3 fold increased chance of reactivation compared to the general population and that would include patients who are malnourished they would include patients who have diabetes and even patients whose risk factor is only and I shouldn't say only perhaps with smoking so those can all increase the chance of tuberculosis emerging from its latent or dormant state and becoming reactivated and what's the increase for HIV transplant I read drug use probably about tenfold or at least tenfold some of them are actually it's not gonna be up to 70 fold that certainly greater than 10 fold so the final thing I'd like to say about secondary tuberculosis is that much of it results from reactivated disease but you can also have secondary tuberculosis because you get reinfected that means that it's not your own latent TB that's reactivated and cause secondary disease that you've been exposed to yet another person infected with tuberculosis and your secondary disease results from that reinfection that new exposure and then once you get that new exposure or the reactivation of your own latent TB then you can progress sort of down the same pathway of symptoms exactly you can have local progression as you've indicated or if you're severely depressed immunologically you may get more of the disseminated infection including a miliary pattern and so forth so just to end like to show the two promise pictures the picture that is all pink is a zoomed in microscopic view of a granuloma and there are a couple of features to point out first of all in the very middle of this granuloma is some very pink very homogeneous material that probably represents dead macrophages and other debris that have eventually been resorbed and formed this dense core sometimes that becomes calcified over time and that may show up on an x-ray such as x-ray picture we show here as a calcified spot a white spot in the lung we'll come back to that the other part of the granuloma to point out is this inflammatory reaction occurring around that dense middle and so all of the cells that are shown in the blue are lymphocytes and monocytes and macrophages and this is the reaction to the infection with the tubercle bacilli sometimes this actually becomes quite necrotic in the center it's not shown so much here and then it's referred to as KC ation because it becomes sort of cottage cheese like the other picture the picture of the x-ray shows the calcific granuloma and that would be again the original granuloma the goon and it also shows some swelling of the lymph nodes at the edge of the heart and so as previously mentioned this lymph node reaction along with that going focus together make up the Gaon complex and that is evidence radiographic evidence that this individual has been previously infected with tuberculosis latent ly infected at risk for subsequent reactivation