Description

Dermatological cases can be highly frustrating due to their often-chronic status as well as frequently having a poor response to therapy.  To try and alleviate these problems it is imperative to have a set protocol which can be followed to reduce the risk of misdiagnosis and therefore ineffective treatment plans.

Transcription

Well, thank you everyone for coming to have a listen about a practical approach to equine dermatological disease. The hope with the lecture today is to go through the general presentation, some of the diagnostics available, and hopefully come up with a treatment plan for the vast majority of cases. When we think about dermatological disease in horses, I think we can break it down into a number of categories, which will hopefully guide us in our treatment plan and, diagnostic modalities.
One of the biggest that we suffer from in the equine industry is prurituss, and we'll go through a few of the diseases associated with that. When you think about some of the scaling where this is normally set due to a secondary, sorry, a primary disease with secondary scaling, whereas pruritus is normally a primary disease. We obviously have oncological manifestations, and we'll come on to sarcoids as I think that is probably the most common oncological manifestation of dermatological disease in horses, although there are plenty of other ones that are out there and should be considered whenever we're looking at any issues with skin.
We're then going to look at the diagnostics, and how they can hopefully really indicate what therapeutics are going to be utilised in, in each case. But why are we interested in skin disease? You know, I think it's one of those diseases that is highly frustrating to a number of clinicians, but it is really important to note that this national equine Health surveillance, indicated that skin disease is one of the most common ailments that, the equine population deal with.
And you can see other than lameness, which is not too far behind, all the other major diseases are, a, a long, long way behind. And when you consider that the skin to includes sarcoids and melanomas, there's a lot of pruritic courses that are making up the vast majority of that. Why do clinicians find these cases difficult?
And I think for me, I still find them slightly frustrating and difficult. Part of it is that often these cases are distressing for both the horse and owner. Skin disease is incredibly uncomfortable and can be life consuming for that animal involved.
Also, I think for me, it's often been that I don't know if I'm going to be able to cure this situation. You know, lots of these skin disease horses really do struggle to come to a resolution and hopefully at best you can manage them rather than cure them. In a lot of cases, there's not going to be the empiric treatment, and by that I mean when you go and see a colic, you know you're going to do X, Y and Z and you're going to give certain drugs in the vast majority of cases.
There are obviously some empiric treatments that we can undertake, but they are not normally curative. Again, they are managing the disease. And it can be emergencies.
I know it's not very common for that to be the case, but I have definitely seen horses present to me that are so severely pruritic, they are, self-mutilating to the point where they are, they are life threatening. For me, with every single disease process, I think the important thing is to have a consistent plan, and a consistent route of options that you're going to take. Now obviously, the first and simplest route that you can take with any disease is to say, OK, I want to just do empiric treatment.
And by that, in these situations, I mean something along the lines of glucocorticoids, or whether you do topical medications, be it a shampoo, or a Medicaid shampoo or a soothing shampoo. And in many cases, that is going to be the right choice when you first start these. But I think really, you've got to look at it a little bit more systematically.
History is absolutely critical to all all cases, but particularly true in your dermatological disease because that's really going to elucidate some of the, hopefully some of the presenting issues with these cases. Clinical examination, going to be vital so that you can document the exact locations of the lesions. And also the type of lesions they are.
And both of those things are hopefully going to lead you to a differential list that is going to then allow you to take the most appropriate diagnostics to lead you to an appropriate treatment modality. I know that is consistent with all diseases, but I think when we look at it for horses, for dermatological disease, we've got to consider some really important things in the history. What is the age of the horse?
And the reason. The reason that I talk about the age of horses is that when you're looking at a very young foal, when they are starting to shed their coat, it can be that they are very itchy at that period. So if they're a yearling coming through the new coat, don't worry.
Also, when you look at things like papillomatis virus on the, on the nose, warts, are they young, in which case you can ignore them, they're they're completely normal. But if actually you've got a 14 year old horse that suddenly has papillomatis virus on its nose, that indicates that there is something else going on with that horse, something that might be immunosuppressive in it. The environment is critical.
So when we look at the environment of the horse, we're considering both its outside world and it's inside world. When we look inside, what is the bedding, what is the feed that horse has been given, how clean is the stable, and all of those sorts of things linked in together. If we're outside, is there running water?
Is there stagnant water more importantly? Is it a very dry win windy place versus a wet, still place? So all of those can play a role in particularly things like insect bite hypersensitivity.
The duration of the clinical signs is vitally important. If this is a very acute onset with nothing leading up to it, then we can consider, say, the mites as a bit more of a problem. Whereas if it's a really insidious onset that's been gradually getting worse, you might lean a little bit more towards neurologic or I'm sorry, oncological or maybe some sort of immune-mediated disease.
As I've mentioned, the bedding is quite important, and paper bedding is probably the least allergenic of all the beddings, and therefore it's one of the ones that we use when we are trying to make a break. So when they come into the hospital and we're trying to get the hives under control, we put them on paper bedding and cut everything else out of their lives. Obviously, it depends on each individual horse, sometimes shavings, sometimes straw will be the problem.
Feed is a difficult one. We don't see too much too many feed allergies in horses. It's not a common clinical complaint.
But we do see a few, and I think what's important is breaking down exactly what that horse is being fed. Is it being fed alfalfa, which some owners do report anecdotally is quite a high risk factor. We also have a really good look at the supplements.
You know, so many of my patients come in and they're on 10 supplements that so and so has said that they need to try this to try and fix the skin. And actually when you break it down, they're getting so many different allergens, whether they're allergic to them or not is a different matter. Being thrown into their body every single day.
It's for me, it's better to wipe those all out. No horse needs a supplement other than racehorses when they're on high energy diets. Have a look at the intacts.
Is this the only horse that is affected or other horses affected at the moment? Because that's gonna give you a good indication if you whether, whether you think this is infectious versus non-infectious. Think about genetics.
Now we don't see too much of this in the UK obviously, but, things like quarter horses can have herda, which is hereditary equine regional dermal asthmia, so where their skin becomes stretchier and can have quite marked clinical signs associated with it. Or they can have things like fragile warm blood syndrome. So there are other problems that are going on that we really need to think about them.
And finally, really grill that client on what the previous treatments have been. So, so many cases will come in that have had hundreds of different shampoos applied to them, and actually, you slowly realise that maybe this owner is just aggravating the skin by washing it every single day with something that's quite caustic. So just be aware that actually it could be an iatrogenic dermatological disease rather than it being a truly infectious or immune-mediated.
We considered the history, which is quite a long history and does generally take time to discuss with the owner. And the examination now is critical. I always run blood work in these cases, and there's two reasons for that.
One is, could this be a perineoplastic syndrome, and we're going to see some abnormalities in the white blood cells or in the liver enzymes. Also, we're going to look for some inflammatory markers. So if this horse truly is infected, you would expect the serum mammaloid A and things like that to be elevated.
You do see some tic causes secondary to liver disease, so I always, excuse me, want to rule that out as early as possible. When assessing the skin lesions themselves, it's really important to document the location of the lesions. It's easy to walk away and think, I'll remember that, but I guarantee I do not remember any of the locations of any of these lesions about two days later.
Photos can be very helpful in these cases if you've got the right IT software in place that you can easily locate it onto the history. Otherwise, drawing diagrams in your clinical notes is, is absolutely fantastic. And with that, I want to know the location of them.
Is it mucocutaneous, which can lead you towards an immune-mediated? Is it facial? Is it dorsal ventral distal limbs?
You know, all those things are going to lead to is it coex? Is it collicoides? What might it be?
And hopefully it's going to start to untangle the picture a little bit for you. Lesion description is quite important. Now, it's quite difficult to go through every single one in in this lecture, but most of the time it doesn't make too much of a difference in the cases we deal with within the equine industry.
Within the human world, it does make a huge difference because each of these has a very different aetiology. And maybe that is naive of me to consider that there is a difference, but it does seem that way. But when considering each lesion, consider whether it is infectious, so maculal papule, does it have pustules in there, or is it some sort of immune-mediated plaque or wheel?
Could it be a vesicle or bullet on a mu mucocutaneous junction, again leading towards immune mediated. And is there alopecia or hypotrichosis? Is it hyperkeratisis or lichenification?
All of these are gonna say, OK, there could have been a one-off insult in the alopecia state or a chronic hyperkeratotic inflammatory state. And then go into your scales and crusts. All of that's gonna hopefully lead you to deciding which diagnostics that you are going to want to use.
So a few of these are very simple and very cheap and quite easy to do. So, sellotape preparations, great if you consider you've got oxyurist aqui. So if you've got any consideration that the horse is scratching its anus, then apply the tape to the perianal region and then plop that tape straight onto a slide with a drop of mineral oil, or if you're considering that choreoptes might be your option, then pop it on with a bit of potassium hydroxide.
I do use sellotape strips sometimes in my choreoptic ones in the feathers, but it has a fairly low strike rate. So a negative doesn't mean it's not there, it just means you haven't had success in finding them. Some of those correoptes though, using a brushing can actually increase your rate of success.
So brushing into a nice pot and collecting the sample. Remember that cooptes are highly mobile, so it is possible for them to try and escape from the pot. So, once you're done, get the lid on there and and make sure you get that to the lab for investigation.
Scrapes can be used, but I find them infrequently required in the equine industry. We don't see the burrowing mites that you see in some of the small animals, so the sarcoptes, scai and things like that. But if you are worried, then it's important to do the technique properly.
There are two types, there's a superficial scrape and then there's the deeper scrape. Superficial is going to be looking more at your epidermis and whether there are achantholytic cells or anything like that, whereas your deeper is looking for the likes of mites. It's important, therefore, if you're doing a deep one, to use a scalpel blade, both the scalpel blades, sorry, but to ensure that you get deep enough through the tissue so that it starts to bleed.
Remember to have that blade at a 45 degree angle and cut away from the actual blade edge so you don't cut into the skin. We're not looking to remove a piece of tissue. Obviously you part the hair because you're not interested in the hair itself.
And then place that sample on a slide with a bit of potassium hydroxide. And that should give you a really good indication as to what might be going on in there. Culture and sensitivity, I think, is one of the most important diagnostic modalities if you really are struggling with skin diseases.
Obviously, I think we have to be slightly cautious with our interpretation because there are a high number of commensals on the skin in all cases anyway. So these have to be interpreted in light of sensible clinical knowledge and also what is growing and how much of it is growing. Are you interested in aerobic versus anaerobic, and the vast majority of cases with this is that it's aerobic.
It's unlikely that there is an anaerobic disease ongoing within the skin unless it is underneath the skin. So I rarely, will submit anything for anaerobic. In many cases, I'll start with a superficial swab, but then I'll move on to a deep culture if I'm not getting the results I I'm interested in.
And for a deep culture, I take a skin biopsy and I submit a part of that for the culture itself. Whether to clean the site or not is quite important. I think if you have a diffuse disease, then cleaning the site is not indicated because you want to know what's going on.
If though you have any pustuar material or anything that's sitting under the skin that you can clean the superficial bacteria off and then express the purulent material, then that's exactly the right thing to do so that you don't get any contamination from the skin. And do you need a medium? The answer is always yes.
The only time you don't is if you're considering a PCR, in which case, the desiccation of the bacteria is not a problem. But if you are considering PCR, say if you're looking for strangles in a submandibular abscess or something along those lines, make sure you don't put it in a charcoal medium because that will affect the PCR negatively, and most of them will come back as a negative result. For, so for the vast majority of them, you're gonna want a bacterial culture, you don't want a viral culture, that's gonna essentially suppress any bacterial growth.
If you're really struggling, then some saline will do, that'll at least keep it wet and stop it desiccating. This was a study that was performed a little while ago looking at what was cultured in skin samples. And it's a very interesting one.
There's there's a couple of different groups doing this sort of work, and this one found that the vast majority, 70% of cultures were in the staff group, Staph aureus intermediate or hiatus. So from that point of view, most of these are going to be relatively sensitive to broad spectrum antibiotics such as TMPS if that's required. What was quite interesting though was another group looked at this and actually found strep streps were the most common in their group.
And therefore, really with that in mind, you really shouldn't be using N refloxacin in any of these cases, because that will not work against strep bacteria. Not that I would ever advocate and refloxac in any way and therefore I think this just really cultivates that view that we should be using things like TMPS or more likely just topical antibiotics in the vast majority of these cases. But what if we're thinking about something along the lines of ringworm, we need to consider hair plucks.
Really important to take them from the edge of the lesion where there's most active disease ongoing. Normally the centre there might be no hairs or they're so far gone that there's absolutely no evidence of DNA present in there anymore. And you have two options now.
One is to submit for either microscopy, with culture or with PCR, one of the two. And there's a big advantage to each one of those. So, well, not much of an advantage to culture, if I'm honest.
So what we found was that, this is a test that was created here at Litook by Andy, and we found it's absolutely as sensitive and specific as culture. So everything we PCR'd positive came back on culture as a ringworm of some sort. And then we missed one that came positive on a culture but not on PCR.
And we're not sure if that was because of a sampling error or if it was because the bacteria, sorry, the the ringworm did not have the right DNA for us to pick up. What we can say though is rather than having to wait for 14 days for a result, you can look at this and say, OK, we get a result within 24 hours, fantastic. The one caveat I have with this test is that if you have treated it recently with a maro or similar, that there may well still be DNA within the hair shaft, which is going to come back as a positive on PCR even though there is no ongoing infection.
So what I normally say in those cases is sample it, and if it's negative, great, you can release that horse from from isolation. But if it's positive, then you can go to culture and and wait for the result from that. So we're now able to say with the ringworm PCR exactly which pathogen, or not exactly, but which group of pathogens are going to be involved.
And a lot of the time this doesn't have a big sway on how we're going to treat or what we're going to do with the information, but what it can say is have a look at it and say, OK, could this be transmitted from another animal, so micros microsporum canus coming from one of the dogs or some of the others coming from horse cattle. So it just gives you that little bit more information that hopefully you can take to the owner and say, OK, where has this come from and how are we going to deal with the problem? Skin biopsy I think is probably one of my favourite techniques when we're looking at skin disease.
A lot of the time it is going to come back with not much that's going to be very useful. It's going to say, OK, there is a nondescript inflammatory process ongoing within this skin. But what it can do is it can rule out other problems that are going to need specific treatments.
I normally use a punch biopsy for a couple of reasons. One is you get a very clean, easy sample. Secondly is that I'm not very good with a scalpel blade anymore as a medicine specialist, so I normally do just use the punch biopsy.
Obviously sedate the horse and do a ring block, but make sure that you don't do any local anaesthetic within the lesion itself, because that is gonna cause severe edoema and completely disrupt any normal architecture. It's imperative you do not prepare the skin, do not scrub, do not do anything to that skin. And that's because you don't want to disrupt that top layer that might give you some more indications of what's going on.
For me, it's important that you do a minimum of a 6 mil, ideally an 8 mil punch biopsy, so it does seem quite big, and ideally do multiple of them. So when I do it, I'd normally do at least 3, if not 4, and I send 3 for histopathology because the price of histopathology includes 3 different sites, and then 1 for deep culture, and I do that in every single case where I am taking biopsies just to be sure that I'm not missing anything. When doing the skin biopsy though, make sure that you twist the punch through the skin in one direction so you're not doing a shearing force backwards and forwards.
And ensure that you are through the epidermis, dermis and subcuters so that you've got through every single layer. Hopefully at that stage, you can do a little scooping action and that's gonna remove all that subcutaneous tissue and allow you to get that biopsy site out without any further intervention. But if it isn't coming, which does happen quite regularly, then ideally skew it with a needle so that you're going to get the least amount of crush artefact within the tissue, and then cut it off.
And I normally do that with a scalpel blade again, so you get the least amount of crush artefact, that it's possible. Place those straight into a 10% formulin as you would with any biopsy, and then some into a plane tube culture. I always suture the incision.
I think probably it isn't necessary. I think most of the time the skin would be absolutely fine, but more often than not, it's helping the clients out because they don't like the look of those multiple holes in their horse. I rarely will use antibiotics unless there is a genuine indication.
So if I'm really concerned there is an infection within that skin, then I will use it, but otherwise I won't give antibiotics. Finally, from the diagnostic point of view, normally we've done all of those, we've got all the answers and we're not quite getting to the the, the result that we want. Then I'm going to start leaning on an intradermal skin test.
What we're doing with an intradermal skin test is we're looking at specifically the IGE that is associated with the allergen that we're talking about within the dermis. And what that's going to do is allowing us to identify potential allergens and therefore hopefully create a positive response, sorry, create an immun immunotherapy vaccine that is going to allow us to treat that horse. What we can say is that having done a lot of these, we do see a lot of positive responses in normal horses and therefore it's really important that if you are doing them, we ship these things out now, you resend the results back to us so that we can interpret them in line with you and with the clinical signs, because some will be positive and not clinically important.
Why not serum testing, serum testing is much, much easier. There's no question about it, you just take some blood and you send it off and you get an answer. What I think is really important is that when you're doing that test, you're not testing for the IGE that's within the dermis, it is going to be causing the clinical problems on the dendritic cells, leading to mast cell activation and histamine release and all the the clinical signs associated with that.
In fact, you're just testing IGE in the blood, which really is quite short-lived. And also there's very little of it. So, how can that, in my mind represent what is going on in the skin?
Also, there's a huge variation in the IG quantification techniques that are used, so each lab is going to have a different technique and therefore give different results. And that has led to poor repeatability, particularly between labs, and even within the lab, you start to see different results if you send the sample in multiple times. And it appears that there is a debatable response to treatment when we have used it.
There's been, there's a recent little study just this year actually, looking at a comparison of intradermal skin testing and serum testing. And so they took 26 horses that had a known insect bite hypersensitivity, and these were assessed. What they did is using intradermal skin testing as the gold standard, they then compared the serological response with multiple allergen simultaneous tests, which is called a mast test, or mast, sorry.
And what they found was that the sensitivity was around 73%, the specificity was around 63%, and the accuracy was around 60, 73%. So in some ways it's not the worst test, you know, on those numbers we do worst tests out there, but at the same time, when you have an option that is better, why would you do the choice that is less appropriate in my opinion. And what we're going to do following intradermal skin test is, having injected our 42 odd allergens, we compare the results of each allergen with the positive.
So in that image, that's circled on on the bottom right, you have to forgive my inability to circle, a, a, a lump. We compare each result to that and based on that we can then say which which allergen is positive. As I said already, we do see repeat offenders that are constantly positive in many horses.
From that though, we can create a specific allergen based immunotherapy that is gonna hopefully help resolve some of the clinical signs. Generally, we see a good response within, if we're going to see one within approximately 2 months, but in some horses it can take up to 1 year to start to see the really good clinical improvement. And in my opinion, there's generally quite a good response.
So this was a small study that was performed that looked at 41 horses all treated for urticaria or pruritis. And what they found was that following starting immunotherapy, 84% of these horses had quite a marked clinical improvement. Of those that had a clinical improvement, 59 were able to stop, or discontinue medications to a point where the owners were very, very happy.
And it might be that they either stopped them completely or reduced the frequency with which they were being given. 40% of the group that responded positively were able to stop immunotherapy after a year. In that group then, 33% had signs reoccur 1 to 12 years later, so quite a big separation there.
And 3 had to restart medications and the signs resolved. But what's really important in that group is that 67% of them, so 2/3 of the ones that improved initially, didn't need any further medications forever, or at least for the length of the study. So what I always recommend is that we start the immunotherapy, treat for at least 20 months, and the reason I say that is that the vials that are produced last for 10 months and 10 months isn't long enough because we know that some horses don't respond for a year.
And after 20 months, as long as we're getting a good response, we then stop the medication and see how the horse does following that. And we did a, we went through our own data recently over the last two years and found that actually we, we were looking at about the same numbers, about a 75% good clinical improvement, and some people stopped the medications a little bit earlier just due to financial constraints. What are the downfalls of both intradermal skin tests and serum testing?
I'm not claiming that intradermal skin testing is the be all and end all. I think it has many problems. And one of the biggest is that cross reactivity or co-reactivity can occur.
Cross reactivity is where there is a shared IgE binding epitoppe. In other words, the IGE that is being produced will bind to different allergens and lead to a positive reaction. Co-reactivity is that they have separate IGEs but they're similar enough that they might respond consistently.
And what we've seen that in horses, sorry, in the bottom point and the group did it recently showed that this is particularly true. There seems to be a, what they surmise a co reactivity because it seems to be consistent in grasses, that this is going to confound some of the results. This was done on serum testing rather than intradermal skin testing, but I would imagine that it's very similar because in dogs, it's been shown that both intradermal skin testing and serum testing have some degree of cross or co reactivity.
And I don't see any reason why it wouldn't be the same for horses. This is one of the diagrams that they produced, and I know it's a lot to take in, but the reds and the oranges are where there is a lot of cross and co reactivity. And what we can see is that right up in that top left corner, the grasses really are quite orange.
And so they are doing a lot of coreactivity, whereas you look down, say, at the moulds, where they had no cross reactivity, that you can get, if you get a positive result, you can be fairly certain it is that one specific allergen. I don't think this would change the way I treat or the way I make my immunotherapies, but I think it just adds a little bit more information to the picture. When we think about prurituss specifically.
It's one of the most common complaints we see in horses, and I think in the vast majority of cases, it's going to be some sort of parasite, whether it's a lice, a mite, oxyuris, is it colooides, insect bite have sensitivity, any of those things. We do then, obviously, once we've ruled those things out, then we've got to lead them down the ATP, the contact or the feed route. And I think it then becomes quite a difficult case when we start having to rely on those as the diagnostic mode diagnosis of choice, because the most common are very easy to treat.
There are some of the less common ones, ringworm is out there obviously, but folliculitis, pemphigus, malacesia, or a systemic disease that's leading to a secondary pruritus, as I mentioned before, liver disease can do that. Me, the first thing I do with all pruic cases is actually I do do an empiric treatment. I do reach for DSX or frontline or something along those lines, and make sure that there are no lice or mites being involved, because there's nothing worse than doing the whole workup, the whole gamut of diagnostics, and then suddenly finding out that all you need to do is spray this horse with DSX.
If though you think about oxyury and we'll come on to that a little bit more, then we've got to consider antalmitic treatments as well. I try and stay away from steroids if the horse is only mildly pruritic. But if that horse is severely pruritic to the point where it is going to be self-mutilating, then we've got to consider getting some steroids on board as soon as possible, so we don't get into that itch scratch cycle, which is very, very difficult to break.
I think in the UK insect bite hypersensitivity is one of the most problem er most problematic diseases that we see. It is a chronic recurrent seasonal disease seen mostly in the spring, maybe a bit in the summer and the autumn. And it's known to affect between 5 and 60% of horses, depending on the, the location, breed, and genetics.
Now obviously it is most frequently associated with coulicoides, but that doesn't mean it's not associated with others such as tabernas and klis. So do make sure that there are other things, other insects that are being checked for. Clinically, most of these horses are affected starting in spring through to the autumn, and horses will often show severe pruritic lesions along the maine and the tail area with a lesser degree some along the midline and face.
Often clinical signs will start with the papules, taria and tufted hair, along with changes in hair structure. And these can be the first indication that you're gonna have a problem. If these are allowed to progress and become severely pruritic, then you're going to see changes that lead to self excoriation due to the severity of the pruritus.
Winter though normally brings relief, and the culicoids are no longer present in the environment. But what can happen is that some of these cases are so clinically affected that the welfare of the horse can be seriously compromised. And this must be assessed and involved in formulating of any treatment plan.
And what's really important is that most horses will have shown clinical signs by the age of around 3.5, but it takes up to 7 years for the vast majority of them to be showing the clinical signs. What we do know though is that these signs will get worse every single year, and therefore getting treatment in and going well is going to be absolutely essential to ensure that this horse suffers the least it possibly can.
But when we look at the insect bite type sensitivity, what is going on and why is it happening? What we're seeing is an IGA IGE mediated immune response within the dermis. And there are two forms of it.
There's the type 1 hypersensitivity that we're all very aware of when we get bitten by some sort of insect, that histamine response leading to an urticarial wheel around that bite. What more is, is more of a problem is the type 4 delayed hypersensitivity that we see in this. So it's gradual worsening of the problem that is going to lead to the ongoing prurituss.
This response is in, this reactivity, sorry, is in response to the proteins within the saliva of coocoides. We know there are about 2 serious proteins involved within the saliva. And what's important is that there are likely variable amounts in each saliva of each collicoides, but also it seems that there's a variable response to each of the proteins involved.
And this plays a role in the creation of an immunotherapy because most of the immunotherapies that are available are based on crushed up micoides, sorry, not based on their saliva. And therefore, we're getting a very poor response because the vast majority of a crushed up collicoides is not saliva. But how are we going to diagnose it?
Realistically, the diagnosis of, insect by type sensitivity is frequently made on clinical signs alone, and they are generally pathonemonic for that disease. But you've obviously got to look at the environment, make sure that everything is, is correct. Intradermal skin testing can be helpful.
I think it can give you that little final push and say, look, it does, does have a response to, looides. But as I've already mentioned, we do get, a lot of poor responders to the treatment, so it doesn't particularly help in making a, a therapy. Biopsies are also very useful, as they can just ensure that there's no other disease ongoing, although you are likely to see quite a profound inflammatory reaction in that tissue.
But again, I do sometimes do it if they're a little bit, confusing and not consistent. Also, you're likely going to see a good change with the seasons and hopefully a response to the treatments that we're going to come onto in a moment. But what are the predisposing factors?
I think most of us are fully aware of them, but still water, low wind, the damp ground and static water allow facilitation and breeding. Only the females of the kulocoides are required to feed on blood for the development of eggs. And those females are generally found in greatest numbers when the horse's grazing area is surrounded by hedges, woodland, as I said, it's a static water, and also be aware that dusk and dawn is the period of the most activity of these guys.
So remember that, moving them in away from those periods can be very helpful. Alsoulicoides are terrible flyers. They just, they don't do well as soon as there's any wind.
So if you can move those horses into a nice windy area, it really does make a difference. Genetics might play a role, and we're gonna really come onto that in in a moment. And as I've mentioned, repeat encounters are the problem.
So these horses may start as a mild disease, but as they keep getting exposed to the colocoidess year after year, the clinical signs will gradually become worse and worse. So firstly, Iceland is absolutely amazing, for, for so many different reasons, but one of them is that there's no colloquoides there, and therefore they have no sweetitch in Iceland, full stop. But what we do know is that Icelandic horses do get Swedish, not when they're in Iceland, obviously.
But what we can see is that those that are born abroad, so what we're looking at in the table is Icelandic horses that are living in Sweden and Norway, and whether they are born in Sweden, Norway or Iceland. And we can see that those that are born in Sweden and Norway have about a 7 or 8% chance of having Swedish. But those born in Iceland and then exported to Sweden or Norway have a much, much higher rate of Swedish, around 27%.
But why is that? Why, why does this happen? And it seems to be that if you're bitten as an adult, sweet itch is much more likely to occur, whereas if you're bitten as a foal, sweet itch is much less likely to occur.
And if we consider the flu vaccine analogy, what we see is we see that actually most foals respond very poorly when they are first exposed to a flu vaccine, when they're very young, and therefore get a very poor response. And is that because the exposure to the antigen, and so hopefully what this is then going to do in our sweetitch cases is that exposure to the antigen in the presence of anti antibodies is going to lead to immuno tolerance. In other words, they are getting exposed to a small amount of antigen when they're a foal, and the body gets used to it and stops worrying about it so much.
And so there is a degree of immunotolerance allowing them to be bitten and probably having a histamine response but not getting into that type 4 hypersensitivity. But what can we do? We can try and avoid moving horses from a low risk to a high risk area as an adult.
So in other words, don't buy a horse from Iceland and move it to a dam still area of England because you're going to risk a very high rate of of wage. How about allowing exposure of false to colooides? I don't know if that's a sensible option, but it might be something that we should consider.
What about the genetics? There is some, but it is pretty limited research out there. So, the genetic components of IBH have been investigated.
And although there seems to be a a genetic involvement, it's a pretty paucity of evidence to confirm if there is a single dominant or recessive mode of inheritance. And without that information, whether it is inherent dominant or recessive, it's very difficult to give any sensible guidance as to what the appropriate breeding should be. When they looked at warm bloods, what they found that there was a 0.65 to 0.78 heritability, so a small heritable factor, but it does indicate there is some degree of it in there.
They do seem to be some other breeds that have some heritability, but they have a much lower heritability indication, so it seems unlikely that that is going to be particularly helpful. And what they found is they can't find any more definitive markers within the genetics to guide us. So one thing is that they found that black Shetlands seem to be more likely to have Swedish than any other horse.
So just an interesting fact, we might be slowly learning a little bit more about that. But how are we going to treat these horses, insect hypersensitivity, horses. There's a lot to deal with and a lot to do.
Treatment, what's really important to get across the owner is treatment and prevention will be lifelong and will require intense management on the part of the owner. And without that, we're gonna have no success because it's going to get worse as I've already mentioned. What's really important is we get a multimodal approach, as one thing alone is unlikely to be the, the, the cure.
So we're going to be looking at repellents, we're going to look at rugs, we're going to look at active stabling fans, mosquito nets, and obviously medications. Peters, in 2014 found that stabling alone resolved clinical signs in 59% of horses, whilst blankets did so in 49% of horses. So this can confirm that the best chance of success is if you use both, because then you're hopefully going to cross over and get the ones that aren't responding.
When, for me, when formulated treatment protocol is with the owner, it's helpful to consider a three-tier approach. And 3, the 3 tiers should include control of the prutic response. So in other words, hopefully you're using some medications to stop, stop that itch, scratch cycle, and therefore the self trauma, because we know that the more they do that, the more likely they are to carry on scratching even when you resolve the problems.
Make sure that you've got resolution of any infections or epithelial trauma, so it might be that you do need antibiotics or topical treatments to get that under control. And finally and most importantly, you're looking at getting a prevention of further exposure to coulicoides. When we consider the medical therapy, it's important to try and control that prutic response.
And for me, that's two ways. One is systemic glucocorticoids, either with prednisolone will make the kick once a day, or dexamethasone if you are struggling with prednisolone. The reason for that is that dexamethasone is a far more potent glucocorticoid than the prednisolone is.
Me antihistamines have very limited response. I very rarely use them. I'll talk about them a little bit more in the atopic section of this lecture.
Tropical treatment though, as long as the hairs are gone, and I think that's really important, it's, they are very helpful. And I really like the spray hydrocortisone such as Cortivans. I think it's, it's non-greasy.
It gets through this hair very well and has a very good job of breaking the scratch cycle. Also, it reduces the risk of any systemic absorption of steroids and therefore any concerns about that. Stomic antibiotics, as I've mentioned, might be required if you are concerned about a con an ongoing infection within the skin.
But we should be obviously considering sensible antibiotic stewardship whenever considering these, and I would more often lean on antimicrobial shampoos than I would on systemic antibiotics. Finally, fatty acid supplements have been shown to have quite a good effect. in in some studies, sorry, and some have had quite a poor effect.
But, a group used flaxseed, and it did seem to mitigate some of the skin test responses to icoides. And it might be worth considering flaxseed supplementation about it was in America, so it's 1 pound per 1000 pounds, so what's that 500 grammes per 500 kg ish, sorry for my poor maths, per day. And that did seem to help.
So it might be that that is an adjunctive therapy is very helpful. Reduction of exposure though, this is where we've really got to, to work hard. So turnout, as I've already said, is probably one of the most important prophylactic treatments we can, can, can undertake.
Proximity to the hedgeos and static water, as I said, is also going to increase the risk of, of, ongoing disease. Chemical repellents or insecticides though can be very effective, and they have to just be maintained and resprayed on very quickly. What they found was that pyrethroid-based insecticides, they're available in the UK, killed about 100% of exposed colooides.
And permethrin-based products, reduced the exposure of horses to colloquoides as well. There are a number of these products on the market and there are variable contents and variable responses. So what I normally recommend is that owners try a multitude of different products, spray it on the rugs, and it's really important to spread it on the rugs because it stays there for longer.
And also on, if you are putting up any mosquito nets, spray it on the mosquito nets. I'm also a big fan of the cattle tags, the ones that have permethrin in them, because they can be put onto the head collar, they can be tied. Plastered into the tail main as well.
And that's gonna really reduce the exposure of, the horse succulicoides. There are a lot of rugs that are out there, and some of them are very expensive, but what we do know is that they do really reduce the incidence of disease. So for me, although they're frustrating for the owner and the hard work, they are absolutely pivotal to treatment if that horse wants to be turned out.
When we consider fans, don't lean on ceiling fans, they're not, they're no good, the mosquitoes get the Kulicoides can fly, through that. But if you put horizontal fans, they don't fly through those, so, really good at reducing the, the rate of exposure. This was again a more recent study that looked at omega 3 fatty acid supplementation with a product called Kerais Smooth.
And what they found is that omega 3 fatty acids, in this case from fish oil, act as a direct anti-inflammatory, but also increased barrier protection on the skin. Also, they've got a very few other products that hopefully reduce the hyperkeratotic skin, and therefore the pruritus associated with that. What they found was they studied 21 horses and they split those horses in half, so half their body was treated with it, half was not.
And they found a statistically dramatic improvement in the clinical signs and pruritus in all those cases. What they then did was they then treated the whole horse after one month, for another month, and overall the whole pruritus and skinneian scores improved dramatically. So again this may play a role in the whole spectrum of treatments.
I hope that what I've proven with insect bite type sensitivity is that you need a multimodal approach to have any chance of success. Atopic dermatitis is when you've kind of ruled everything else out and you have these cases where there is a generalised pruritus. Occasionally it might be localised in one area, but more often than not in my experience, it is over the whole horse.
They'll frequently have urticaria associated with the prurituss. It may be seasonal, it may not be. And really you've got to rule out things like insect bite or hypersensitivity nectar parasites.
And again, this is where you really do lean on your intradermal skin test. So we've ruled everything else out, let's get the intradermal skin test done and hopefully create an immunotherapy. But once you've ruled out all of the other diseases by treating fructose parasites, reducing insect exposure.
If you get an intradermal skin test that is helpful and can guide you, then you can reduce the exposure to certain things, whether it's a food type, a type of bedding, whatever it might be. But if you're not having much luck, which often happens with these cases, we can start to look at the global picture and try and rule out some other problems. As I've said before, bedding is my number one thing to change.
Get rid of it, change it, turn the horse out, whichever one of those things is sensible. Have a look at the rugs. Are they washing them appropriately?
The vast majority of rugs have mites in them. And what washing powder are they using? Have they changed it?
Tests the feed, make sure, as I've said, get rid of all of those supplements, and if anything else, move stables. Move the location of that horse from one place geographically to another geographical location. Obviously not always well taken, but it is an option.
We've mentioned some of these already, the prednisolone, dexamethasone, topical steroids. For me, antihistamines, the only antihistamine in these cases that might be interesting is hydroxyzine. And you're looking at about 1 milligramme per kilogramme every 8 to 24 hours.
I normally start twice a day and then increase up to 3 times a day if required. The one thing is that some of these, along with the neck, the tricyclic antidepressants, is that some of these horses do become a little bit sedate with the treatment. Oxapin is a really good one, I think, the one problem is that it is most of the time cost prohibitive, and can really suppress the itch scratch cycle, so, it's very, very helpful in a number of cases.
And finally, topical treatments, antimicrobials for bacterial or yeast, malaceb is very good to try and get rid of, yeast if you are concerned. I would say yeast seems to play a very limited role in the majority of cases. I really like ethylactate compounds, so etidderm, and the reason for that is that the ethyl lactate penetrates into the follicles and continues to work even after you've finished washing it off.
And that's gonna really resolve any bacterial infections, that's all it's going to treat within those follicles. When we consider the vast majority of potic horses, so the lice, mites and irritating creatures, and I consider our interns as irritating creatures, hence their pictures there. Choreoptic mange is probably one of the most common when we look at the horse.
Very common in feathered animals, the lesions can be extensive, including crusting, scaling pruritis, and serum moves. The vast majority though are going to be those really hairy horses that have, itchy feathers and pastterns, stamping continuously. With those, obviously the first thing you're gonna do is clip them up and try and get all that hair away and treat them topically with DSect or something along those lines.
More often than not, again, this is where I lean on empiric treatment without getting a diagnosis. I think most people know well enough what these horses look like, without needing to get cellotape strips or brushings. The COPG SKBI is something that theoretically seems to be coming into the fore a little bit more, and I'm not sure why that is happening.
I have never seen a case of it though, but these sources are obviously going to be intensely potic around the head, neck and legs, rather than the main and the tail base. What's really important though is it's contagious and zoonotic, but it does respond to Amin, so oral supplement, oral medication with ivermectins, tins is going to help and cure these cases, hopefully. Might be that they need multiple treatments though.
Its great so are really helpful but can be useful in some of these cases, Scoptes, trambiculi, seroptes, Demodex, but again, I don't see that much use of it. House dust mites they play a really big role in our atopic dermatitis cases. And I would say the vast majority of my horses that I do see have some degree of allergic response to house dust mites.
There's a group that looked at the rugs, and trying to work out if if that could be the source of them, and 50% of rugs had mites in them. All mite negative rugs had been washed and sun dried, and that's the really important thing, that washing alone doesn't do it, but washing and sun dried with the UV light really does affect it. And what I've found is that there's a really good response.
Once you A, deal with the rugs, and B, continue with immunotherapy, that they do seem to respond very well and hopefully come off all medications. This is an interesting thing that I came across the other day when I was doing my research and preparing for this lecture. Scopy scabia is relatively frequent to humans, as is Rosaia, which is a chronic skin disease of unknown aetiology.
But some recent work in the human field has shown that they respond to a topical 1% ivermectin treatment, which is in America, where obviously most people are paying for their medications, it is quite expensive. And what they've found is that a huge number of people are now starting to self-prescribe equine Dwormers to apply to their skin. I doubt very much that this is gonna happen to any of our clients and our patients, but it's just something to be aware of that is out there.
Well here is Equi is a pain in the backside, literally, and is a really difficult thing to treat. So, diagnosis is via sellotape and strips and clinical signs. But how are we going to treat it?
Treatment is always a poor response to augments. Do you do two ivermectins? Do you do 2 parentals, do you do 2 and benzils?
Is there any point in perianal washes? The perianal washes, I don't see much point because it's the adults who are depositing eggs that are going to be exiting the eggs rather than the active worms, and they normally die once they have deposited the eggs. So these guys looked at 21 horses, with no treatment versus parental double dose versus eithermectin, and then did a postmortem two weeks later.
What they can, what you can see is that those treated with ivermectins had the lowest presence of adults and larvae, parentals, had a some response. So really, overall pretty poor. We're looking at quite small numbers, that's the important thing here, but .
I think the multimodal approach is again very sensible, so I normally treat with parental followed by an ivermectin if they're still bad, and even a a rectum er treatment as well. So scaly encrusting is normally a secondary lesion, reflecting an increased turnover of skin due to ongoing inflammation within that skin. So obviously what we're going to be looking for is, is there an ongoing problem within that skin, that we can treat?
Are there oral plaques, cannon keratosis, near keratosis, any of those things that might be causing it? The more likely is we're going to see some sort of bacterial or fungal disease. Often these will start around taxites or under rugs, and will start with a fliculitis within the hair follicle.
And then it's gonna spread and become a pharunculosis, an infection within the dermis. Now most bacterial infections are generally not contagious, so we don't as a human involved, have to be too worried. But there isn't ever increasing evidence the MRSA is present within the vast majority of our equine population.
So do be conscious of that, especially if you are dealing with people who are immunocompromised and try and get a swab if you're worried or not getting the response you want. Fungal bacteria often, sorry, is is secondary as well just to trauma, whereas fungal is quite likely going to be a primary pathogen. Abrasions are going to help that infection get in place, but they're not required.
And often these are contagious. So do be aware of that when you're talking to those horses, to those owners, sorry. And some immunity will build up as well in the face of ongoing fungal treatment.
First and foremost, treatment, is going to be cleaning all the tack and the rugs. As I've already mentioned, Eiddem, ethyl lactate for me is the best thing to use. I'm not a big fan of Malaseb unless I'm absolutely certain there is a yeast infection.
. And if I'm worried about a fungus, about ringworm or anything like that, I'm gonna lean on him Maro, diluters are 1 in 50. I would say I pretty much never recommend systemic treatment with TMPS or similar, unless that horse is actively sick. And I would say there are very, very few skin disease cases that are actively sick that will require ongoing systemic antibiotics.
But how do we escape fungus, you know, we, we've decided that we've taken our hair plugs, we've got a PCR, we've confirmed that this horse has ringwormer of some sort. How are we going to prove, and it's been treated with a maro, sorry. How are we going to prove that this horse is no longer contagious?
The problem is that they may only produce spores for a short period, but they can remain as a fomite for a very, very long time. So sensible approach and sensible conversations have to be had. One option is saying, OK, 2 weeks beyond the new hair growth, once it's treated, but that's gonna take a long time for that hair to start coming in.
Repeat culture is very good, but obviously it is fallible. And again, as I said, repeat PCR is, fallible to a false positive. My general advice is get a PCR.
If it's negative, you're fine, and we'll take that risk. If it's positive, do a culture, and if that then comes back as negative, you're fine. .
I think waiting for 2 weeks beyond hair growth is, is probably going to lead to a political nightmare within that that group. Just a few interesting diseases that I can do a slide on each just to round this off, to think about a few other options. Dermatophilous rain scold is a very common disease, leading to a lot of scaling, a lot of the sort of paintbrush little clumps of hair coming out, involved with damp environments and, that exacerbate and encourage the growth of the bacteria.
Tomatous dermainophili congaleni is congalensis, sorry, is the the pathogen involved. And generally those clinical signs are going to be very widespread, normally along the dorsal aspect of the horse, and, you know, pathonemonically those lesions are going to have these crusts that come off as paintbrush, paintbrushes. First and foremost, the treatment is going to be keep these sources dry, remove those crusts, use a anti-ic product to hopefully clean that skin and remove anything that's gonna hold on to the the pathogen.
And then treat topically. So, some systemic, sorry, again, meaning on the ethyl lactate or something on those lines or the malaceb, would, this would be an indication for that. Such plastic vasculopathy, I think, are one of the most frustrating diseases that we have out there because they're very difficult to treat.
First and foremost, coming back to our examination right at the beginning, get some blood work, rule out a hepatopathy that's a photo sensitization. If though that's negative, what we're looking at is these horses having white skin only affected, so normally on the distal limbs. They're very painful with oozing, erosions and crustings that are just like this picture.
And then occasionally edoema within the limb as well. Normally it's seen worse in the summer than it is the winter due to the increased UV light. And for me, most of the time diagnosis is based on clinical signs, but I do normally try and get a histopathology again just to confirm my diagnosis so we know exactly what we're dealing with and what the prognosis is.
As I mentioned, the cause is multimodal, so UV light being one of the most common causes, but it can be secondary to a contact dermatitis or an initial and ongoing bacterial infection. So it's really important that we do a multi-modal treatment as well. For me, getting rid of the crust is number one problem.
And a very random resident study from a few years ago looked at how the best way to get rid of canon keratosis was, and they found that, topical application of KY was the most appropriate and quickest to remove it. So I applied KY in very high levels, cling filled them for 12 hours, and then washed that off with Eidderm. Once they're all off, treat any secondary infections with topical antibiotics and then use topical steroids such as cortidovans.
What is absolutely imperative throughout all of this is that these horses or their legs are kept out of light. And by that I mean every time they walk outside the stable, they are kept out of light with wraps, or they're kept in the stable the whole time. Until you do that, you are not going to get resolution of the clinical signs.
Finally, I'm just gonna do a brief comment on sarcoids because I think you can never do a Durban theological lecture without looking at these. They are a tumour that is induced tumour of fibroblasts, and it's important to remember that they are tumours. They are going to keep growing and they're not going to get better until they are removed or dealt with.
They seem to be closely associated with bovine papillomavirus one or two, depending on if you're in England, Europe or America. Not that that seems to have any effect on the clinical outcome. There seems to be a slight increased risk in your thoroughbreds, your quarter horses, Arabs, Appaloosas, and most horses, most sarcoids are against developing those horses that are over 4 years old, sorry.
So 70% of sarcoids occur in that age older age category. Hospital slug, the name at the bottom, sorry for the poor pronunciation, found that there does seem to be that Snoxiss Calcitrans, your normal house fly, are able to carry the BPV virus. They found it on the feet of them following exposure to horses with sarcoids.
So it could well be that they act as a vector and therefore fly control is going to be imperative to these treatments, to these cases. Firstly, when you look at them, going back to that first discussion on location and naming them, this is where I think it really is important to localise them and also to discuss what type they are, because each of these has a very different, different outcome and prognosis. Nodular, very easy, malignant, much harder.
So do just be aware of these different types and make sure that you report them to whoever is going to be treating it. But how are we going to treat them? Obviously, in the UK, most people are using the, the Liverpool cream, the AW 5 cream, and that does seem to have a good response.
One thing to say is that the research is limited because, the team who make it are unwilling to release what the ingredients are and therefore, this will never be published. What we found, have found though is that there's about a 73% success rate with just laser excision radiotherapy. Cryosurgery on its own is actually a very poor response rate.
Another study showed about 81% with laser therapy, so really quite a good response to those cases. I've, I know the picture below is a melanoma, but it's the only laser one I could find. What they did find though was that 38% of those cases had recurrence at the sites of neoplasia with laser only.
So what can be important is to consider, do you need to use chemotherapy afterwards. So Taon in 2007 looked at intramural chemotherapy with cisplatin, and what they had was a 93.3% cure rate at four years.
And that's, that's fantastic. The one problem with cisplatin is that it's much harder in the UK to deal with due to health and safety reasons. It's not a very nice product, and can have quite severe effects on people as well.
Well, they also found with Justiceplattin, and a few others on its own, is that 96% had cure rate with Justice platin, and also it worked very well in lymphoma, squamous cell carcinomas, melanomas. Electric chemotherapy has become a bit of a buzzword, but realistically as you can see, the success rate is no different. And for me, the problem with electro chemotherapy is that you need to have that horse under general anaesthesia without question, so it doesn't really add a lot to it.
But with sarcoids, what's really important is that you get on it. You do not sit and wait and say it's a sarcoid, it will be fine. So if you ever get the diagnosis, get them off as soon as possible.
So to summarise, I think for me it's really important that you are consistent in your workup. Have a routine that you undertake and make sure you stick to it because then you won't miss things. It is quite important sometimes to trial empiric treatments in these cases because I think lots of them will respond to DSect or similar.
But if that's not working, then get onto your diagnostic samples and be patient. Lots of these horses will take time to respond, and don't be surprised if it doesn't happen in a day. Don't be surprised if it happens in a few months.
Thank you very much for listening.

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