Well, thank you very much for the introduction. And as I've said, it's a very topical conversation and lecture that we'll have today. The vast majority of it is going to be based around sort of more the inflammatory airway diseases, because that's where initially this lecture started.
But obviously I'm going to bring some of the more up to-date bits in at the end on equine influenza, and hopefully if you guys have got any good questions or any questions at all, then. I can try and field them although I'm sure you're all a little bit sick of hearing about it really. So through this talk, we're gonna go through a bit of a differential list first and foremost, to see what's out there.
Gonna have a little bit of a discussion about the nomenclature, particularly around in airway inflammatory disease rather than infectious disease. Look at some of the investigation techniques, why we use some rather than others, and finally discuss some of the treatment options. And in those last two, we're going to bring out in some nice research that's been occurring in the last, sort of 18 months or so.
So when we see any horse with a cough, our first question obviously is, is this infectious or is it inflammatory? Now, in the UK obviously we're mostly going to be looking at inflammatory in the normal year. And so we're going to be leaning towards the equine asthmas, the IAD, the RAO or the summer pasture associated RAO.
Now, normally, I would be talking more on the viral EHV 1 or 4, but I've kind of pushed some of that out of the discussion today in preference for equine influenza. So from that point of view, just a little comment on the EHV, particularly for, is that it is ubiquitous, both of them are, and actually EH4 run right through a barn, but actually not cause too much of a problem to those horses. And when testing, and this I think is the important part of EHB, any of them, is to understand that EHB 5 particularly is absolutely in pretty much every single horse.
So testing for that, unless you are specifically looking for equine multi nodular pulmonary fibrosis. It's not really going to be particularly interesting or rewarding and will end up getting yourself in a situation where you continuously get a positive result. That said, EHP 1 and 4 are both very helpful to, to sample for.
From the bacterial point of view, there are multiple different bacteria and we'll come on to some of those when it's relating to track wash. Aspiration pneumonia obviously has to play a particular role when you're talking about choke episodes, or anything with pharyngeal weakness, particularly some of the folds that are born with that. There's some of the more nebulous ones looking at interstitial disease, which really doesn't often have a diagnosis, but actually can be pretty fatal or, life changing to those horses.
EIPH I really won't touch upon today. That's a whole another topic in itself, one with lots of controversy. And then finally, neoplasia does sit in there, but again, it's rare, and, you know, we, I see once, one every sort of six months or so in this hospital.
Did you call this unfidi, I think has to be mentioned, although frankly, I'm not sure it's a real disease most of the time in our patients. As of yet, I've never diagnosed it, and I think I spoke to Andy the other day about it, and he has diagnosed one in his whole career. So, obviously something to always think about, but diagnosis is based on track washing the, the larvae within that sample.
So when we come on to the actual pathogenesis of this, and I'm gonna really touch on this a little bit later on, the most important things that we're looking about that are gonna separate the allergic and the non-septic in or allergic and non-septic information is that what we're dealing with is a bronchoconstriction, mostly within those lower sort of bronchi, excessive mucus production. And that can be caused also by things like inhalation of foreign materials, noxious gases. So we see this in smoke inhalations following bonfires or, you know, when, when I was out in California, those the brush fires out there.
Also, we do see pulmonary edoema, and we've had a little run of those here at the hospital that all secondary to congestive heart failure, but those horses are going into a non-septic massive inflammation in their airways, which in that case needs furosemide. But the the other opportunity for that to occur is when there's absolute. Yeah, complete paralysis of the larynx or something blocking the upper trachea, leading to huge negative pressures as they're trying to breathe in, leading to edoema within the tissues.
And you do see that following liver disease, is one of the main ones and theoretically foreign bodies, although I've never seen anything like that. When we see one of these horses, I think the, the examination is absolutely critical to deciding what we're going to do, what tests we're going to recommend, and how to move forward. So obviously, I think the history is going to give you the biggest clue as to what is going on in this horse.
So are we talking about some cob that lives in a In a stable, in a dusty environment, those ones where you walk in and you slightly shudder at the stable, or are we talking about a racehorse that's just coming into exercise? Or is it something different? And that's gonna really guide you as to what you next do.
Obviously a basic physical examination is, is pivotal. And then auscultation, as I'll come on to in a moment, it's not that great. So a rebreathing examination and nicely advertising nook in the bag.
But I do find that a hugely beneficial technique when I don't have an ultrasound scanner to hand. And that's going to really increase the the noises going through those lungs, particularly as you remove the the lung the bag and allow that horse to take a very, very deep breath. Endoscopy, both upper and lower airway can be very useful.
And therefore, I'll go through a video of that in a second. Do we do a tracheal wash, do we do a trans tracheal wash, or do we go straight to a BAL? And do we add nasal or nasopharyngeal swabs into that?
Frankly, there's very few incidences when I would recommend a nasal swab, unless you are literally testing for a PCR for strangles. Otherwise, culture of a nasal swab is pointless. But it is still amazing how many of those nasal swabs we get coming through this lab on a regular basis.
Ultrasound and radiography obviously play a huge role in that, and I'm gonna show you some pictures of what I particularly am interested in that. So auscultation, . Now certain sounds can obviously be indicative of diseases.
Things like crackles and wheezes can indicate some sort of parentchimal disease, but also the lack of sound is as important as the presence of sounds, as it can indicate a pleural effusion, that will need to be further investigated by ultrasonography. Now remember that for me, if there is a lot of environmental noise going on outside, so the wind is high or anything like that, then you're going to get absolutely no noises, er, no respiratory noises at the best of times. He's also, my picture here showing the different dots is to show, obviously we're all going to listen to the lung in multiple places, but don't forget that trachea.
Now, there are plenty of times when you're going to get a lot of lower respiratory noise based on fluid within the trachea or an upper airway noise. So again, liver diseases will cause a lot of noise around the, the lung, sorry, around the larynx. There was a study, now this wasn't calves, but it seems to be very true of horses as well, that showed there's only about a 5% correlation of the ultrasonographic findings with auscultation.
In other words, auscultation dramatically decrease or underestimate, sorry, the severity of clinical signs or lesions within those lungs. Be patient. Remembering when a horse only breathes 12 times, a minute, you just to do that one side you're looking at, you've got to do that over a good 30 to maybe a minute to hear a breath in each location.
Obviously listening to both sides. And for me, when you're doing that rebreathing, it's essential to listen on that final inspiration and do it on both sides. So this is a case where temperature is obviously really, really important.
Now, if it's, the horse is pyrexic, is it infected? And this was a case that just sort of brought to the fore for me, that actually it's not always an infection that causes a temperature. This horse was in severe tachypnea due to cardiac disease and actually had a pyrexia because it was breathing so hard and so fast and only just staying alive.
So just remember that it can be an acute allergic disease, respiratory disease that you'll see these pyrexias. Also, neoplasia can cause a pyorexia due to the high or the release of cytokines and interleukins, leading to the a pyrexia that is not truly associated with infection. Also we see it in respiratory sorry I've said that.
We also see it in Tip near in foals, so falls that are really agitated or get up and get going very quickly, obviously can, get a pyorexia as well. On the flip side as well, normothermic horses do happen when there is an upper respiratory tract infection because it can be so localised to the upper respiratory tract that there's no systemic disease. So for me, don't rely on temperature as the only thing to .
Lead you as to whether there is a disease or not, an infection or not. Therefore, we bring in another string of our diagnostics, with haematology being very, very important. What we're looking for is a neutrophilia probably, that's going to be indicative of a, either a very acute viral disease or an ongoing bacterial disease.
But often in the acute phase of these diseases, there can be a neutropenia due to sequestration of those bacteria into the pleural cavity. Now neutrophilia said is typical of acute viral and chronic bacterial disease or even neoplastic disease. .
Whereas neutropenia can also occur in a more chronic viral disease as well. So it's obviously has to be slightly taken with a pinch of salt for every disease. His inhyium may be also evident in an acute infection, but can also be marked elevated in a very marked, parasitism or allergic disease.
Now as I said before, parasites are exceedingly unlikely if analmenttics have been administered appropriately. Also, it's important to note that in Rhodococcus equi cases, that those biochemical and haematological parameters really do underestimate the severity of the disease and therefore, by haematology cannot be relied upon for the diagnosis of REI whatsoever. We also see hypoalbuinemia in these cases most frequently due to a hypoglobulinemia, so there's that secondary acute negative acute phase protein.
Within the biochemistry, you also look at serum amyloid A elevation and serum, iron decrease. Now, at Li, we don't run the fibrogen anymore due to issues with both the control and also it being a very non-specific test. So we've leant towards iron, serum iron as a more specific marker of inflammation.
And we're very happy that that is, is the case. So far we've done quite a few diagnostics, and we, I would hope at this stage that most people are looking and knowing what disease they're going to be dealing with through the clinical examination, auscultation, your auxiliary diagnostics. But obviously, we want to make sure we get to that final diagnosis and make sure we fully understand whatever is going on in that case.
So for me, if we're truly thinking again, as I said before, we, we're leaning more towards our inflammatory airway diseases rather than our infectious in this case. So, I would always recommend a thorough upper airway endoscopy, and this has got to take into account your nasal passages, your sinus drainage angle, and your laryngeal function. This is just a video of me performing one and we're we're looking up towards the ethmoid turbinates, and sorry for everyone who's probably knows this very well.
And we've got nice clean ethmoid turbates, no obvious issues there, and further back, we'd be looking at the drainage angle as well. As I tell somebody to correct it. Now we look up at a dorsal pharyngeal recess and look back and we can see a bit of lymphoid hyperplasia in this case.
Not too dramatic, but obviously, it is very much present. Sit there and monitor and watch the larynge. Function and make sure it is normal.
And in that case, it was relatively normal, although there is a slight decrease movement in the right atenoid cartilage, most likely due to sedation in this patient. So if you're ever worried about laryngeal function, make sure that you do this in an unsedated horse. So the next thing is obviously going to be coming into our guttural pouches and it's really important to know your anatomy as we look in this guttural pouch so that we can really assess it.
This is a basic diagram showing some of the major aspects of it. What we're looking for more in our infe in these respiratory cases is, is their strangles. That's our first and foremost answer.
So there are there any chondroids in the bottom? Is there actually a puddle of purulent material or anything like that? Also, though, if you are concerned that there could be laryngeal paralysis or something along those lines, we want to be looking on the, on the right hand side of the image at all those cranial nerves that will have an effect.
So the vagus is very much in control of your atenoids. And if you have a fungal plaque sitting on that internal, the medial pouch of it sitting over the internal carotid, then you could have damage to that vagus without any problems. So having a good look around is, is very important.
Next is obviously having a look down the trachea and making a sensible discussion as to and plan as to what's going on. And I think what's really useful is this was a paper that was produced a while ago, ago in 2004, but really did look at trying to categorise the changes seen within the within the trachea. And the advantage of that is not only do you do a better job of really imaging and making sure you know what you see, but also it makes it much easier for then referring or passing this on to one of your colleagues.
So grading that mucus accumulation, grading the blood in an EIPH case is absolutely fantastic. So now in this examination, the endoscopic examination, we've gone into both guttural pouches, and I personally find it easier to go into the left and right nostrils to look in guttural pouches individually, especially if you're going to look at both nasal passages, but it is possible to scoot across from one to the other if you're just looking for strangles. Then we move on down and into the trachea, and as we run down the trachea, we've looked at the mucus.
And finally, as we get to the bottom, we want to look at the thickening of that carina, the bifurcation into the two lungs. The left images are relatively normal. I wouldn't say it's 100% normal, but I don't get to scope many normal lungs, frankly.
Whereas the one on the right shows quite a marked thickening of that carina and therefore, indication of inflammation in that area. Therefore, leading you to want to do more diagnostics in, in the lower airway. So the one thing that I would say is if you are considering doing a BAL at any stage, then don't go down into that carina with the endoscope until you've done your BAL.
Otherwise you're going to complete the . Sorry, you go down that far, if you can do a track wash, sorry, because if you go down that far, your scope is going to go down the trachea taking any contaminants with it and contaminate your tracheal wash. So why are we going to do one or the other, because both the trachea wash and the bronchialveolar lavage play a very pivotal role in our examination.
So the traquil wash is actually a highly, highly sensitive test for lower airway disease, but it is very, very bad at dis distinguishing between which inflammatory disease it is. It has very little correlation with the BAL fluid, but it is absolutely essential for a culture if you think there might be an infection. So for me, it's very useful for infectious diseases, or if you are just trying to get an overview of the whole lung field.
Now, I normally do both at all times because The BALA is limited to use in bacteriology, but also you can get a false negative result because the tube pretty much always when you're doing it blind, will go into the right, dorsal lung field. So if that's not affected, you may get a negative result. But if you get a good lower airway sample, then it's gonna really represent that lower airway pathology and also able to focus on a particular area.
And so if you know you have lesions in the right or the left cranial ventral lung field, then use a gastroscope, obviously cleaned, and enter down into that area and then take a sample sample from there. There's been some recent work by a group called Rossi or Rossi and L who have looked at the traquill wash and the BAL. And what they found is that the traquial wash is far more sensitive than the, sorry, more sensitive and specific than the BAL, but that it is not a specific on the aetiology.
And so what they found there is that there's a very good crossover between a BAL with The, with greater than 5% neutrophils and track wash of greater than 20% and also at the other end, so we're seeing very few false negatives or positives in either category. What they also found was that we should maybe reconsider our cutoffs for these. So they found that for very highly specific sensitivity and specificity, the track was should be about 17.7%, and the BAL should be about 7%.
Now, I think that's not too concerning when we come to the laboratory because Actually, there's a lot of crossover between them anyway, and also you take those results in place with your with your clinical examination. Doing the tracheal wash, it's a very simple technique and something that I think can easily be done as long as you have an endoscope. So I used to do a lot of trans traquial washes when they came from America, and now I've leant towards the traquial washes for, for a couple of reasons.
One is the tracheal wash is very easy. We can do that in a mildly sedated horse. There's no clipping, there's nothing to be done, and you can walk away with the owner's very happy.
The problem is that often you will get a falsely contaminated sample and therefore the bacterial culture may not be a true representation of the disease process ongoing in that horse, most likely because the horse has coughed and put that fluid over the end of the endoscope, or there's been a little bit of an exuberant driving and you've plunged into the the fluid in the the thoracic inlet. Transtracheal washes though completely avoid those problems by entering through a sterile area on the trachea and then passing a tube into the trachea itself. But the problem with that is obviously you're clipping an area, you are inserting a needle into the throat, and I've definitely had a few infections in that site following it.
I still reserve it for those cases where I absolutely need to know what that bacteria involved is without any question. So when performing this sample, you enter the proximal trachea and advance your catheter beyond the end of the the the endoscope. You then instil 10 to 20 mLs of fluids down the trachea and make sure that that head is being held up high, otherwise that fluid's gonna run straight back out of the trachea and the whole process has been a waste of time.
Advance the endoscope carefully so that you don't enter that fluid and then aspirate it back. So that sample then is going to be going on for cytology and also culture. So this is me performing the test and letting it run down.
You can see a few of those nobles that you see in a few horses, which, who knows what they are in most cases. And then you also saw the horse cough at me and cover the endoscope. So that's other than the coughing, is how it should be done, but, doesn't always exactly go to plan.
So we've submitted the sample for culture and also cytology, and we'll come onto the cell counts in a second. But cytology, this is a list that's in the Libook lab book and it's very, very useful to say, OK, when you get those bacteria grown, which one's really important, which one isn't? And there are a lot that you're going to get.
The vast majority of gramme negative commensals of the nasopharynx, and therefore absolutely aren't a problem. They're just because your scope has gone through the trachea, sorry, through the, the nasopharynx. Now, if there has been an aspiration pneumonia, then that changes the story, absolutely.
So again, with everything to do with laboratory work, take the piece of paper with the horse as well. So the bronchoalveolar lavage, as I've mentioned already, essential for any lower airway inflammation investigation and without it, I don't think you can do a proper job, advise the owners on what the disease is and also what the prognosis is. In the vast majority of cases, I would do a blind versus guided, because I think most of the time you just need a section of lungs rather than a specific.
But as I mentioned before, if you've ultrasounded and found something or X-rayed, then use your gastroscope and get in there. So when doing blind or guided, there's a recent study whether the salbutamol administration would increase your return of fluid or not. And Bowser and his team assessed that technique and found that the cellular acquisition during the BAL, when horses were suffering from equine asthma, so they didn't look in normal horses, only horses affected by excuse me, affected by asthma.
Found that busarpan made no difference to the acquisition of cells. But the pre-treatment with salbutamol at 100 mcg per 100 kilogrammes, and most, inhalers are about 250 mcg per actuation, increase the rate of recovery of fluid. They also found that the use of a mechanical pump rather than gentle aspiration by hand was a negative effect, which decrease the number of cells and also increase the number of red blood cells.
So I don't, I've never heard of anyone in the UK doing that, but, avoid it if you can. First, when you're doing blind, make sure you're in trachea. A couple of ways to do that.
One is to rattle the trachea and make sure that you are in the right place. And the second is to aspirate through that tube with an empty syringe and make sure that you get no negative pressure. Normally I'm following a trachea wash when I've done this, so I've instilled lidocaine into the trachea and at the carina.
But if you haven't done that already, then you can instil it at that stage and keep advancing until you feel resistance at the the lungs. Now I inflate with about 5 mLs of air because I've found that I get better acquisition of fluid with the the cuff in place. But that said, I didn't do it for many years and got plenty of good samples without a problem.
You want to instil about 250 to 300 mLs of saline, depending on the study that you look at and aspirate that. Then place that both in a red top and a purple top. Now, I only ever do cytology on it unless I'm specifically looking for, again, for a bacteria that I want, or if I think this could be an equine multinodular pulmonary fibrosis, in which case I'm going to be sending that sample for a PCR for EHV5.
So when we look at the normal cytology of these cells, . What we, a group, sorry, this is just a slightest side on it, found that there is quite a relationship between the cell morphology of the neutrophils and the possibility of an infectious process going on in that trachea. So if we are saying that the cells are degenerate, then there is likely to be associated with an infectious bacteria that is deemed clinically significant by the authors.
Also that they found that there was an association with age. So those younger horses, 1 to 3 year olds, were more likely to be affected with degenerate neutrals. And also the spring, summer, sorry, the autumn winter had a lower chance of higher chance of degenerate neutral.
So winter increased risk of degenerate neutrophils. Sorry, I got my words mixed up then. When we look at the normal cytology, though, we're looking at a tracheal wash, and the main ones we want to know about are the neutrophils, which should be less than 20%, and the BAL should be less than 5%.
The vast majority of the remaining cellular count should be made up of macrophages and lymphocytes. Now, the exact ratio between those is very much up for debate. Normally it's highly macrophages rather than lymphocytes.
But nobody's ever found a correlation between one there being a swap in that, that ratio leading to a specific disease. Also, the earsinophils and the mast cells should be very low. So when we look at the BAL cytology, what are we looking for that's important?
First and foremost in an IAD you're looking at a slight inflammatory neutrophil count of about 5 to 20%. Put an elevation in your ears infills and also your mast cells. So that's the important part, whereas you can get a slight increase in your neutrals in an early RAO if that's, if that's what we're gonna call it.
Whereas in REO you're going to be looking at a neutral count of greater than 20%, quite often up into your 80s or 90%, so they're normally pretty obvious. This is some histopathology looking at the pathogenesis of these cases, that a group run, led by Bone and this year, or sorry, last year, undertook. And the reason I've added this in is to obviously point out that the lower airway inflammation diseases are not only allergic, but they're inflammatory and that they end up leading to chronic changes that are, that are going to be life threatening in, in a minority of cases.
So what they found was that the lower airway inflammation was asso that was associated with the neutrophilia correlated well with postmortem changes. And they were most marked obviously in the lungs, and the severity of that neutrophilia was also associated with the severity of the changes histopathologically. And what they show is that there's quite a lot of interstitial fibrosis, and this is the section that we are not going to be able to do anything about with our treatment.
There's also mucosal cell hyperplasia, which hopefully we will be able to do something about because we're gonna slowly reduce the inflammation, clear the mucus out of there. There's peribronchial metaplasia, so it's quite a lot of inflammation that's gonna change those cells. And finally, mucousstasis.
So that's gonna be what's gonna cause a lot of alveolar damage with the increased pressures that will be associated with it. So all of these changes when put together can easily explain the obstructive nature of this disease process and why some of these cases are essentially fatal. So a group in Denmark recently looked at the possibility that they actually, some of these changes that we see in our neutral counts could be seasonal.
They, they felt very much on their anecdotal experience that that was the case. Well, they found that there was an increase in the mucus score in the November period rather than the May period, but that it was not statistically significant. And the only abnormality that was significant was your neutrophil count.
Now as you can see that change in neutral count is fairly mild from 3.5 to 6.1%.
So you are leading into the inflammatory airway disease stage at 6.1. But I would struggle to get too excited when I was advising on that.
So Yeah, the, the other thing that was mentioned in that paper was that during the November period, there was a statistically significant change in the light levels, so decreased light levels, decreased temperature, and also decreased increased humidity compared with May. So is that slight change due to environmental increase of allergens of fungal particles and things like that? So when we're looking at our cytological samples that come into the lab, there are a few other things that we're going to comment on and whether they are important or not.
So cellular clumping with mucus is going to really alter the ability to diagnose the, the cytology and the numbers perfectly. So we have started instigating a new technique that's going to allow for the breaking up of that mucus and hopefully a more specific and accurate answer. Hemosiderin is obviously important because that may indicate EIPH.
Now there's no other reason really get hemosiderin other than bleeding, so something is going on if you see that. If you're reading these samples by yourself, then pollen is a really common. Problem that people see as fungal spores, and in fact, most of the time that's not the case.
As I've already mentioned, parasites really aren't very common. Fungal spores on the other hand, I think are an absolutely fantastic thing to find to be able to guide the owner appropriately as to what to do. So 55 in a study by De Villiers, 55% of samples that were submitted had fungi that were cultured.
And what they found was that those fungal elements led to it about or were associated with a 2 times greater chance of IAD. And the bedding on straw historically had an increased risk of fungal fungi in the sample. So, from that, I think what we can take is that remove straw, obviously from the bedding, I think we hope all know that.
But also that if we see fungal spores or hyphae on a slide, take them seriously and talk to the owners about the environmental changes that would be appropriate. There've also been a couple of other studies that I, I think one's not very interesting, 1 may be interesting in the future. So Bazzano, and sorry, if I'm pronouncing either of these names incorrectly, assessed metabolomics on the tracheal wash and exhaled breath condensates.
And what they found was that Based on that, they can actually diagnose inflammatory airway diseases because about 10 out of the 38 metabolites were significantly different between normal and horses that were affected. And in that group of different metabolites, both histamine and oxidant agents were, which is unsurprising considering the clinical signs. Therefore, that may well become a clinical modality as we move forward in time, although at the moment the equipment is obviously very expensive.
The other study was one, by, I won't even try their name, where they assessed histological examination of bronchial mucosa that was taken by a grab biopsy. There was an earlier study about 4 years ago that found it was very useful. These guys didn't find it useful.
My experience has been that it's incredibly difficult to get an accurate sample, so I don't do it anymore. So other diagnostics that we should really be considering. Naso, nasal nasopharyngeal swabs, I've already mentioned the nasal swab scenario for me, that if you're gonna culture it it's absolutely pointless.
If you're looking for something specific, then it is useful. Not gonna talk about the minefield of strangles, that's again a whole different topic, and we're gonna come on to influenza. Talks about EHB1 being very important, obviously for any respiratory or neurologic diseases.
EHB 4 is absolutely important for it running right through a barn, but most of the time those horses are going to end up actually doing just fine, although they are slightly. More prone to bacterial infections because you've knocked out the type 1 pneumocytes and you've got a type 2 cuboidal pneumocytes sitting in there, which is not going to be anywhere near as effective at protecting the lungs and the system, the systemic, blood flow from bacteria. As I mentioned, DHB 5 is pointless, as it's ubiquitous in all animals, in all horses.
The ultrasound is something that I think a lot of people are very scared of when it comes to lungs, and I think actually it's one of the easiest areas to ultrasound in the horse. For me, it is all about being systematic, and that's true of not only thoracic ultrasound, but any ultrasound. I always start from the back because I find it much more helpful to be able to count from the 17th intercostal space.
Just remember in Arabs, they have an extra rib, so they're often 18 intercostal spaces. When you're scanning, make sure you're not scanning the ribs. Sounds silly, but it's easy to do that bright white line of hyper ecogenicity is both true for lungs and for bone.
To watch it move. And remember that some comet tailing in that top picture is very normal if the horse is older, so don't get really excited by that, especially if you're using a tendon probe or similar. But remember that bottom picture, if you see that then you know you're in trouble.
There's a lot of consolidation, probably an abscessation or something similar. Remember though that ultrasound is only good for the surface of the lungs. It's only gonna give you that top millimetres unless you have an abscess.
And so you're going to need to rely on tra radiography. Now we get a lot of samples sent in to us, sorry, a lot of ultrasound sent into us. And a few tips I'd just like to, to make sure I'm sure all of you know how to ultrasound scan.
Obviously, get your name in there. If we're assessing an ultrasound and we're expected to pass any true judgement on it, we need a name on there, otherwise we wouldn't be able to pass judgement on it. Make sure your depth is right.
Don't scan at 30 centimetres because you've been doing that on the abdomen because you're gonna really lose the detail of the lung. Make sure your focus is in an appropriate place. Now, you may bring that focus down or deeper 1 centimetre in this one, but it, it often just affects the the view a little bit.
Label where you are because otherwise if next week you go back to scan, you can't find an abnormality, you need to know exactly where you're meant to be. And then finally, just make sure you've got a good frequency going on. So radiography is your final step in the diagnostic tools I think at this stage.
And obviously it's very, very difficult to do in the field unless you have an absolutely gargantuan generator, and I don't think most people do, especially as you need a grid, and a bucket to hold the plate. Make sure that when you are doing them that nobody is holding that plate because the, the scatter and the level of X-rays you're using is so high that it's a, it is a risk to human, health. What it allows you to do though is to assess the complete lung field for that horse.
And you're going to obviously be looking at the different patterns and deciding whether it's interstitial, it's bronchial, it's alveola. And from there, you can then also look at equine multinodular pulmonary fibrosis, so you're gonna look at these little cotton wool balls all throughout the lung. EIPH is likely going to affect the quad dorsal tip.
So are you gonna have some consolidation up there? Aspiration pneumonia, though, is completely the opposite, so it's gonna be the cranio ventral lung field. And doing bilateral radiographs is going to allow you to see if one side has a mass that is bigger than the other side.
So for me, it's very important to do both sides. Also, you're going to be able to assess for a pleural pneumonia or a pneumothorax. Hopefully, either of those you've already got an answer for with your ultrasound, but you want to assess the severity or if there might be something else.
If you do have a pleural pneumonia, then I would recommend draining that before doing any X-rays because you won't see any abscessation in that lung field. OK. So we've gone a long way through our diagnostics at this stage and we're getting to the point where we need to make a plan.
We've hopefully come up with a, a diagnosis. So to start with, we're going to look at our RAO and our IAD. So our recurrent airway obstructions are severe equine asthma versus a mild equine asthma.
You'll see that I haven't quite changed mine in amenclature. And the reason for that is I, I really struggle with a disease name that already has an adjective in it. So, at the, with severe equine asthma.
How do you decide if it's a bad or a good one, because you can't say severe severe equine asthma. That's me on my soapbox, so I'll, I'll step off that for now. RAO though, is generally greater than 5 years old on in the vast majority of cases.
And you're gonna see most of these horses with dyspnea, but they may have subclinical diseases in the early stages. Whereas IAD is generally your younger thoroughbred horses that are coming into exercise and really starting to push themselves. And that this is subclinical by nature until there is an exercise induced or exercise intolerance reduced performance.
Both of them though, the essential situation is that there's airway inflammation, there may be, there's coughing in REO, there may be coughing and IAD. There's poor performance, and there might be nasal discharge. So there's quite a big crossover between the two, but there's quite a difference in the prognosis for them.
So recurrent airway obstruction. Most of you will know the clinical signs, but most of them, most of these horses will have a heave line as in the picture above. They'll also mostly be coughing.
And they are obviously exercise intolerant, even at a walk or a trot in some cases. As I've already mentioned, a BAL is very important, but there is a lack of correlation between the neutrophilia and the histopathology in those samples. What is important to note though is that don't expect magic when you start treating these cases.
So don't be surprised if that BAL does not respond as you would like. And that's been shown time after time in in research projects. So in fact, the best mode of ongoing monitoring is what is the horse doing, how is it doing clinically.
And I do normally recommend at least one more BAL to make sure we're at least trending in the right direction. When it comes to treatment, there are lots of options out there. I think the crux of the matter in both of these airway diseases is change the environment, don't, don't rely on drugs, don't rely on anything else, change the environment.
When we look at systemic versus inhaled steroids, They both do an absolutely fantastic job, and I'm gonna come onto that a little bit more with some specific, steroids. Mucolytics do play, can play a role. Bronchodilators do as well.
And again, I'll touch on that in a moment. And omega 3 was an interesting research project that showed that that really does decrease in neutrophils. Inflammatory airway disease, as I've already mentioned, is the younger horse, exercise intolerant, and these are the ones that have a much, much better prognosis compared to your REOs.
They're quick to respond and hopefully succeed with the treatment. The one thing also I forgot to mention with the RAO is that the longer you don't treat it, the poorer the prognosis will be once they do decide. So if you do see these horses, push with the owners to say, OK, if you leave it for another year, we're going to be in a situation where we might not be able to bring this all back to normality.
Diagnostics are again a BAL to get the specific diagnosis and the treatments are exactly the same. So this is why it's important to get that diagnosis so you can say, OK, this horse is gonna do well, this one is not. So when it comes to environmental management, what are we looking at?
Ventilation is absolutely essential to any treatment of these cases. So stable hygiene is imperative, dust-free bedding is one of the best things to use. I always recommend with these cases that you turn out when mucking out either that just that horse is stable or any other horse's stables.
Turn out during peak activity when the horses are coming and going, and also reduce the dust load in the stables. A lot of work for the owner, but frankly, or sadly for them, that is the only thing that's gonna really help these horses. Feed obviously plays a big role as well, so always recommend soaked or steamed hay or even haulage.
Now, when we talk about soak, we're not talking about having to overnight soak it for a laminitis to reduce the water or non-structural carbohydrates in there. We're purely talking to remove the dust. So as long as it's been in there for 5, 10 minutes, really permeating through all those fibres, then we should be absolutely fine.
Sometimes don't forget the outside spaces in the hot summers, you know, last year we saw a huge upsurge of these cases during the really dry weather. And I think partly because there's no reprieve for these horses when they're outside it's dusty, when they're inside, it's dusty. So just be aware of that as well.
And also pollen and environmental allergens. There's been some more research saying actually doing intradermal skin testing in these cases might help because you might be able to find an allergen and use an immunotherapy. So if the owner is absolutely adamant, it happens when the oak trees are flowering, then it is well worth doing an intradermal skin test in those cases.
If we do have another summer summer, then I would recommend using water to dampen down any outside schools, or even spraying mineral oil on bedding and things like that, which will really keep the dust down, makes them shiny as well. So Drugs, what are we gonna do? First of all, change the environment.
I don't think I can push that one far enough. Bronchodilators, though, are sometimes absolutely essential. So in your really acute severe, asthma attacks, your anticholinergics such as atropine will be essential.
You can also use Buscopan as a much shorter acting one. With fewer side effects. So if you're not sure what's going on, lean towards the buskpan.
If you're certain, get the atropine on board, and don't mess around. The chances of an impaction occurring from atrophine aren't too high, but they are very much there. Beta 2 agonist, they are going to be more your friend when it comes to treatment.
And you've got Clembuterol, so Ventolin, ventapomin, salbutamol or salmetrol. Lembuterrool inventapomin has about a 5 day efficacy. So in other words, don't give it for more than 5 days because it's not really going to work in those cases beyond that.
Salbutamol has a very short acting, so really, really useful as a pre premedication before giving any further inhalational steroids, cos it's gonna cause a massive dilation. But it's not very good for actual ongoing bronchodilation. Salmeterol has about a 4 hour, .
Bronchodilatory effects and I'll come on to some newer ones that might actually play an interesting role. As I mentioned, there's down regulation of the, clobuterol, but it does give short term relief, so it, it really is a helpful drug in some cases. So then we're looking at the anti-inflammatories, and I think steroids are going to be your main, main play.
There's not really any point in non-steroidals, they're not going to have an effect. So, prednisolone is going to be your, your main player, and I generally go 1 milligramme per kilogramme, once a day. And the arisolone is licenced for a 10 day course and so normally has a pretty good effect with your IADs and getting some of your RAOs under control.
Dexamethasone, though, I do use as a rescue therapy in those cases that really are not responding appropriately. And I start normally, I, I go in at 1.1 migs a gig IV once a day.
Now, if that's not possible, you can lean towards giving the IV formulation orally off licence, of course, and it should be in a cascade manner. But if you're doing that, increase your dose by about 30% to deal with the decreased bioavailability that you're gonna see with the dexamethasone. Prednisone, there's absolutely no point, .
And what they found that despite the improvement that you see with these glucocorticoids, despite the very clinical sign improvement with the glucocorticoids, the lung function and inflammation actually doesn't change all that much. But what they have shown is that regulatory T cells, so there's ones that keep the inflammation under control, and have an anti-inflammatory property. Play a huge role in all of these diseases and actually following administration of glucocorticoids, these start to be up regulated and play probably quite a significant role in keeping the RAO under control.
So that I think is where we're seeing good improvement. When we look at inhale versus systemic, which one should we lean upon? Systemic obviously is absolutely fantastic, but comes with some side effects, the increased risk of laminitis is the the main one.
What they found though, was that overall, overall steroids in general, led to a 30% improvement in clinical signs, and that they found there's no difference between the response to inhale versus systemic, and therefore careful consideration should be given to you the most appropriate route. . I feel that anecdotally, both have a much better than 30% improvement in clinical signs in the vast majority of cases.
So I, I would take that study with a pinch of salt, but I think what's important is inhaled is essentially as good as systemic in them. Now there's a new product or a new drug that's been researched, called budesonide, which seems to have a very good effect, pretty much comparable to dexamethasone. So it'll be interesting to see if that starts coming out.
It was a boring, funded study, so it'll be interesting to see what, what they've got in the pipeline. Eucalytics, I, to be honest, I, I could take them or leave them. I know a lot of people really like sputallosin, and it may be useful in the early stages, but again, I, I think the, the other treatments are more important.
So, there's some new treatment modalities out there that are really coming around and I I I think it's good to just bring a few of them up. Now this first paper by Junior in 2018, I take it with a bit of a pinch of salt, it really wasn't a very good study, but what they found was that pre and probiotics showed a reduction in the sinophil count and tracheal wash. So it may well be that giving these drugs, changing the gut flora has an effect on the respiratory tract.
And we know that's true within the human medicine, so why shouldn't it be true in the equine world? So I think it's something that actually, I haven't really started bringing into my own treatment, my doubts, but I really think that it's a good thing to start looking at. Another one is these nanoparticles.
It's a new therapeutic strategy trying to modulate the immune response, in both human and equine allergic asthma cases. And it's quite, it's quite under quite a lot of extensive investigation. What they found that it was the immunomodulating agents stimulated the regulatory cells, as ones that we were just talking about a moment ago.
And that these treatments could offer a new option beyond the conventional symptomatic treatments that are out there. And The aim of the study that was taken by Clare Cle showed was, sorry, the aim of it was to evaluate whether the nebulized nanoparticulates would improve the sciences, and they did. So this could become something very important.
Now, at this time, this is very much in the research world, but I hope that we're going to start seeing some of these come out into the real world. There's a tamoxifen, which is a breast cancer treatment, a selective oestrogen receptor modulator, and what it did do was that it decreased airway neutrophil, neutrophilia, and improved clinical signs in experiment, experimental models of equine asthma. And also induce neutrophilic apoptosis in, in vitro.
But the statistics weren't great, so I wouldn't be personally desperate to lean on tamoxifen as a, a very expensive medication to try and help these cases. This final one was just a short aside that actually they, in the really acute RAO cases, they found that an infusion of magnesium sulphate massively decreased the clinical signs. So a 2.2 Migs per gig per minute for 20 minutes caused a massive reduction in inflammation within the lungs.
And so quite an interesting one for those severe cases when you're struggling to get under control. So when we look at the treatment plan, some of pasture associated often responds very well to the initial treatment, and obviously it's gonna get better in winter. RAO I generally try and do a decreasing dose of oral steroids following the initial, dose and move them on to inhaled steroids.
And then indefinitely be on steroids. Now, most of the time, the clients are able to wean their drugs off and hopefully get them to a better place. IAD though has a decreasing inhaled or oral steroids and normally do very well.
And frankly, antibiotics are not needed in the vast majority of cases. They inhaled steroids, I've already mentioned that they have a very equal treatment outcome compared to systemic steroids and therefore, I personally lean on them in the chronic cases. They theoretically have a better penetration at the site of the problem, hence why I like them.
And I generally nebulize rather than me a dose inhaled, obviously I couldn't find a picture of me doing it with a horse, so we have me doing it with a cow, and a horrific moustache, so sorry about that. But the metre dose inhalers I find really don't work very well in these horses. They breath hold, the smell is quite intense, whereas nebulizers, they can't escape it, so it works much, much better in my opinion.
So, the Flexeneb, this is just here for to show what they're available. They have a whole list of all the different drugs. Please don't use a lot of them, you know, cefquinone, cefivefu, we shouldn't be using unless there's a really good indication.
But from the drug point of view, salbutamol, and dexamethasone are very important. Now, with dexamethasone, you've got to, dilute it 1 to 1 with saline. Or if you are using one of the others, so do forcort or something similar like that, remember to alter that dose 2 to 1 with more saline.
From the inhaled other drug point of view, I generally, I would love to use fluticasone, but it is generally too cost prohibitive in most cases, so I lean on Becklamethasone if I, this is if I'm not able to nebulize, sorry. . And becylmethasone has a pretty good effect, but just not quite as good as fluticasone.
Ventippomin, we already talked about and salbutamol I have as well, just put these up for the, the doses and the atropine, the emergency dose is there, frankly, if you've got a true emergency, don't bother with the lower, just go to the 0.01 mix but kick. So hopefully that's covered a lot of our airway inflammatory diseases, and obviously if you've got questions, I think I saw a couple pop up, then we'll go through those in a second.
But equine influenza. I think hopefully everyone is sick of it, and the next sort of 5 minutes or so will be fairly quick. Obviously, clinical signs, cough, nasal discharge, pyrexia, lethargy and appetences, all of those things that are fairly non-specific and we see on a regular basis with things like EHV4, strangles, and non-specific respiratory disease.
Obviously it's a highly contagious disease, shed for about 10 days in the vast majority of non-vaccinated horses. Whereas in the vaccinated horses, you're looking at approximately a day of shedding in the vast majority of cases. Isolation is absolutely essential to all of this, as we've seen with the racing.
If we can, if we catch it early, we can deal with it. That first case that occurred went to a race meet where there were 75 different trainers that then spread out throughout the country. So you can understand why one race meet in one part of the country has led to this dissemination in this picture.
Map on the left hand side is the most recent one from yesterday I think it was that the AHT have been producing, they're doing a fantastic job of keeping us all up to date and ideas know what's going on. There has been one fatal case as far as I am aware, which was a non-vaccinated horse, whereas every other vaccinated horse has had a very good outcome. In this outbreak, we're looking at Florida clade one.
And what's interesting is that Florida clade 2 is the more common that we have seen incursions of in 2019, 2009, then again, I think in 2014, I want, I think I want to say, whereas Florida clade 1 has been circulating far more in Europe and causing a lot of problem over there as well as here. Again, this is the AHT information and what's interesting, is that, as I say, all of these cases that were vaccinated had very short diseases and there were no spread on those sites. So it's, it's quite useful to be able to say to owners, although it doesn't stop disease completely, it massively reduces the rate of infection or the severity of infection as well.
And why, why else is it important? Because at the moment we're seeing a lot of it in Europe, so it, it has been in France, it's, it's been all over the place really. And it, there appears to be a link rather than a link between the Irish cases that started a little while ago and then those in Europe.
So it appears that it has spread from Ireland to France, Belgium and the Netherlands. And again they're seeing it in vaccinated and unvaccinated horses. And from the vaccine point of view, that's gotta be the biggest discussion at the moment, is which vaccination to use.
With the clade one involvement in these cases, it is only sensible to recommend use of a vaccine that has a clade one strain in it. And the two that have that are Protec and proquenza. Equip has shown some degree in a scientific research paper of having some antibody production to clade 1 and clade 2.
But they haven't, as far as I'm aware, produced a paper showing. A challenge study where they are. They have a good outcome to a clade one's challenge.
So sense has got to be applied and use one of the other two. When it comes to transitioning from equipped to proquenza or Protech, at this stage, whilst we're in the acute phases, it seems, recommended that you just re-vaccinate, and there will be some sort of cross protection increase in immunity. There are studies that show that as well.
And then moving on to a normal vaccination protocol following that. Otherwise, at the moment, the recommendation is if the horse hasn't been vaccinated for anything over 6 months, then we vaccinate. Last two slides on the flu.
This is just to show how complicated the flu vaccination protocols are that there are different recommendations by all these different regulatory bodies with regard to, first boosters, subsequent boosters, rules post vaccination, and all those sorts of things. So the Animal Health Trust has tried to consolidate all this information and try and bring it into a slightly more coherent and understandable protocol. And the proposed new plan is that for the primary course, you've got a 21 to 56 day window, and the first booster is 121 to 185 days, the latter being shorter than the previously recommended course.
And then the subsequent boosters, other than for the HBLB sorry, the VHA, is that there's been an an annual minimum. . What they're also recommending is that there's a concession that anything that goes beyond 14 days beyond that vaccination is actually allowed to continue, rather than having to start a whole new process, because really, it doesn't seem sensible that there's, because there's no scientific data saying these horses have a poorer immunity following that.
So hopefully these present, this is being presented to all the different governing bodies on agreement with the vaccine companies. So hopefully we're going to start to get that. The other important thing is the racing situation at the moment, that if a horse has not been vaccinated within, it cannot race after 7 days, 7 days after a vaccination, and that is true, whoever is the racer.
So it really is strict at the moment that if you vaccinate today, that horse cannot race for another 7 days. So Obviously, if you've got any questions about equine influenza, please post them. We've been discussing it a lot over the last few days.
But to conclude from the inflammatory side of point of view, airway inflammation most often associated with housing, it's unlikely gonna require antibiotics, but proper diagnostics are really going to give you the best chance of success when it comes to treatment and prognosis as well. And that inhaled drugs are as useful as . Systemic drugs in the vast majority of of cases.
Well, thank you very much for listening and I think that's virtually the hour, so if anyone's got any questions, I'll happily field them. Brilliant, thank you very much, Jamie. It was a really, really good talk, and I a little update of equine influenza.
It does sound as if it would be quite good if there was some kind of cohesion between the vaccine guidelines between all the different, kind of companies and different authorities and things as well. Yeah, cos at the moment we're actually running off licence when we adhere to the BHA recommended, third booster. But could that leave vets open to legal action?
Well, I don't, it's been a discussion actually. I, I'm sure a few of you are on the equine veterinary Group and Phil Ivins and and Richard Newton have been discussing it, and their feeling is no that it wouldn't leave the vets open, it would, because it's BHA guidelines, but it would give the vaccine companies wiggle room to not help out if there is a breakdown in in the disease. Yeah.
Fair enough. OK. So, there's a question regarding, in like saline inhalers, they seem to be pop up all over the place.
Yes, so there's a good study a little while ago that I think it was in the Netherlands where they created a stable that was essentially a big nebulizing room, and they had a huge improvement in our REO cases to the point where they didn't actually need to do any medications. Now, that's not normally sensible, but I often will add saline in the course, and it seems to really help break down the mucus and, and help out. So often, as part of the cleaning process of those flexing nebs, you have to run saline through them about 10 mL.
So I normally get the owners to run the saline through whilst the horse is breathing it. And it does, does seem to help them cough up a bit more mucus. OK, cool.
And then just, so regarding bacterial combination, contamination with track washes, does doing a transtracheal wash then minimise how much . Absolutely, yeah, so transtracheal washes completely negate the, the risk of, of contamination as long as you've sterilely prepped, . Yes, absolutely beneficial in some cases.
OK, brilliant. That's, I'm afraid that's sort of time we've got time for. So thank you very much, Jamie.
That was a really, really interesting, interesting talk. Thanks to everyone, for, for listening, and also thanks to Baileys who have, sponsored this webinar as well. So thank you, everyone, and hopefully, well, see you back soon on a, on a webinar.
Good night. Good night.
