Hi and thank you for joining me for this webinar. This is going to be on the investigation and management of weight loss in horses. So we'll look at the causes of weight loss, a diagnostic approach to weight loss and the management of weight loss.
We'll start with the causes. I think for most of us, most easily coming to mind will be systemic diseases and diseases of specific organs like the intestine, but I think it's important that we take a systematic approach with these cases, particularly at the stage of taking our clinical history and performing our clinical examination so that we don't miss anything, especially as these cases can sometimes be multifactorial. So we'll think about the access to food right through to maintaining weight once it's been gained, so accessing food, prehension, mastication, swallowing, digesting, absorbing, assimilating and maintaining.
So we'll think about the factors affecting access to nutrition. Factors affecting intake or absorption of nutrition. Factors increasing nutritional demands.
Altered metabolism causing cachexia. And primary muscle loss. So let's look at factors affecting access to nutrition.
The simplest, of course, is inadequate feed provision. But there can also be difficulty accessing the nutrition for the horse, and that might be due to hayrack space if multiple animals are present, bullying, lameness, or or even neck pain which can affect the ability to graze or to use a hay net. Unpalatable food might be declined, so even if there's plenty presents, and actually unpalatable food doesn't always look abnormal.
I find it quite interesting the way horses sometimes know when there's toxins in food, even though it seems to look and smell perfectly normal to us, but particularly if hay is, or if they're just poor quality, mouldy or evidently grossly contaminated, then that should be a concern. An appetite might be affected by pain, pyrexia, other elements of illness, or fear. Factors directly affecting nutritional intake.
So these can include prehension due to reduced lip function, which can be due to neurological lesions or local lesions in the lips. Things affecting mastication, such as dental pathology. Oral soft tissue lesions, mascar muscle disease, or temporomandibular joint disease.
And swallowing so lesions of the tongue, pharynx, or oesophagus could be relevant here, or neurological dysfunction. And for me, I think with these cases, it's helpful to watch the horse prehend, masticate and swallow to gain an assessment for ourselves as to whether they can do that normally or not. Factors affecting digestion and absorption.
Normal digestion absorption requires good gastric function, hepatic and pancreatic function, and healthy intestinal mucosa and transit. So for example, this little horse here had proliferative enteropathy and so absorption across that intestinal mucosa and transit of nutrition was significantly affected. Factors increasing nutritional demands.
Physiologic factors such as exercise, late gestation, or lactation. And it wouldn't be the first time if someone was called out to a horse that was losing weight, that was actually about to have a fall, and no one knew the horse was in fall. So I think factors like this, yes, they're not the most common reasons, but they're worth bearing in mind too.
Pathologic factors, a variety of disease states can increase nutritional demand. And particularly and perhaps most commonly, severe respiratory disease, such as severe equine asthma can involve a significant amount of physical work of breathing. Sepsis also.
And some neoplastic diseases. Altered metabolism causing cachexia.cachexia is a multifactorial syndrome, secondary to an underlying illness.
And it's usually associated with skeletal muscle loss, and fat loss may also accompany that too. Metabolism is abnormal and appetite is decreased. There are multiple mechanisms here, such as the presence of catabolic inflammatory cytokines, leading to muscle breakdown, physiologic stress or pain, leading to catecholamine and cortisol production, which leads to metabolism, and again muscle breakdown.
The weight loss cannot be fully corrected by adequate nutritional provision in these cases. And it's especially seen with neoplasia, chronic renal failure or cardiac failure. So I think about primary muscle loss too.
This can be seen with this use. So for example in an animal that was previously exercising a lot, that's now you know, on box rested for example. Neurogenic wasting.
So for example, secondary to equine motor neuron disease, and then they quite advanced presentation, we might see that classic elephant on the drum posture like we see in this photograph here. Primary muscle disease can also lead to muscle loss, for example, polysaccharide polysaccharide storage biopsy. And PPID can also lead to primary muscle loss too, and I'll talk about that a little bit more later.
So the common causes of weight loss will be different, I think in different populations in different geographic areas, but in the area where I work, most typically it would be parasitism, PPID, hepatopathy, or equine gastric ulcer syndrome. So we'll start by thinking about parasitism briefly. So this would be typically the large and small strongiles causing weight loss, typically in animals over 6 months of age.
So those small strongiles being also known as the small red worms or cystoins. That becomes relevant more so when we talk about diagnostics such as serology. Asteroids can also contribute significantly to weight loss, and they're most typically seen in animals over 3 months old, but up to 3 years of age.
Although we do see them again in older or immunocompromised animals. And mixed burdens of all of these can be present too. Deep worms, although not usually associated with weight loss, can lead to this when heavy burdens are present.
So back to PPID. It's a neurogenerative disease, leading to proliferation of tissue in the pars intermediate in the brain. And this leads to the production of endocrinologically active peptides.
And we're most familiar perhaps with ACTH as this is what we use in the diagnosis, but actually there are a number of different peptides abnormally produced in PPID cases, and they contribute, we think, to the development of most of the clinical signs. And interestingly, I think the age at which this can be clinically relevant is younger than is often thought. So in animals over 7 years of age, this could be a consideration.
And decreased muscle and fat redistribution contribute to the impression of overall weight loss. Thinking now about hepatopathy. Many of these cases will be idiopathic, but that is, I think, in part because we don't always have the opportunity to investigate these in a comprehensive manner as we might like due to various constraints.
But toxic plants certainly thought to be one of the more common causes, and again, causes will be different or slightly different in different areas, frequencies of certain issues will be more or less common. Microtoxins are probably an undiagnosed issue, and we can assess food sources for these. There are bacterial causes, although in adult horses, bacterial hepatopathy is uncommon.
It can be seen usually secondary to something else. So for example, a ascending cholangio hepatitis in a horse that's had a small intestinal obstruction. Can also see it with leptospirosis or in falls with Clostridium piliforma infection.
Viral causes, I've put a question mark here because there are a number of viruses that are known to increase hepatic enzyme concentrations in horses and therefore are hepatotropic and causing a degree of damage. But for the majority of them, it would be uncommon or unreported for them to cause a hepatopathy significant enough to cause weight loss. But one that could potentially do this could be equine parvovirus.
Fasciola hepatica does affect horses, including in the UK and again this may well be something that's underdiagnosed. Metabolic. So here I've put a question mark, because I think it would be uncommon for metabolic causes of hepatopathy to cause weight loss.
But here we're thinking really about a horse with advanced EMS insulin dysregulation with significant hepatic lipiddosis leading to significant hepatopathy. Some of these occasional, occasionally some of these patients will be in a diabetic state so there may also be an element of weight loss to that in that regard to this would typically be Shetlands or possibly Welsh section A. Neoplastic disease of equine liver is not common.
We can see primary disease such as carcinomas, but also multisystemic neoplasia or, or, neoplasia that's metastasized, such as with lymphoma. Infiltrative disease, again is not common, but can be seen, for example, in Mead, multisystemic eosinophilic epitheliotropic disease, but we'd expect to see other changes too. And heavy metal toxicosis can also cause hepatopathy and weight loss.
Thinking still about some of these common causes, let's take a look at equine rastacle syndrome. My first comment would be, let's not forget the unlikely candidates, because I think often the sort of either currently racing or ex-racing thoroughbred or the competitive sports horse, this might be something that might be relatively high up our list. But actually also, we can see significant disease causing clinical, clinical signs in ponies, including those that aren't ridden, and in in brood mares too.
Weight loss is commonly observed in affected animals, but the relationship's not been clearly elucidated because although reduced appetite is frequently reported and might contribute, there are other factors too, I think. So possibly altered metabolism due to inflammatory cytokines. And I think this is relevant because what we don't want to do is exclude gastric ulceration based on the fact that a horse might be eating normally and have a normal appetite.
So we can move on now to investigating weight loss. So the clinical examination will be our next step after taking our clinical history. And some useful considerations might include is are we seeing muscle or fat loss or both?
Is there any evidence of edoema? If there is perhaps protein losing conditions such as various forms of intestinal disease might be higher off our list. Are the vital parameters normal?
Are there any respiratory signs? Does the thyroid palpate normally, as hyperthyroidism can cause weight loss? Are there any neurological signs which might be affecting the ability to eat or swallow?
Is there any laminattis, which might increase our suspicion of inflammatory conditions, insulin dysregulation, well, of those two really. I think it's worth seeing a faecal exam in these cases. It will be not particularly useful for the majority of the time, I would say.
But every now and then you do find something useful and it can point us in the right direction. It's cheap, it's straightforward, and it's quick. So, things that we might see that could be relevant could include inadequately masticated and digested food pipers, parasites, or sand.
It takes quite significant pathology, I think, for a horse to be losing weight because of oral pathology, but I still think it's a vital part of the assessment of a horse with weight loss. Haematology and biochemistry can provide us with really valuable information, information. And you'll notice here I've got plus or minus against all of these things because for any given type of disease, we don't always see the characteristic changes or we might see some of them.
So with liver disease, we could see increases in GDT GLDH, AST or ALP. And with intestinal disease, we might, but might not see increases in ALP fibrinogen, and then a decrease in albumin. But as I'll mention again a bit later, not all cases with weight loss and intestinal disease have hyperaluminemia.
With kidney disease, we might see increases in urea and creatinine, but again, not always. And with muscle disease, we might see increases in CK and AST but not always. Parasitology, I think is important in these cases, even if they have been recently dewormed, as antalytic resistance could be, you know, a possibility that could be relevant.
We'll come to talking about sort of parasitological diagnostics a bit more again later. PPID testing. So PPID and concurrent disease processes is common.
So I think if we do identify PPID, I wouldn't always stop looking at that point. I think it's still worth considering some of these other basic forms of assessment too. The basal ACTH will be increased in about 75% of cases with PPID and and probably more than that in those that have weight loss, but not absolutely all of them.
And sometimes TRH stimulation test can be useful, it's more sensitive, but we can see false positives and false negatives at certain times of the year, and, in some instances, a per glide trial might be worth consideration. So moving from these blue ones, which are ones that I would consider in the majority of of cases with weight loss to these more grey boxes as we go around. Sooscopy, of course, can be highly valuable in cases with weight loss.
And if we do see ulceration or disease, then could this be primary or secondary? Again, it's not always that we should stop looking when we find gastric ulcers, because this might be secondary to something else. And abdominal ultrasonography.
So we can gain further assessment of organs shown to be affected. So for example, if we identified through our biochemistry that liver or kidney disease was affected, we might be able to get information from this scan about what's going on there. Similarly, if we have a second intestinal wall, we'd be able to gain an idea about the severity and location.
And the new identification of affected organs might be able to happen, as for example, the spleen doesn't have any specific changes on serum biochemistry, so this could give us a bit more information about organs such as that, where we don't have that organ specific biochemistry. And rectal palpation, so we might be able to identify thickened vastinal wall. Left renal pathology as we can can palpate there, but, but not the right kidney.
We might feel masses or lymphadenopathy, or occasionally other strange things like foreign body granulomas. And sometimes depending on the case, there'll be other specific diagnostics that might be useful to us. So let's look at the identification or recognition of chronic protein losing enteropathy.
And I'm just going to pause briefly to look at the nomenclature together. This is not well defined, and I think different publications, different people will use slightly different definitions, but I wanted to just add a bit of clarity as to what I'm I'm speaking about here, because I think it can be confusing otherwise and misleading. So the term protein losing enteropathy is the same as protein losing intestinal disease.
I would say they're interchangeable terms, and it's a general term to describe disease of the intestine where protein loss is occurring. And this is not interchangeable though, with idiopathic inflammatory bowel disease. Although idiopathic inflammatory bowel disease covers multiple syndromes, such as eosinophilic enterocolitis or granulocytic enterocolitis, and these are inflammatory and often protein losing.
So this would sort of come under the umbrella of types of protein using enteropathy. But just to make it a little bit more complicated, horses with protein losing enteropathy don't always have a low protein or albumin concentration. There can be different reasons for that.
So, for example, if we think about a normal albumin concentration in a horse being from about 28, you know, upwards by approximately 20 grammes per litre. If that has fallen by, you know, say 10 grammes per litre in that animal, it might still not have dropped out of the reference interval for our laboratory. So not necessarily that this horse isn't losing intestinal protein contributing to weight loss, but we just might not necessarily see that on our serum biochemistry.
And similarly, if the horse is hypovolemic at the time of presentation, we might see a sort of slightly falsely increased protein and albumin concentration too. So now let's move forward to identification of chronic protein isentropathy. So we may or may not have concurrent clinical signs such as recurrent colic or diarrhoea.
And as I said already, we may or may not see changes in serum biochemistry, such as changes in albumin, ALP, fibrinogen, sometimes SAA. If we're talking about weight loss, we'll often we're talking about chronic intestinal disease, and often these diseases, even though we've got inflammation ongoing, SAA does sort of peter off with time and we may not necessarily still see an increase there. And we might see loss of electrolytes if we've got significant intestinal tissue damage too.
That's the the sodium chloride, the calcium can be low just as a direct consequence of a low albumin affecting calcium binding. We might see thickened gut or feel thickened gut on rectal palpation. And we might observe they could go on our abdominal stenography.
If we do if we do a glucose absorption test, which is not always necessary, or a xylose absorption test, then we may or may not see changes in that too. If a small intestine is affected, we often will, but if it's predominantly large colon, then not necessarily, as those are absorbed in the small intestine. So what about the causes of protein losing and toy?
We have infectious causes, toxic causes, and other causes. So we've got the insisted cystoins, and these are widely spread throughout the globe and are involved not only because they're one of the most common causes, but because they're the, the main cause really of, of chronic, well, although they do cause acute too, but we're talking really here about chronic protein losing antthropathy with weight loss. Salmonella species, and mycobacterial species, I've not gotten brackets.
The brackets are really predominantly acute causes of, of PLA, but when it comes to chronic, the salmonella and the mycobacterial are not going to be common causes of of weight loss without other signs. So salmonella is relatively common, but would most typically be seen with loose faeces as well. And the mycobacterial disease is really quite uncommon.
I've included Gastrodius aegyptius, particularly as a as a reminder really. So this is an intestinal fluke that is present in various different parts of the world, including South Africa and India, and it can contribute significantly to weight loss. But I say as a reminder because there may be different things that can cause weight loss in this infectious category, depending on whereabouts in the world you're practising.
When it comes to toxic causes, I would say non-steroidal anti-inflammatory drug associated toxicity would be the most common, and this can occur not just with chronic use or high dosage use, but can be just after a single reasonable dose of these drugs, this can develop in some animals. Mercury and aluminium are described as causes of intestinal disease, but again they're not thought to be common. And oak or other plants would more be associated with acute protein using y.
In our other category, we've got idiopathic inflammatory bowel disease. I've also gluten sensitivity, which is interesting and and worth consideration here. There's only actually sort of this been really looked at in the literature once, .
There was a case that had gluten dependent antibodies and histological changes consistent with celiac disease. And then when the gluten-containing feed was removed from that horse's diet, then again, the horse resolved clinically and then on follow-up histology, they could see that those changes had resolved. So it seems quite likely that horses can develop gluten sensitivity, although testing is not sort of routinely practised at the moment.
Neoplasia can of course cause chronic protein losing infainal disease. And sand enteropathy too, which can present in a variety of different ways, from acute colic to weight loss to chronic diarrhoea. So let's think about investigating the cause of protein losing thropathy.
So when it comes to parasites, a faecal count will be our primary diagnostic test. And with cystoins, serology could also be useful, and we'll come back to look at this in a bit more detail. Sand testing, so actually on auscultation caudal to the sternum, on the ventral abdomen, we might be able to hear sand.
We might also pick this up by faecal sedimentation testing, although the sensitivity of this is not particularly high. Or we could use imaging, particularly if we have a high suspicion of this. So we might see sand radiographically in the large scale one.
Oh we, we probably would if the horse had had done a sound andropathy. And sometimes it can also be seen ultrasonographically too. Salmonella and other bacteria can be identified by faecal pathogen testing.
And we'll come back to that too. We've talked a bit about the dietary antigens. And gluten-dependent antibodies.
But what about other dietary antigens causing entropathy? This is something that's really poorly understood in the horse, and there's very little published information about and really very little known about how frequently or whether they even do develop allergic type intestinal disease to non-gluten, . Allergens.
So it's possible that we can consider using serum allergy testing in these cases, but the relevance of those findings and how well they extrapolates clinical diseases is poorly understood. Neoplasia, if we are suspicious of this, then biopsy histology could be useful to us. And occasionally we may be able to make use of gastroscopic, gastric or duodenal biopsies or rectal mucosal biopsies, but often in order to get a diagnosis, we'd need to get either a laparoscopic or via a surgical laparotomy sample in order to get a definitive diagnosis.
If we were looking for mycobacteria, then using a specific stain, a zeal nusin stain on a full sickness tissue biopsy from the intestine probably be required. I say probably because there's no reports that I've been asked to find of the use of mycobacterial faecal PCRs in horses, but certainly this can be useful in other species. So if we had a case where we were suspicious or concerned about this, then it could be something that we could consider.
And in specific cases, there might be other things that could also be useful to us. So I'll just make some key points about the use of cystoin, small red worm serology. The main use of this test is to give confidence that animals with low management risks and low faecal accounts do not need an autumn treatment.
That's autumn in the UK. It's not primarily designed for use in clinical cases. The antibodies is measured and not only to insisted stages.
But for some cases with low fe collect counts, it can potentially be useful in a clinical setting. So low faecal accounts do not exclude the presence of a relevant cysto and burden. But the test is not to be used within 4 months of treatment because it takes a while for antiorticitiss to decline following treatment.
And the sensitivity is greater than 90% for high burdens, so when I say it could be useful for some cases with low ey counts, this is because if we do this serology in those cases and there's a low result, that does make a high burden unlikely. Although it's possible that we can get false negatives on this serology, so the manufacturers report that hyalinemia and, potentially immunosuppression could lead to sort of falsely low circulating IgG levels. So we could get those results and interpret that as a low burden, but actually it might be that there's a high burden without those titers, seemingly being increased.
Anecdotally though, that doesn't seem to be something that we see or see commonly, and we certainly see high serological titis in a significant number of cases with marked hyperarinemia, but I think it's, it's still a relevant, at least theoretical consideration. Not all animals with high scores will develop disease. So, if we have an animal with a high score, it doesn't necessarily mean that it's the cause or the only cause of weight loss.
So let's move on to look at salmonella species. So if we want to test faeces for salmonella and we're going to use culture, ideally we want 3 to 5 separate faecal cultures. Compromise would be at least 3 pool cultures.
But it will be suboptimal to use only a single faecal culture, and there's a reasonable likelihood of us not detecting the presence of relevant salmonella if we're only doing one faecal culture. I think we also can consider enriched QPCR which we'll talk about here further. So what is enrichment?
So enrichment before a QPCR means when the faecal sample is put in through a specific process, so often that will be in a selenite broth that increases the likelihood of salmonella being able to be sort of isolated from that sample. And if a faecal sample is processed in that way, there's a much, much greater likelihood of getting a positive PCR when salmonella was in that sample than if one just tries to do a salmonella PCR on a faecal sample. So, you might think that all labs would, would therefore do that, but that's not always the case.
So, be aware if you're sending a faecal sample for salmonel PCR is that lab using a validated enrichment technique, because if it's not, if they're not, then the sensitivity of that test probably actually be lower than culture rather than significantly higher. And when using QPCR, how many samples should we submit? We don't know, I think it's the short answer.
I would not feel comfortable ruling Salmonella out of one alone, but there's no definitive answer to that really. I like to think about investigating hepatopathy. So when it comes to investigating hepatopathy, we've got the potential causes here as a reminder, and the ones involved are ones which might affect more than one animal in that population at a time.
So when we assess these animals, I think the clinical history is a really important part of getting to the bottom of what might be causing the issue here. And then establishing by considering testing the other animals on the property, whether there's only one affected or not. And often clients will say, oh well, all the others seem fine, but actually when you do test them, multiple of them might have abnormal serum and biochemistry as well.
So when finances allow, I think that can be really worthwhile. It's about ultrasonography. Well, it could tell us if there's biliary obstruction, what that cause might be.
So for example here we've got some hip attalysts pointed to by the white arrows. Or it could help us to identify a possible focal lesion. So for example, if there was a neoplasm or an abscess.
That wouldn't be that common, but when those types of lesions are present, they're usually highly relevant. So I think ultrasonography does play an important role in the assessment of a horse with a hepatopathy. It can also tell us if there's an end stage appearance, so you'd be thinking about a smaller liver with an increased ecogenicity due to the development of fibrosis.
And that whilst it doesn't tell us really anything about the cause, that could give us some quite valuable prognostic, poor prognostic information. So what about mycotoxins? Well, we can test, as I mentioned earlier, feed for those.
For fasciola hepatica infection, there's a serological test and we can also do faecal sedimentation to, to look for the presence of ova in the faeces. We wouldn't typically expect to see these on a normal faecal count. But there are reported cases where clinically significant fasciola hepatic infection has been present.
And the serological titers have been low or normal and the faecal sedimentation is not demonstrated over. So for me, if I've got a clinical case where I think there's a high suspicion of this, so for example, with co-grazing with ruminants or on a wet, low lying pasture, and we don't think the other causes seem likely, then I think triclobendazole therapy empirically can be reasonable. And when it comes to hepatotropic viral infections, there are PCR tests that can be done on blood or hepatic biopsy specimens.
So biopsy histology can be useful to us. It can allow us to gain a definitive diagnosis of hepatic disease. But perhaps we, we usually know that when at the time of doing that biopsy, but of course it may give us some information about.
So for example, we might see the presence of . Sort of features characteristic of either rat toxicity or microtoxin toxicosis, we might see the presence of of heavy metal deposition with certain stains. It can also give us prognostic ability to, there's a scoring system developed by Andy Durham that can be used when looking attic biopsies to determine the likely survival time or the likelihood of making it to certain stages following.
That identification of that diagnosis. Perps one of the key questions is when should we do a liver biopsy and when should we not. So for me, it's when I've got acute severe enzyme changes where I think this is really bad and we need to get a diagnosis as to what's causing this as soon as possible to optimise the likelihood of or you know, maximise the likelihood of survival.
Or if we've got a sort of less severe case that's failing to improve over the space of, sort of, well, usually often give mild cases 2 to 3 weeks at least and if their enzyme changes and clinical signs are improving, then often I think histology is not necessarily indicated, but if it isn't, then it may be more pertinent. What about biopsy culture? Well, I personally always try and take an additional biopsy call to submit for culture, because whilst bacterial disease is uncommon, what we don't want is to get our histology back, find it's consistent with bacterial disease and have not taken a sample of culture.
Because if we, we'd either have to resample, or if we took a call and didn't submit it until we got the histology back, it may well be non-diagnostic by that point. So let's move forward and take a look at how we're going to manage these different conditions and weight loss in general. This of course will depend on the underlying cause, and we can think about alleviation and direct treatment of the the driving driving cause or also, and also specific supportive care for that underlying cause.
And then nutritional support is going to be relevant in most cases as well, and not being excessive about that is important. So let's look at the management of protein losing antthropathy. So we can divide this sort of a bit like the last slide really into specific treatment for any diagnosed cause.
Specific management changes that we can make for any of those diag diagnosed calls, and supportive care. So if we have some enteropathy, there's a recognised successful, or usually successful treatment protocol for that, involving 1 gramme per kg of psyllium and 1 gramme per kg of magnesium sulphate via as a gastric tube once a day for 4 days, and subsequently followed by infeed psyllium supplementation. And I'll put a question mark by the 1 gramme kg of magnesium sulphate, because whilst that is in the published protocol, a different study that looked at the use of magnesium sulphate for the treatment of just normal large colon infections found that a number of animals did develop magnesium toxicity at that dosage.
So, I think many people off the back of that have decided to decrease their standard dosage to 0.5 grammes per kilo of magnesium sulphate. Now whether that is as useful in the treatment of sand enteropathy or not, I don't know, but certainly, personally, I would reduce that dosage to 0.5 grammes per kilo of body weight.
But the sins, oral oxidectin therapy is usually effective unless, now this doesn't affect the efficacy, but if these animals are extremely thin, I would be reluctant to give moxidectin as we could in theory see toxicosis associated with that as the moxidectin is stored and metabolised into . Like fat stores, so if we haven't really got any, we can end up with a much higher circulating oxodectin level than would have otherwise been the case. So in those animals, I would consider 5 days of fenbendazole, although at least as a starting point, although we know that resistance is widespread to fenbendazo.
Or we could consider Irmexin therapy, which will not treat as many stages of cythotonins as moxidectin, but would potentially decrease the overall burden. With NSAID toxicity, mesoprostol therapy could potentially be helpful, helping to reduce GI tract inflammation and increase local blood flow. So which can IT like?
So what about specific treatment for idiopathic IBD? Recommendations for idiopathic, equine inflammatory intestinal diseases are not available, so there's very little guidance on this. But corticosteroid therapy represents a mainstay, and but it's efficacy is variable.
I've just made a note here that you know there may be implications to that pregnancy if we were giving. Got the thyroid stoma during pregnancy. Azathioprine is another consideration.
Sometimes azathioprine can be effective in cases where corticosteroids are not proving adequately efficacious, and you may consider adding them in addition, or instead, particularly if we've got cases that can't cope with corticosteroids, from a metabolic perspective. And again, a pregnancy warning, but not just for the mayor, but also for clients that are pregnant. We don't want them to be exposed to Azyprine.
Methotrexate, is another possibility. It's called anti-metabolite medication. It's used in humans for immune-mediated diseases.
And there's been some sort of recent discussion about the use of this for idiopathic IBD in horses. It's thought that it probably depends, and this is actually similar with azathioprine, on the type of cellular infiltrate that's present, . And ultimately, you know, potentially in more detail about what's going, what's driving that type of IBD, but of course they're idiopathic, so there's not, as I say, much or really any guidance on this, but these are considerations.
Again, we don't want pregnant clients to be exposed to methotrexate, nor is it suitable in pregnant mares and probably not in lactating mares either for azaprine or methotrexate. There are a number of quite significant drug interactions with methotrexate, so it'd be worth looking into that if you're thinking about using alongside other medications. Thinking about specific management rather than treatment now for for intestinal diseases where we've got a specific diagnosis.
Feeding roughage from a rubber matted area is a helpful thing for horses with sand enteropathy. They're obviously gaining sand during their grazing or consumption of roughage. So if they can be fed hay in the field from a rubber matted surface, potentially replacing some of the time that they're spending grazing to, then that can be helpful.
Besides the stonings, a lot of it's about pasture management really, so poop picking at least twice weekly. Having a muck heap kept away from the grazing, such as the one demonstrated in the picture here, because yo stoneman stages can crawl and migrate a significant distance on grass, so they can, you know, under the soft surfaces, they can, basically crawl out of muck keeps next pastures back onto the pasture again. So keeping that at a distance can be helpful.
Ruminant co-grazing can be a consideration too, so they can consume some of the infectious stages without developing disease. But it's important to remember that they can bring other challenges too, such as fasciola hepatic or infection. With doing feca counts, we've got, and we know that we've got particularly high egg shedders within that group of horses, then these could be kept separately to prevent them exposing the other horses too.
And, and preferably if there are a number of them, they could also be kept together too. But equally those horses are then going to be exposed to an even higher burden. So particularly the other considerations such as ruminant co grazing might be helpful there.
And if we have underlying health conditions that are affecting this horse's immunity and potentially intestinal health, then managing those might help resources to have improved immunity to parasites. The non-steroidal anti-inflammatory drug toxicity, discontinuing the NSAIDs, is an important part of not propagating that disease process. And I'm sure it goes without saying really that if we've got suspected gluten sensitivity, then removing gluten from the diet is worthwhile.
So what's about nutritional considerations and weight loss cases? Ad-lib good quality palatable roughage is important and useful in the majority of cases. And short, soft roughage may decrease the risk of impactions in horses with concurrent recurrent colic.
So horses with inflamed intestine are predisposed to impactions, and also potentially spasmodic type colics and gas accumulation that can lead to displacements. So having that short soft roughage can, can be helpful when it comes to those impactions. And when it comes to recurrent colicers, also, Sort of low sugar levels can be particularly important and consistent, diets without changes.
Some of those animals don't tolerate grazing very well either. So unfortunately some of those will be better managed without that. And that's where the pelleted roughage, I think, can particularly come in as useful.
Also helpful if we've got horses with poor teeth that's contributing to impactions often concurrently with enteropathy. So these can make up some or all of the diet. It can be soaked prior to feeding.
Can divide it into at least 3 meals per day. And any dietary changes introduced should be made over 7 to 10 days, allowing the resident intestinal microflora time to adapt that we don't precipitate colic signs. It's not supportive care, a balance sort of concentrates is going to be useful in most cases to help regain weight.
But if we are giving concentrates, it's helpful if they're high protein, excuse me, high protein, avoiding an excessive starch and fat can also be added to the diet or a high fat concentrate given to support weight gain as we're trying to not avoid an excessive starch. The stabilised rice bran can be a particularly helpful component as a source of moderately soluble fibre and fat. Let's look at specific management and treatment for liver disease.
Removing the source if we've got a toxic cause for our liver disease, goes, you know, without saying that that's that's worth doing, that can sometimes be expensive if for example we've got whole batches of roughage but worthwhile. If we've got fasciola hepatic infection, then try tobal therapy, which is off licence, certainly in the UK. It's the treatment of choice.
And like I said before, bacterial disease is uncommon. Therefore, antimicrobial therapy should not be a routine part of treatment of hepatitis C. But in the cases where we have got that, so for example, it falls with Clostridium piliformy, metronisal therapy might be helpful in those cases, or if we've got evidence of bacterial disease on our.
Histology, we've got a useful culture result that targeted antimicrobial therapy would be indicated there. What about non-specific therapy for liver disease? Time and monitoring can sometimes be adequate.
A number of cases do, you know, plenty of cases do recover once the insult is removed and the driving calls removed. They can recover without further intervention. Many people will recommend hepatic support supplements.
Is there any, sort of efficacy data to support this? Well, I can see there's only one paper, which demonstrated an improvement in hepatic health in horses in an experimental setting, and that contained milk thistle and an artichoke type of artichoke. So there's some evidence to support that combination.
There's no sort of published safety data for these, so there's little information about that in these cases, but anecdotally, certainly they, they do seem to help sometimes and I do often recommend them. What about corticosteroids? These are, I think, quite frequently used, sometimes I think with little merit.
They can reduce inflammation, certainly. And if inflammation itself is a significant part of that disease process, so particularly if we've seen that on a biopsy, then maybe something we want to do. But they can exacerbate the condition in horses with a metabolic reason for hepatopathy and potentially if we had a bacterial component like hepatopathy too.
Nutritional management is an important part of liver disease if we've got weight loss, and so concentrates little and often would be recommended alongside the roughage. Used to be that protein restriction was recommended. Now that's only recommended if we've got advanced disease where hepatic encephalopathy is present, or if we think the horse is at imminent risk of that.
And certainly, giving the the concentrates little and often helps to prevent a spike of . Of protein challenge, which can help precipitate that disease that heart disease. Let's move now to specific therapy for equine squamous gastric disease.
There's a high success rate with oral omeprazole alone in these cases, which is great. 75% of cases resolved within 28 days with the omeprazole therapy alone at 4 mg per kick pers once a day. Specific therapy for equine glandular gastric disease is unfortunately much less straightforward.
There's a low healing rate using oral omeprazole monotherapy. There's a higher success rate when you're combining that omeprazole with sacralfate. And there are other potential treatments such as injectable or omeprazole.
Now this is not a licenced treatment, . But there is data to support it. So how, how and when you can use this is probably going to depend on where in the world you're practising.
And I think the cascade is interpreted slightly differently by different people when it comes to this subject. My interpretation of it is that not all equine glandular gastric disease has an ulcerative component. When it does have an ulcerative component, we're obliged to use.
Oral omeprazole, as it is a licenced product for gastric ulceration. But when there's not an ulcerative component, I don't believe that we do need to, to use the oral omeprazole first line. So injectable omeprazole might be an option in those cases, or in cases that have not responded adequately to or omeprazole.
It's unclear whether adding sucralfate alongside injectable therapy is beneficial. There's also published data to support the use of misoprostol, but again there's not a licenced product. And whether or not it should be used with scrafate or is it better used with scraphate is also unknown.
And misoprostol should be avoided in pregnant animals and should not be handled by pregnant ladies. Corticosteroids, what's not usually a component, if we think we've got an underlying infiltrative inflammatory components, particularly if we think we've got, infiltrative inflammatory disease of the intestine as well that's idiopathic in origin, then or immune mediated origin, then cortic steroids may well be a helpful component in the management here. So when it comes to nutritional recommendations for equine gastric ulcer syndrome, pasture turnout has long since been recommended, but actually the literature supporting this is quite conflicting.
I think it's likely that access to turnout is going to be helpful in these cases. Constant access to roughage is also recommended. Feeding less than 2 grammes per kg per body weight of starch per day is recognised as, well, put it the other way round, I think makes the most sense.
If you increase, if you, sorry, I'll start again. If you feed more than 2 grammes per kilo of body weight, starch per day, there's an increased risk of equine squamous gastric disease. Over or equal to grow 2 out of 5.
So that doesn't equate to necessarily that that feeding more starch. It's bad in these cases, but I think it's likely that it is. So to that end, I personally would try and avoid feeding, feeding this amount of starch.
So this equates to, roughly for a 500 kg horse, 3 kg of your average competition mix per day or less. It's also recommended to feed 1 gramme per kilo of body weight of starch per meal or less, and that equates to, for a 500 kg horse, about 1.5 kgs of.
Concentrate a meal, approximately or less. So we'll move now to the treatment of PPID which is thankfully, usually relatively straightforward. So Pergolide forms the mainstay of therapy, and there are licenced products.
I won't go into the detail of how to use it as is explained well on the data sheet. But there are sometimes cases that don't respond adequately to Pergolide as per the data sheet, and potentially some of those cases will benefit from Pergolide twice a day, or if not, cyproheptadine or could be considered in addition to Pergolide or Cabergoline injections could be an alternative. It's worth just recognising that with the ciproheptadine, it can cause sedation, so those animals won't always necessarily be safe to ride.
And management of concurrent and secondary issues is important in cases of PPID. So as I mentioned before, there could well be other elements which are contributing to the clinical signs, and horses are predisposed to other issues such as, poor health, poor skin health, or dental health, when they have PPID. So managing those is is also important.
So as we wrap up this webinar, I'd just like to go over the key points. Firstly, I think it's helpful for us to always consider the mechanisms that lead to weight loss when we're taking our clinical history and performing our clinical exam. So thinking about factors that could lead to reduced access to nutrition.
Reduced intake or absorption of nutrition. Factors increasing nutritional demands. Things that could cause altered metabolism and cachexia.
Things that could cause primary muscle loss. If there's intestinal disease, I'd always recommend investigating the cause. Effective management often includes specific therapy, non-specific therapy, and management changes and supportive care.
Thank you very much for listening. If you do have any questions, then please don't hesitate to contact me.
