Well, folks, this is Dr. Steve McLaughlin, Dr. Zuku, and we're back at HootCamp, and I'm going to do the thing where we talk a little bit about what our topics are today. Then we're going to do a little warm up. You may remember from the first session, we promised that each new session will have a warm up based on the last topic. So what was our last topic that we had on session one? It was a bovine thing. There it is, yeah, LDAs. Good job. 

So, we're going to start with a warmup. We'll be hearing from Dr. Brock about the small ruminant classic case. I'll be talking soon about your next study strategy topic, which is no zebras. And we'll learn what that is in just a minute. And don't forget at the end of every session, we always have a low stakes quiz on the topic of the day. So there will be a low stakes quiz on some of the basic things we heard today from Dr. Brock. Finally at the end, I'll give you a super short assignment, something you can work on in the coming week. 

The warm-ups, why do we do these? Why are we going back to something we did in the previous session? The whole purpose of Hoot Camp is to model the learning process and to model for you what we want you to try to do as a habit when you do your own studies for the NAVLE®. So the idea here is we'll cover a topic, we'll give you some questions on it and then you'll see it again in a few days when we do the warmup session, okay? This idea of pulling answers from recent memory, that's the foundation of learning and reinforcing what you're trying to get to stick in your head. That retrieval practice is the fundamental building block of improving your understanding of clinical medicine. 

So here's our first warmup question based on last Sunday's topic. You diagnose a recently fresh dairy cow with a simple left displaced abomasum, which choice is the most appropriate initial treatment option. Emergency surgery to prevent shock, oral calcium, transfaunation and gastric stimulants, immediate IV hypertonic saline and dextrose, treat the concurrent diseases first, or E, a standing right paralumbar fossa omentopexy. So take a few minutes and see what you think of that. And if you feel like it, feel free to put your answers in chat. I'm going to check out the chat room. How are we doing? Okay, people are all over this one. Excellent. Okay, and the answer is, B. So what you want to go for is oral calcium, transfaunation and gastric stimulants, okay, as an initial treatment. It's not the ultimate treatment, but it's where you start. 

Question two, which of the following diagnostic findings is most suggestive of a displaced abomasum in a recently fresh dairy cow? Hyperchloremic, hyperkalemic, metabolic acidosis with ketosis. Severe ketoneuria on urine dipstick. A high-pitched ping between the left elbow and the tuber coxae at ribs 9 and 13. Bradycardia and rumen hypomotility. And finally a firm mass palpated in the left paralumbar fossa. So take a moment have a look at that. If you know the answer you pick it. If your not sure, hide the choices you think are wrong, narrow it down to two and take a guess. And our answer is C. A high-pitched ping between the left elbow and the tuber coxae, that's the hip, at the ribs nine through 13. So you draw a line between that elbow on the left side and the hip bone on the left side, put your stethoscope there and whack with your finger and you should hear a high- pitched ping if you've got a bona fide LDA. 

Which management practice is effective in reducing the incidence of displaced abomasum in a dairy herd? So we want a management practice here. It's common on NAVLE® questions where they give you a presentation of some kind and they ask you to make a mental leap. What are we gonna do to manage? Increasing the calcium content of the lactating cow ration. Feeding high-energy rations immediately following post-calving. Restricting access to forage pre-partum. Balanced prepartum nutrition to minimize negative energy balance. Administering oral electrolytes during the dry period to increase the dietary cation-anion difference. All right. All right, lots of answers flowing in here. This is excellent to see. Good job. So what are we going to do if we're going to prevent this kind of on a herd-wide level? When I clicked the button, it didn't change color. Bear with me. There it is. D, balance pre-partum nutrition to minimize negative energy balance. Do you see the connection between this disease and the disease that we're going to cover tonight? Think about it, okay? Pregnancy toxemia. 

Finally, question four, this should be familiar to you now. High producing dairy cow, freshened three weeks ago. Today they're off feed. On physical, her heart and respiratory rates are within normal limits. Here's your TPR. Remember on the real NAVLE®, you will get the normal values given to you if they give you the TPR or the blood work. There's decreased rumen motility and a urine ketone test. Uh, urine test for ketone bodies is positive. So she's ketotic, which you would expect with off feed. There's no evidence of mastitis and uterus is clear of infection. On the left side, there's a high pitch musical ping that you can hear via stethoscope during percussion over the ribs between the line between the elbow and tuber coxae, what acid base abnormality is most like. By now, this hopefully is familiar. Does the acid-base abnormality depend on the degree of displacement? Is the acid-base abnormality respiratory acidosis? Is it respiratory alkalosis? Is it metabolic acidosis? Or is it metabolic alkalosis. What's your choice? So if you've attended the first class, this is now the third time you will have seen this question. And if it feels easy to you, that's because we're trying to model how repetition can help you get things to stick in your head, okay? That plus understanding. And the answer is, I see it, people are definitely getting this one. It's metabolic alkalosis. Remember that this is the true glandular stomach of the cow, the abomasum, but it's twisted up. And so it's sequestering all that hydrochloric acid on the inside away from the rest of the body and the body responds with a metabolic alkalosis. 

Great. So, hello everyone and welcome back if you were here on Sunday to talk about cows. Today we're going to talk to us about the littler versions of cows, small ruminants, sheep and goats predominantly. So we're gonna dive right in here. 

So here's our case. In these short little tidbits, we're always going to start with a case. Um, and so here we go. As always, you know, a good veterinarian, the very first thing you're gonna do is take a great history. So our history for this case is this is a three-year-old Dorper ewe who presents, she's 142 days pregnant and she's a member of a 50 ewe flock. So this is not like a backyard just has three sheep operation. This is a commercial sheep operation that has quite a few ewes and lambs out pretty frequently. She was diagnosed pregnant at 50 days gestation with a chemical pregnancy test. She has had progressive lethargy over the last three days. So her energy has been tanking just sort of seeming dopey and separated from the herd over the last three days and the owner notes that she's also been selectively anorexic specifically for grain. No interest in eating her grain will sort of nibble at hay. The farmer client recently moved a whole bunch of pregnant ewes to a new pen on the farm, sort of shuffled a whole bunch of different ewes into a new grouping and moved them to another pasture on the facility. And she is currently being fed a pregnant ewe grain mix and free choice hay. So in theory, good nutrition. 

We do our examination and find that she has a body condition score of five out of five. So she's a chunky monkey. She is depressed, so pretty lethargic and kind of just not really with it like you would expect a ewe to be. Usually they're very prey species and so they would be ready to run away from you and she's just sort of looking at you giving the side eye. She's pretty dehydrated, about 8% dehydrated and she's grinding her teeth in this sort of unpleasant way. And you notice that when she's laying down, she has sort of that opisthotonos, kind of turned neck position when she's laying down when you're not bothering her. So what is your top differential diagnosis? I'm gonna open up my chat box here. Let's hear it. Write it into the chat. What do you think is going on? If you did your homework from Dr. Steve then you already know what's going on. Yeah, so wicked good. Yeah, you guys are crushing this, folks. You're crushing this. Pregnancy toxemia, hypocalcemia, definitely both high on your differential list at this point. 

So pregnancy toxemia. Late stage, pregnant animal that won't get up and is dumpy, pregnancy toxemia is top of your list. So, what is pregnancy toxemia? Essentially, it's simply ketosis, simply, not good for the sheep, but simply ketoses and hepatic lipidosis that happens in late gestation. So what happens? Most of the fetal development, so most of the fetal growth happens in the last trimester. And so if you imagine, there's a lot of glucose demand to grow a fetus inside the womb in the last trimester of gestation. So the liver increases gluconeogenesis during this time and starts to mobilize fat stores to help with glucose demand. However, that combination of effects of increased gluconeogensis and mobilization of fat stores can sometimes overwhelm the capacity of the liver to actually convert fat to glucose. The result of that is fat deposition inside the liver, hepatic lipidosis. And when you have that fat that deposits in the liver it basically screws up the liver function and overwhelms its capacity. This can coincide with inadequate nutrition. So if we're not feeding pregnant ewes appropriately they're more prone to this disease. Why is it so bad? To some extent, what happens is they end up with a hypoglycemic encephalopathy. So their brain is not getting enough sugar, and they become more comatose as the condition worsens. It is more common in sheep, but it can occur in does. So when you're sitting there for boards, if the question is a sheep, late pregnancy, weird symptoms, you're definitely going to think pregnancy toxemia. If it was doe's, oftentimes they get this disease postpartum. Um, so it'd be a little tiny bit lower, pregnancy toxemia would be a little bit lower on my differential list if it was a goat. 

Okay. So what do they look like, right? Classic case, late gestation, last one to three weeks of gestation for sure. The does or the ewes and does can be either over conditioned or under conditioned. So they can be like a one out of five body condition or a five out of five. They're never going to be a three. So what is the pathology here? Why can they be thin or fat? If they're thin, then they're thin for a reason. Either they're not being fed appropriately, they have bad teeth, they have some other underlying disease condition that's making them not eat, and they end up in this hepatic lipidosis because they're literally just don't have enough groceries to make glucose for the babies. If they are over-conditioned, They often have a decreased appetite because the uterus is taking up so much room in the abdomen that you have decreased rumen fill. They have just less room to eat. And then they will also mobilize more fat if they're heavier, if they are a bigger body condition. They also are sometimes insulin resistant when they're over conditioned. What are they, multiple fetuses is the other key indicator. So if you know for sure that the ewe is carrying more than one fetus, again, it's gonna drive the risk for this condition. Again, that's just because more babies, more glucose demand. They will present with partial anorexia. So they go off grain first. They'll sometimes still be nibbling at hay, but they will not eat grain. They'll be depressed and they'll separate themselves from the flock. Any sick sheep is going to separate herself from the flock. They will grind their teeth and drool. There's some evidence to suggest that this condition is painful, and we think that that's probably why those two things happen. As the condition progresses, it will go to pacing, sort of wandering around aimlessly, muscle tremors in the face that you can sometimes see and that twisted neck condition. The last stages, obviously the worst stages, they'll have central blindness, they'll be ataxic, they will not get up, they will go into a coma and die. 

Okay, so let's go back to our case. How are we going to diagnose pregnancy toxemia in our case ewe? So obviously the clinical signs, anytime we're doing large animal medicine, clinical signs is one of our diagnostic clues because we don't have a lot of diagnostic tools available to us. So relevant blood work in this case, we can just do blood or urine ketones. So blood BHBA or urine ketones will be indicative of ketosis, obviously. So in this case, our blood BHBA is elevated, 2.5 millimoles per deciliter, normal is less than one. We could also run chemistry and we did in this case she was hypoglycemic. Just on the border of being hypocalcemic, about 20% of these guys will be hypocalcemic as well. Hypokalemic, and this is simply usually due to inappetite. So any ruminant that stops eating will be low in potassium. And then her wonky liver values, right? So AST and GGT are through the roof and that's because this is what the liver looks like. Sorry, this is what the liver looks like over here. These big, huge vacuoles of fat that have been deposited inside the hepatic plates and are screwing up the function of the liver. 

Again, just to think about diagnostics here, ketone meters are really helpful. We can detect that elevated BHBA in the blood or in urine. Urine is sometimes easier in small ruminants to get than a blood sample. Hypoglycemia is a less reliable measure. They can actually be normoglycemic. And so it's not always as indicative as just measuring the ketones in the blood. The level of hypoglycemia doesn't necessarily correlate to the severity of the disease either. So, you know, they can be normoglycemic and still really sick. Let's see, hypocalcemic, that's always worthwhile to check because if they're low in calcium, then that's going to continue to be a problem. Often times if they're not eating appropriately, they can be low in calcium as well, and we would want to correct that. Hypomagnesemia, same difference if not eating correctly. You can measure NIFAs. I was trying to think if they would ask you that on a board question, exam question. It's not commonly done. It certainly wouldn't be asked in a clinical case because it would take two weeks to get back, and by that point the sheep would be dead. You can measure NIFAs and they would likely be elevated because of the hepatic lipidosis, but ketosis is just as good a measure. 

All right, so how did we treat this lovely sheep? Here I am in my lovely Boston Red Sox hat treating the sheep. We penned her separately, so separated her from the herd, but she's still with an eyesight of the flock. And the reason for this is we want her to have all of the access to the feed that she wants. We want her have zero competition for feed. But we want to not stress her out so that she can still see her flock mates, but she's got kind of her own space to live in. Access to super highly palatable feed, anything that we think that is gonna be tasty for her, the best thing, obviously, we want her to do is eat. And then in this case, we started oral propylene glycol twice a day for five days. We also gave her a little hit of calcium sub-Q once and that was because her ionized calcium levels were just on the touch of low, but not like scary low. And then we drenched her with some oral electrolytes because of that dehydration, provided flunixin meglumine, a couple doses of that because of the teeth grinding that we saw and because we presume that this condition is painful. And then she was starting to show some improvement, but was close enough to gestation that we decided to induce labor at 146 days of gestation. We induced with dexamethasone and delivered two very large stillborn ram lambs. The ewe did make a full recovery. 

Okay, so let's talk about what we did for treatment here. What are we gonna do to treat the ewe? Obviously the goal is to get her body to start making glucose again. So the ways in which we do that is to get her to eat. So providing something that's tasty is first and foremost a great idea. Propolyne glycol is a glucose precursor in the rumen. So it's an opportunity to provide a substrate for which the rumen microbes can turn that into VFAs and then the liver will then turn it into glucose. The downside of propylene glycol is that it's, well, for you all as veterinarians, it's messy to give. And for the sheep's perspective, it not tasty. So we want her to eat and we're giving her something that kind of makes her not want to eat because it doesn't taste good. So we have to be a little bit cautious in how frequently we give this. It can also damage the rumen microflora if we give too much too often. Calcium is one of those plus or minus. It's probably not wrong to give these guys a little hit of either sub-Q or oral calcium, because again, they're often hypocalcemic. There does seem to be some evidence in the literature that NSAIDs are helpful and improve the viability not only of the ewe, but also the lambs or kids. And so I think that that's pretty safe and warranted in these cases. And then oral fluids as needed to help with dehydration. There's debate in the small ruminant world about whether or not we try to get the fetuses out, right? Because the reason this is happening is because the fetal demand for glucose is so high and she can't meet that demand. And so there's a logical thought of, well, let's get the babies out. The problem is that if we are trying to induce labor too far away from the gestation date, the viability of those offspring is pretty low. And the part of the problem is that as the liver becomes damaged, her body stops making glucose, the fetuses wind up dying, and she subsequently gets enderotoxic septicemia from those dead fetuses. And so we certainly don't want to put her through a cesarean section if she's already on the way to being septic and has dead fetuses inside. So it's, I don't know, it's one of those catch-22s. I'm not sure that there's a right answer on a board's question. If there is a board question about trying to get fetuses out, the things, the nuggets that I would tell you to think about is, did they say it's a valuable ewe? Did they use that language? Like, this is a show animal. It's a really important, a really valuable animal that we want to make sure she survives. Are the fetuses alive? Do we have evidence on like Doppler ultrasound that the fetus are living and are we within three days of the due date? In those cases, then a cesarean section might be warranted. If the fetusses are dead or the ewe is further away from the end of her gestation, you could consider inducing with steroids. Remember that sheep are non-CL dependent species. So you can't just give them prostaglandin to induce them. You have to give them dexamethasone. Inducing them could, again, help her kick the babies out and help her recover quicker from the pregnancy toxemia. 

Okay, so what's the outcome of these guys? If you catch them quick and they're still ambulatory, the prognosis is pretty good with just the supportive care. You can usually nurse them through this period of, oh crap, there's not enough glucose and get them to deliver their babies in a normal, a normal gestation, a normal window. If the animals recumbent by the time you start treatment, the progosis worsens. So the worse the, obviously clinical signs, the worse the prognosis. The fatality rate for this disease can be upwards of about 40%. So you definitely want to warn owners that there's a risk for that, regardless of what you do, the sheep might die. Lots of great tips for prevention and lots of great fodder for NAVLE® questions like how would you prevent pregnancy toxemia? First and foremost, we wanna maintain ewes in the appropriate body condition score. So that's 2.5 to 3.5 right in the middle is appropriate. We don't want them too skinny and we don't want them too fat. Definitely monitor for concurrent disease. So anything that is gonna make her go off feed is gonna be a problem and that can include deworming. So we think about nematodes and trematodes. We probably wanna do some fecal eggs counts and things like that during gestation to make sure that her worm burden isn't too high and that that could impact the amount of glucose she can make for those babies. Nutrition, obviously, I think that probably goes without saying. When we think about good feeding management, that's gonna include adequate space at your feeders, grouping by gestation. By gestation size, so you've got all of your late stage gestation sheep in one pen, for example. You could group based on size, based on age, based on body conditions score, so that you make sure that you're feeding appropriate rations to each individual population of animals. You maybe didn't catch this little nugget in the history, but this herd had done pregnancy detection through a chemical pregnancy test, which just gives you a yes, she's pregnant, or no, she is not. It doesn't tell you how many offspring the ewe is carrying. So ultrasound is helpful in managing for this disease because if you do ultrasound at a young enough gestation, you can count fetuses and then you can know that she's carrying twins or triplets and manage her appropriately. You can also do a screening of the flock, BHB levels. So you can actually start taking blood BHB, you know, within the last two weeks of gestation if you had a big flock to monitor for subclinical ketosis that's happening and that way you can catch it quicker and treat it sooner before it gets to be an issue. 

Okay, to sum up, I think I talked really fast. That's the problem of me giving a talk at eight o'clock at night. Summing up, right? Inadequate nutrition in late gestation results in hepatic lipidosis and ketosis in the ewe, okay? We diagnose this disease with clinical signs and just a BHB, blood BHB or urine ketones. Super simple. Treatment. Propylene glycol, give them a glucose precursor, something that the body can make glucose out of quickly and easily. Prevent with good feeding and appropriate body condition score. This is a disease of body condition score badness. Okay, so just keep that in your mind. Outcome is pretty good if we catch it early and they've got mild clinical signs, it worsens the worse the clinical signs become. Interestingly, a ewe can have this disease in one pregnancy and be completely fine in the next one. So it really has to do with what is her body condition score, what other concurrent diseases she has, what is she being fed right now, how many fetuses is she carrying? This is a incidental disease based on each individual pregnancy. And I think that is it. This is... I had to put this picture in. It's fantastic. I'm gonna give you a 10 second version of what this is. My neighbor has sheep and I farm sit for him on occasion. This is Penny. She was a bottle lamb. And so she was very friendly, but she had to eat her grain outside of her pen. And my dog, Tuca, tried to befriend her, thought she was a wonderful puppy playmate and was doing his little play dance to say, will you play with me? And she was not interested, but he was very sad. 

Right. Great job everybody, really great job. I really love seeing how well you guys are doing on these. Alright. So tonight, as we move into the topic of study strategy, I want to really encourage everybody to give yourselves permission to triage the things you study. Don't try to study everything. Remember the old veterinary saying, if you hear hoofbeats, think horse, not zebra. You don't want to study the weird... The zebra diseases, the rare things to prepare for NAVLE®. You wanna prioritize the species that cover the most points on the NAVLE® and you wanna prioritize the clinical topics and diseases that are the most common. Not zebras, horse, all right? Do the big stuff first. You're gonna hear this over and over as we go through Hoot Camp. The NAVLE® is about knowledge that can be reasonably expected of a first-year graduate from veterinary school. You do not need to be an expert, and you should not try to obsess about a lot of tiny, tiny little details. You should stick to the big stuff. Okay? 

Remember, we spoke about this last week, and those of you who've heard my talks about study strategies have heard this very often. The NAVLE® breaks down to 300 questions to count, but over 78% of those questions are in only four species, dog, cat, horse, cow. If you do well enough on those four species you will pass your NAVLE®, no matter what happens in the other species. This is what you do first. Triage. If you want to look for other places to invest your energy, I think pigs are worth some time. Okay? Most of us don't know much about pigs. So anything we do to study pigs or maybe chickens is gonna help right? You don't need a hundred to pass this test You're basically shooting for a 75% Okay, you do that. You're likely to pass your NAVLE®. Alright? All these other topics You know, these smaller topics can be your best friend. If they can only ask you one question, or two questions, or three questions about reptiles, it's gonna be the biggest of the biggest problems. So should you be studying heartworm in dogs? Absolutely. Should you be study some weird monkey parasite? Probably not, okay? Do the big stuff first. And even if, um, Even if you don't study fish very hard, if you complete the Zuku material, you will get fish questions. You will get the non-species questions, things like ethics, things like professional and professional communication and management. You will the chicken questions, okay? So it's not like you're gonna be walking in that test with nothing to help you, but prioritize your best attention to the big four plus pigs. 

So what does that look like? Well, at Zuku, we got all of our veterinarians together, and we also asked different consultants that we knew who were experts in their field, what did they consider to be the most important diseases? And among ourselves, we kind of agreed as a group, we think these are the 20 biggies. And another group of 10 veterinarians might come up with a very slightly different group of diseases, but I bet you anything. Most vets who practice clinical medicine for cats would agree feline leukemia is on the list. FIV makes the list, hyperthyroidism should be on that list, hepatic lipidosis, chronic renal, one of the classic chronic older cat diseases you can ever see. You'll see these every week or two of your life. FUS diseases in cats, very important. Diabetes mellitus. Cats are the poster children for diabetes. Well that and some fat dogs. Some of the key cancers. A few toxicities because cats seem to be vulnerable to every toxicity on the planet and then let's say hypertrophic cardiomyopathy Could you study more? Sure you could, but home in on the big stuff first, okay? Now I'm just gonna pop through some other examples of what these diseases might look like I would not worry one bit about trying to memorize this particular list. All of these things can be found on Zuku. But it's very common sense, okay? You want to do the big diseases, not the weirdos, okay. 

So if that's kitty cats, what's dogs? Here's 20 diseases we thought were important, but it's nothing that's going to surprise you. Diabetes, Cushing's disease, IMHA, heart failure, heartworm is huge. Ethylene glycol toxicity, parvo, GDV, hypothyroid, on and on. If you knew what the classic presentation looked like, a classic case of these 20 diseases were for dogs and cats, and you knew roughly how to test for those 20 diseases in dogs and cat, and roughly how to treat those diseases in dogs and cats that's 50% of NAVLE® right there. It's not impossible. You can totally do that. You don't have to learn everything, but if you do study, study the big stuff. 

What about the other guys? Horses? Pigs? Chickens? Sheep? Cattle? Once again, do the big stuff first. The most points are gonna be in cows and horses. Then you got your pigs, then you get your chickens and sheep and goats. Now, for me personally, I like to think of sheep and goat along with cattle because there's some overlap metabolically. Remember, as we've talked tonight about pregnancy toxemia, there's an overlap with the negative energy balance that kind of correlates with some of that negative energy balance stuff we saw to prevent LDAs in cattle. So they kind of go together in my opinion. But nearly one third of your NAVLE® is gonna be horses and cows. And I don't care if you are, you know, God's gift to cat doctors or dog doctors, if you're uncomfortable with horse and cows, you should at least try to tune up for NAVLE® on this because it'll help you, okay? And if you're really strong on horses and cow, good for you, but you better pay attention to dogs and cats. 

Um, if I had to pick, I'm not a horse guy, but here's what, uh, the whole Zuku review vet team thought about equine priorities, another 20 diseases. These are easy to find in Zuku, but, you know, some biggies in my book would have to be something like colic, strangles, viral respiratory disease, like flu and, um, things like that. Laminitis. There's others, no question, but it's not a list of a thousand things. It's a list of 20 things, and for the big four, 20 is a good number. Bovine top 20, you know with cattle, we think mostly of production diseases, okay, particularly with dairy cattle because they're metabolically complex. But if you hear hoofbeats, think cow, not what to see. Cattle, I think of things like bovine lymphosarcoma, ketosis, DAs, hardware disease, that's traumatic reticuloperitonitis, calf diarrhea is classic, classic NAVLE® question, mastitis, just for some example. 

And people always get stressed. I mean, I'm seeing some questions popping up on the chat box. Like, oh my God, are these diseases guaranteed to be on my test? Guaranteed? No. Likely? Yeah, pretty likely, okay? These are the big topics. They are asking you questions to evaluate if you know what can be reasonably expected of a first-year graduate. That's why you stick to the big diseases, okay. It's getting a little dark in here, so I'm gonna give myself some light just a second. There we go, all right, that's better. 

If I look at pigs, I don't know anything to speak of about pigs so I'm going to rely on my list and here's what we came up with was 10 good pig diseases plus one, okay. If you studied five or six of these to prepare for your NAVLE®, you're not going to get 100 on the pig questions, but you're probably going to do okay on the pig questions and that's good enough. Biggies, I always think about neonatal diahhrea. Think about classical swine fever, also known as hog cholera. Think about these subclinical diseases like mycoplasmal pneumonia. Think about TGE, these projectile vomiting pigs, never good. If you subscribe to Zuku Premium, we have videos on all this stuff by an expert. 

Small ruminants, gotta love them. They're lovely to work on. They're really interesting animals, particularly goats, very smart animals. Big things I think about, parasitism is a big issue in these animals. For goats, we think about CAE, caprine arthritis encephalitis, pregtoxemia, we just talked about. Ureolithiasis is a deal in the males. 

Finally, chickens. I don't know what to tell you. There's gonna be six questions that count on the NAVLE®. I wouldn't obsess about chickens. I mean, if you really love chickens, good for you. That's awesome. But you only have to get six questions right on NAVLE® to get all the chicken questions right. If you pick three or four good diseases on chickens and you knew them well, you can be okay on chickens. I always like to say you can wing on chickens, you're gonna be okay. It's a foul pun. Newcastle's a biggie, Marek's is a biggy, Influenza is a biggie. But if you picked any four of these, it's going to help you. Okay, you don't have to be an expert. 

People always ask, they say, well, where are all these NAVLE® diagnosis options come from? Like, I mean, what if I want to know everything? You heard me say this before, don't try to know everything, that's impossible. You'll drive yourself crazy. And it's not the name of the game. The name of game is to learn enough to help you do better in clinics and pass the test. It's a pass fail test. So where those diagnoses come from is the ICVA every seven or nine years, they'll do a big survey for what are the common conditions that clinicians are treating and they update their NAVLE® species and diagnosis list. You can find this online. There's a link to it there, but if you Google this, anybody can find this list and it's great, except it's over a thousand conditions. So for all the species, if you add it all up, there's over a thousand conditions that technically are fair game for the NAVLE®. You don't have time to study that, and nobody does, okay? That's why we boil it down to the top 10 or the top 20 conditions, and we try to make sure we're on good solid ground with those, and that's enough. It's definitely enough to pass. 

So people look at this and their minds get blown, they're like, oh my God, how the heck do I study all this? Well, the good news is it's not rocket science. We don't study all of it. We triage and we study the big stuff, okay? Boil it down to the big stuff and forget about everything else. And the big stuff is always the same. The biggest diseases per species, and then within that, Can I identify a classic case? How do I test for it? How do it treat? If you wanted to add one more thing, maybe you would say, how do I prevent it? Which is good for like the food animals. 

People still get scared and stressed out. They're like, yes, but how do I start? Well, a good place to start is to make your own notes. Literally take a half a sheet of paper, write the name of the disease on top, and in your own handwriting, write down what does a classic case look like? How do I test? How do treat? Slap a picture on the side and now you've got some notes. And then remember we talked about, we'll talk about this more, but remember we've talked about this before, make your independent study of notes active. So you write this stuff down, stick a picture in it, study it a little bit, and then turn it over and then quiz yourself. Okay, a classic case of pregnancy toxemia or whatever it is, looks like this. How do I test for it? How do I treat? You're making your study active. People resist this, they don't want to do it. They're like, I don't wanna do that, I'm just gonna read somebody else's notes. You can do that, but if you're not careful, just reading somebody else's notes is pretty passive. And passive isn't the way to succeed. By writing it down and making your own stuff in your own handwriting, and then quizzing yourself on it, you're making it active. If you are not willing to write it down, at least take the notes you studied from somewhere else, it could be Zuku, and make that active by quizzing your self on it. 

Let's just try one so you can see what that looks like. So let's try Listeriosis. This is a cow disease. Okay, this is cool. See this in ruminants, you can see it in small ruminants too. So remember, we like images. Images are sticky. To images you can hang information. We're looking at Listerosis in a bull. You can see like a droopy ear on one side. You see his ptosis, the eyelid is dropped and we're wondering what his history is. Silage fed adult cow, big clue. It's got a head tilt, circling, asymmetric sensation loss to the face. So if you touch them on the side with the arrows, they don't feel anything. You see this in adult animals, sheep and goats, animals that are kept indoors for the winter with a history of being fed silage. Test of choice. Frankly, on the farm, it's typically clinicalsigns plus or minus a CSF analysis. Um, culture is pretty difficult and it's not always successful. So, you know, we do the best we can on the farm. Treatment. Treatment is simple, antibiotics. Um, sometimes people treat with a high dose of steroids. Sometimes they don't. That's controversial. Guess what? Controversial is not going to be on the NAVLE®. Okay. Maybe be aware of it, but that's not going be, it's just not going, to be on your NAVLE®, okay. If they have bloat, you have to address bloat because bloat will kill them. And then you give a lot of supportive care, basically fluids, dietary maintenance, things like that. Bonus fact, not a great prognosis. So you might wanna be careful in a food animal about giving them a bunch of antibiotics because the withdrawal times might mean that they can't send that animal to slaughter if they're carrying antibiotics, at least not for human consumption. So if all you did was learn those three points for 100 of the most important diseases and species, dog, cat, horse, cow, pig, small ruminant, you're gonna do great on the NAVLE®, okay? You really are, okay, that's a super foundation and that's doable, totally doable. 

And people still get stressed. They're like, okay, I made some notes. What do I do now? Well, what you do is you repeat. You review and quiz yourself. Review and quiz yourself. And you find ways to make that part of your habit. All right, I'm running out of light, so I'm going to turn the light on and then we'll go on to the next topic. Right there. There's your case. All right, a little light on the subject. Three-year-old Charolais Bull, 2100 pounds. He's a big boy. Found in the pasture, walking in circles. Neurologic. This is an enormous clue that you're thinking about something like Listeria. He's been fed ensiled chicken litter. Sileage, big clue, in addition to winter pasture. You get your TPR here. What you notice is this animal is febrile. Okay, heart rate, low. Doesn't tell you very much, respiratory rate, normal, no big, no big conclusion there. He's depressed, anorectic drooling, head tilt, right ear and eyelid both droop. He's ataxic, predominantly a right-sided proprioceptive deficit. What test do you, what test will help confirm the clinical diagnosis? This is real life and this is what NAVLE®'s like. They're not going to necessarily ask you what is it. They are going to assume you have a pretty good idea that this is Listeria and they're going to make you do a mental leap and say what are you going to do? The more of that you can do the better you will perform on the NAVLE® and also the better you'll perform on the real-life cases that you see. In Zuku, we built an enormous number of clinical cases across the species on this format, because if you learn to do this on NAVLE®, it's going to help you in real life, okay? So who can remember what are some tests we do to confirm a clinical diagnosis? Remember these are farm animals. We're usually not putting them through like an MRI or anything like that. And chat room says, there we go. Um, clinical signs, yes. Clinical signs, yes, and also a CSF tap sometimes if you've got like a valuable animal and it's worth confirming the diagnosis. How are we gonna treat this? And treatment as you think about it, remember, it's simple, antibiotics, supportive care, which means IV fluids typically or fluids and nutritional supplementation. What's our prognosis? Not great. Okay. So what do we just do? We just modeled what I want you to do, whether you're doing practice questions or whether you are doing your notes review or video review. You review a thing and then you quiz yourself. Okay? That repetition and that retrieval practice, that is the foundation of excelling on these tests and in a real clinical practice. 

That's how we really learn, okay? It's not by studying really hard one day and expecting to memorize and know it three months from now. It's by study and then ask yourself some questions. Review a little bit more and then quiz yourself a little more. Review one more time and then have your friends quiz you. That's the way you reach mastery. They call it working memory. And you can read any number of objective research, peer-reviewed studies about why this works. All right, let's do one more and then call it a night. Let's talk about p-tenuous. Parelaphostrongylus tenuous, we're going to talk about a camelid disease. If you live anywhere in the Northeast of the United States or Canada, you may have seen this, okay? Here we see a llama and the llama is affected and clinical. And here we see, looks like a deer and the deer is not clinical, okay. They're asymptomatic hosts, but the camelids get sick. So this could be a llama, it could be sheep or a goat. Once again, we have neurologic disease. They've got ataxia, they're stumbling around. You may see pelvic limb weakness. They go down in the hind end. Sometimes they circle, so that could look like listeria, right? Sometimes they appear stiff or lame. You can get a scoliosis, kind of a curve to the spine. It's common to see temporary remission. Like maybe you hit them with some steroids or something and suddenly they feel better for a few days. You know, kind not a surprise, right. But they don't get better for long. Test of choice. There is no good ante-mortem test. Not a simple, easy ante-mortem test, basically we make these diagnoses by clinical signs and a CSF tap, okay? Does that sound familiar? Does it sound a little bit like Listeria? Don't try to memorize everything as if it's a hundred different things, try to put things together. Oh yeah, LDAs. And pregnancy toxemia, those are diseases associated with a negative energy balance in the pregnant animal or the animal that just freshened. In this case, ah, neurologic signs circling in these adult ruminants, or in this case a camelid, could be listeria, and if there's no fever, I'm starting to wonder about P tenuous, right? And what do I do? I go by my clinical signs and my CSF. But for ways to clump it together. If you do necropsy, you can take biopsies then, and you can get a diagnosis. Treatment of choice. Just like the test, there's no definitive treatment. People have tried Phenbendazole, they've tried ivermectin. There apparently is anti-helminthic resistance to this bug. It's tough. This may be an easier condition to prevent than it is to treat. So people talk about things like deer-proof fencing around valuable llamas. A deer- proof fence is usually really high. 9-10 feet high. And then they'll give these animals anti-helminthics every 30 or 45 days from spring to fall. Not easy. Sometimes there's not a good treatment. Sometimes there is not a good diagnostic and we do what we can. I think I've got a picture, oh, a bonus fact if the animal goes down, bad prognosis. 

Okay, a couple of quick quiz questions. Remember, we're modeling what we do as we have our study habit. We study and then we quiz ourselves. So what species are aberrant hosts for P. Tenuis? Aberrant hosts means they get sick. Exactly, camelids, good job, good jobs. Camelids, sheep and goats, actually. I've never seen this in a small ruminant myself. What are five clinical signs of p-tenuous you might see in affected llama? Remember there was a whole kind of a grab bag, a mixed bag, but we're thinking here of things like what, ataxia, yeah, right, weakness in the hind end, maybe circling. What else was there? Well, I got three out of five. Let's see what you guys can tell me. Stiffness yeah that's a good one stiffness maybe they might appear lame. Scoliosis that's right so you get the bent spine. Good job. All right let's see what we can get out of this. Okay, there we go. Good job, everybody. Good job. What's our treatment of choice? Remember this one? There isn't one. There's no definitive treatment of choice for this condition, at least not right now. Remember, this one may be easier to prevent than treat, so you try to exclude the deer from where the llamas live. You know, llamas cost a lot more money than a sheep or a goat, so somebody might want to invest in that. 

Good job, everybody. All right. That was a whirlwind tour of no zebras. And the whole, if all you did was get a take home message today that I'm not gonna learn everything. I'm gonna pick the biggest diseases. I'm going to tune up on three basic things about each one of those big diseases in the big species and that's gonna be my mantra. That's a good way to go. Remember, one third of your study time in any given week should be independent study on those topics. Two thirds of your time in any given week, roughly. You want to give it to your practice testing or your timed testing, and you want to prioritize the big species. Remember, one of the big things we do in Hootcamp is we're now going to do a low-stakes quiz about our big clinical topic tonight. Our big clinical topic was pregnancy toxemia. So here's your quick review quiz. You've got a six-year-old pregnant ewe in late gestation carrying triplets. The ewe is presented with mild depression and anorexia. You suspect pregnancy toxemia. What's the most practical next step for confirming your clinical suspicion in a field setting? You're on the farm, you're not in a laboratory. So what's a practical next step to quickly try to confirm what you're worried about in this six-year-old pregnant ewe late gestation with triplets? Are you going to check urine ketones with a dipstick? Are you gonna submit a liver biopsy for histopath? Perform a CSF analysis? Send the serum to a reference lab to measure BHBA? Or evaluate hepatic enzymes on serum chemistry? This is a little bit of a softball on purpose, we want to give you an easy one to start with. So any ruminant that's off feed, what are you thinking? I hope you're thinking ketosis, and if you're worried about pregnancy toxemia, I hope you're wondering about the possibility of ketosis. So you want to check the urine for ketones with a dipstick. Quick, easy, fast. Question number two, you're treating a moderately affected goat for pregnancy toxemia with oral propylene glycol. Which choice is the most appropriate caution regarding this treatment with oral propylene glycol? So what are you gonna be careful about with this particular treatment? Once again, on the real test, just like in real life, They're trying to get you to make a mental leap. What do I have to be mindful of? Are we going to avoid use in animals with hepatic lipidosis? So avoid the use of propylene glycol in animals with hepastic lipidosis. Are we gonna try to not use propylene glycol concurrently with calcium? Are we going to give it only via IV for maximum effect? Are we going to limit duration because you can supress rumen microflora? Or finally, is it inappropriate to use this treatment in goats with twins? It's a little bit of another softball, because some of these answer choices kind of contradict what's up in the question, and that'll help you. On the real NAVLE®, they won't do that. But just for practice and low stakes here, we want you guys to simply home in on the main answer. Basically, you want to limit your duration of treatment with oral propylene glycol, because we don't want to suppress the rumen microflora. You want that to be a happy microbiome in the rumen. And our last question for the night, or no, I think it's our last question, I might've misnumbered. A client presents a valuable ewe that is heavily pregnant due to lamb in about a week. She's not eating well in the last few days and she's now recumbent and seems unaware of her surroundings. Her temperature pulse and respiration are normal. A urine dipstick is positive for ketones. Ultrasound shows dead twin lambs. What's the best option to save this ewe? Antibiotics and anti-inflammatories. Induce labor with dexamethasone. Supportive care until the ewe goes into labor on her own. Thiamine supplementation. Tube feeding with IV calcium. Okay, what do you guys think? And the answer is... So in this case, we have a valuable ewe. We're gonna try to save her life. And the correct answer in this particular situation where you know you've got dead lambs, you know it's a valuable ewe, would be to induce labor with dexamethasone. It's a little more gentle. Final question, which choice is the most effective herd level prevention strategy for pregnancy, toxemia in small ruminants? So now we're talking about prevention strategies in a herd. Prophylactic administration of calcium to all pregnant animals in the last trimester. Routinely deworm in late gestation. Feed grain formulated for pregnancy to all dams. Administer NSAIDs prophylactically in late-gestation. I think i've got one more. Group animals by fetal number and body condition for tailored feeding. All right, great. Great answers everybody. I really like what I'm seeing. Good job. So this should be E. You want to group the animals by fetal number and then fetal number and the body condition of the ewe and then you want to do tailored feeding. So if these questions felt a little comfortable and easy to you, that's because we want this to be low stakes, learning experience, okay? You'll notice in Zuku, the further you go, sometimes questions can start to feel a little harder because we're trying to help everybody be as ready as possible for the real NAVLE®. 

All right, here's a quick assignment for session three. Remember, there's no session next Sunday. You can all take the weekend off. And here's your review assignment. We're gonna do a quick review of pregnancy toxemia because we gonna do a warmup with some preg toxemia questions next Tuesday night, okay? And your tuneup topics, we have two, and one of those will be our topic for next Tuesday. To do a quick tuneup on either, both hypertrophic cardiomyopathy, HCM in cats, and heartworm primarily in dogs. And what do you wanna know? A quick tune up just means, what's a classic case look like? What's my test of choice? How do I treat? I don't recommend you use something like Chat GPT to answer those questions for you because that's passive. Be active, be your own best teacher, and go to the Merck and find the information there or go to something like Cotay's Clinical Vet Advisor book and find it there, okay? I'll post this up in chat right now so you can all see it and then we're going to call it a night and... We'll answer any questions you guys have left over. Oopsie, that's not it. All right, I will post that. I guess I don't have a way to post it. Okay, so onto our last slide. Thank you very much, everybody. It's been a real pleasure. Dr. Brock, that was an excellent presentation. Thank you so much. Really appreciate all your help. It's always so fun to be with you all. I appreciate you.