Good evening everybody and welcome to the webinar vet. My name is Bruce Stevenson and I have the honour and privilege of chairing tonight's session. It is a session with a difference for our regular Thursday night members who have joined us, We have no question and answer session in tonight, but you will tomorrow be sent an email with all the details on, for how to pose questions.

So even though we're not dealing with them tonight, you will have the opportunity. Tonight's presentation has been pre-recorded. So, I'm basically alone without a presenter, but just the recording and of course my controller Dawn in the background who as always will help us to make things run smoothly.

So tonight's session, is sponsored by Bohringer Ingelheim, and a huge big thank you to Boringa for their sponsorship, which has allowed us to open this up, for everybody to attend. Our presenter tonight is, Simon Tappan, who graduated from the University of Cambridge, and after 2 years in practise, he undertook a residency at the University of Bristol in small animal medicine and intensive care. That resulted in the fact that he gained his European diploma in small animal medicine.

He's currently head of internal medicines at Dick White Referrals, where he sees cases in all areas of internal medicine. Dawn, if you will start the recording for us, please. Hello everyone, and welcome to the webinar.

We're going to be talking about lone worm today, so not letting lone worm catch you out and how we manage and strolais in practise. So, there's lots to talk about. And strongylosis is something that we've seen with increasing incidents over the last few years.

So we're gonna talk about where it's found, how it's spread through the UK, and it's now a more prevalent problem in parts of the UK where perhaps we hadn't thought about it being a problem previously. We'll talk about how it's spread, so the pathogenesis and the life cycle of antistroullus. And we'll also talk about the clinical disease that antitrolus wasorum causes.

So, essentially that's what we mean by antistrongylosis, this set of clinical signs that come as a result of parasitic infection. And then we'll talk about how it can catch us out, because it's one of those diseases that has quite a wide spectrum of clinical signs that are associated with it. And there are also some other parasitic diseases that can look quite similar.

So not every lung worm larvae that we'll find on washes will be antistroullus. There are some other, parasitic respiratory infections that can look very similar. So we'll talk about those.

And we'll talk about how we can diagnose antistroussorum as a specific infection. So we can have we differentiate those parasites, how we can look at the different larvae, and what other tests that we have, to help us make sure that we are right that and stronggus. Is what's causing the, clinical signs that are in front of us.

And then we'll finish off talking through a case. It's an old case that I saw during my residency, so it's about 10 years old. But it's essentially talking through how we would make a diagnosis and how we would approach an antithrodus case, and then we'll think about how we would treat that case and what the best treatment strategies are, and how we might think about preventing the disease, because wherever we, are able to prevent It's gonna be better than cure.

And if we can prevent parasitic infections from causing clinical disease and developing into, clinical signs, then that's gonna be much better for our patients. So, hopefully, you'll find that the next hour or so interesting. If there's any questions that come up, you're very welcome to get in touch after you've listened to the webinar.

My email address is here, so [email protected].

I'm very happy to answer any questions at any point in the future when you're listening. Perfect. So antos strongylosis is caused by antistrolosfizorum, which is.

A parasitic infection, with the, host is the, dog, the life cycle goes through slugs and snails, and we see these, worms living in the right side of the hearth in the pulmonary vasculature. It has a number of other different names. It used to be called French heartworm, which is a colloquial name for it.

It's not quite correct to call it a heartworm. This isn't the worms that sort of live in the heart chambers, the big long, dihylaria immatous worms that we see that are sort of 25 to 30 centimetres in length. These are smaller worms for about 2.5.

After 3 centimetres. And they usually cause signs of respiratory disease through larvae moving through the lungs, causing, a verminous pneumonia. So, irritation, coughing, respiratory signs associated with, dyspnea, tachypnea, exercise intolerance.

But more recently, we have noted signs of bleeding deaths. So sudden onset bleeding, which can be quite severe. And in those cases, we can see sudden death as a result.

So it's a, a potentially very serious disease entity when we think about it in that sort of context. And it's fairly widespread through Europe, through Asia, through Africa, sporadic reports, in the US and Canada. So it's not quite so established there.

But it's, it's geographic incidence is changing through, the UK. So we know that there are areas where we're seeing an increased incidence. So, historically, we've seen it down in the southwest, and around the home counties, so south of London, but we know that the disease in is moving northwards.

So we're seeing cases in more northern and more easterly parts of the UK up into Scotland, in Northern Ireland, in areas where historically we haven't seen those cases. And we also know that locally, geographic incidence is changing, so we know that there are some practises in one town or city that see a lot of ANO cases and other practises that perhaps don't, and we'll talk about some of those different reasons for that when I see some of the papers in a, in a second. And so this is something we need to be aware of, and I think everyone's sort of heard of the increasing incidence of lungro as a result of that, with this increasing frequency, over the last few years.

So where do we find? It's always really difficult when we're thinking about infectious diseases because we don't have good records of clinical infections, and so we're relying on looking at lab data or reported cases to try and get an understanding as to where these cases are. And this is some data from, from IDEX just looking at chemically reported cases for them, and the darker the red colour, the, the more anti stronglus cases that are seen in those areas.

So historically, we know from the sort of 60s and 70s, there were hotspots of antistrolus for all and down in the southwest in Devon and Cornwall. And then through sort of 80s and 90s, we picked up cases that were present more in the home counties and through the south of Wales type areas, which is where the darker red areas here are on the map. But over the last 10 years or so, we know that there's been a northward increase in those.

Infections, and we're starting to see, infections in, in all areas of the UK, in Scotland, and Northern Ireland, as you said. So this needs to be a, a, a differential that we have on our list, regardless of the geographical area that we're in, because this is something where, where we see, locally, but also dogs travelling through lots of different areas and, and potentially picking up infection in that route as well. So it is a fairly, UK wide, parasitic infection, although there will be local geographical differences in the incidence that we see.

So, we've talked a little bit about the life cycle in that the adults live in the pulmonary arteries and the right side of the heart. And dogs become infected with Androstrorus azorum after eating molluscs, so slugs and snails. And we know that there are quite a lot of slug and snail species that can act as the intermediate host for Androstrolus visorum, and some of these can be really small.

So, the little picture down here on the left is a, a tiny little slug, you know, that we wouldn't necessarily, see. If the dog had ingested that, that, that could potentially then, be the source of infection. And the L3 larvae is the infectious form that is within that slug or, or snail, but when the dog ingests that larvae, it will become present within the GI tract.

It migrates through the intestine, through the body to the lung. And as it's present within the pulmonary vasculature, it will then mature, into the adult, worms, and as, at that point, will produce. The IV and, and, and larvae that then develop in the pulmonary capillaries, and it's that migration of that L1 larvae through the, respiratory, system that causes the coughing and respiratory signs that we see in association with androstrogulosis.

Those larvae are then coughed up, and, and swallowed, so they move back into the GI tract and they're passed out in faeces. So the L1 form is then infectious to slugs and snails, and, and that's how the life cycle is then completed. Casing we'll also see that there are paraitic cos involved, so slugs, can be eaten by frogs and other amphibious creatures that can then also come into contact with dogs to, to sort of complete the life cycle, but it's unusual for that to happen.

So the adults are, sort of slender pinkish worms. As we said, they're about 2 centimetres in length, so they're a lot smaller than the true heartworms that we see. And they do have quite a long lifespan in the definitive hosts, so they can live for several years in the dogs.

So they can act as a, a quite, you know, potent reservoir of infection within the host. So there's a, a lengthy time that they can be producing, OVNL1 larvae to potentially infect the more lost population. And we also know that there's the potential for the L3 larvae to be present in the slime trails that slugs and snails leave behind.

And I'm not sure what the technical name for the slime trail that a slug and a snail leaves behind, but the, we know that the L3 larvae can be present in the right, environmental conditions within that slime trail, for up to about 15 days. So if it's warm and wet, that slime trail can act as a focus for the L3 infection. So snails, and slugs moving over food bowls, over toys, just over vegetation, which the dog later made.

Come into contact with could be the source of infection. It's not been well characterised as part of the pathogenesis, so we don't know what impact that plays. But when we're thinking about roots of infection for an stronglus, typically, we would think about ingestion of the slug or the snail itself.

But this presence of the infectious health 3 form within the slime trail and the, contamination of environmental factors like the, the bowls, the, the toys and then the vegetation. And also potentially act as a source of infection as well. So there doesn't have to be a history of ingestion of a slug or a snail for us to see clinical signs of antis strongylosis developing, and removal of food bowls and toys from external outside environments is, is really sensible when we're thinking about ways that we might want to, to try to prevent infection.

Now we know that the definitive host for And stronggus wassorum is, is the dog, but we also see that foxes can act as a reservoir host, and this is thought to be the main reason why we're seeing that androstrongullus cases are increasing over the last 10 to 20 years, that the, reservoir population. And strong within the fox population, and the fox population itself is increasing within the UK and we're seeing an increasingly urbanised population of foxes, and increasing numbers, and, and that is thought to be the reason why we're starting to see, that there are more cases in, in areas of the UK. We'll come back to those later and I'll show you some some papers and data as to what's happening with those, but just really wanted to go through the life cycle a little bit more detail just so that we're clear, because it's really important when we think about preventative strategies as to what's actually happening during the infectious phase.

So we've said that the L3 larvae is the infectious form for the dog. So here's the L3 larvae here, and this would be ingested by the dog as the dog comes into contact with a slug or a snail, so it ingests one of the mollusks or potentially come into contact with the slime trail that we've talked about. The ingestion of that L3 larvae then means that we have the development of that larvae through the L4 to L5 to the adult form.

So we have the larvae maturing. In the pulmonary arteries and the heart. As we have those adults in place, they produce legs, and those eggs are washed into pulmary vascature and develop into the L1 larvae.

So this is the L1 larvae here, which is then coughed up and passed in the faeces, which comes into contact with the slugs and the snails and the life cycle is completed through this stage. The L1 larvae then develops to the L2 to the L3 form, and then the L3 form then is then infectious when another dog would be coming into contact with that mollusk to, be able to then pass on the infection. Obviously, this takes a little bit of time, and there are different parts of the life cycle.

We know from the ingestion of the L3 larvae, so from the infection with Androschondrosposorum, through to the point where the, larvae are being excreted in the, in the faeces, what we call the pre-patent period. It takes between about, 6 to 8 weeks. It's sometimes a little bit longer than that.

It sometimes can be a bit quicker, depends on geographic conditions and the type of long one that we're looking at, but it's around that 6 to 8 week mark. We know that the development post infection. Sort of progresses through that.

And then the completion of the life cycle from the L1 infectious form through to the, L3 larvae takes about 3 weeks in the slug and mollusks, but the L3 form in the slug and mollusk, is infectious there for at least sort of 6 months or so. So they have a fairly lengthy lifespan, in the mollusk as a reservoir for infection. So from the point of infection with the L3 larvae to the point that we have adults present within the pulmonary vacature in the lungs is around about 33 days, so it's around about 1 month after the point of infection.

And then we know to the point where there are L1 larvae being present within the faeces. It's about 44 days. So this sort of 6 to 8 weeks that we talked through, in terms of, of the post-infection and the pre-patent period.

And it's this period where we're seeing that there are over being produced and L1 larvae developing within the lung, but we mainly see clinical signs of disease, where we have that verminous. Ammonia, these L1 larvae moving through the primary brachima that are causing the signs of respiratory disease and associated changes. So really what we're wanting to, to try to do is to, to stop that development of the adult worms to the point where they're able to produce those IV and larvae developing within the pulmonary vascature and, and causing clinical signs of disease.

So if we're worming animals on a monthly basis, we're gonna break the life cycle. So if we're worming them every 30 days or so, we're going to be stopping that development post that 33 days where we have the adults developing within the within the pulmonary vascuture and seeing signs of clinical disease. So it's really important that we do have regular worming on a monthly basis to try and break that life cycle.

And this is just trying to sort of visualise that and showing where we are in terms of, of what would happen with those treatments on a monthly basis. If we have an infestation on, on day one with the, the worming treatments that we give, there, there is some residual action of some of the products, but we don't, we don't see a huge protective effect over, over time. So what we would want to do is to make sure that we do give the preventative on a monthly basis.

So if we, start with infestation on day one, for example, we will have development of that to an adult population and patency that takes a 6. So 8 weeks that we talked about and this patency where we have the production of infectious cell wall larvae would be associated with clinical disease. But if we're worming on a monthly basis, so after, you know, our 30, 31 days of, of that month, we're going to stop the development of that, infection.

We're not going to see that there are clinical signs associated with that. If there's another infestation at that point, then we're gonna need to wait, you know, another 6 to 8 weeks for the development of the adult population, see clinical signs of potency. So, at different points during that month, we might get Different types of infestation, we may have multiple exposures to slugs and and snails.

This is something environmentally that we're going to see all of the time. It's not just going to be a one-off incidents. So if we're worming at a monthly interval, we're going to stop all of those stages of development from developing into the signs of clinical disease.

So it helps us to break the cycle where we see there is development onto the clinical signs. So, monthly worming is, is really important. It's essential in preventing infections and this progression to clinical disease and patency.

So, why am I talking a lot about foxes? Well, when we look at these studies looking at reservoir hosts in foxes, we do see that the incidence of, of Androstroososorum in foxes, has gone up quite a lot over the last, 10 to 15 years. And there are various postmortem studies of foxes that have shown that the incidence of, of androstrolus infection within the fox population has increased quite markedly over that period of time.

This is a study from the University of Bristol, so, Eric Morgan and Richard Wall's group looking at the fox population in the UK, and this is a postmortem study where they looked at the fox population at two points in time and compared the incidence of infection, across that period. And they looked at the distribution of foxes, and these were foxes that came in through, road traffic. Incidents and, and culling, so they were able to, to look at the geographical incidences, and to compare the incidence of And stronglus at these two time points.

So the first time point was, 2005, 2006. The second time point, is about 10 years later, so just before the paper was published. And what they could see was there was quite a marked increase in the anti Strongus, population, the antis stronglus, infection rate within those different areas.

And they broke it down into different geographical areas. So they looked at the prevalence in those areas, the open bars of the prevalence in the graph here of the North, the Midlands, the south, east, and the Southeast. At the first time points, so 2005, and then the darker incidents in, the second study about 10 years later, where we do see that there's quite a mark.

Increase in the number of cases that have that have been increased. So you can see that that's kind of effectively double in lots of those areas, the area in the Southeast, you know, which is thought to be more of an angios hotspot. Incidents gone up from 25% to up to about 50%.

So quite a big jump of infection rates and prevalence within the fox population as a result of that. So we are seeing An increased incidence within the fox population, but also that that's increasingly moving northwards, that we're seeing that there are foxes that are infected within the north of England that weren't present before the Midlands has kind of increased in that regard, and moving into the eastern parts of the UK as well. So, that reservoir and the urbanisation of the fox population probably is a a significant factor in the increase in antis strongse cases that we're seeing.

We also talked about the differences in different geographic locations within quite close environments. And we know that there are differences with the incidence of and stronggus infection within different gastropod populations within really quite close geographical incidences. And this is another paper from Merrit Morgan.

Group at the University of Bristol looking at anti stronggus infection within the gastropod population. So there's the mollusks of slugs and snails that act as the intermediate host within two cities in the UK. So this is looking at Bristol and Swansea, but also looking at different environments within those areas, so rural, suburban, and urban areas within those two cities to look to see what the incidence, of infection with Androstrongylus L1 larvae was, sorry, 3 larvae within that gastropod population was as to how likely it would be if the dog came into contact with that mollusk, that they would potentially be able to develop androstromlus infection.

So they looked at these two areas and, and looked at different, different parts of the city. So the, the urban areas in red, the suburban areas in blue, and the rural areas in green, and looked at the incidence of the antistronggus infection of that gastropod population in those different areas. And interestingly, they found very little infection with andros stronglus.

Within Bristol, which, having been a resident at the University of Bristol is, is surprising because we saw a lot of injury cases there. But when they looked at Swansea, they found that there were different geographical incidences in different areas that were quite close together. So, the urban areas, they found an incidence of about 30%.

In the suburban areas, they found an incidence that was quite, you know, dramatically different. So Underhill Park about 60%, but West Cross down about 30%, and then the rural areas, and we've got about sort of 15 to 5% depending on which of those areas that you look at. So there are definitely different areas where you would be potentially walking your dog, and the risk of coming into contact with a slug or snail that is infected with Androstrouss is going to be quite markedly different.

For example, in Underhill Park, that's sort of 60% of the molluscs that the dogs are gonna come into contact with have, they are positive for antitrossum and therefore a potential effect for the. Disease. Whereas if we're taking our dog for a walk on Pilton Green, for example, that's gonna be less than, you know, 10%.

It's gonna be much less of a, a potential risk if the dog was to ingest a, a snail or mollusk, but that risk is obviously still there. So, this goes some way to explain that there are differences within the gastropod population as to the risk and the incidence of disease, given the prevalence of the disease and places and the potential infections within that gastric population. So it's, it's really interesting to see that there are different geographical incidences in those areas and certain hotspots, and that's certainly something that we've kind of picked up from a clinical perspective, that we do see, that there is clinical disease in certain areas as a result of a, a quite high infection pressure within the, the gastropod population.

So, let's go back to sort of thinking about things from a clinical perspective and what we're actually going to see in the clinic, which doctors does Androstromullus affect? Well, the honest answer to that question is, is it can affect any dog. There, there isn't sort of your classic predisposition for, for, for anti strongullus.

So, we can see it in any, any breed, at any age of any sex. It's not going to be something where, we're going to be looking for a specific, signalment, which is causing the problem. So that's something that we will find in, in specific, Breeds in specific ages.

It is more common in younger dogs. So about half the cases that have been reported have been less than a year of age. But the, the cases are reported in very young dogs.

There are cases that are reported in quite old dogs. This kind of, thought that mollusk eaters will be more at risk is certainly, you know, something that we do see if dogs eat slugs and snails, then we're going to see, you know, more cases in them. So that's going to be something that, you know, potentially we, we, we, we do, worry about.

But it's not something that is going to have to be a historical factor when we're looking for the, sort of differential list. We're not gonna be able to rule out antos strongylosis without having a history of mollusk congestion, as we said previously. And there are some breed predispositions that come through.

They're not huge, but Cavalier and she spaniels and staffy were more prevalent in the initial studies. This may have something to do with the immune response that we see in that breed, and then the IgG, IGE response being perhaps less good. But it's not clear why those breeds are a bit predisposed, but we're not going to be thinking or worrying about them more than other breeds, but it's certainly something that we see, from the papers that were slide predispositions for those breeds.

So what clinical signs do we see associated with antroussorum? Well, there's a huge sort of spectrum of disease that we see. And as you said, the most common signs will be respiratory disease or bleeding diaphysis, where we see bleeding as a result of anthrolus infection.

The respiratory signs tend to come from that migration of the L1 larvae, so this verminus pneumonia, where we see the migration of the L1 larvae through the lung, the damage that's caused as a result of that and the inflammation associated with that migration. So, we will see coughing, tachypnea, signs potentially of, of pulmonary hypertension, as the, it becomes harder for blood to move through the, the lungs as a result of that inflammatory process. So signs of exercise intolerance and, and just sort of listening to some lethargy as a result of that.

And all the associated signs that we see as a result of inflammatory disease, so inappotents, just not being quite right, are all signs that we would see in association with that erinous pneumonia. And then the bleeding diathesis, which we'll talk about in a second, are difficult, so we don't really know what the underlying cause of that bleeding diathesis is or what the triggering part of the understrobus or an infection causes that. But bleeding can occur in lots of different areas, so we can see, you know, just overt bleeding, within the, the central.

Of a system, which would be perhaps one of the more common sites for bleeding. We can see that post-surgery, or we can just see that as, as unexplained bleeding where the animals had some trauma or just comes in as a potential, bleeding for its mouth, has hematosis has bleeding from mouth, GI tract, and we don't know what the cause of that is. And we can also see unexplained bleeding after surgery and in some areas of the UK, for example, you know, South South Wales, for example, A is quite prevalent, looking to try to exclude and stronguss before routine surgeries.

It can be quite helpful because we can see that these animals have, unexplained but, but, some clinical coagulopathies until we have an intervention, there aren't signs of bleeding, so we need to be aware of that, and also really guard against that in areas where antithrombosis is quite prevalent. So these are just some clinical pictures of, of dogs that have signs of antis stronglus. This is a dog that has retinal haemorrhage associated with, with antis stronggus infections, so these haemorrhages are are present within the retina.

This is a dog that had larval migration, so this is an ab larval migration of an L, . Through larvae, so this is an infectious form that's moved and is added up in the anterior chamber of the eye. This isn't something that we see very often.

Aberrant larval migration is, is not a common cause of things like central nervous system disease or other inflammatory, manifestations. But we do occasionally see it. This larvae was removed through acrocentesis, so, puncture into the anterior chamber and the larvae was removed and the very well as a result of that.

But you know probably the only Manifestation where we can clinically see where the larval infection is from, from the, clinical exam that we've, that we've done. And then a lot of the signs that we'll see will be because of this bleeding and bleeding at distant sites. So this is haemorrhage within the, braculum of the brain.

And we can also see problems where we have, spinal cord bleeding andhyligotaxia, as we see in this dog as a result of, of spinal cord bleeding in association with androstrolus as well. This is another dog that, we saw fairly recently, where I work, which came in with a hemoabdomen, which is suspicious that this dog might have a rupturespleic mass or a coagulopathy. This dog did turn out to have angiostronglus infection.

It didn't have anything, horrendously horrible like a hemangiosar. Poor, but it was bleeding into its abdomen, and this is, what's called colo sign. This is blood that is leaking through where the umbilical opening is.

So you see this sort of bruising, this dark area around that is, it's quite a, a nice sign to be suspicious of a, a hemoabdomen if you see it. But that dog responded really nicely to treatment for anthrombulosis and, and didn't require any surgery as a result of that. So, it's certainly something that needs to be on the differential list as to, a possible cause when we're thinking about unexplained bleeding.

So why does this bleeding cause a problem? Why, why do we see coagulopathies and, and the bleeding sis and associated with antitroullosis? Well, the, the honest answer is it's not completely understood, and there are probably multiple factors that are involved, and the, the trigger with the parasitic infection as to why it forms, hasn't been completely established.

But when we look at patients that have antistroulosis. We see that they have a, a mild increase in their coagulation times. They usually have slight reduction in their platelet numbers, and we can see bleeding, as a result of them, actually having completely normal coagulation parameters when we're looking at things on our blood tests.

So the platelet numbers being normal and also seeing that the coagulation times are normal as well. So, it's, it's sometimes hard to fully understand why these dogs are bleeding. There are some cases in the literature which have immune-mediated thrombocytopenia, so the infection has triggered the immune system to destroy platelets.

And there are some cases which have sort of been acquired from Vilivan's factor deficiency again as a result of antistrobus infection, and those have resolved and got back to normal after the antistrongylosis has been treated. But in experimental infection, as we see there is a consumption of factor 5 and factor 8, and these signs are really consistent with the state of compensated disseminated intravascular coagulation. This has been quite nicely showing.

A paper from, Sophie Aamantos, and Amanda Bo and colleagues that were looking at thromboolastography, so global coagulation, that the clot formation, clot stability and clot breakdown seems to be a lot less, stable in these patients with anthrombusy as one with infection. So they're, they're sort of hypercoagulable in the sense that they're more likely to cause, a clot, that that clot is broken down more quickly and there's increased fibro analysis as a result of that. So, clots.

Stability was, was definitely something that was a problem in those patients and this, global disseminated and vascular coagulation is, is why these patients are bleeding as a result of that. Usually treatment of the infection, alongside treatment of the coagulopathy with, freshhold blood or thinking about fresh frozen plasma, will help improve things quite quickly. So it doesn't tend to be something that is an ongoing infection, but it's certainly something that can be really difficult to try and treat because you can see really quite marked bleeding and associated with the infection that's present.

So what can, what can catch us out? So we've talked about the kind of presentation, the clinical presentation that can catch us out, because there isn't sort of a set, clinical presentation that kind of comes in and says, I've got along with. And yes, if the dog is coughing or respiratory disease, that may be something that makes us think about it, but we may see the bleeding that's causing clinical signs that it's not overtly obvious that the dog is bleeding.

It may be that the animals come in with, with another person. And it's not until we start investigating that we find that antrola should be on our differential list. But there are several types of circulator and respiratory strongula that can infect dogs and cause similar signs.

So we need to be aware of those. And is the only circulatory one in the UK, in Southern Europe, diphylaromatous is another, vascular heartworm, but it doesn't tend to cause those, clinical. Signs of, of bleeding deaths and so forth.

And then we also have some other respiratory worms that are present in the UK as well. So chronosome of Opus and oscius osseri that, can also cause respiratory signs in a fairly similar way to, to antitroosorum. So even if we have a dog that is coming in and is coughing, and we're, you know, really suspicious that this may be a parasitic respiratory infection.

It doesn't just mean that that's gonna be an andros stronggus infection. There are these other respiratory parasites that we need to consider, and this may be why we have some difficulty in sometimes making a diagnosis, because we get very hung up looking for antis strongylus. There are some other pulmonary parasites that we also need to be respiratory parasites that we need to be looking at, or looking for that, perhaps we forget about on, on some occasions.

So, chrosomma ulpes, as you might imagine from the uluss part is the fox, lung worm has a life cycle that's very. Similar to antitrolasorum with slugs and snails acting as the intermediate host. But the signs of recursomus is, is less, they're less marked.

So we usually see sort of mild signs of, of coughing, sort of more kind of chronic bronchial inflammation. So this can be very similar to sort of mild chronic bronchitis cases. But in more severe infections, we see, you know, really quite harsh expectorant coughing, and we can see dyspnea association with that.

So it is, possible. To see a more advanced disease as a result of that. So Cronos obvious infection in dogs is certainly something that will have signs that mimic, they're both signs of anti stronglus, but also, potentially signs of more sort of kennel cough type signs in that respect, but can be progressive to, to much more marked respiratory disease, in some instances.

And also, so, slightly different life cycle to strongbus fororum, the adults are in the trachea and the bronchi, but they're Presence in, in the airway itself. And they produce these large tracheal bronchial nodules that are present within the airway, which when you do endoscopy, you can see these kind of lumpy round areas that are present in the trachea and the bronchial themselves, they cause some signs of obstructive change. These tend to cause quite mark sort of tracheal bronchitis, so irritative type change, and we see kind of harsh coughing fits as a result of that, and we can see some obstructive changes as a result of the size of the nodules.

So that's going to affect dogs that have smaller airways more than it does with dogs that have larger airways, so we're gonna see irritation as a result of that. So being aware of both of those parasites as potential differentials is, is gonna be really important. And when we look at the sort of prevalence of that in the fox population, we've, we've already said that androstrousshosorum is, is quite prevalent in the fox population, you know, in the UK.

We take that as an average, you know, 20% of the fox population has angiostrous posorum, about 10%. 11% have chromosomal ulpes. But if you look in specific areas, so in the Southeast, for example, it's getting close to 51% have androthrombus infection, about 25% have chromosomal vulpes.

So we will see that there is quite high incidence in that fox population. So that, that would potentially then be a reservoir for infection of slug and moss population, which means that we're potentially going to see infection within the canine population as well as a result of that infectious process. So how do we make a diagnosis where we may have a, a clinical suspicion of, of disease on the basis of the way that that animal is presented.

And of course, we have to have a list of differentials that includes all those other respiratory parasites and all those other causes of coagulopathies and all those other things to take into account. So you're gonna want to do a more general investigation to look at the patient and we'll talk about that a little bit more perhaps when we come to the case in a second. But looking at specific diagnostic tests that we can do for antiau and we're gonna start with our general blood tests and with haematology, we may see a sinophilia, which we see with infectious processes caused by parasites.

So these cells that have these really bright red, granules within them as the oinophilic content, and they're signs consistent with blood loss, so anaemia and coagulopathy, so thrombocytopenia, coagullate reduction in or extension in coagulation times is a reduction in coagulation factors that are present, and bleeding as a result of that. And then we will see in chronic cases of infection because the adults can be present for quite long periods of time, that there is an inflammatory process. So we may see that the CRP is is elevated, and we may see that globulins are elevated as a result of that as a result of chronic inflammatory response.

And interestingly, there are a number of cases of an stronglus that also have hypercalcemia. And hypercalcemia is obviously differential for hypercalcemia, we think of neoplasia, we would think of hyperparathyroidism, but we always have on that list of potential differentials, infectious diseases, and usually when we think of those infectious diseases, we're thinking about weird and wonderful things that don't happen in the UK very often. So a lot of the fungal diseases that happen in the states like blastomycosis, cryptomycosis, those sorts of things, but and stronger.

Can cause chronic granulomas inflammation, which can cause an elevation in calcium. So there are some nice case theories looking to show that hypercalcemia can be caused by anthrombolysis. It's not a marked hypercalcemia, so we're not talking about calcium elevations that are dramatic, but consistent and mild to moderate increases in calcium and have been reported in association with Androtrogus infections.

So it's quite, quite good to sort of bear that in mind. So these are some of general tests that might give us suspicion that we have and stronggus, but of course we're gonna be wanting to make a specific diagnosis that we have and stronggus wasorum present and that's the cause of the clinical signs that we're seeing. So we're gonna be wanting to look for evidence that the parasitic infection is present.

So we can do that in a number of ways. And one of the ways we can do is to look for the L1 larvae that are present. So we can do that by looking, using faecal tests.

We can do that looking at sputum, we can do that looking at rectal, wipes, trying to find evidence that the, larvae are present. And it's one of the things that we, we sort of have a, a, increasing. Prevalence of those larvae aren't always, prevalent.

So they're not always present and being passed. So they're not always present in every faecal sample that is present, and they're quite lazy larvae, so it's sometimes quite hard to actually find them when we're looking for them. So making a diagnosis of antirombus is, is essentially trying to build a clinical picture and put lots of pieces of jigsaw puzzle together to try and make it a diagnosis.

The gold standard, when we're thinking about diagnosis and thinking about faecal samples would be to do bare and floatation. So to collect faeces over a number of days, so if possible over 3 days to try and overcome the intermittent, excretion of the larvae, pull those samples and then to do the bain, floatation. And that allows us to look at the larvae themselves, and for us to maintain the larval, integrity and the larval structure so we can hopefully identify them, very nicely.

So it's a very specific test. If we find them, we know that. There, but if they're not there, the sensitivity isn't, isn't as, as good, because we, we may not be able to find them in, in the flotation where actually there, there is a patent infection that is present.

So, if we do find the infection, we know that it's present, but if, if, if we don't find them, we can't rule it out. And that, that's one of the difficulties. Once it's a gold standard, and we find that we have positive results, we probably do have a lot of larvae that are present.

If we have lower or more chronic infections, then the number of larvae are probably aren't going to be quite as high and that makes it a little bit difficult for us to find them. So flirtations take a little bit of time and they're quite sort of intricate, we have to take samples away to the lab or spend a bit of time doing them. So if we have an animal that's in front of us where we want to make a more rapid diagnosis, then we can do a direct faecal smear.

There's a nice paper from the group at London looking at this, looking at a small piece of faeces, so usually described as the size of a piece of a lentil, something like that, where we make a, a slurry as a result, we put it on a slide, and we look to try and examine where the larvae are, and they found that, you know, even with inexperienced operators, they could tell about half the time whether the infection. The sensitivity was, was about 50%, so about half of the infections were, were documented, through this route. So even without experience, it was, it was good to be able to tell that they were present.

So that's a, a quick and easy way of trying to do that. But it is, it is a little bit tricky because there are lots of, of potential, larvae that are present that can look very similar to Androstroullus. So these are some of the worms that we've talked about before, socrinosoma, Androstrolus, and oslos oslora.

And just looking at those, you know, my paracytology is, is not so good. But just looking at those, it's quite hard to tell which is which. And, you know, these are the best pictures that people can find in terms of trying to, to make this talk.

So, these are really nice examples. So, you know, when you've got an animal in front of you on a Friday night and it's not really doing very well, and you're trying to look down the microscope and trying to tell, you know, is this anrondos, isn't it antirodus, it can be quite difficult to try and make this diagnosis. So this is, chromosomal olpis, this is antistrobus sorum, and then, on the, on the left is osososterri.

And the key part is looking at the, the tail detail and the crooky. kink that's present in the tail. And we need to have really good morphology to be able to identify that species because they can look very similar.

And if we're not sure, then doing an adjunctive test to try and prove which of the paracystic infections is present, like a, an angiodetector, a serology test, or a PCR test to try and prove which one of those parasites is present, is gonna be really important in that regard. So, this is just looking at antistrooszorum and crinozoma in a little bit more detail, and it's this kind of really sort of kink that we see at the base of the tail, that's really important in terms of being able to say that this is Andrew strong dust tends to have this quite curled appearance, and when we look at it, has a, a sort of more pointed tail and doesn't have the hook that is present. But it's, it's sometimes tricky to be able to see that unless you've got absolutely good preservation of those, largely when you're looking at them under the microscope.

So it's really important, to be able to tell that. And if we're not sure, then we shouldn't really assume that it's Androstro infection. Of course, we can treat.

For it, whilst we're waiting for results to come back, but doing, a serology test and angio test or potentially a PCR test, that would be really helpful to enable us to, to differentiate that. And, really important that we use the Bin technique for other flotations that, essentially dehydrate or, change the shape of the larvae can make, morphology really hard to distinguish. So bamin would be the, the best way to, to do that because we can sometimes have, false results and, and get caught out if we're not able to do that.

So what are these other tests that we've talked about? Well, the angio test is, is a nice test because this is a blood test, so we don't have to have a faecal sample or have anything to do with faeces to be able to make a definitive diagnosis. And this detects adults antigens.

So it's a lateral flow, in the chiaographic test. So you put the blood on and you look to see that there's the anti In presence and you get a line that gives you a positive or negative result. And the sensitivity and specificity is, is really good with this test.

This is, I'm shown in a number of different papers. It does depend a little bit on the, paper that you read, but is in the highlighted specificity and sensitivity for all of those papers where it's been compared to Bearman. Bearman, obviously, you need to have quite a, a, a high incidence of infection, a lot of larvae being produced for that to be present.

And there are some studies that show that that perhaps there are some, suggestions that the sensitivity may be less in clinical infections where there's a low grade infection. So there's a couple of papers that reported slightly lower sensitivities, and there's a recent Javen paper that has suggested that, actually the end test was negative in some cases that did have and strong, but compared with the other tests that we use in veteran medicine, this is a very, very good test. And gives us a good indication as to whether antrolu is present or not.

But in the rare instances where we still think angio might be present, then we need to use another test to be able to, to look. So we would do a Bearman or another investigation, so a PCR for example. And we also need to bear in mind that the angiotect test does, doesn't cross react against other nematodes, so we won't get a positive result with chronosoma, for example, as a result of that.

So the take home message really is that no test is 100% accurate. I guess we know that from when we're thinking about diagnosis of Cushing's disease, we use tests to help us build a clinical picture, same with and stronglus that yes, the, the high sensitivity and specificity is very likely to give us yes or no results, but if our clinic clinical suspicion is still quite high and we're getting a result that doesn't fit, consider using a different test or to treat speculatively, if we're not going to get those results back and, and, and don't worry about completely. But just keep a bit of an open mind and consider that there might be some alternative explanations to the clinical signs for respiratory disease, whether the chronos might renoso might be present with chronosoma volpis, or whether there may be another cause of, of, bleeding deathsis that we haven't considered in that respect as well.

So angio test is a really good test, but, there, there is more we can do to try and further diagnosis if we're, if we're not sure. And generally, the best test is to, to use a QPCR test, which is extremely sensitive. Which is something you need to do on faeces, on, bronchial washes or sputum that's been brought up, and it does differentiate between antiscasorum and other nematodes.

And it may detect them earlier in the, the sort of process and the infection, then, when we're thinking about using the anti detector test, it may actually find earlier infections, but it will help us to differentiate between those things. And this is something that's become more available more recently in the last few years. It hasn't something that's been historically available, but it's, it's really helping to change the way we're able to, differentiate between those parasitic infections.

And be more sure when we've got negative, angio results and we're still thinking that that may be a potential differential type basis. So use the PCR test to help you, to understand things. And if there's suspicion of strongness for a negative negative angiotect test, then I would still do this on, on bronchial washes, and it will also help you to understand, you know, whether there's other respiratory, parasitic infections that might be present that we need to look at or treat specifically in that regard as well.

So those are the, the sort of blood tests, the more definitive tests where we're looking for some infection. Of course when we're thinking about respiratory disease and we're thinking about respiratory signs, we'll usually start to think about taking some X-rays to try and understand what's happening in the thoracic cavity. And angio has a quite wide range of signs that it can cause on X-ray.

So we can see that there's alveolar changes, we can see bronchial thickening, we can see generalised interstitial patterns. So it's very difficult sometimes to be sure when we're looking at radiographs as to whether Androstrolus is present or not. Now the classic pattern that we see with Androstroos wasorum is this peripheral alveolar pattern.

So if we think about the infection, we've got. Adult worms in the right side of the heart of the pulmonary vascature. They're releasing, OV into the, the lungs, so they're gonna get washed into the capillary bed.

We're gonna see inflammation around the edges of the lung. So, here we've got this kind of alveolar pattern that is present in the caudal dorsal lung fields, but also around the edges of the lung here as we've got the ovum and L1 larvae being washed into those areas. So, peripheral alveolar pattern is something we see with non-cardiogenic edoema.

There's not many different credentials for that are usually fairly obvious. So things like, you know, strangulation, drowning, electric shocks, those sorts of things. So usually there's a fairly obvious history if that's the case.

So if we see this peripheral alveolar pattern, then anti strongozorum would be quite high up on a list of differentials. But we can also see that there are a number of other sort of presentations in terms of different patterns that are present. So this kind of peripheral pattern is fairly obvious when we look on the lateral, when we look The dorsal ventral because of the difficulty in blood moving through the lung with that verminous pneumonia, we do see some cardiac changes.

So this reverse D shape with the heart, so this straightened border on the left side and roundedness through to the right side of the chest, but also a fairly prominent, pulmonary bulge up here. So you can see that's a rounded shadow up at the top here, which is, as a result of pulmonary hypertension, and becoming more difficult for the heart to pump blood through the lungs. And then there's a, a number of different, sort of presentations.

So this is a dog that had androstronglus, it's got quite an interstitial pattern, so it's kind of got this hazy opacity through the lung here, so it's quite difficult to see what's causing the problem. This is a different dog with androstronglus infection. Well, we've got more of a bronchial pattern, so you can see the sort of doughnuts of the bronchial inflammation, and the tram lines caused by the bronchial markings being more thickened and more obvious in that respect.

And we've got much Evidence of the alveolar pattern or, or, in the distal and the periphery of the lung field. And then this is another dog that had Androtro. So this is a really bad X-ray.

This is from my residency at Bristol, so about 20 years ago. But we've got a dog that had Androstrolus and had these parasitic granulomas that are present in the chest. So you can see these nodular areas that are present.

And these are parasitic granulomas in association with Androstrobus. So obviously, when we see nodules like that within the chest, we're going to be worried about. Near plastic, cancerous processes, but this dog did very well with treatment for parasites, and those granulomas resolved and, and did very well.

So this is another potential presentation. But that classic presentation, this peripheral alveolar pattern is, is very common, and it's something that would make us think of androstroglu, but don't get caught out. If you're not seeing that peripheral alveolar pattern, it doesn't mean that you don't have an angiostroglu infection, and I would go looking to see whether you might have parasites in in other areas.

So this is the sort of pattern that we see, and these X-rays belong to a dog called Travis, and I just want to spend the last 15 minutes or so when we're thinking about treatment of an strongdus, thinking about how this dog presented and how we moved through treatment. So Travis was a 16 month old male mutter cocker spaniel. And he had a castration about 3 weeks prior to our seeing him, and there'd been some oozing associated with his castration site.

And then when he came to see us, he become really dull, depressed, and had this scleral bleeding around his eyes. You can see in the picture here that they're really quite red and quite, bloodshot, and a lot. This sort of scleral haemorrhage under the edges of the eyes around the edge of the whites of the eyes that is really quite marked.

This is quite one of the signs that we sometimes see in association and strong so say it's common, but it would be definitely making me think that and strongbus might be the cause of a problem here. And we had a grade 2 heart murmur that hadn't been picked up when he'd been castrated previously. That was a right-sided heart murmur, so it's not something that we often will hear.

So it's making us think about what might be happening with the tricuspid valve. And listening over the chest, there were moist crackles in, in all areas of the lungs, and this is a, sort of suggestion that we've got, a pneumonia of some kind and that the alveoli are snapping open and closed, as we've got more fluid that's present in the alveol than we'd expect. So we're gonna do some blood work, and our haematology shows that we've got a mild but regenerative anaemia, so it suggests that we've got some blood loss over a period of time for that regenerative response to develop.

We've got a mild thrombocytopenia, so it's not marked enough for it to be the cause of the bleeding, but suggests that there's a consumptive process that is present, so it's lower than we would normally expect to this is being consumed in some way, but it's not low enough for it to be the cause of the bleeding. And then on biochemistry, we've got an elevation in globulins, so essentially showing us that we've got an inflammatory response of some kind, although we can see that in respect of cancer changes so inholiy disease, plasma cytomas, those sorts of things, but inflammatory infectious diseases would be most common. And we've got a mild increase in calcium as well, which would be potentially something we see with some antistrous cases, as we said, as a result of granulomais inflammation.

And we did an SPE in the dog as well, because of the elevation in Goblin, and you can see this is an SPU trace here. We don't run these very often, but you put blood on one end, apply electrical current, and depending on the size of the protein, depends on the, distance that those proteins travel from where you've put them on. So this spike here is albumin because it's quite small, it gets quite a long way.

The alpha 1 and alpha 2 proteins, beta 1 and beta 2, so these all are acute phase proteins, so things like alpha 1 microglobulin and haptoglobin. So, our, our defence against bacterial infections. And then this is our I IGG spike at the end, which is the, the larger antibodies.

And this is quite a broad-based spike. So this is suggesting we've got chronic inflammation against a wide range of targets, and would be very characteristic that we have an infectious disease that the body is responding to. So, intend to do them very often, but it kind of helps to support this might be a response to, inflammation and infection rather than this being a cancerous process.

Because we're seeing signs of bleeding, then we're gonna want to do some coagulation work and PT and APTT were normal here, so we haven't got signs of a secondary coagulopathy. Platelets are normal and our bucking mucosal bleeding time is normal, so our primary platelet function and platelet numbers seem to be OK. And the dis are also OK, which is sort of a marker of tertiary, clot breakdown, doesn't seem to be Increasing clot breakdown.

So there's no obvious explanation as to why this dog is bleeding. There doesn't seem to be an obvious documented quite a lot that we can see in this patient. So, of course, being in an area where angiostrouss was quite present, seen in my residency, so University of Bristol a said an area where we saw a lot of angiostrous cases, suspicious that this might be an angiostroris case.

And at that point, we didn't have an angio test that was easy for us to use. So we're going to want to, to do a faecal wipe and a rectal sample and try and see if we can find any L1 larvae, which we didn't. The dog took some time to pass some faeces, and we'd actually speculatively started treating the dog at that point, so we didn't find the larvae when we did when we did the bain flotation.

So we're gonna want to think of other ways that we can try and make that diagnosis. Now, of course, with the angio test and the PCR. It would be a bit easier in terms of trying to make that diagnosis, but, we want to go looking to try and see if we can see evidence of the infection.

It's quite nice to be able to document what we found, but obviously things historically are a little bit different from what we're able to do now. So, in this story, we obviously took our chest X-rays, which shows we've got this nice peripheral alveolar pattern. We've got the reverse D shape to the heart, which obviously is, is suggesting that we've got some signs of pulmonary hypertension, so wanting to do an echo and and look at the heart and try to understand.

And what's causing that. And we did have signs of pulmonary hypertension. It was harder for the blood to go through the lungs because of the inflammation that was present there.

And as a result of that, the pressure in the right-sided vessels was increased. We have tricuspid and pulmonary regurgitation as a result of that, which is causing us to have, the murmur that we can document on our clinical examination. So it's quite nice to be able to, to fit all of those things together to show that the pulmonary hypertension was the cause of the murmur that was present.

So we wouldn't necessarily do this, but because they still had signs of, of, inflammation, so the, half the pattern that was present was obviously bleeding, was suspicious of an stronglus. We did do bronchoscopy to go down and look into the lung and try and understand what was causing the change. And as we go into the airway, you can see that there's some bleeding there.

The airway looks inflamed more than we would expect it to do. So the mucosa is quite hyperemic. We've got some Blood clots that are present within the airway.

You see, it's obviously during my residency, because the scope is upside down. The dorso tracheal membrane is at the bottom of the screen, so we'd usually turn it up the other way. But you can see that there's mucus, there's blood, there's bleeding.

There's quite a lot of airway inflammation as a result of that. So, looking on our, BALs, our, our washes from the lung, you can see that there are a lot of L1 larvae. And, and this is the, the difficulty in terms.

Of making a diagnosis, these are quite coiled larvae, so we would be suspicious of about strongullus, but you can't see the detail there to be able to see the hook tail as as you would clearly want to, to be able to document this is and stronglus was all so PCR testing this dog would be really nice to be able to prove that, this treatment response to treatment, the treatment for a lot of the parasitic ferris is fairly similar, so in that respect, we would be able to try and understand what the cause of the problem is, and be able to, to try to, to make sure we treat things effectively. So from the BAL samples, we would be fairly happy that this is a an anstrous infection within the context of, of the things that we've talked through. So we're gonna want to think about how we might treat angiostrongylosis, and that's gonna be supportive as well as specific to try and treat the infection that's present.

So the supportive and symptomatic things are really trying to support the coagulopathy that's present, so trying to give coagulation factors, so things like fresh frozen plasma, whole blood, if there's active bleeding. When we have signs of pulmonary hypertension, then Cedillaphil will be helpful to try and reduce the pulmonary pressures. Obviously that's not licenced for use in the dog, but that's how it was developed in people, and does have some good action anecdotally, and to consider whether we would give anti-inflammatories like steroids or non-steroidals to reduce the inflammation that's caused by that from from this pneumonia, where we've got the L1 larvae moving through the lung.

And we also need to treat the parasitic infection. So this was 2008, so there And to licence product at that point. So we use fambendazole, which obviously isn't licenced for use against strong poo at the moment.

It does somehow have some activity and there's some papers that sort of support that, but it's not a current licence product. So, historical case, and there are now licenced products, which we'll talk through in a second, that would be better choices, in terms of having treated this dog. But we obviously started treating the dog with, with flambeazole, to treatment for an strongdu, unfortunately, his mentation rapidly deteriorated.

We do. From some mit trying to reduce, cerebral pressure, he had some pressure some plasma, but he started to have some seizures, and really didn't do very well. His own is very sensibly elected that he would be euthanized and also very kindly agreed that we could do a postmortem, to try and understand what was going on.

And he had really massive soft tissue haemorrhage through his muscles, through his brain, through many organs, and, and really large numbers of angiostrongullus worms in the pulmonary vessels. So from a dog that had been, really quite well a couple. Of days prior to presentation, and gone through its castration quite well and not had a problem.

It's one of those cases that really made me think about and strongullus as a potential cause of clinical disease and how dogs can have a quite marked supplemental infection would do very well with that and for that situation to suddenly change and the degree of Toshi haemorrhage and inflammation that we see associated with that haemorrhage can be really quite difficult for us to manage. So, it's really kind of a bit of an eye opener and a sad story to, to make us think that Androtroulus. It's a really important disease that we need to think about, and, and can really be quite devastating in those instances where we're not able to get on top of it with treatment.

So, that was a little while ago. So how do we treat and stronglus in 2021? How do we try to, treat those infections in a, in a better way?

Well, we now have some licenced products, in the form of moxystatin within the Cloprid, so for example, Advocate, which would give a single dose and maybe repeat it after 30 days, or Milammycin with Pasil, so things like bides, for example, which are dosed on a weekly, basis for 4 doses, through the course of infection. And they're slightly different in terms of the format that these treatments are given. The oxytocinrod is given as a spot on, whereas the nomycin products are given as a tablet.

The dose frequency is slightly different. You give a single treatment with the oxytocin followed up a month later, whereas the normycin needs to be given on a weekly basis for the 4 doses. Usually suggested that the, first dose is the normyin Prazorantal on the 1st 2nd.

For those that are given with a mono product, which there isn't available in the UK, but we know that the effectiveness of those treatments in terms of treating clinical disease with both of those moxiexinycin products is very good. They're they're both very good products in treating clinical and strong infection and have, have been supported anecdotally and with a limited amount of literature that they're They're good products for treatment. So it's quite hard comparing them in terms of where we are and a lot of the comparison comes perhaps from all the practicalities from how they're used rather than the efficacy, because the efficacy of both of those products, is very good and they're both very good, robust options for treatment of antistromullosis, at the moment.

So we reduce one of those products, as we've said, to, to enable us to be able to treat the disease. Where possible, prevention is going to be better than cure, and we have several more licenced products for prevention of androstrongulus, infection and antrogulosis in the UK, now than we did historically. So we can have mectin products, in the form of spot on treatments within the cloprid or oral treatments with parental and soulana, and then there are megamycin products as well with ouroxan or.

The clientele to given orally in that regard. And these, we need to give monthly, as we said before, and I'll I'll come on to explain again why we need to do that, and we would try to treat every dog on a monthly basis for the lifetime, because we can say this is a disease that we see throughout the dog's lifetime, and they will come into contact with and strongest on a very regular basis. Consider treating all the dogs in the same environment, because that's going to be a potential problem.

And also considered the environment as well, as we said at the beginning, the molluscs, the slugs and snails that are moving through the environment over toys and food bowls, can act as a source of the infection. It may not be the slugs and snails themselves, that are actually passing on the infection, the L3 larvae that are left behind in that slide trail, may, may be acting as a focus of infection and may also pass on the disease, and we, we don't have to see those slugs and snails, to be able to, to document that we have infection of androstromullosis. So this monthly prevention is, is really essential and we showed this side before in terms of making sure that we give this monthly treatment to try and stop the patency of infection and the development of the infection developing into clinical disease.

So giving treatment on a monthly basis stops this patency, regardless of where during that month the infestation occurs, because we can't. Stop the infestation from happening, we need to treat on a monthly basis to stop the infection from developing, and we really would want to to try to make sure that we monthly dose these patients and to really try and prevent the progression to clinical disease and patency, and that's, that's really important when we're considering long worm prevention. It doesn't really matter which product we use as long as we give it on a monthly basis.

It will be something that helps to prevent clinical disease and patency. We've talked about a couple of different products, we've talked about oxidetin and gamycin in terms of those, those products, in terms of, you know, which one should I use in terms of we've got a choice of, of different things, we've got spots, we've got oral treatments, what, what is the evidence as to, to which of those products might be better and the difficulty is that we don't have a, a good selection of papers or literature to be able to look at to try and help. Us to, to understand that question, and the answer to, to it really in, in the summary is that both of these products and both of those drug products are very good in the prevention of, of the development of antithrombus infection to the point where we see clinical disease.

They just work in slightly different ways and, and there are some nuances to, to what's been published in that regard. So there are two papers that people usually refer to when we're talking about Strong prevention in terms of looking at moro oxidectin and the oral administration of romycin in terms of the development of the disease and those of the papers that are here. And both of these papers show that both of these products are are very effective in the prevention of androstroulosis, and so the invention the development of the clinical disease that's caused by androtrolus infection.

So just to take a little bit of a look at these papers in a bit more detail just to understand what's been done, don't want to labour the point. It would take us too long to go all the way through it, but the, the moxidectin paper, which is the spot on product with immoclod amoxidectin, was given as a prevention study. So dogs were infected with lung worm on day 0, and then given the oxidectin inoc product either on day 4 or day 32.

And that was found to have a 100% efficacy reported as a Result of that, when they looked at the lung worm larvae that were excreted at the end of that study, so day, day 60 at the end of that process, larval excretion was completely reduced, and clinical science and pathology were less severe in the dogs that were treated early on in the disease course, which kind of makes sense than the ones that were treated later. So, topical min and very effective at the prevention of the development of, of, of antifisa and infection to the point where it. Sandros strongylosis.

The other paper is looking at oral mmycin of the foxella. This is another prevention study. It's a slightly different model to the one that we're talking about for the spot on moxiddexinin crop product in that it's a trickle challenge.

So the dogs are infected with lung worm on a fairly regular basis, so every 2 weeks during the study, and then treated with the oralmycin product, every 28 days through that study to kind of Or mimic what's happening with natural infection. And really good efficacy was reported as a result of that. So 95% efficacy reported larval excution reduced dramatically through the, through the course of the study, and no clinical signs of thrombolysis were developed, observed and developing during the treatment group.

So slightly different, studies in terms of how they're designed, but overall, the efficacy is, is really good in terms of the oral milk yin or foxy product. So when we're comparing these two things, it's, it's obviously really difficult. These are two very different studies designed, so we can't, compare directly those results and to actually compare these two sorts of products, these two types of approaches in terms of all treatment versus spot ons, different drugs, would be quite difficult for us to perform.

It would be quite unethical really to, compare those products because we always had to have licenced products that we know that would work. So, you know, it wouldn't be fair to the animals that would be needed to. Able to do that.

But I think the take home message is that both of these products show prevention that is efficacious. So we've got greater than 90% efficacy with both of these two, products and both of these two formats. This is the threshold that's needed for regulated authorities to demonstrate that they're affected products.

So when we're choosing the product, we want to choose the product that's most appropriate considering all of the overall needs of the patients. So whether that's topical or or product, that's gonna be a little bit of owner, . Preference as well as owner compliance, and really the essential take home message from today is if we want to prevent that one, we need to give that treatment regularly every month to try and stop the development of antis strongylosis.

So, so we're not gonna stop the, infection, but what we're trying to do is to stop the development through, to a patent infection that can be associated with clinical signs of disease. So just to, to finish off, thanks for, for getting to the end this is the last slide, but and fungus azorum is increasing in prevalence in the UK, increasing northwards, eastwards, to areas where we haven't seen it previously. We know there are some geographic hotspots that exist even in the local areas, and that's due to the gastro or population as we talked through.

These respiratory and coagulation signs are most commonly reported, so we, we know that in terms of the respiratory disease, the coughing, ermous pneumonia, coagulation signs as a result of this disseminated and dramatic coagulation. Some death can occur as a result of those bleeding diathesses, so that's really important that we recognise. Diagnosis is best achieved using the angiodetect test, but if we're unsure, then a PCR test or by positively and being absolutely sure that we're identifying the faecal R1 larvae, can, can help us, but we need to take care that we're not confusing Andropozorum with razavolus or osos or.

You know, sometimes things even like, other, other, strong doses that have become, desiccated or sometimes even fibre can look very odd like those. So being absolutely certain it's really important. If we see clinical disease and we treat it with a licenced product, so that's gonna be a spot on moxidectin or a novamycin product.

So using those treatment regimes where we give them oxidectin month for first treatment and then second treatment a month later. And Nomycin on a weekly basis for 4 treatments. But if we're preventing the disease, which is really key to trying to stop these things from happening, then lifelong monthly disease prevention is essential and we need to give that on a regular basis.

And essentially what we're trying to do is to break the life cycle before those worms can cause clinical disease and we get to patency and either nomycin or moxetin have been shown to be very effective in trying to do that. So thanks very much for listening. I hope you found that this all interesting.

It's provided some information as to where we are with your cases. If there's anything that I've said that isn't clear or any questions that you want to ask, or any cases that you've seen that are interesting, then please get in touch. My email address is here, so [email protected], and I'd be very happy to hear from you.

Thanks for listening. Folks, that brings us to the end of this recorded session. For those of you that missed it in the beginning, tonight's webinar was recorded, so we're not doing any Q&A sessions tonight.

However, there will be an email that goes out to everybody that attended tonight, with the, instructions on how to ask your questions. So Frank and the others that have asked questions. If you could just repeat those questions based on the email tomorrow, then, Simon will get back to you with those answers.

In his absence, a huge big thank you to Simon Tappan for yet again a fantastic presentation. He really is a a very valuable asset and and a source of knowledge for our profession. So thank you, Simon.

And of course, a huge thank you to Bohringer Ingelheim for sponsoring tonight. Yeah, as Simon said, it's really important to prevent this condition and our sponsors Bohringer make some fantastic products that can help us along the lines with that. So to all of you for attending tonight, a big thank you to you as well and as always to Dawn, my controller in the background.

Thank you for playing the video for us tonight. And from myself, Bruce Stevenson, it's goodnight.