Hello, good evening, good morning, good afternoon, wherever you are in the world. Thank you so much for coming on our webinar this evening, which is all part of the virtual Congress 2021 incorporating column vet over in Latin America. Again, thank you to all of the sponsors who've made it possible for us to to run this conference this year.

And I'm super thrilled to have one of my ex lecturers on, Derek Notten Bell, who's going to be speaking about equine uveitis. I think I have some credit to pay for, Derek's stellar career because, when I first met him, it was out in Zimbabwe where I was doing an elective. And I think he liked me and the group of Liverpool students so much that he decided to follow us back to Liverpool, and of course had a stellar career there.

I think one of his high points was when he had me at finals explaining the, the equine I to him, and it's all been a bit downhill since then, hasn't it really, Derek? I passed anyway, that was the main thing. I got through, which, which was a thrill.

So thrilled to have you on. You were loved very much by us. We were your first year and and you were such a breath of fresh air.

We were so fortunate in the equine department. With the great Barry Johnson there as well, Barry Edwards there as well. And so it's a thrill to have you on.

I'm really looking forward to the, the bits that I didn't talk to you about when I was on that finals many, many years ago. So over to you, Derek. Good.

Well, thank you very much, Antony. Thanks, Steph for your setup for me this evening. I'm very grateful to you all for inviting me.

And, and, it's, it's a, humbling thing for us to talk across the world like this, at this very difficult time. And most of all, I just hope that everybody is well and, we can keep ourselves safe and do the right thing by our neighbours and our friends and our countries and our world really, both environmentally and in respect of COVID, of course. In any case, we've got to talk about something.

Serious now, called equine uveitis. And the problem with equine uveitis, we all know what it is. We all, we all understand the word, but we don't understand the disease.

And, the problem with that is that it always creates a problem, therefore, because we, if you know what something is, but you don't know how it works or what it does, it's a problem. Can you imagine getting into a car, you know what a car is, but you have no idea. The controls are, you've no idea how the engine works.

You don't even know what makes it go forward or back. It can be dangerous apart from, a problem. So, it, it's important.

And I just put a picture at the bottom here of the Tyndall effect. And this is the, the effect where the shafts of sunlight beaming through a barn window like this is sunlight coming through, and you can see the dust particles and you'll see why I've put that there later on because it is a fundamental. Part of the diagnosis of uveitis, that same Tyndall effect where the light beams highlight the little particles of, of dust and so on in the air.

So we'll come back to that later on. It's important for me to recognise those people who helped me with bits and pieces of slides, bits and pieces of ideas, and of course, a lot of education. Fernando Malala at Liverpool, Josh Slater now in Melbourne, David Wilkie and Dennis Brook.

In USA and of course, Tandy Matthews, who really drove the, the original concepts of Uveitis and, and its immune-mediated background. So, you know, all these guys have helped me, they've taught me stuff, and I've kind of, I suppose I've cheated really because I'm not a card-carrying ophthalmologist. I just got interested in the disease and, and these guys have guided me through it and helped me enormously.

So thank you guys. So what is uveitis? Well, uveitis is inflammation of the uvea.

Well, that's not surprising. You know, when you have tonsillitis, you've got inflammation of the tonsils. It's easy to understand that.

But what is the uvea? Well, the uvea is the pigmented layer lying between the inner retina and outer fibrous layer of the sclero and cornea. So it's the, the, the, the inflammatory change, the, the area where blood vessels are prominent.

And of course, all the pigmented vascular structures, including the Irish ciliary body and the cord, and that's really where the majority of the problem comes from. UVI is always an emergency because anything that happens in the eye has a disproportionate. Long term harm on the structure and function of the eye.

So whenever you have a horse reported to you that it's got a painful eye, I view that as a clinical emergency and needs dealing with now, not tomorrow, now. And because 12 hours with a painful eye often results in damage that is irretrievable in the end. And we know, as you'll see a bit later on, that if you deal with these things early, you can usually Resolve them.

Whether you cure them is another matter, but at least it brings them under control. We divide uveitis into three different sections. I think for practical purposes, this may be a bit theoretical, I suppose, but you know, iritis, which is inflammatory change which occurs in the iris itself, yitis, which is inflammation.

Of the of the ciliary body and then choroiditis, which is inflammation of the choroid, which runs all the way around the eye. So, if we understand that, we can combine these into three different syndromes or we can combine them into anterior uveitis, which is the first two, and posterior uveitis, which is the second two combined. So, we'll be dealing with both of those two forms of uveitis, in a little while.

So, uveitis like laminitis really, it, it's lots of triggers and lots of causes with one endpoint. You know, there's a, there are a whole heap of conditions which result in uveitis, just like there are a whole heap of conditions that result in laminitis. Lots of triggers with one.

A clinical outcome that looks the same no matter what the cause. It's a very poorly understood disease. It's very bad for the horse, of course we know that because there are very serious sequelae to this.

So if you have Damage to the cornea, damage to the iris, damage to the lens, damage to the retina. All this has a catastrophic and disproportionate effect upon the function of the eye, and I don't know about all of you guys listening, but you know my eyes are important to me. Yeah, I, I, I don't want to lose my eye.

Somebody couldn't buy one of my eyes for $100 million. I would not sell them my one eye. So, so a horse feels the same.

And so he doesn't want to be left with a damaged eye that's never going to be recoverable because I want to try to encourage people to do for a horse what they would wish to be done for themselves. The problem with uveitis, just like laminitis, is there's variable responses to therapy, and mostly it's symptomatic treatment that we use. You know, we give a laminitic painkiller, we give a uveitic horse a painkiller.

We give them, medication to try to improve the circulation. We try to counteract the cause if we can. But because the eye has multiple things involved with it, You know, it's a difficult balance to draw because sometimes you can harm one site while helping another.

And in my view, this condition never goes away. It stays with the horse and the vast majority of cases of uveitis, in particular the, the common immune mediated uveitis will be the most, the biggest part of this talk, is that it never goes away. And I just think we shouldn't call it, you know, a recurrent uveitis.

Maybe we should call it equine persistent uveitis because actually even in quiescent times, there are still changes going on that could be triggered into something much more obvious at any stage. So here you see this accumulation of plasma in here you can see the iris is constricted. The iris itself has lost its characteristic colour.

Here you see a painful eye. You don't know what's going on. There, very painful disease.

And here you see the consequences of damaged, aqueous production. In other words, that there's no nutrition in the aqueous and therefore, the endothelium doesn't function. And that leads me to what else it's like.

It's sort of kind of similar to mastitis. So if an organ is not healthy, it can't function properly. Mastitis causes infection, of course, it causes pain, it causes severe inflammation and long-term damage.

But more importantly, for the calf, at least, it causes altered milk secretion, which is not nutritious. It's full of water, it's full of pus, it's full of bacteria. So it's not nutritious, so the calf won't grow.

And the same applies when you come to look at uveitis. Here we have infection, we Pain and it triggers an immune response now and of course more importantly altered aqueous secretion both in quantity and in quality so the aqueous becomes poor quality. It's like mastitis milk that's not nutritious and therefore the endothelium, which is heavily reliant or actually totally reliant on the nutritional content of aqueous.

Can't function. And so it affects the cornea as well. So you can see the problem with this is that unless we understand this, you know, we, we tend to think of aqueous as being aqueous water, just, just a bit of water, but actually how can it be water when it nourishes and and supports the the corneal endothelium which keeps the cornea clear.

So that's really why you have this sort of milky appearance here as you see, there's a bit of hyperpyin in the bottom here, iris spasm, loss of pigment and colour of the iris itself, and of course, a lot of congestion. Pain pulls the eye back, the eyelids close, lachrymation is profuse, and now suddenly you see all the clinical signs of uveitis developing. So I think if you view it laminitis for having lots of causes and mastitis for having lots of consequences, then I think you'll get a better idea of where we are with it.

It is the commonest cause of equine blindness. There are multiple causes, as we said before, and therefore this uveitis itself should be described as a syndrome, in other words, a sign of disease, not a disease in itself, unless we add extra. Titles to that like immune mediated uveitis.

Now it becomes a specific disease. It can be traumatic. You bash the eye, you'll get uveitis, of course you will.

Just like if you bash your skin, you'll get dermatitis, you know, you'll get inflammation. It's, there are responsive forms, immune-mediated forms, you know, there are responsive ones are those where there's secondary changes going on. In other words, it's reacting to something else.

You know, like a different kind of insult, like the cornea's got an ulcer, for example. That does that mean it's got uveitis? Well, maybe, maybe that that's just a reflex meiosis, but anyway, that's these responsive uvetic changes and then the common one, which is the immune-mediated one, and then the infections, of course.

And so here you see the kind of things that we see. These are all uic cases. So here you see A cornea, that's slightly cloudy.

The pupil is constricted and abnormal in shape, as well as the loss of granular ridica. And you also see that the iris has got a prominent loss of its of its natural structure. It's become very thin, it's become very poor in quality and in colour.

Lots of pigment change, loss of pigment, which is a very cardinal feature. This is ocular leptospirosis. And of course, you can see the flash here is very blurred.

The flash is not normal. That's because the eye is soft. Why is the eye soft?

Because the uattic, the, the ciliary body is not producing enough aqueous, therefore, the pressure of the eye drops. So it's a low pressure. The corneas becomes instead of nice and tight like a drum with a nice smooth outline, it starts crinkling because it shrinks back a little bit.

Lenses go cloudy, you know, ulcers develop on the surface because the cornea is not healthy and becomes edematous. So you can understand all of this, and it's a complex pathologies that lead to these signs, but clinical subsets are recognisable, so different kinds of things, as you can see here, this is an immune. Mediated uveitis.

There's ocular leptospirosis, a post trauma traumatic uveitis, a chronic very long-standing degenerative uattic change, and then of course, the cornea with its attendant problems of staining, of ulcers and staining of abnormal precorneal tear films. So all these are recognisable. So it, it, this is the, the classic, disease, I suppose, which classifies as, this kind of, kind of pathology.

The classification, well, here we got our equine recurrent, you know, maybe equine persistent. Maybe we should combine those two together. Anterior uveitis, which affects the front part of the eye, posterior uveitis, which affects the back part of the eye with the Axillary body being the barrier between the two.

Reflex uveitis or reflex meiosis, spelling wrong there, corneal ulcers, corneal surgery, blunt globe trauma, all these kind of things, and then systemic disease where uveitis is part of the syndrome. We think immediately of leptospirosis, ocular leptospirosis, a very characteristic feature. Brucellosis causes uveitis.

Streptococcus ei, strangles causes uveitis, and of course rhodococcus ei. So bacterial infection seemed to do this much more for the, for the classic forms of uveitis, but inflammation of the retina can also be caused by herpes viruses. We know, we know that.

So, these are the things. So if you look at this, you know, we've, we've got these, these barriers here. So virus infections, bacterial infections, protozoal infections, parasitic infections also cause all this.

But the ones that we're mostly interested in when we talk about uveitis in the normal sense of the word, is this condition, equine recurrent uveitis. And that is, an immunological response that links infection. To immune-mediated changes or autoimmune disease within the eye.

In other words, the eye has structures within it where it loses its immune privilege. In other words, now it's, it's going to react to its own tissues, and this is triggered by a very complex, set of immunological changes which take place. These have been well classified.

But it's, it's, it's a, it's a complicated business. I don't really pretend to, to understand it all by any manner of means. Andy Matthews drove it and Fernando Malala and Dennis Brooks and, and David Wilkie, all these guys, Alison Clode in, in America, all these people are working on this disease and trying to find more about the understanding of the, of the trigger and the mechanisms behind it so that we can target therapy a little bit better.

So what are the early signs? Well, meiosis, closure of the pupil, you can see that here very prominently, ocular pain, so the eye gets closed. The larymation is a reflex lachrymation.

Of course, the eye gets pulled back into the socket, so it appears to be soft, but it is soft because there is low. Intraocular pressure. So the low intraocular pressure doesn't help.

You can measure that by whatever means you like, or you can just feel them and actually it's not a good test because it doesn't give you a numerical value, but it does give you some idea of whether the eye is soft or not. Pain responsive to topical atropine, that, that means that the iris, you're, you're relieving iris spasm. By using this, by using atropine, you know, a midriatic.

So you're using a midriatic opens the iris, and the pain goes away. So that's a cardinal feature of uveitis. So where that happens.

And then, of course, you get Aqueous flare, as we said before, with accumulation of inflammatory debris, cells, bits and pieces of protein aggregates and so on in the aqueous which float to the bottom, not float to the bottom, they sink to the bottom. And of course, as you can see here, this iris, this cornea doesn't look normal either because it's soft, it's soft. And then of course reflexly you get a lot of hyperemia of the conjunctiva as well.

So those are the sort of early signs and of course Irish changes as we showed you before. It's a very nice slide from Dennis Brooks. Very kindly lent me this with a lot of fibrin here.

You see the fibrin inside the aqueous. That can't be right. You know, this is, this is like a mastitis cow producing stuff that isn't nutritious.

So you can see, you know, the blood vessels aren't normal, the pigment is not normal, here at all. But If you treat it correctly, you can see how things can start to come back to something like normal. This is more like the normal original colour.

It's not normal, but it's more like it. Much less inflamed, much more pigmented. But of course, the pupil is abnormal, the granularridica have gone, all these things are cardinal features of iritis or inflammation.

Of the iris itself. Cylitis, well, this is inflammation of the cillary body. So atropine responsive, causes reduced pain, slightly low intraocular pressure, and a trace of flare.

So when you look with a slit lamp, you get that kind of yindle effect through the, through the, through the area, through the aqueous. You see that exact same thing. It should be black, it should be completely clear, of course.

But the moment you put a slit on it and look at it from an angle, you can see that it's grey and sometimes you can even see these particles vortexing and floating around, within, within the aqueas itself. And of course that floats up along the back of the back of the eye and then down across the front and so it dumps protein up against the corneal endothelium and that stops it functional. So, so, .

Usually there's some hyper pine, but not always, and possibly some cloudy cornea as a consequence of that, and you can see that in these cases here. Corroiditis is a little bit different. There's a vitriol degenerative change.

So this is the one that occurs in the back of the eye. Now, the choroid becomes inflamed and usually this produces plasma leakage and plasma leakage produces a greenish colour in the back of the eye. So I've got a little video here which you can take.

You can take these videos yourself, by the way, just with your smartphone. It's fine. And this is a very typical case.

All right, it's a little bitty. I don't know where the volume thing is gone, but anyway, you can see here, you can see that the back of the eye, there's a lot of greenish colour at the back. There's a lot of plasma exudation and it's abnormal.

You can see it's rough and congregated inside the eye. So this is the kind of thing that you see. So if you look in the eye and you see it's green, Patently green like this, it is usually a bad sign, so be very careful of this.

Remember that there are very few pain receptors in the posterior segment of the eye, and so pain is not a feature of this particular form of uveitis, and little or no lachrymation as a consequence, if they don't feel pain, then they don't produce tears. So, it's, it's quite an interesting, part of the syndrome. OK, so there's the green colour.

OK, so this is the biggest single cause of equine blindness and it's the most common equine eye disease of all. Remember what we said, it's a syndrome with subsets, not a single disease. Infections, trauma, and immune-mediated conditions, all responsible for causing it.

You don't diagnose what the cause is, your, your treatment. Bound to be compromised in some way unless you just use polypharmacy where you hit everything with everything and hope for the best that one of them is going to be the right thing. It seems counterproductive and sometimes it's actually harmful when you think that you may have active infection like ocular leptospirosis like this and you give them some steroid.

That's not a great thing to do. So you have to control the infection first under those circumstances. But if you give antibiotics to a standard immune-mediated or recurrent or persistent UVI, it doesn't necessarily help you because it's an immune-mediated condition.

Maybe it does help a little bit because maybe it's triggered by bacterial infection. That's common in Europe, not so common in the United Kingdom, for example. Maybe common in your area.

You've got other things that cause it as well. So this equine Current UVI it's been known for many years. In fact, it's been found on the, on, in the pyramids.

I'm not going to translate this hieroglyphics here and I don't pretend it means that it's the right text. But what it means is that the ancient Egyptians reported the identical disorder. You know, and they called it Oculus lunaticus, not lunatic oculi, but that could be the case, of course.

But it's, it's been present for many, many years, thousands of years, and probably as long as horses have lived, and it remains even to this day, an enigmatic and difficult disease to understand. and, but nevertheless, we have this equine recurrent or persistent UVitis syndrome. We have the classic form, very common.

A lot of pain associated with it like this, you know, these kind of things which are very classic. We have the low grade ones which are the insidious ones which you find very hard to see and sometimes all you see is a few iris rests on the, on the, on the anterior capsule of the lens where the iris is stuck temporarily and then released and left. A little bit of the pigmented epithelium behind and then you get the recurrent ones on the posterior side.

These are the posterior segment ones where there are no pain but has this green appearance. So I think if we divide it up into those three, I think we, we'll probably get a better understanding of the disease. So what's its aetiology?

Well, it's a broad name to a group of diseases suspecting insighted stimuli can include any bacterial infections, toxoplasma, of course, protozoal infection, EHV 1 and 4, Lyme disease, others, African horse sickness, all these kind of things. Anything can ostensibly at least cause a uvetic change, and it's just a balance of trying to say, is this a classic syndrome or is it, has it got a specific cause that we need to address and try to overcome in our own way. There's usually a lymphocytic thing.

I'm quite interested in lymphocytes and why lymphocytic inflammatory responses are present, and it's that which has given me some fresh ideas on mechanisms to treat this disease because we have to try to find things that alter the immune process in some way or another. We tend to use steroids, of course, because that's the easy thing to do. But is it?

The best thing, it's not quite the same thing, but you know the lymphocyte infiltrations like this, you know, very common, and then you ask why is it there? The, the condition is bilateral in approximately 20% of non-Appalusa cases. So, whilst you can say, well, 11 eye has been where the other's gone, gone anyway.

I mean, the horse doesn't leave one eye at home while it goes for a, for a, for a ride, does it? Take them both with them and so you'd expect all the insults to be identical, but the fact is it's only 20% of normal ordinary non-Appalusa horses where the condition is bilateral, whereas in Appaloosas it's 80%. and of course, you know, this is, this is an extraordinary, difference in my opinion, and you know, there may be reasons for this.

We know that Apaloosa are very prone to this. They're most prone, they're the most prone breed, I suppose, and the Rocky Mountain spotted horses, same thing, of course. 8 times more likely than other breeds to have this disease.

There's a genetic predisposition and of course specific colours of Appaloosa are more liable to it. So brown eyes are more liable than blue eyes or heterochromic eyes, and there's a high incidence also in German and Dutch warmblood horses. So it begs the question as to whether there are breed susceptibilities or breed.

Or, or heritable, aspects to this disease. Not that they will get it, but that they have a genetic susceptibility to the disease. And then if that's superimposed on the cause, then you get the disease.

There's a circumstantial relationship with intraocular leptospiral infection, sometimes, like in continental Europe, for example, and I know in several other countries in the world, some parts of Africa, some parts of South America, very, very common to have, active leptospiral infections. So if you were to, to remove the vitreous, you can culture leptospira out of that. So if they, if they're active, then you They, they may go down and they may go up and they may go down and they may go up, but they actually continue to trigger an immune response.

So that's a little bit different from the so-called autoimmune forms, which are perhaps more difficult to understand. But in any case, bacteria, protozo, and parasites can all be involved. So the location of the, of the inflammatory response dictates what kind of UVIis we have.

So those are the things we mentioned before, trauma. That's OK. We understand that anterior uveitis, posterior uveitis, and pan uveitis.

Pan uveitis means that everything. So the whole eye is affected. Of course, you only know that.

Mostly you're only going to know that from histology and hopefully, you, you're gonna save the eye. You're not going to be doing pathology on it, but you know, the fact is that many of these animals, do lose their eyes. It's a multi-etiology, multi-feature disease.

And so this idea that every single case has to Look identical and I'll just put up some cases here for you to see that they, they're very different. They look very different and you could be mistaken for thinking they're very different conditions. And, and, and it just illustrates the point that there are multiple features of this disease with multiple etiologies like mastitis, like laminitis, all these kind of things.

They're all different. What does an owner see first? Well, the owner calls you out of course for ocular pain, you know, Eothalus eyes pulled back into the socket, eye closed, or sometimes rubs the eye, sometimes causes, an ulcer on the surface.

Maybe the ulcer is caused by the disease, not so much by the, by the rubbing, but one way or another, the presence of ulceration is a serious complication to this, to the treatment of this disease. Obviously, as you, as we'll work out in a minute, lachrymation, photophobia, they don't like going in the bright light. They, they, they resent bright light, so you keep them in the dark, they're excessively blinking all the time and lachrymation keeps coming out, sometimes swelling of the eyelids themselves, the loss of the dorsal orbital sulcus, you know, swelling indication of the eye, the eye talking to all the other structures around and about because it talks to them.

One part of the eye talks to everything around it and says, Look, I'm sick guys, so be sick a bit yourself, and you know, and protect me a little bit. And that sounds a bit simplistic, I know, but, but it, it's quite uncanny. They can even talk to the other eye actually and change the precorneal tear film and so on.

So, if you see any of these signs, or any of these signs are reported to you, you must examine the horse. And then, as I said before, I view this as an emergency. So, all the clinical signs that we mentioned before, here they all are.

This is the list of much more prominent clinical signs. So this is from your aspect. This is what you're going to see, not what the owner will necessarily see.

So you'll see the layri spasm. See the, the, the eyelashes will be down, whereas the normal eye will be, will be normal, of course, and the eyelids, the eyelashes will be horizontal in the normal way. But as soon as the eye becomes painful, the eyelashes go down.

Of course, that's because the eye is drawn into the socket a little bit and it drops down on top of it. So, ocular discharge, you can see that here very prominently dripping out of the eye. Episcleral congestion, you can see the congestion of the, of these epicleral blood vessels, 360 degree neovascularization around the limbus, that's a very common feature, corneal edoema.

So you get this cloudy cornea, sometimes quite bad in the And with a lot of charatic precipitates within it, of course, because that's what happens if you leave it there for long enough. Aqueous flare, so this cloudiness of the aqueous which you can see with a slit lamp, a fibrin clot which we showed you a picture of earlier on, meiosis, constriction of the pupil like this, for example, and like this and like this, sometimes a fixed pupil like this. A loss of iris pigment, yeah, yeah, it's not here, but you've shown you pictures of that.

And then inflammatory deposits on the corneal endothelium and here these inflammatory deposits are found here. And then blood. So sometimes you even see patent blood within the aqueous itself and you can see that the flash again here is abnormal simply because the eye is soft.

The cornea is thick and the eye is soft because the endothelium is not able to function properly. The chronic signs, the ultimate outcome from these, of course, is that the horses go blind. So this is a blinding disorder.

It's, it's blindingly obvious that it's a blindingly obvious disease, and, and the corneal opacity. Amentation is something which compromises the, the vision. Iris hypoplasia, the iris becomes thin, often with white pigment within it, leukocoria, atrophy of the granular erydica, and of course posterior synechia and iris rest.

So the iris sticks to the lens. And of course, then that leads, of course, ultimately to the failure of the lens production and cataract formation. So here you see iris adhesion, the whole of the iris all the way around adhes to the capsule of the lens, and then an iris, a cataract develops behind it.

Sometimes with with dislocation of the lens behind it. So here you see one that's dislocated the lens, as well. The thysis bulbbie where the eye shrinks back and becomes very Small and very damaged like this, very shrunken eye, and of course ultimately some cases of glaucoma where there's stretching of the eye of the cornea with scarring, the so-called ho's stray, not to be confused with the little linear lines that are very common, commonly found in some corneas in normality.

So, and then ultimately retinal detachment. So all of this is the things that you can detect. So when you see all these, you know, it's pretty bad news for the horse.

Diagnosis, well, firstly, it recurs. So ask the question, has this happened before? Oh yes, it happens every month or every 6 weeks, or he got better 2 weeks ago and now it's bad again.

Remember, if it's an Appaloosa, walk in the box and have a look at the eye. Don't matter whether it's got lameness, you know, at least look in the eye because you need to check them because it's not always very obvious, as we said before. Painful tearing, hypoteny, all the kind of things that you're going to use as indicators that this is a, a bad state of affairs and that UVIis is the likely diagnosis.

Investigative measures. What can you do? Well, you can, you can examine the eye.

Sometimes you have to do nerve blocks to do this, you know, the auricular palpibral nerve, which you can do here below the, just below the ear. You can do it just over the zygomatic arch as well, very effectively just here as well. So there are 3 sites where you can do that.

Very nice thing to do because it enables you to free up the, the upper eyelid, and now the horse doesn't resent you opening it because actually horses have more muscles in their eyelid. Than you have in your biceps and you know, if a horse doesn't want to open its eye, it's not going to open it. And the worst thing you can do is to try to force it because then you're pressing the eye, you're going to cause a lot more damage.

So don't do that. Do some tonometry if you're lucky enough to have a toometer of some description. I don't like the, the, the, the, the inclination one.

I like the rebound one like this. It's very much more accurate and the new one, the turn of it plus or the new one. It is a very useful instrument, very good, giving very reliable results.

aqueous aspiration, oh, ultrasonography you can do. You can scan the eye, you can see this is a scanned eye and you can see the pupils very strictly constricted, really help you with much else, but it, it does confirm to you that this is a very stric very constricted pupil. And sometimes you see the, the iris is very thick.

Sometimes very thin, sometimes you'll see stuff floating about inside the vitreousis, well, inflammatory debris, I suppose it's best called. You can aspirate the aqueous and you can see if it's got proteins and cells in it. You can fluoresce stain the surface of the eye because actually every single painful eye must be stained.

It doesn't matter. I don't care. It's got to be stained.

So if the horse has got a painful eye, it's stained. Even if you can see the ulcer, it's got to be stained because you've got to understand what the ulcer actually is doing. Because as we said before, one of the most important things is if there's a corneal ulcer, the therapy of UVI test becomes more problematic.

So use sedation, use the nerve blocks, and examine the eye very, very carefully. Don't say anything until you've examined the whole eye and make sure that you understand what components are involved and therefore, what kind of UVI test you have present. The differential diagnosis for this of course lots of things, that look like it, you know, so corneal lacerations, corneal ulcers, you know, tumours, you know, all sorts of things.

This is the same eye as this one, a foreign body. You know, you, you tend to think, oh, hang on a minute, this is all, this is all very obvious. But actually, quite commonly people think, oh, it's got uveitis because it's got pus coming out of its eye and they don't look at the eye.

When you open the eye, you've paralysed the eyelid, you've opened the And here you find a foreign body. Of course, it's got uveitis. You can see that the pupils very constricted.

This is the reflex uveitis. In this case, reflex genuine uveitis because it's got stuff in the anterior chamber of the eye and it damaged the ciliary body as well. And so this is a genuine re trauma related uveitis rather than just a reflex meiosis, which happens in some cases where they get a corneal ulcer, for example.

So, lots of different diseases, discoids and systemic lupus erythematosis syndromes, purprareica, African sickness, conjunctivitis, neoplasia, all these kind of things can be mistaken for uveitis both in, maybe sometimes they're together. You know, there's no, no reason why they shouldn't be together. You can imagine a horse that gets an ulcer.

And of course, may have an ulcer secondarily to the uveitis, but you don't notice the UVI test until the ulcer is gone. So try to remember that comorbidity can exist as well. So, this is just to show you a few of the, this is lupus-related uveitis.

This horse had all the signs of lupus erythematosis. You can see it had scaling on its coat here. And then this way, this was the eye at the time of presentation, this was 24 hours after steroid injection.

So you can see it's a very prominent cause of UVI it's commonly forgotten. You know, so don't forget to look at the horse. You know, just because it has a painful eye doesn't mean you don't look at the horse.

In fact, It makes it even the more important to look at the horse, to make sure that you're treating the right thing. So where you have multi-systemic disorders like this that affect different parts of the horse's anatomy, and its physiology, then be very careful with it. So you may want to do that.

This is discoid lupus now and you can see this has got UVI. You can see it's got keratiti as well, solar-induced keratitis, but of course, it's got the characteristic features of discoid lupus as well. So you can see that here.

There's a different case here. But it illustrates the point that there are diseases in which Uveitis is a distinctive component. Now, the problem is, is it that or is it comorbidity, and that's something which you have to establish yourself and you have to be satisfied with what you're doing.

So how do you manage this disease? Well, examine the animal, you know, if there's a donkey, donkeys can get it as well. By the way, don't think that the donkey is exempt, although the number of donkeys I've seen with this, and maybe there's somebody out there who can.

Tell us, you know, how common uveitis is in donkeys, but it seems to me the immune-mediated forms seem to be very rare in my experience. I've not much experience of donkeys compared to horses, of course. So examine the eye, eliminate other forms of uveitis, eliminate corneal ulceration because if corneal ulceration is present, You can't use steroids topically and you can't use them systemically.

So you have to use non-steroidal drugs. So that's using Ocufe or diclofenac and these kind of topical non-steroidals as well as systemic non-steroidal treatment to try to reduce the inflammation. But you have to control the ulcer.

You can't put these animals on steroids because you're just going to wreck them. So be very careful, the treatment differs if corneal ulceration is present. General the therapeutic objectives control the pain.

We have to do that. And there's a way of doing that, of course, by reduction in intraocular inflammation, non-steroidals, and corticosteroids, reduction of iris spasm, meiosis by atropine. Don't try to treat these with tropeamide and other stuff like this, and it just doesn't work.

You need atropine. Of course atropine is not without its hazard. You may find that an individual horse may have a, a strong intestinal response to the atropine, even administered on the eye.

So I think, Dennis Brooks describes quite a few of these and that we, I don't see them very often in the United Kingdom, but that may be because we're using slightly different forms of the. Drug or that the disease we're dealing with is a different form of disease. So, prevent self-inflicted trauma because these animals rub their eyes a lot and cause ulceration and cause damage.

And then our objective is to limit long-term ocular damage and preserve vision. That's what we have to set out to achieve. And then Of course, ideally, we want to prevent more episodes because each time we get an episode, we go back to this again and then we get, we tumble down the pathway towards a catastrophic outcome.

We've got to preserve vision. I mean, that's what we're all about here. You know, it's easy to take the eye out.

If the eye is irretrievable and it's painful, well, then remove it. You know, there's no problem with that. I don't have a problem, but if you can save the eye, then the horse will be grateful to you because just like me, I want two eyes.

I don't want one, but what I don't want is a blind, painful eye, even if It has to go because that's counterproductive and you may just have to tolerate that and understand what's going on here. So we need to minimise the progression and minimise recurrence. So, we need to be aggressive.

So we've got to, you've got an acute case, a very severe case like this where this has happened. There wasn't anything yesterday and now it's like this. OK, you've got all the signs of a very acute change, you know.

This is, this is things that you've got to tackle immediately. You've got to try and pounce on this and really hammer it. Keep the horse in the dark, you know, relieve the, the layro spasm by dilating the pupil.

Try to reduce the amount of lachrymation by reducing the pain, by non-steroidal systemically and corticosteroids topically if you have to, and then make sure that you persist with it until the condition has resolved. So make sure you're treating the right sort of uveitis. You know, make sure the treatment is applied properly.

Make sure it's early and aggressive. Make sure that your management is contributing towards the success of the treatment. So don't put the horse out into bright sunshine.

You know, you've got to put it in the dark, not pitch black. But in the dark, so that the eye, so that there's no photophobia, you've got to overcome that. You've got to treat it properly and you've got to treat it hard and you've got to treat it for a long time.

Here's the slit lamp showing the Tinder effect as you can see, here's a very nice picture from Dennis. He lent me this and I'm very grateful to him for that. But you know, don't forget to examine the eye.

I always look with bright lights and try to do this, but remember now. Blocks, be kind to the horse. Don't try and force the eye open.

Use all the science you can and try to understand what's going on. Try to feel the pressure of the eye if you haven't got a tinometer. Not many people have gottenometers, you know, they're rare actually, regrettably, because they're very expensive bit of equipment that you may only need once a year, and that's of course, that makes it a little bit more problematic.

So once you've identified the type of disease, well then that gives you a chance, doesn't it? You know, it gives you a chance. All the things that you can apply to the eye or to systemically, you, you know, you can control active infections with antibiotics.

You can modify immunity, you know, by steroids, by intracameral injection, intra-e injection. Of small doses of triamcinolone, very small, you know, 1 or 2 milligrammes of triamcinolone, into the back of the eye sometimes helps enormously. But if there's active infection, is that a great idea?

Probably not. And so you do need to be careful. And then, of course, there are cyclosporin implants, you know, these can be put in as well.

This is a new idea, well, relatively new, and Brian Gilger developed this and a great guy, Brian and, and, and has driven equine ophthalmology. If you want a book, you know, then buy his book, but you also buy Dennis's little handbook, which is just amazing. Both of these are very helpful for just ordinary people out in practise who want to get more information about some of these more difficult conditions.

Yeah. Oh, hang on. That was, that was not good.

Just to remember that you can inject into the eye. OK. So remember you can put some chemicals into here if you like.

Yes, corticosteroids for the most part and antibiotics. So you can either inject into the vitreous, you can inject into the aqueous, you can sample the aqueous. You can do a lot of things to try to help you understand what's going on.

The fact is, It's difficult and not every horse responds in the same way as every other one. In fact, my experience is that there are no horses that respond in the same way every time. So every single case I've ever seen has got a different kind of response.

So early strong intervention and persistence, you have to drive on and drive on and drive on. And of course, Owners get tired of trying, you know, and horses get tired of trying. They don't want you.

The first day they love you because you've killed the pain. Second day, they're not so happy with you. And the 3rd and 4th day, there's a problem.

So you may have to use some long term management methods such as the placement of naso of, of subpalpebr the vast systems of varying descriptions. Cruiser and Miller make very good lavar systems. Don't try and make them yourself.

My experience is if you make these yourself, they're almost always a disaster. So get the commercial ones and just have one handy, whenever you need it because they do make long-term management much more practical. Analgesia, of course, you're going to use flunixin, that's usually the way topical maxetrol, ointment or drops, and then atropine.

Atropine is in my view, the most important single thing of all, because that relieves the pain associated with iris spasm. Reduction of meiosis with topical atropine is good, but just remember to watch for the colic watch. Sometimes people report it happens a lot, but in my experience, it hardly ever happens.

I, I mean, I use 1% atropine. I, I agree, I don't use 4%. very often anyway, and when I do, then I am very careful.

But, but for the most part, you can add with a little phenylephrine if you want to try to get it to dilate the pupil and you persist until the pupil is dilated and you keep it dilated. That, to me, that's probably the most important single thing of all. There's no point in using tropicamide.

It's too weak and it, it doesn't help at all, but atropine is great. Because it dilates the pupil, the eye gets back to normal, the horse feels very much more comfortable. And now you can start to take some other action, including corticosteroids.

So, reduction of intraocular inflammation, be careful if you see an ulcer, be very careful. Remember, all painful eyes must be stained, OK? And you only use corticosteroids in the absence of ulceration.

So you can do it topically or subconjunctially or subtenins injections, or you can do it. Peremptorily by oral prednisolone, administered daily, low dose, continued prednisolone. No problem with it, but be careful which the case is and make sure that you are getting a response.

Pain control, flunixin, or the phenob non-steroidals. We, we don't use much else, I think, and everyone will be, be very familiar with these drugs, I am sure. Cyclosporin, interesting, interesting topical medication.

I'm not really Very convinced that it does very much, to be honest, and, my experience is very poor, but intraocular implants do do improve the delivery, and there's several ways in which this can be done all again. Courtesy, Brian Gilger, who's developed the subs, sclero choroidal implantations here, supracorroidal implants. You put these little implants in, and then suture the thing back, and then it dispenses the, the, the cyclosporin into the back of the eye, into the eye itself over months or even years, and that does bring about a considerable improvement.

Pain control topically, Voltarol, you know, diclofenac and these kind of things, florirofen, Ocufen, aspirin, topical anaesthetics. I, I don't fancy topical anaesthetics because it masks a lot. Sometimes it's necessary, particularly when you're examining the eye, but I try to avoid it if you can.

Systemic corticosteroids, prednisolone or dexamethasone, you can do one or the other. And then sometimes you need to remove the clot, from the aqueous because that's sometimes a block to the improvement of the horse and you just inject a little bit of tissue plasminogen activator, into the eye. It helps a lot.

It's very very expensive, but it's a spec. Spectacular response as you can see just in a few hours, this is the consequence. So you can see how much of an improvement you can get very quickly with this in clearing the eye.

There are patient compliant, patient and owner compliance difficulties. Owners get tired of doing it, horses get tired of receiving it. be very careful when this is the case because the horse, unless you can medicate effectively, it's, you're doomed.

You know, it's not going to solve the problem. You have to have a facility to keep this going as long as it's necessary. You may have to change the treatment from time to time.

Therapeutic deficiencies usually because we have got drugs that are poor for horses. They're not. Made for horses and we apply tropical drops that wash out because there's a lot of lachrymation.

We apply creams because we think that's better, but they actually they don't deliver enough long enough. So you can see there are all these practical difficulties associated with it. Intracameral injection, gives you a high concentration of the drug, but you need to be very careful, you know, the, the, mostly, we use TPA or we use triamcinolone and gentamicin, but please don't use too much, you know, get the doses exactly right, you know, Very low doses, consult with a specialist before you do this.

You know, don't go around injecting horse's eyes with these things without consulting someone who can give you guidance on this. That's why I'm not going to go into too much detail with this. Shouldn't really be sticking needles in eyes unless you know what you're doing.

It is possible, of course, to use 4 milligrammes of preservative-free gentamicin. If you use more than this, you could kill the eye. So you've got to put a very small dose, into the, into the vitreous, sometimes with some, with 1 milligramme of triamcinolone as well.

That's a good mixture to give a dramatic improvement, but does it solve the problem? Almost never. Other treatments, antibiotics, well, not so sure.

They're much use to us. Preservation of vision, you know, you've got to set out to do that, really, OK, by preventing recurrence and by maintaining the medication to the point where the eye is as normal as possible. Remember what I said at the beginning?

You know, the most important thing is that you've got to get to the end of this. You know, you've got to try to get to the point where the horse is comfortable, but don't trust this disease. I, I think the message I try to put across is never trust the disease.

It's not going to go away. You're Gonna be sitting waiting till your back is turned to come back. So you've got to limit cataract formation, you know, try to avoid all that if you can.

Lots of other treatments have been tried, acupuncture, all sorts of other things, you know, damage the good eye for a sympathetic effect was published in 1867. So if the animals got damage in this eye, you go and hit the other eye with a spike or something, and that makes it open to this eye. Well, it's not.

Point is it? Homoeopathic remedies are universally rubbish, and never worked anyway, and neither are they ever going to work. magnet magnet polarities and all sorts of stuff that's out there.

In practise, medical treatment is the only real practical option and it works, but you have to be aggressive and you have to be early with the treatment. So this is a horse that Dennis treated and you can see the, the consequences of the treatment. It's an improvement and it's very good.

Cyclosporin A implants are difficult to get and please be careful. Don't go thinking that you can just plonk these in. You know, refer your case to someone who's used to doing it.

It's, it's not as easy as it seems, and Brian has developed different kinds of implants, but they are very useful because they do tend to give you long-term control of the disease. You can do a surgical vatrectomy, with it, and I'll show you one that we did, when I used to do these things. This is the vatrectomy working here.

You can see all the crud in the back of the eye, all the inflammatory stuff, the fibrin inside the vitreous being aspirated out. And, but there are dangers with this, you know, you can have all sorts of difficulties with it. So contact someone who knows how to do it, you know, don't try and do it yourself.

Of course, the lens is cloudy or the cornea is cloudy, you have to have a second camera inside the, the, the posterior segment of the eye, and that's difficult when you've got two ports to manage at the same time. Reasons for therapeutic failure, you know, taking too long to get there. You know, it's, owners call you, you go.

It's as simple as that. Fact is, when you ask the owner when did it start to sale, 2 weeks ago, but I've been putting cold tea or barracic powder or golden eye ointment in the eye, you know, you know, you're in trouble from the start, you know, and, you remember, you've got to try to get ahead of the game, OK? And obviously, if the wrong drugs, wrong routes, wrong doses, and wrong intervals are used, then of course, it's going to fail.

Got to assess progress, OK, try to follow it through. Some cases require lifelong treatment, management, and preventive measures. So I'm going to stop there now because my time has run out, and I would very much welcome, any questions.

But the most important message we're trying to get across, get to it early, examine the horse, establish the diagnosis, and hammer the treatment until you get control appropriately. Thank you. Thanks, Derek, that was splendid, thank you so much.

We, we've got a few fans in the room, ex-L Liverpool graduates like myself who are saying hello, so they're they're virtually waving at you. So, yeah, that's great. Just while we're waiting for people to come up with any questions, it, it looks that we've got a really mixed group from all over the world on, so it'd be lovely just if we've got anybody from Africa, Derek obviously, South African born.

Then bred in in there but then up to Zimbabwe, he spent a lot of his time there, so it'd be lovely to see where people are listening in from if you want to just . To to put where you're listening in from. So Victoria, who I think is one of your ex-stents, is listening in from Sweden.

Oh yeah, hi, hi Victoria. Victoria from Sweden, let's see if there's any anywhere else from Romania. Yeah.

And I'm sure a few more will come through. Virginia, US, and I know Jenny is an extent as well, I think so. Right, let's see if there are any questions.

Are the Netherlands, there we go. Ellen from the Netherlands. Angie says she's from South Africa with strong Zimbabwean connections.

Thank you for a great talk. We've got Egler from Lithuania, Anna from Houston, Teresa from Portugal, so all over. Yeah, it's great, it's great.

Rachel's saying, hello from Texas, you mentioned that you cannot use systemic steroids in a horse with a corneal ulcer when trying to treat other disease such as autoimmune disease. Why isn't the cornea? Why isn't the cornea a privileged area where systemic drugs don't really easily reach?

So should systemic steroids be OK to use? I, I, I, I, I understand the argument. I mean, you know, that's the, the argument is, of course, that when you give steroids systemically, it doesn't get into, into the, into the tears and it doesn't get into the cornea because the cornea doesn't have a potent blood supply.

The problem is that in many cases it develops a blood supply. And that's one of the problems with, with the, with the more recurrent forms of uveitis. So the moment they get this, 360 degree neovascularization that's invading the cornea that reflects the body's, I suppose simplistically, the body's willingness.

To try to reconstitute the function of the cornea, to try to get the function of the endothelium right again. as soon as you get that, now you're delivering the steroid to where the ulcer is, and I, I, I think we just always have a slightly uncomfortable feeling about it. That said, I have done it, simply because sometimes there's no option.

You know, the, the nonsteroidals, they're not working, you know, you can't get non-steroidals onto the site. You need something to break the cycle of deterioration, and, and I do understand that. In fact, in some ways, although we always say, you know, if a horse has, has, has a corneoser, should never ever use steroids.

There are occasions when there's a perverse logic to it. Because the steroid, the, the, the ulcer may be caused by inflammatory cells that you want to get rid of, but if you're prepared to manage that, you know, and make sure that there's no fungus and no bacteria that are going to destroy the eye as a consequence of it, then maybe a single dose doesn't necessarily always do harm. But as a general rule, you know, that's the, the sort of Thing, you know, we just simply don't and you've always got to be a bit you've got to be careful using them, haven't you?

But we're fortunate, we've also got David Mags who I noticed was listening into the webinar and of course David is a very famous small animal ophthalmologist, David will be giving lectures later on in. The in the week, along with Ron Offrey, who are two of the authors from the splendid ophthalmology bible that if you're interested in from a small animal perspective, it's a great book, so, free to come in on those. Well, I think absolutely, thank you.

I mean one of the things is that you know. Sure they will both recognise the difficulty of understanding this this this complex disease in horses, but I know that uveitis occurs in as a panel, as a part of a lot of other diseases in small animals as well. I'm not a card carrying ophthalmologist by any manner of means.

I've just been interested in the disease. 51 years now, and, and, and I've just managed to soak up some of the information from some amazing people. And it just strikes me as a practitioner myself, that, that I, I still struggle with the disease.

I still have failures and they really just stress. Me, you know, where you start out, you get a little bit of an improvement. Oh, the owner's happy with you.

Everything's fine. Then 4 days later it's bad again, worse, you know, and the thing starts slipping down again. You start hammering it harder and then the horse becomes non-compliant and resentful because a painful eye makes a horse unmanageable.

You know, they, they become very sore and they hide in the corner. They want to kick you as soon as look at you because they know you're going to do something that's going to make them even soreer. So I, I think, you know, these guys, you guys and small animals, you'll, you'll appreciate this.

I know you will, and the difficulty of dealing with the disease. And I think that's the, the great thing, you know, when you came to Liverpool with that practitioner's hat on, you just bring a different perspective than somebody who's been, you know, in university the whole time, so it's great to have that mixture, you know, at any level, isn't it really? Well, I think, you know, we, we all have to be practical and at the end of the day, you know, when you, when you haven't got a tenometer, you know, it's no good saying, well, you have to have a tenometer in order to get an impression as to whether the eye is hypertonic or not, you know, whether it's got glaucoma, because glaucoma, very common sequel to this, cataracts, glaucoma, all these things are sequels to this, and you, you need to know which stage of this you're at.

You know, and, and just by using your hands, you know, even if you touch your own eyes, you know, press on your own eyes 5 or 10 times with your middle finger, with your middle finger, just like that, and press, and then press on the, on the eyes of the horse and bounce the two together. You know, you'll get an impression as to whether it's soft or not, you know, and oh God, this is soft. Sometimes when you put a scanner on the eye, you can tell whether they're hard or not, you know, where the, where the scanner doesn't indent the cornea.

You know, when you press on a scanner, you could get a flat surface because if it flattens completely, you know, you know it's low. If it doesn't flatten at all, you know it's high. So it's it, but it's all a question of just learning little practical skills that, that make it possible to treat this disease in genuine practise, you know, but there are some circumstances when referral becomes necessary or at least consultation with a genuine specialist, and I heard, you know, I, I contact people.

Regularly because even though I've been at this for many years, there's still cases where I say, oh, this is not going right, you know, what can I do? And I phone a friend, you know, and, and, and we, and we get information from them and they say, Well, why didn't you try this or try that? You know, I've been trying to treat the disease with methotrexate with very considerable success actually, which is something.

Which I'm just interested in continuing with, but you know, that's at the very early stages of the treatment. It's an immune modifier, of course, but it's an anti-metabolite, so that's a very safe drug to use, but we don't know very much about it in horses. I don't know if they use it in small animals, but it's quite a, it's a forgotten drug for veterinary medicine, you know, and, and it seems to work quite well with some of these cases, not all of them by any manner of means, but some, at least.

Got a few more comments. We've got . Tracey listening in from Canada.

The problem, as you know, with webinars is you can't hear the tumultuous applause, Derek. So Tracey says thank you very much. And we've got Joyce listening in from Zambia.

Henrietta's saying she's in Northern Ireland, she's not sure whether that that's a part of the UK or the EU, and I think we all share that, quandary, don't we? I think it's still the UK at the moment, Henrietta, but who knows for how long. Not for long.

Anyway, we're not gonna talk about politics. We, we have enough of that on the telly anyway. Natalie says hello, vet student from Kosiki in, Slovakia, of course.

As an owner of a horse with uveysis and recently been to an ophthalmologist, excessive blinking is considered a sign of pain, but atropine is applied to relieve pain from meiosis. Would excessive blinking after atropine applications suggest continued pain or an issue of inability to adjust the eye to daylight? Not when putting in maxotron mass the rest of the time.

Yeah, I think, I think you be with a bright light, it's going to be and you'll see that. I mean, if if you ever have atropine in your eye and you go outside from the, you know, if you ever have that or even tropiamide, and your pupil is dilated, you know, you, you can't really hold your eye open, but that should be closed then and held closed. They shouldn't.

Continue to blink. In my experience, if they continue to blink, they continue to be in pain. And then you have to just make sure that the cornea is normal, you know, that you've not got something else that is not only the iris spasm, which is the sole source of the pain because it can be corneal ulceration, even punctate ulceration, or, you know, there could be something else associated with it.

But this business of the structures of the eye talking to each other, I think is quite a nice concept, you know, and, and you change. Just the lachrymation on the other side as well to try to give it some protection, you know, just a natural response mechanism for eye protection because the eyes to any animal, you know, if you don't have eyes, you know, and you're in the wild, you're a sandwich for a lion double quick, you know, and, and, and I suppose that's just evolution, I suppose even losing one eye if because of the way the horse is, if they come on the part of you that you're still a sandwich, aren't you? Yeah, well, you, you are, and I think, you know, you know, I just think if two eyes are important to you, then two eyes are important to a horse, and, and, and, and I think we've got to set out to preserve vision and preserve, first you've got to preserve the eye because if you don't preserve the eye, of course, then the vision's gone anyway.

But, but first to preserve the eye and then to try to find ways of preserving vision by preventing progression. So you can prevent the progression of the disease to go further down this path. So, you know, try to get, avoid the, the long term sequels to uveitis, which are glaucoma, cataract, retinal detachment, thysis bulbie with a knackered eye, you know, massive corneal precipitates, you know, infiltrative cornea corneal.

Conditions, dislocation of the lens, you know, all the things that go with the catastrophic outcome, and I, if it gets to that, you know, then remove the eye. You know, because it's not, it's not, the horse will be relieved for having a, a, a non-painful blind blind eye as opposed to a painful blind eye. You know, it doesn't make any difference to it.

This is a blind horse, by the way. Just in case anybody else has any questions, just a a few announcements. Tomorrow we've got 8 a.m.

UK time, we've got large animal surgery basics with Doctor Paul Woods. At 1 till 2, we've got into cat tension with one of my good friends, Doctor Sarah Heath, and then 7 p.m.

A practical approach to diagnosis and treatment of feline herpes virus. And I think that is David Mike's actually, who's going to be giving that talk. So I'm, I'm looking forward to all of those tomorrow.

They should be cracking talks to spoil the day tomorrow. A few people on Hoover have been asking me, I've been, Derek, playing my guitar on Facebook during. Lockdown and people say that if they record it, it's a great way of keeping the birds off the garden.

So I am going to do a little, a couple of tunes on Facebook Live about 100 tomorrow. So if you really want to have a miserable evening, then feel free to find me on Facebook. But, .

Derek, thanks again, loved having you on. It's always a joy to listen to you. And you know, who knows if we go back to that, final exam again, I might, I might do a bit better than last time.

I'm sure you did great. To be honest, my memory has gone to hell, but I, but I wouldn't have passed you if you didn't deserve it. You've done a few finals in your time, haven't you?

Thank you very much. Thanks very much, Derek, thanks everyone for listening and we'll look forward to seeing you on one of the webinars and obviously do go on to the to look at the on-demand stuff as well. Take care everyone, good night.

Thank you very much bye bye. Thanks again, Derek, bye bye.