103: Spirochetes and TB – If these have you confused, let’s get it sorted it out

Hello and welcome to the Physician Assistant Exam Review Podcast, Season 2, Episode 103. We’re going to be talking about Mycobacterium and Spirochetes today. My name is Brian Wallace, the founder and creator here at Physician Assistant Exam Review, where we teach core medical content and how to dominate PA school and ultimately pass the PANCE. Those are not the same thing, by the way, right? Dominating PA school and medical content are two different subjects. And I’m seeing that more and more clearly as I work more with individual students and groups of students, how that affects their studies, how that affects their work, that there’s certainly a large portion of medical content that has to be learned. There’s absolutely no doubt about that.

There’s so much medicine to cover. But because of that, there are different techniques, methods, ways of learning and retaining that information. There are different techniques, ways and methods for getting that information to stick in your brain and then to get that information out of your brain and onto the paper. And like I said, as I’m working with more and more groups of PA students, I’m finding that there’s a lot of space in those skills that people can improve at. And really dramatically show how much medical knowledge they have. They’re just having trouble getting it out on the paper. One of the reasons I do this show is to teach the medical content, of course.

And we do that in such a way that I’m optimistic, I’m trying to, my plan anyway, is to get you to understand a little bit different ways of thinking, a little bit different methods for retaining the information, for going after it. Just reading your books after class is not going to be enough. You’ve got to do more. You’ve got to change the way you’re studying. You have to change the way you’re thinking, especially if you’re not getting the results that you’ve gotten before or the results that you would like to be getting. You’ve got to make some changes, right? And I hope that you see the way I present the information, the way I talk about the information.

There’s a specific style to it, a specific way I do it. Not to say that that’s the best way to do it, but for most of you, it’s a slightly different way of approaching the material than you’re used to. And I hope you have your eyes open and you’re looking out for some different ways to, again, one, get the information into your brain, and then two, get it out of your brain and onto the paper, and that you’re always testing these different methods. Anyway, let’s go on and get started with our priming questions for today. We wouldn’t want to hesitate in our approach to mycobacterium and spirochetes.

All right, question one. My question mentions dark field microscopy. What is the likely diagnosis? If you see dark field microscopy, what should you be thinking? What is the organism that causes Lyme disease? What is the organism that causes Lyme disease? What side effect should you look for with ethambutol?

What side effect should you be aware of if you prescribe ethambutol? Drenching night sweats is the hallmark of which disease? Drenching night sweats is the hallmark of which disease? And then here’s a tough one we’re going to go through today. Describe a Ranke complex. Describe a Ranke complex. We’ll get to that one in a little bit.

We’re going to start with spirochetes today. So number one is going to be, that’s going to be Lyme disease and syphilis are the two we’re going to focus on. So Lyme disease. Borrelia burgdorferi is the organism that causes Lyme disease, right? It’s transmitted by a deer tick. These are teeny tiny little pinhead size ticks. I don’t know if you’ve ever seen one, if you’ve ever seen pictures of one, if you’ve ever seeing pictures of the scale of the size of a deer tick.

I mean, they are incredibly small. I did pull one off my youngest son over the summer. He actually pointed it out after taking a shower. It’s like, dad, this seems kind of weird. And I looked at it and sure enough, it was a deer tick. This little thing was tiny. So they’re easily overlooked.

And that’s part of the problem. It takes between 36 and 48 hours to transfer the bacteria from the vector, from the deer tick into the human, right? That seems like a long time, but because they’re so small, they’re easily, I mean, this was on his belly. It was a little black dot and he still was easily missed. If it was in your hair or somewhere on your back, somewhere harder to see, you certainly would never, probably never would. Deer ticks, for those of you who don’t know, are found in high grass or wooded areas. Most of the cases for Lyme disease in the United States are in the Northeast from Maine to Virginia.

But Lyme disease has now been found all over the world and all over the country. Signs and symptoms. So at the site of the bite, it says early localized stage. And this is the part that everyone thinks about and looks for, right, is the erythema migrans. This is a bullseye rash that comes out about a week after the bite. And it usually grows. And you get that white, you get the red middle with a white ring and then a red outside of it.

That’s your bullseye rash. You can get a fever, malaise, and flu-like symptoms. You can get early disseminated disease, which takes a few weeks, muscle and joint pain, facial or Bell’s palsy, severe headaches and neck stiffness due to the inflammation of the spinal cord, pain and swelling in large joints. Usually this is the knees. You can get pericarditis and arrhythmias. You can get shooting pains. And then lastly, it can move into a late disseminated stage, and this is months out.

You can begin to develop significant arthritis. Again, this tends to be in the knees, but it’s in the larger joints. You can get polyneuropathy, numbness and tingling in the hands or feet, mood changes, memory loss, fatigue. And if left completely untreated, diseases can have significant cognitive and psychological manifestations. And most of them don’t progress to this point, right? Physical exam findings, again, that erythema migrans is going to be the thing that really points it out to you. This is a small red bump may appear at the site of the tick bite, which later the redness expands, forming a rash in a bullseye pattern with an outer ring surrounding a clear area.

That’s really going to be the significant finding out of the gate. You’re really going to want that evidence of the erythema migrans. So you may not get it, of course, but you’re going to want it. So the diagnosis here is going to be a lot based off of that clinical exam and the patient history. You’re looking for a history of possible tick exposure, right? So someone who has been outside, been out hiking, been out in an area or a place where there’s an increased risk for this, right? So if you get someone who is, presents in Arizona, there’s a low likelihood that they’re going to have Lyme disease.

Is it possible? And again, I have to say this caveat because I don’t want to get emails from people saying, you know, my cousin’s brother had Lyme disease and he lived in Arizona. It’s certainly possible, right? Could it be on your test? Again, possible, but I don’t see them doing that to you, right? I think they’re going to give you a person in Maine who’s been hiking, a person in New Hampshire who’s been hiking. Something along those lines is going to be a more obvious clue, and that’s likely the direction they’re going to go on your test.

But you want that erythema migrans and you want that history of someone who has exposure to a possible tick, right? Most people, like I said, won’t have a memory of the tick bite, won’t have pulled the tick off of them the way that we did. They’ll present with just that erythema migrans or just some fever-like symptoms, and then you can ask them about questions that might lead to if they had any exposure. And the reason that you want that information is because the blood tests aren’t fantastic. There are many cross-reaction issues with false positives, so a diagnosis needs to consist of history and physical and multiple lab results. So you can do an ELISA enzyme-linked immunosorbent assay, which will detect antibodies to Borrelia burgdorferi, but will get false negatives in the early stage of Lyme disease. And then you’re going to follow that up with a Western blot.

This will detect antibodies to several proteins from Borrelia burgdorferi. And you can also do a PCR, polymerase chain reaction. And this is most helpful if you’re testing joint fluid, if you’re looking for it specifically for arthritis. Treatment. Number one thing here is going to be prevention, right? We talked about how you get this. You get this from a deer tick.

So you get this from being out and exposed to this insect, which is the vector, right? So protective clothing, if you’re going to be out in an area that has a good population of ticks, I guess is the best way to say it. So protective clothing, some things that are light colored, you’re going to want long sleeves and long pants tucked into your socks, things like that. That will be physical barriers to the entry. And then use of insect repellent is also helpful.

Now, how do we treat this? Doxycycline is going to be the antibiotic of choice, but not in children or pregnant women. You’re going to want to use amoxicillin in those cases. And NSAIDs for pain. And at some point there was a vaccination, but that is no longer in production. So that was Lyme disease.

Now, what are you going to run into? So again, how is that question going to be written? How is that question going to come across to you on your exam? Right? Can you think about how you would write a question about a patient who walks in the door Lyme disease? Certainly, you’re going to need to know the treatment. You’re going to need to know amoxicillin’s first line and amoxicillin’s second line.

But what’s that presentation going to look like? What’s the story going to be?

Next, we have syphilis. Syphilis is a highly contagious sexually transmitted disease, including oral and anal sex, caused by the spirochete bacterium Treponema pallidum, subspecies pallidum. Males have this greater than females. Now there’s a couple different ways why syphilis is confusing to people and that’s kind of like Lyme disease. Patients have trouble clearing it, and then it goes into a couple different manifestations. So you get a primary disease, which is typically acquired by direct sexual contact with an infectious lesion of another person, and you wind up with lesions. We’ll get to that in just a second.

From there, you move into secondary syphilis, which occurs approximately 4 to 10 weeks after the primary infection. Then you move into latent syphilis, which is having a serological proof of infection without any symptoms. And lastly, tertiary disease, which thankfully has become pretty uncommon, occurs approximately 3 to 15 years after the initial infection. And then you can break that down into gummatous syphilis, late neurosyphilis, and cardiovascular syphilis. Those are your tertiary… So, if this hangs around a long time in the body, you can get a couple different manifestations. Gummatous syphilis is a slow growing inflammatory mass that destroys local tissue.

Neurosyphilis is obviously it affects the meninges and the brain. And cardiovascular syphilis is it affects the cardiovascular system. You can also get congenital syphilis, which is a transmission from the mother to the fetus during pregnancy.

All right. So, let’s break this down a little bit more clearly now. Primary. So, three days to three months after contact, you wind up with primary syphilis, which is the chancre scores, sores, lesions where the bacteria appear at the point of contact. You get a single, firm, usually painless, non itchy ulceration. It is a clean base and clear borders. Right.

So, that description is key. That’s the description you’re looking for, both in your patients and on your exams. A single, firm, painless, non itchy ulceration. It has a clean base and clear borders. You may also find lymph node enlargement in these patients. Secondary syphilis, of course, occurs four to ten weeks after primary syphilis. Right?

Makes sense. In this case, you get a symmetrical reddish pink rash on the trunk and extremities, including the palms and soles of the feet. It is a maculopapular rash that is usually painless and does not itch. So, again, I would use those to stick together in my head, saying that the initial ulcer is painless and not itchy, and now our rash is painless and not itchy. So I can put those together. The other thing obviously here is that including the palms and the soles is another indicator. Patients get fever, sore throat, malaise, weight loss, hair loss, and headache.

And again, I’ve talked about this before. All that’s helpful and colorful background, but lots of things cause fever and headache and malaise and those aren’t incredibly helpful. They tell you the person’s sick, right? But it’s that first ulcer for primary and then it’s this rash for secondary that really lock you in.

Now, what are you going to see in the latent phase of syphilis? Well, we said earlier in the name, in the latent phase, you’re not going to get any symptoms, but you may pick it up on routine screening. And for tertiary syphilis, I’m not really going to go deeper into that because there are multiple presentations and multiple effects for tertiary syphilis. I think that’s deeper than you probably need to go. I think you need to be aware there are neurological aspects, there are cardiology aspects, and to understand what gummatous syphilis is. But that’s about as far as I’m going to go down that road.

Now, how do you diagnose this? This is one of the questions I asked early. Dark field microscopy is the most sensitive diagnostic test, but technically difficult and not usually available. So if you see dark field microscopy, you would definitely be thinking syphilis. There are blood tests. There are basically two categories, treponemal and non-treponemal. Non-treponemal is positive at four to six weeks and during primary and secondary syphilis, but are negative during tertiary phase.

It’s good for screening, but not very specific. So these are a little bit cheaper, a little bit easier to do, but there may be cross-reactions and false positives. So you can do a VDRL, which is a venereal disease research laboratory, or rapid plasma reagin test, or RPR. Those are the non-treponemal blood tests. The treponemal blood tests detect antibodies and are very specific. So you can do a TPHA, which is a Treponema pallidum particle agglutination test, and that’s used after the VDRL to confirm positive results. There’s also the FTA-ABS, fluorescent treponemal antibody absorption test, similarly used after a positive VDRL or RPR to prove your results.

Once you get into tertiary syphilis, you can do things like lumbar puncture or joint aspiration or tissue biopsies to see what’s going on. Treatment, this should be a pretty easy one. And that is, it’s going to be benzathine penicillin G administered intramuscular single dose during the early stage of infection. It’s definitely something you should be aware of. That’s an easy one to get right and hopefully you nail it. You could also use doxycycline, tetracycline, or ceftriaxone if you need to. Two important parts to this, though, are sexual abstinence and treatment of all sexual partners.

Treatment of all sexual partners, that’s important. And syphilis needs to be reported to the CDC.

Now, one thing I wanted to stop and talk about before we move on to mycobacterium is a Jarisch-Herxheimer reaction. This applies to both syphilis and Lyme disease. And this is an immune response the materials released by the destruction of the spirochetes. So, you give antibiotics, and very soon after that, the patient gets worse. They get fevers, chills, muscle pain, headaches, and they look sicker. What’s happening is the destruction of the spirochetes is releasing antigens, and your immune system is going nuts. That’s called a Jarisch-Herxheimer reaction.

It typically resolves in 24 hours, and there’s no reason to stop treatment. It’s not a reaction to the antibiotic. It’s a reaction to the dying spirochetes. So definitely be aware of that.

Next, we have tuberculosis. So we’re going to move into our mycobacterium discussions. In this case, we’re going to talk about tuberculosis and atypical mycobacterial disease. The bulk of this is tuberculosis, though. Mycobacterium tuberculosis is a slow-growing bacteria. Mode of transmission is droplet and contact. And this is the part that’s interesting to me and the part that creates this story and this better picture for you of how TB works.

About 10% of people exposed will develop primary tuberculosis. 50% of those will go on to progressive tuberculosis. Right? So, although those numbers are very high, it’s not everybody, right? So, 10% of people exposed will develop a primary issue, and then 50% of those will clear it, clear that primary issue so they don’t have a problem, and 50% will go on to a progressive disease.

All right, I’m going to come at this from a few different angles. So, stick with me to the end, because there’s a few ways to talk about tuberculosis. So, one place to begin with is there’s active disease and there’s latent disease. Most people will move into a latent phase will never have had any symptoms. And in a latent phase, they’re not infectious. But here’s the problem. They can have a reactivation, especially in an immunocompromised state.

So, what happens is the tuberculosis moves in. Usually, it moves into the lungs. You get a focus of infection. And then a granuloma forms around that focus of infection within the lung. The granulomas are white blood cells attacking that focus of infection and walling it off. This is called a Ghon focus. It’s that walled off TB infection.

Your white blood cells are basically just packing in around it, making a sphere, and then closing it. These are caseating granulomas, which is a tough term for a lot of people, especially when we throw in a bunch of words like Ghon, Ranke, granuloma. Now we throw in caseating just to make a bunch of words you don’t recognize or understand. Caseating means it looks like cheese inside because what happens is that walled off area becomes necrotic and dies. So, you have this necrotic, gross, cheesy looking tissue inside of this thing. That’s why it’s called a caseating granuloma. So, let me back up for a second.

So, think about it. You get a TB infection. This material gets inhaled. It moves down into the lungs. You get a focus of infection.

Let’s just pretend the TB is built up this little area that it’s attacking from. Your white blood cells move in, surround it, wall it off. That’s called a granuloma, and this specific one is called a Ghon focus. This Ghon focus plus the hilar lymph node right next to it having the same issue is called a Ghon complex. So, you can picture that some of the material from that TB focus has moved into the lymph nodes because it’s been carried over that direction. So now we surround that lymph node and wall that off. That’s called a Ghon complex.

Now, let’s pretend that your immune system wins the war. You have this caseating granuloma, this walled-off area, small area of your lung, and this walled-off lymph node. Your immune system wins, and it clears the TB. Right? That’s what we said, and about 10% of people exposed will develop primary TB, but only 50% will go on to progressive issues. So that’s a good chunk of people who are going to solve their own problem with their immune system walling off and creating this granuloma, this caseating granuloma, called a Ghon complex. But what happens to that tissue after the infection?

Well, it’s kind of thick and gross and necrotic, right? So it doesn’t reabsorb well. What happens is it gets fibrotic and calcified. That calcified Ghon-Ranke, I’m sorry, Ghon complex is called a Ranke complex. And you can see that on x-ray. So it’s evidence of a previous TB infection. So I hope that story helps a little bit.

I know it was super confusing for me when I was in school. I didn’t spend a lot of time on this particular idea. But that’s all it is. It’s a way to look at an x-ray and see something that’ll say, whoa, that looks very distinct and looks a lot like this person has had TB. So the Ranke complex is just that fibrotic calcified Ghon complex after the body has walled off and tried to destroy that TB focus within the lung.

Okay, so it’s also possible that you can get infections outside of the lung. Because if that primary is not, if you don’t successfully clear it, well, then the infection can spread. It can spread into the pleura. It can spread into the central nervous system and the meninges. It can spread to the lymphatic system. It can spread to the genitourinary system. Pott’s disease is TB in the spine.

And it can move to other bones and joints. You can get abscesses through the skin and then you can get disseminated TB or miliary tuberculosis. That seems to be the one that I’ve seen the most questions on, but that doesn’t, I don’t know what value that has, but it’s what I’ve seen. So those are extra pulmonary tuberculosis infections.

Okay, so again, and I told you this would take a little while to go back and forth on. So hopefully you can kind of see where you can get a primary infection, a latent infection, where you get that system where you’ve walled off the focus of TB, but you haven’t actually cleared it. But it’s not really doing any damage. It’s just kind of hanging out there. I like to think of it sort of like varicella, sort of like chickenpox and shingles, right? Because what happens is your immune system fights off the chickenpox and the varicella virus. And it does a good job.

But it doesn’t completely clear it. That virus still lives inside your body. Waiting for a time when your immune system is weak to then begin the attack again and fight back. That’s kind of what happens here with latent TB. Latent TB is walled off. And you get this granuloma, but it doesn’t completely clear it. So it’s just sitting there doing nothing.

Your immune system is fighting it off and doing a fine job and really has little effect on you. No symptoms, no real issues. The problem becomes if you become immunocompromised or become, for some reason, your immune system is weakened, even just as you get older, this can become a bigger problem because you start to lose that fight.

All right, let’s talk about the clinical presentation, the way people look when they come in with a TB infection. So it’s a cough with thick, cloudy, bloody sputum for more than two weeks. That blood in the sputum should be a good indicator, right? That’s one that should kind of throw up some red flags that points you towards TB. You also can get shortness of breath, chest pain, and then drenching night sweats is the other one that should definitely stand out to you. Bloody sputum with drenching night sweats should make you think TB on any exam or in any clinical exam. Fatigue, fatigue is a big one.

Generalized weakness, loss of appetite is a big one, unexplained weight loss, and you can get nail clubbing. But to me, it’s the unexplained weight loss, the drenching night sweats, and the bloody sputum. Those are the three that would ring this. If I’m writing a question, I’m going to include at least two of those three, but probably three of those three. Physical exam findings, apical post-tussive rales, and the look of chronic illness and weight loss. So these people will have characteristic changes in the way that they look.

All right, the diagnosis gets a little funny with this as well. Because it’s such a slow-growing organisms, right? That makes it so you can culture it, but it takes six to eight weeks to provide results. So that’s kind of helpful. It’s helpful for proof and helpful to make sure you’re on the right treatment plan, but it’s not helpful the day the patient walks into your door and you have to decide what to do with them. So most of you have had the purified protein derivative skin test, right? The PPD.

This does not differentiate between active infection and latent infection. And this is where they put that protein underneath your skin and then read it at 48 to 72 hours after the initial injection. And the positive test is based on the size of the induration. Right? The based on the size of how, basically how big and red it gets outside from where you were injected. And it shows your body have an immune reaction to those proteins at the site of the inoculation. These numbers are worth knowing because it’s so easy to write a test question on.

It’s something that I’ve seen come up. So if a person has no risk factors whatsoever for TB, and you do this test on them, the redness and swelling have to be greater than 15 millimeters for a positive test. That’s a lot, right? One and a half centimeters, 15 millimeters. Medium risk factors. So people who have traveled from area high in TB, injection drug users, healthcare workers, patients with diabetes or renal failure, they’re at medium risk, and the induration then needs to be greater than 10 millimeters. Now what would put you in a high-risk category?

High risk for TB. Any immunosuppressants, HIV, or evidence of TB on a chest x-ray. That would throw you into the high-risk category, and then anything greater than 5 millimeters you’d want to be thinking like, okay, it looks like this person probably has it. Right? It’s not clear cut. And I know everyone likes things that are really clear cut, yes or no. But that’s kind of how this works.

If a person has a lot of risk factors and they’re high risk, then a small reaction becomes an important indicator. If they have zero risk factors, you’re going to want a pretty big reaction to make you think that it’s an issue. So there are some other tests out there. There’s an interferon gamma release assay, IGRA. The nice thing about this is it’s a blood test, so it doesn’t need to be checked again. It’s just blood work. So there’s no follow-up, which is huge.

It’s also more specific to TB, so it does not give a false positive with the TB vaccination, which is not used in this country, but is used in a lot of places around the world. You know, I’ve talked about this before. There was a student from Ghana in our class, and she had had the TB vaccine. So everywhere she went, her PPD came out positive, right? It’s frustrating. So this test doesn’t cause that. The problem is it’s expensive and harder to get.

So that’s the drawback. All right. So, a definitive diagnosis, like I said before, could be sputum with acid fast bacilli. The problem is that takes 6 to 8 weeks to get your results. You could also do a DNA or RNA amplification test and get results a little bit faster in a couple of days. Chest x-ray you may see those nodular infiltrates, hilar and tracheal lymph node enlargement, and then the Ranke complex as I talked about before. Do you remember what those were?

I know that was just a minute ago. If you remember, that was one of our priming questions was what’s a Ranke complex? You know, it’s going to come up again at the end of the show. Another way to test for this is the biopsy of the caseating granuloma. And then it’s going to be different for all the extra pulmonary tuberculosis diagnoses, right? So you may do a biopsy. You may do a urine culture.

You may do a lumbar puncture. A CT scan may be valuable. An MRI may be valuable. Depends on where you’re looking and what you’re trying to accomplish.

Now, unfortunately, the treatments don’t get any more clear. TB is a little tough to understand, and then they make it harder by throwing in different treatments, right? But if you understand, to me, it’s always about that base, that understanding the principle, the story, the way it sounds, the way it presents, the way the bacteria affects your body, that makes all of this easier. So if you can hold on to that picture of breathing in those droplets, having them plant and create a small little fortress inside your lungs, and then that fortress becomes under attack, and we call that a granuloma, a walled-off granuloma, and then the material inside either lives or dies, but is walled off. And then it moves from there.

All right. So there’s a couple of different medications. We can, a bunch of different medications we use to treat this because one, it’s difficult to treat. And two, there’s concern about antibiotic resistance, significant concern about antibiotic resistance. And we’re not going to go into it here, but in different areas, different bugs are resistant to different antibiotics. So you have to consider that depending on what area you are working in, living in. So the standard treatment begins with an intensive two months of four antibiotics.

Isoniazid, INH, rifampin, RIF, ethambutol, EMB, and pyrazinamide, PZA. So that’s two months for antibiotics. This is followed by another two to seven months of INH and RIF. So isoniazid and rifampin, in most cases, they usually drop the other two after the first two months. That two to seven months depends on how the cultures come back, how the patient is, if they’re doing better, if they’re doing worse, all of those other factors come into play. Maybe we want to keep more antibiotics on board. Maybe we can drop down to those two, but that’s the standard decision-making point.

Another key with tuberculosis treatment is called directly observed therapy, which means someone monitors the patient taking the medications. The medications have some significant side effects and are not pleasant to take. The problem is if you take if you don’t take them correctly, right we push these bacteria into becoming drug resistant. And that’s obvious for obvious problems and for reasons I’m not going to here, but a TB tends to be one that they look for someone to monitor that medication intake. It’s also a long course, right? Two to seven months of taking this is hard for people. So, that also helps there.

Now some side effects you need to know about. Isoniazid can have peripheral neuropathy. B6 can help to reduce that. Rifampin can cause hepatitis, flu-like symptoms, and orange body fluid. That’s a good one, right? Easy to ask a test question on. Orange body fluid, meaning urine.

Ethambutol can cause optic neuritis and a red-green vision loss. Again, that’s an easy one just to link that one together, ethambutol optic neuritis. I would definitely know those side effects. And I would go back through, because these are funny names, they’re hard to remember, but it’s really not that difficult. Like I said, it’s four antibiotics that you should know for this. You treat with all four for the first two months, then you drop off the last two after that most likely. And then know the side effects.

All right, not to worry. We’re moving on to atypical mycobacterial disease. And this is a little bit more, excuse me, a little bit more, I don’t want to say straightforward, but I think there’s a little bit, there’s definitely less to know than what you needed for tuberculosis. So this is also known as non-tuberculosis mycobacteria, NTM. The most common organism is mycobacterium avium. I think the number I came across was there’s 170 different organisms in this class. So knowing all of them and knowing the details behind all of them seems insane.

We’re not going to do that. We’re going to do a very high overview of this. So patients can have an increased risk of developing problems with atypical mycobacterial bacterium if they have things that will put them, they’ll have an increased risk if they have things that put them at risk. That’s a great sentence, Bri.

All right. Things like cystic fibrosis or immune compromise, longstanding lung issues that will cause a problem with clearing immune issues within the lungs, and then immune compromise can do, can, will increase their risk here. The most common is a pulmonary disease. You can also get lymphadenitis with this, and then skin and soft tissue disease. So, three different presentations. Again, the pulmonary disease is the most common. Your clinical presentation would be things like cough, weight loss, coughing up blood or mucus.

So again, kind of like TB, weakness or fatigue, fever and chills, night sweats, lack of appetite and weight loss. So, it’s hard to differentiate based on that from TB, right? Lymphadenopathy. You can get cervical and submandibular lymphadenopathies. Diagnosis is a sputum culture or a tissue culture, depending on what we’re looking at. Again, we know that the cultures are going to be a little tough. You can do PCR and a chest x-ray looking for radiographic findings that may indicate this disease.

Treatment here is also going to be tough, right? It depends on the tissue being affected. But you’re going to use things like clarithromycin, azithromycin for lung infections. For your lymphadenitis, you’re going to do an excisional biopsy that usually tends to be curative. And for a cutaneous infection, they recommend doxycycline or there’s a couple different cutaneous infections that are possible. And again, I don’t want to go too far down that road, doxycycline or for the other one, it was rifampin with streptomycin. But again, I think you want to be careful how far you take that path.

You can certainly keep going. I am not, I’m not going to here. I don’t think as far as your PANCE is concerned, it’s not something I personally would spend more time on.

All right. Well, that was a long one, right? So I don’t want to, what am I?

All right. So this is a little longer than I was expecting, but we’ll skip the study skills section for today. I think I talked a little bit about that at the beginning, regardless, about having different approaches, different ideas, different seeing things differently, seeing how other people study, seeing how other people take tests, which isn’t as easy. We’ve been covering a lot of that in the 33 Days program. And I think it’s been a world of difference for some people who don’t realize what’s out there. So that’ll be our study tip for today.

All right. Let’s get into answering our priming questions. A question mentions dark field microscopy. What is the likely diagnosis? Hopefully you’ve nailed that one. Syphilis. What is the organism that causes Lyme disease all the way back at the beginning?

Borrelia burgdorferi. What side effects should you look for with ethambutol? We just did this. What side effects should you look for with ethambutol? Optic neuritis. Drenching night sweats is the hallmark of which disease? Tuberculosis.

All right, now here’s a tough one. Describe a Ranke complex. Don’t wait for me to do it. You do it right now. Stop and think. Describe and picture a Ranke complex. I’m going to give you a few seconds to do that.

All right, so remember, a Ghon focus is a granuloma formed around that active TB. They’re caseating, meaning they just look like dead cheese inside, rotten cheese, because they’re necrotic inside. The Ghon focus plus that nearby lymph node with the same issue going on is called a Ghon complex. Over time, that complex gets fibrotic and calcified. And we call that a Ranke complex. Hopefully you nailed that. You have a solid understanding of tuberculosis and you’re feeling good about moving forward.

All right, excellent work. This is a long one, but this can be a tough one to get your head around a lot of these. You may want to listen to it a couple of times. I think that probably makes sense. Until you have a real clear picture of how TB works, how spirochetes work, how all that stuff functions, what it looks like, what that picture is in your mind, so it stays longer. Don’t just memorize the lists, right? Hold that image in your mind, tell the stories, understand how it comes across.

We’re much better remembering stories than we are remembering lists.

All right, if you haven’t done so yet and you get a lot of information out of this and you’re enjoying the content, please go over to the website, physicianassistantexamreview.com. Sign up for the email list. I put out daily emails with solid information to help you get through PA school, help you get through your PANCE. I email a lot of methods, a lot of my methods, a lot of the ways I do things. It’s constant contact there. So please go over and hop on that if you haven’t. Also, I am running a November cohort for the 33 Days to Pass Your PANCE program.

I had not expected to be doing a November cohort. I had two planned for this year and three planned for this year. And those went so well. I was actually blown away by the April cohort, by the June cohort. I haven’t gotten results back for the September cohort yet. We just wrapped up on October 3rd. So I haven’t heard a whole lot of test results yet, although I do have a lot of people who feel like they’re in a great, great position.

But the results have been spectacular, quite, you know, to be perfectly honest, they’ve just blown me out of the water. And I’ve had a lot of people reaching out to me saying, hey, I failed. Hey, I’m struggling here. Hey, I’ve been in school and my grades have been okay, but I’m a little worried about my PANCE. And because I’ve had so many people reaching out and we’ve had such great success and the students have gone on to do really well, I decided to open up a cohort for November. So if you’re interested in that, definitely get on the email list to get more information. The place to register is physicianassistantexamreview.com/33, just the number’s 33.

And that will give you some information on the program, but it’s not as thorough as you’re going to get from being on the emails and seeing exactly what we do inside of that program. And I think you’re going to be blown away if you decide to join us in there for the November cohort. I will be offering those more in 2023. So if your test is, I probably won’t be offering one before February. So if your test is December or January, then this is definitely the time to get on board. I, as of right now, I have plans to offer one in February. I don’t know if that’ll happen or not, or if I’ll push it back to March.

I’m going to make those decisions pretty soon. But as of right now, if you have your test in December or January and you want to do everything you possibly can to get through this thing, then I would love to see you inside the 33 Days program.

All right. I’m going to wrap it up there for today. Thank you so much for being a part of the community. Thank you so much for sharing the show for sharing all the things we do here. I really do appreciate that because that’s how people find out about this. I don’t do any advertising, right? That’s all just word of mouth from you telling other people that you found a great resource and it was really helpful for you.

So I appreciate that. And I’m hoping you continue to do that. Thank you so much. Take care. Have a great week. Thank you.