Good evening, everyone, and thank you very much for joining us for tonight's BCVA webinar. My name is Sara Peterson from the BCVA board, and I'll be chairing tonight. We have a fantastic speaker lined up tonight, and I'm sure that there are going to be loads of questions, so please type any that you may have in the Q&A box during the webinar, and I'll save them for the end of the presentation.

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So that's enough for the housekeeping. Tonight it's my great pleasure to introduce Ben Strugnell as our speaker. Ben qualified from Edinburgh in 2002 and spent several years both in mixed practise in North Yorkshire and then at the then VLA in Thirsk.

In 2014, with help from AHDB, he undertook a pilot project to establish a carcass-based PME service at a fall and stock collection centre in northeast England. And he's still there to this day, which just shows you what a success it was. During the last 6 years since Ben has been based there, he's examined over 8000 carcasses and written and presented widely on these findings which he's going to share with us tonight.

You may not know this, but when he's not doing postmortem examinations, he has kept us entertained during lockdown with his singing. So he's not here for tonight for that, unfortunately, although maybe we may get a bit later on, Ben. But he will instead be taking us through postmortem examination of the calf.

And, he, I think you'll agree he's perfect speaker for tonight. So now I'll hand over to you, Ben. OK, well thank you for having me.

We had better crack on, that's, that's the introduction I was going to do, so that's basically the area of the country that we cover and . Admirable introduction there by Sarah. What I thought I would do tonight was a brief run through top to tail of how to approach the postmortem examination, and common lesions by organ system, which are all interlinked with each other.

So there'd be a bit of deviation from the organ system when I, for example, find a lesion. Which leads you on to other lesions and other lesions. Try to understand the pathogenesis of the lesions, and when you see a lesion, which diseases they suggest, which samples to take to confirm your diagnosis, and then a few top tips hopefully, along the way.

And divided roughly in by organ system, as you can see there. That's the p.m.

Room. So the aim. Is to turn with the picture on the left here, which is a dead calf, er, into what you can actually make a diagnosis on the basis of which is the gear here.

So how do you get from that to that? You can do them on the floor. Like that, in situ, so that everything is left in situ.

But if you do do that, it's very important to remove the pluck here, to remove the pluck, the, oesophagus, trachea, and larynx, so that you can examine that separately and so that it remains attached to the pluck and you don't cut it off at the thoracic inlet there. It's a reasonable way of getting to see the organs in situ, that is, but generally speaking, I prefer to hang them up as I'll show you later on. So we start off with the skin and subcutaneous tissues, and this is just an example of how one lesion leads to other lesions.

You see those lesions, you think, hm, they look a bit strange. Around the rest of the carcass is those lesions, and you start to think cutaneous, lymph that was actually a case of cute. Lymphosarcoma, which, in other parts of the carcass, you see an enlarged thymus there when you open up the thoracic inlet.

This is the thoracic inlet here, there's the rest of the neck. Bunches of lymph nodes like grapes and multifocal, white lesions throughout the heart. So, One lesion leads you on to another set of lesions which you might, suspect.

There's another cutaneous lymph, there's another lymphosarcoma with a great big thymus, at the front part of the thoracic, cavity there. Then you go into the, subcutaneous tissues, and the aim here is to, see some lesions and start to think about what could be causing those lesions. So, I.

Always have a good look at the subcutaneous tissues because coalescing haemorrhages and engorged subcutaneous blood vessels almost always mean something, usually an endotoxic or septicaemic or enterotoxemic process going on. So never ignore the subcutaneous tissues and what they're telling you. This will be DIC multifocal haemorrhage or endotoxemia.

And in a calf, it'll be something like septicmic, salmonella, it'll be blackleg, it'll be pneumonia that spread to systemic bacterial dissemination. Other important things in the subcutaneous tissues, are edoema, and the textbooks tell you you get sternal edoema. Well, it's definitely true.

Here's a little calf with, widespread subcutaneous edoema. Here's a closer up version of the same thing. That's not postmortem change, that's real subcutaneous edoema.

Here's the same thing, and it's almost always congestive heart failure, which in calves, you're already starting to think, this is something hearty going on here. So. It could be a wire, it could be dilated cardiomyopathy.

There you can see a great big heart and a small set of lungs in there. It could be a ventricular septal defect, of which more later, or it could be endocarditis. But already, just from the subcutaneous tissues, you're already starting to think about the pathogenesis.

Of those lesions and thinking what could be underlying and what could be causing them. The other thing you'll look out for is, nutmeg liver as part of the congestive heart failure set of lesions. And people often say, well, the heart was a bit big.

OK, the heart might be a bit big, it doesn't mean anything until you have other signs of congestive heart failure and or a reason within the heart why it might be big. But the other signs and the putting the whole package together is the most important thing. Here we have another example of lesion, subcutaneous tissue lesions that are gonna lead you directly to the diagnosis.

Here's a. 10 day old calf with lots of subcutaneous subcutaneous haemorrhages without the engorgement of the blood vessels. So all you have here is petigations.

It's not so much a fevered carcass, more like a a a consumptive coagulopathy carcass, and this was a and here, here are the other lesions throughout the carcass. Which gives you a bigger clue of what was going on, massive haemorrhages in the lungs here in the inter interlobular spaces and haemorrhages all over the serosal surface of the jujunum and the heart, epicardial haemorrhages, . In bovine neonatal pancytopenia, which is nowhere near as clear as common as it was in the days of Pragshaw, but does still happen rarely, with other vaccines, especially BVD vaccines, and are normally worth, undertaking a, a pharmacovigilance investigation, and the sample of choice you'll need is a fixed bone marrow.

For, to demonstrate the trilineage hypoplasia, which is the reason for the haemorrhage is because the first, cell type to go are the thrombocytes, also spleen in case of BVD type 2, and also while you're putting the, bone marrow into formulin, you may as well stick some other tissues in case it's a, consumptive coagulopathy and sepsis. . So that's how the subcutaneous tissues can lead you off in directions.

The other thing is, not as commonly in, in sheep, but in cattle, you do see subcutaneous jaundice, for which the cases, the, the, it's quite neat. The common causes will be a hemolytic crisis, pre-hemolytic jaundice, usually with . Copper poisoning here on the right, but in that case, you all, the first thing you want to look for in a jaundiced carcass is, is there or isn't there hemoglobinuria?

If there is hemoglobinuria, it'll be a hemolytic crisis. Most commonly probably short of massive hemolysis. It'll be, copper poisoning, which can happen if calves dairy cows are come out preloaded with copper and then get fed something or rare, probably genetic abnormalities like Bedlington terriers.

But hemoglobinuria is more suggestive of, hemolytic crisis, which is more suggestive of, . copper poisoning, whereas if there's no haemoglobin urea, the other, more common differential would be salmonella Dublin, in which case you often see big splenomegaly, and you often see, polyceroitis with pericarditis here and. Septic pleurisy.

And the other, post renal or sort of semi-post renal disease would be this, chronic cholangio hepatopathy of suckler calves, which remains, cause of which remains. Unknown as it is. Anyway, the point is, you see jaundice and already a, a sort of differential list starts to form in your head and your, the steps to rule each possibility in or possibility out, start to happen.

In all cases of jaundice, you'll never go wrong if you take fresh liver, fresh kidney and fix both. And keep them. So then, .

This is how I remove the pluck. I prefer personally to do the any calf, any calf bigger than about a month old, hung up and then I reflect the skin back either side and . Open up, free out all the tissues up here so that I can post them through the thoracic inlet.

And it also gives me a good opportunity to have a good look at the subcutaneous tissues for the reasons that I explained earlier, because they lead you in directions and start ruling in and ruling out differential diagnoses. The next step once you've reflected those tissues back is to post your tongue through the thoracic inlet. Through there and through there, and then you're going to go underneath the into the thoracic.

Once you've removed the guts, you pull the tongue and the pluck with the trachea here, cut behind and pull it out, saves you going through any ribs. I think it's much easier and it gives you the chance to lay all the organs out on the table, as I showed earlier on. So once you've laid it out, you're left with the .

The pluck removed, the the larynx, tongue, trachea, oesophagus, all that stuff. You have a quick look at the cleft, at the hard palate and soft palate, and make sure there's no dosing gun injury, make sure there's no cleft palate, and in particular, you want to check the hard palate for multifocal erosions, which this was a Case of mucosal disease, which sometimes that's all you see. Thyroids briefly will remain attached to the thorax or to the trachea, either side, so you don't have to worry about them when you're chopping it out.

It's quite difficult to accidentally, remove them, and it's just quickly to mention that. All I tend to do is put them into formalin and let them do the, let the epistop pathologist do the rest, and then subsequently differentiate between normal colloid goitre and hyperplastic goitre. And that's all they ever tend to do with thyroids in the cases of stillbirths.

So, Now the job is to have a look at the pluck. When you've laid the pluck on the table, as I showed you earlier on, you grab the larynx in one hand, you can just see my thumb there disappearing er into the . Oesophagus, and you want to personally run your knife all the way down the oesophagus down there, expose the mucosa of the oesophagus, you, otherwise you'll miss esophageal ulceration, which is almost always present in a mucosal disease, and malignant cataral fever.

You'll also see, if it's present, a quite, quite clear esophageal. Bloat lines there, which is often present, and we're going off on another tangent here in cases of ruinal acidosis or ruminal bloat. In those cases, personally, I think rumin pH is OK, not too bad.

If you've got a rumin pH of 4, you're OK, unequivocally incompatible with life. If you've got a ruin pH of 5, in some animals, it might be OK. In some it might not.

I do like taking room and wall histopathology because you can get an unequivocal diagnosis of, if there's been any ulceration or damage to the ruminal epithelium, you can also get a reasonable idea of are there any protozoa remaining or are there allgram positive, . Bacteria being overgrown because of the, have overgrown because of the acidosis. So I'd like to take room in histopathology if the, his autosis isn't too bad.

The other thing that your mind will be wondering about at this stage to find unequivocal evidence of acidosis will be other organs like liver. You'll be wanting to Look at the liver for ruminal a ruminal liver abscessation, I should say, multifocal liver abscessation there and there and there in this case. Plus, flip the liver over, have a look at the back at the corra vena cava.

If you've got a cordra vena cava septal septic thrombus, unequivocal evidence of liver abscessation, most likely due to ruinal acidosis. In particular reference to cars, calves, suckler cars outside fed creep, . Quite often get acidosis, and it can be quite an art to feed them without them getting acidosis.

And I think I find people are often in denial about it. And the more unequivocal you can be, including rhean histopath, pH, and those downstream effects of rheuman acidosis, the better, in my view. Anyway, back to the oesophagus.

Here's an oesophagus damaged by a stomach tube, by a farmer. This is a useful thing to show to a farmer. You've got, haemorrhages there, haemorrhages there, and erosion of the surface, and all that was needed there was the stomach tube was getting a bit old and, hard and not very.

Flexible, needs to be replaced. So, that's the, that's the oesophagus when you've got the pluck in your hand. Once you've finished with the oesophagus, you, I normally then, switch to the respiratory tract because that's also in the pluck.

Then start with the, larynx, open it up, you'll see larynochondritis if you, if it's there. This is a Belgian blue calf with a fatal laryngeochondritis. You can see the .

Complete obstruction of the airway there, then working your way down the trachea, obviously IBR tends not to happen in cars less than 6 months old, but it's unequivocal, obviously if it's there, important to look for ulceration here, and that when you . When you Just erode the surface of the trachea with your finger. It's got to be ulceration under it, otherwise it could just be cough mucopus coughed up from further down the lungs.

The other thing you'll sometimes see in the trachea in cattle outside is obviously lung worms, and that's the main reason I suppose in cattle outside for looking in it. The caveat being. That if you don't see any lung worms in the main stem bronchi and further down, it doesn't mean that it isn't lung worm, because lung worm can arrive in the caudal lobes first and often really, all you see is cordo dorsal emphysema and sub plural gas bubble accumulation like this .

In the pre-patent phase of lung worm, before you get to any adult or immature lung worms being present in the main stem, bronchi. So, lack of adult lung worms in the main stem bronchi does not rule out lung worm because it could still be prepaid and they just want putting in formal in some of those lungs. While we're on the subject of lungs, I think it's important to say that not all lungs, not all lung lesions are caused by respiratory disease.

Here is a case of dilated cardiomyopathy with a markedly enlarged heart here, and by the way, it did have those, other. Sorry, signs of congestive heart failure that you look for when you're starting off the postmortem, subcutaneous edoema and nutmeg liver. But here, you've got marked edoema in the interlobular spaces here.

No consolidation, no emphysema. That's purely caused by congestive heart failure, you know, volume overload, that sort of thing. So not all lung lesions are caused by primary, respiratory disease.

And here is another example of a, of a systemic disease with pulmonary manifestations. Here, you've got fairly, well-defined yellow exudate, stroke. Edoema in the interlobular regions of the lungs.

Nothing to do with, primary respiratory disease, this isn't. It's everything to do with Clostridium perfringence type D enterotoxemia, basically pulpy kidney in lambs, which is a, an intoxication. And basically, that makes blood vessels leaky, gives you, lung edoema primarily, no consolidation, nothing else.

And then you want to take the, small intestinal contents from the epsilon toxin, and ideally you want to remove the brain into formalin, to, . identify those passnemonic lesions there, but, you're allowed to use the word edoema, you're allowed to use the word consolidation. You're not allowed to use the word congestion because it's generally, meaningless.

And those are two examples of edoema, with nothing to do with, primary respiratory disease. The other thing to say when looking at lungs is that it isn't always consolidation, and the lack of consolidation doesn't mean it can't be a primary lung. Disease.

Here's a, a good case of marked generalised hyperinflation and hyper, yeah, hyperinflation and emphysema with subplural gas bubble accumulation, and this I think was a case of idiopathic interstitial pneumonia. Very little in the way of consolidation, but still a primary lung. Pathogenesis, that you could see similar changes with RSV and with pre-patent, lung worm.

We can't have a a, a, a talk on calf postmortem examination without mentioning, calf respiratory disease, especially at this time of year, but I won't dwell on it because we've had other talks, you've probably had other talks, on the same subject, only to say that. By the time of death, it often is the end of a longish process, as in there'll be cranioventral consolidation. There might be called a dorsal hyperinflation.

You might not be able to say an awful lot more than that, but I still think postmortem examination and histopathology is useful because we'll just concentrate on the ones on the left here. You can divide the, type of respiratory pathology into those five, Categories which all have a different on farm action, and I'll briefly try and go over them now. Cutting into the lung, you can often see that there's a two phase disease process here.

You can see distorted airways and fibrosis and consolidation there, and you can see more recent bacterial bronchopneumonia, here, . Basically, in those cases where you've got cranio ventral consolidation, the approach, I never do any bacteriology because it isn't going to really tell me anything I don't already know, I don't think, and it's likely to be contaminated. By far and away the most useful thing in those cases is going to be histopathology.

It'll tell you, is it viral plus bacterial? Is it viral plus mycoplasma plus bacterial? Is it only bacterial, is it acute RSV?

Is it interstitial pneumonia? Is it lung worm? the, so, so basically the, the, the, action there is to put that into histopathology.

Specific lesions that you might see, are acute hyperinflation of the lungs here and here and here. You can see air bully there, you can see, interlobular edoema emphysema, specifically in, RSV which is. Diagnosis should be easy enough to make histologically, but it might be worth taking a fresh bit of lung for PCR from various parts of the lung to confirm the diagnosis of RSV.

Mycoplasma bovis, similarly, the lesions are pretty, pathenemonic when they are pathenemonic. If you see what I mean, but easily, confirmed, histologically, by these, when you have a suspicion of it from these grossly these Caseus, lesions here and then. Idiopathic interstitial pneumonia does a very good impression of RSV and is almost indistinguishable grossly, I think.

But another reason for sending the histopathology to the lab, because it will easily differentiate between RSV and idiopathic interstitial pneumonia, which is a, an incompletely understood, pathogenesis, similar to fog fever, and, . But worth knowing, because it isn't infectious and it isn't really a broncho pneumonia. The other type of bacteria is a primary bacterial bronchopneumonia, where you see very stiff, the stiffest consolidation you'll ever see, often with pleurisy.

And it's a different plan for this if it's inside or outside. If you have, what looks like a primary bacterial bronchop pneumonia in calves inside, the main focus should probably be on ventilation here. Here are the calves at the bottom.

This is like a dwarf in a lift when someone farts. The, stack effect is working nicely at the top here, but at the bottom, the air is a bit stagnant and not much air movement there, and that can sometimes, on, . Muggy days, cause bacteria bron a primary bacteria or bronchop pneumonia with no need for viral, predisposing airway damage.

The other possibility is if it's bacterial pneumonia outside in, cycloars. You may get something like this, where the calf, the, the cow when it's inside, is eating unsupplemented silage and the calf when it's in the womb, relies almost entirely on its dam for its copper and selenium. There's not much copper and selenium going across the placenta there.

The calf is born, gets turned out. The calf has access to one of these cure all miracle free access lick bolus buckets, which may get enough cop it into the cow to get it back in calf, but there's very little copper and selenium goes through the milk into the calf. So if it's borne deficient, the calf.

Gets born, turned out, it becomes more and more and more deficient, and by this time of year, these suckler cars are often running on empty, so then they tend to die of opportunistic bacteria or bronchan pneumonia, which you can tell grossly, because it looks like that, because they've got no copper and selenium in them and therefore they're immunocompromised. And that accounts for this little spike of, what looks like bacteria bronchial pneumonia in suck the calves, outside. The, the, the, the cure being to make sure that cows receive Ebolus when they're pregnant, so that calves come out pre-loaded with the, minerals, rather than, you know, waiting till they've been born.

The reason all this makes a difference is because each of those various diagnoses of pneumonia, stroke, bronchial pneumonia, have a different on-farm action. So the, the most useful thing you can do is histopathology, I think, but it all must relate back to the situation, on farm. I hope that makes sense.

So that's a brief overview of the lungs. The next, organ in the pluck is the heart, and basically, you, I, I often try to remove the heart from the lungs once, I've looked at the lungs, and I lay it on the table like this. I, I identify which is the right ventricle and which is the left ventricle.

I'll run my knife, just through the free ventricular wall of the right ventricular wall here on this side to open it out so that I can see the tricuspid AV valves here. And this is where your endocarditis lesion's going to be on these leaflets here. And then I look to the right and up a bit, and I can see the pulmonary valve in there.

And then I, and, and briefly, while I'm there, I check for, VSDs and things like that. Then I flip it over, and I run my knife through the free ventricular wall of the left ventricle. I look at the, mitral valve in there.

He's the leaflets of the mitral valve there. And then just behind. The mitral valve here, the bit joins.

I run my knife up, up the way with a sharp bit pointing towards me, and that'll take me up the aorta, and then here you can see the aortic valve here. So you want to go through all four of those valves, sorry. Tricuspid, pulmonary, turn it over, mitral, then, aortic.

And they also, while you're in the left ventricle, you want to try and run your finger, see if you can find any holes and poke your finger through into the, right ventricle while you're in the left ventricle. If you can't, then there aren't any . VSDs.

The other way, the other advantage of this system is it gives you quite a good view of the myocardium in there to check for myocardial lab cessation, and, myocardial necrosis, that sort of thing. . So congenital heart defects are reasonably common in cattle, and again, just to say, the heart is enlarged, I don't think it's, good enough.

It must fit in with gross suggestion earlier on in the postmortem of. Congestive heart failure. So here's a case of .

A ventricular septal defect, where I've opened up the heart in the way that I described, and there's my scissors poking through the BSD there. And here is a, a dilated cardiomyopathy, where the right ventricular myocardium is noticeably thin, and you can open it right up. Here is truncus arteriosis, where you can see a marked bulging of the .

Two vessels joined together. I'll tell you a story about that later if we have time. And here's the reason why it's a good idea to follow the the great vessels, this, in this case, the pulmonary artery, for as long as you can sort of reach around with your knife, because here, this is like endocarditis, but it's of the pulmonary artery and .

Credit to Toby Floyd at APHA for finding this, Legion I sent in this heart, which reminds me to tell you that often if you can see a heart is grossly abnormal, it's a good idea to open it up as described. Don't know what else is wrong with it. Cut it off so that the great vessels are as long as you can possibly get them and plop it into a bucket of formalin, let it fix for a week, and then send it to someone clever, which is what I did with this, and that's how we found this, .

Arterittis. Here, as I said, once you cut the myocardium like that, you can find myocardial abscessation there and there, which is just a manifestation of, yemia. Sorry.

So here what happens is your heart relaxes in diastole and then, beats in systole, and then during diastole again, the blood comes back round the little holes at the bases of the great vessels to go into the myocardium. Once the piamic, spread has occurred into the myocardium, the, the, the myocardium is basically a big lump of muscle with not a lot of immune system, there, so these, . Abscesses can basically have a bit of a pub crawl in the, myocardium and off they go.

And then just to say that doing it this way will enable you to look at all four valves, and you can see endocarditis on the tricuspid valve here, which is probably the commonest valve for endocarditis to be on because it drains the systemic circulation and the pulmonary, the AV valves here. And there's an example of endocarditis on the pulmonary valve there. Another thing to be mindful of, especially in calves, is the cardiac form of black leg, where you'll get a definite multifocal .

Fibrinous proliferation on the epicardium here and when you oops. Sorry, and when you cut into the . When you cut into the substance of the myocardium itself, you can see definite black lesions within it, black, dry, often emphysematous lesions in the substance of the myocardium.

They all the more reason for looking into the myocardium, but as I said earlier on, the, the, the initial lesion, these very fine, fibrinous epicarditis gives you a clue that there may be a bit of cardiac black leg going on there. So that is basically the pluck where you're looking at bronchop pneumonia, other lung changes, and then a gross examination, of the various, cardiac pathology. Then we're into the abdomen, which, normally if the car is hung up, it just flops down by gravity, but before it does that, you can have a quick look to see is there any peritonitis.

And usually in cars, it's one of three things that go through your mind, and have a nasal ulcer. Surprisingly common in suckler calves out of grass for reasons unknown, navale, or possibly, salmonellosis. But with, salmonosis, you'll generally have .

Pluriy and pericarditis as well as just peritonitis, whereas with the other two, you'll generally only have peritonitis. So the first thing, if I see peritonitis like that in a suckler calf out of grass, generally the first place I go and look is going to be the, Abemam before I lose it. And then very often you'll see a full thickness perforation like this and .

That's your diagnosis made. When you cut into the Abermasal mucosa, you can often see sort of emphysematous change and erythema a bit like that. Exact reason unknown, but probably you only get.

One, but I do think it's commoner when you've got borderline acidosis, and, creep feeding probably does make it commoner, I think. Here is an old ulcer. There in the corner.

The other, the other place to look obviously in failing, finding and have a nasal ulcer, would be the remains of the navel, which remember, goes two ways when it first comes in the navel. They get the onphallic vessels that head towards the bladder, which is what I think these are, is the. What I've cut away from the umbilicus, and then it's headed all the way to the bladder here with pus and necrotic material all the way up, with a tendant peritonitis all the way.

And then when I cut into it, there's necrosis and haemorrhage and all sorts of horribleness, unequivocal case of navalil. Yeah, often, I think navalil is a very good thing to show, farmers there and then, because, however, It looks from the outside, it's always worse inside, and there's the sort of strands of fibrin that you see in cases of naval il when you follow it all the way to the end. Then briefly talking about the, what flops out at you when you first open the abdomen of suckler cars, intestinal torsions are not that uncommon, .

I think it's probably to do with a a slug of carbohydrates from either clover or grass or even grain, somehow gets through the room and without causing bloat, then goes into the distal, jujunum, gets rapidly fermented by bacteria that are there increasingly the more you go distally. Rapid fermentation, rapid gas formation, gut instability flips over, and then you just get this segmental purple, discoloration. And normally there's a predisposing factor, even if it isn't obvious.

. So then once the guts have plopped out, we have a better look at the Abemazum. This is a common, a reasonably common presentation in dairy cows with emphysematous abbemazitis where something's gone wrong with the milk feeding. This is what the mucosa generally tends to look like, purple, red, emphysematous, and .

Often with badly clotted milk and a foul sort of pungent smell, often leads to a frank ulceration of the, Abemaz itself, and often to Abemas or torsion, which may be the cause of death. And under and the cause isn't exactly known as far as I know it, but I. It tend to work on the basis that it's an overgrowth of bacteria on the mucosa of the surface of the Amazin for whatever reason, be that, a bad milk feeding regime, be that hygiene, generally speaking.

And in my limited experience of asking people how they dealt with it, if they commit the sin of putting clawtet into the milk, it tends to go away, which tends to be . A proxy for bad hygiene and it can be used as a stick to say, well, your hygiene needs to be improved and this will go away. Next, on the list is room and drinking, and this is well worth looking at in calves, because often these are calves that have had every, investigation for scour or intermittent scour or looking pot-bellied or looking a bit crap under the sun, until one dies, probably of pneumonia or something unrelated.

And you find when you open up the abdomen that they, they, you've got sour, unclotted milk in the rumen, which is here, and a big Abemam also full of not very clotted milk. So obviously the gastric groove isn't working and the milk is staying in the rumen and not going into the Abemazm. There's another example of a not very, pleasant rumen with milk in it that shouldn't be in it, .

And again, and sometimes this is the rumen actually, and sometimes it can lead to these fungal plaques. This was candida, I think, fungal plaques in chronic rumen drinking where something was going wrong with the milk feeding regime, the long and short of which meant that the gastric groove wasn't closing, and, the rumen was . Containing milk, it shouldn't have.

Contained. But the only way I think you're ever going to diagnose that and cure it is by, postmortem examination. Still on the subject of, Abemas, but in calves out of grass now, it's always any poor doing calf out at grass.

Usually weaned calves, doesn't tend to happen in suckler calves for whatever reason, but usually weaned calves, or second season grazing calves. You always, always, always want to look at their Abama because ostetasia is very common and you get this obviously Morocco leather thickening. Often the actual worm egg counts aren't as high as you certainly aren't as high as you see in lambs.

Might have been high and . can be sometimes a bit disappointing, but if you look at the Amaz, you won't be far wrong, with that. And then we moved down to the jujunum, and this is a case of necrotic enteritis of suckler calves, tends to be a spring thing rather than a an autumn thing, but the other, this is a a side on view of the jujunum, just looks horrible and thickened and and necrotic inside.

And here's another one, thickened, necrotic, thickened, just to remind me to tell you in this, case that it often also has extra intestinal consequences because it's They don't know obviously what causes it, but it does involve some degree of bone marrow suppression. So it's another one where you need to take some bone marrow into formalin to confirm it. And often you see other lesions.

This is a case of, necrotic enteritis, because you've got bone marrow suppression, you've got neutropenia, and you've got these septic thrombi in the liver, and then these multiple thrombi in the heart, sorry, in the lungs, which was probably the cause of death through, sepsis. And then what can I tell you about coccidiosis? Nothing much apart from the.

Gross postmortem findings are fairly, variable. If you've got clots in the colon, that's quite a big clue. And also to say that coccidia are reasonably resistant to autolysis or remain, if the thing's been dead more hours than if you're looking for the epithelium.

So histopathology isn't necessarily, . A dead duck, if the thing's a bit too a, it's worth taking anyway, because obviously, you know, the, the, the peak of coccidalosis shedding doesn't necessarily coincide with death. You can get, it can happen before or it can have to happen afterwards, but histopathology is a good way of putting the the pathogen at the scene of the crime by .

you know, by definitely confirming that that's what it is, and it isn't really that expensive. We'll just whiz through, so that's the guts, and then the the the other organs on our table at the beginning were the liver. So we'll run through the, quickly run through my top liver pathological slide.

This is a case of naval ill, complications of naval i. There's a naval dripping pus and there's a, abscess, in consequence. That's black disease, we tend to see in older cattle, but can see it in younger ones, central necrotic core and then black, halo.

There's another one, central necrotic core, and then black halo. Nutmeg liver, we've done 99 times out of 100, it's congestive heart failure, so have a real good look at the heart. Or, the other, the other, or at least it's cardiovascular, sometimes you can get a strategically placed liver abscess in the corrivena ca thrombosis, and that can put pressure on the corriven thrombo er sorry.

Cavena caver, I should say, that can put pressure on the corvena caver leading to nutmeg liver in the same way as, congestive heart failure would. So if the heart doesn't look abnormal, have a look at the corre being in a caver and see if that's the reason. Otherwise, it could be toxic, and it's, as I say, it is often caused by endotoxemia.

. Copper poisoning we mentioned earlier on, you get a really marked orange liver often not necessarily gunmetal grey kidneys like you do in sheep, but sometimes, but always with hemoglobinuria and often with jaundice, as I mentioned earlier on, I think we'll skip over this. On the subject of livers, if you can find liver abscessation, always acidosis and a good way to, relieve farmers from being in denial about sailing too close to the wind, with how much grain that they're feeding their cattle. Here's a quick whiz over kidneys.

Multifocal renal abscessation is a sign of, yemia. This is some, cattle that had very bad, foot lesions outside and manifested as renal abscessation. And then white spotted kidneys in calves is a sign of prior, bacteremia that has settled out in the kidneys and caused an interstitial, nephritis.

May or may not be the cause of death, but is a sign that something might have been going wrong, wrong, earlier on in life, i.e. Colostrum, navels, that sort of thing.

That's white spotted kidneys there, . Then we're onto the musculoskeletal system once we go back to the carcass still hung up, just to say that if you're going to diagnose black leg, it has to be right within the muscle belly itself. It has to be black, dark, emphysematous, cannot be around it, it has to be in it.

There's another one. Unmistakable when you see it. If you're if you're looking at a lesion and saying, is it black leg or isn't it, it probably isn't, because it really is unmistakable right in the muscle belly itself.

You usually have to cut through quite a few muscle. Bellies to find it. That's very common.

In contrast, white muscle disease, I think is not very common, even though everybody thinks it's very common. Here is a case that wasn't white muscle disease, but had very white muscles, and, I don't think it's. You cannot cause something white muscle disease unless you have histological evidence of muscular degeneration, which if you have low selenium or vitamin E, you can then call nutritional muscular degeneration, but until then, you can't do a postmortem and say those muscles are white, therefore, it's white muscle disease, because 96 times out of 10, it won't be.

then, we sort of move on to the musculoskeletal neurological system, and just to mention that arthroglyposis. As in this case, and in this case, is not always caused by Spallenberg, because here is a case of arthroglyposis, which was caused by Arnold Chiari syndrome, which when I took the lid off the brain, the cerebellum has gone, and the occipital. The lobe is pushed through the back of the brain, through the, enlarged foramen magnum, and spinal cord.

There's the remains of the cerebellum there, and there's the small spinal cord. You only, we only would, and it also had spina bifida, but you, you would might have assumed that this is Schmalenberg, which is what the farmer did, but on further investigation, it was not Schmalenberg, so there's a small risk of Schmalenberg being overdiagnosed if the emotions aren't gone through and The brain isn't properly, you know, removed and the spinal cord, which brings us on to the nervous system. I think it's not that difficult to get a clamp that can remove brains.

In fact, I, I think it's often a very important part of the postmortem examination, the brain and the tissues around the brain, here's an abscess, of, the long acting, . Cephalosporin too close to the brain cause a an abscess which was enough to put this calf off its legs, . Sometimes there are no gross lesions in the brain, but sometimes there are.

It's always, always worth having a good look at the back of the brain stem to see if there's any edoema there. That's a sign that when you send it away, you're going to get a result from the histopathologist. This is, and always worth looking in the pituitary fossa, because pituitary abscessation is pretty common.

In calves. And then when you take the brain out, you can see poly meningitis there, which probably means you can save the fellow some money and not send it away, to the lab. Always look for a cerebellum, which this one hasn't got.

This was a case with Schmellenberg, I think. And then I'm just going to show you quickly this video, if it'll play. This was a calf that was born like this and.

Get up, despite 3 or 4 weeks of . TLC from the farmer. This is all it can do, do super, despite a lot of help doing that.

Didn't ever do any better than that, so got a one way trip to farm postmortems, . That's it. When I removed his brain, this is to show that sometimes there are growth brain lesions.

This was the brain of his mate, which was just a ball of fluid, with not much, with no cerebellum. This was his brain with no cerebellum, whatsoever. This turned out to be, when I sent off, I said to him, this will be BVD, because it, that's what I thought it would be, .

The blood that I took from that calf before I killed it were negative by PCR. The immunohistochemistry, the IHC on the brain was negative. The serology on that calf was strongly zero positive.

So, he said to me, how do you know it's BVD? You can't show any BVD here in the You can't show any BVD in the brain, and that could have been maternally acquired antibodies. How do you know it's a BVD?

I said, go back and bleed some younger calves, which he did do and managed to find a PI in some younger calves. And it turned out that this, he'd bought in some cattle. And just about the time that this calf was 120 days or thereabouts in the in, in, in utero, its dam was exposed to some PI cattle or turned out to be PI cattle.

So the calf did manage to clear the BVD from its, system, but in doing so, its immune system also removed its Cerebellum and some other parts of its brain. So it sort of won the battle but lost the war, because it cleared the BVD, but it also cleared the infected cells in most of its brain, which left it without much brain and un unable to stand up. So, we said to him, you need to vaccinate for BVD and do a PI hunt.

He said, Yeah, yeah, yeah, I'll do that, and never He did, and then 12 months later, he had a group of 20 fattening balls, of which 5 decided to die, and he, and they sort of had read the textbooks and had multifocal, esophageal ulceration here with, mucosal disease in their colon as well. That probably says more about pharmacyology than it does about, Pathology, but there was the question, and those were the gross lesions to go with it. That is.

The end of the talking. A brief run through of lesions. So Sarah, over to you for questions.

How are we doing for time? We're doing great for time. We've got 10 minutes for questions.

I just want to thank you, Ben. That was a really great presentation with loads and loads of insight into what you find, during postmortem examination of calves. We have got lots of questions already, but before we go to those, could I just ask everyone that's watching just to spare 30 seconds before they log off tonight, just to complete the feedback form that should have popped up in your browser, .

But we do, we do listen to your feedback. We do get speakers based on that feedback. So please, give us your feedback on tonight and also what you'd like to hear about in future.

If you can't see, what's popped up in your browser, then, you can also email us directly with your feedback to the BCVA office at cattle at cattlebet.co.uk.

So now, over to our, our first questions. I'm just going to, to share a slide here just for a few dates for your diary, just for, for upcoming webinars and also for anybody that's got the RCVS one CPD app, you can actually put the details of tonight's talk directly into your app, just by using that. QA code, QR code, sorry, there.

So, just a reminder that any questions, please, could you pop them into the, Q&A box, because I can't actually see the chat, when we move towards, question sessions. So just please pop them in there so we can make sure that they get answered. Right, Ben, for the first question.

Question here that came in earlier on in the presentation. What causes laryngeal I can't say it, Corronitronitis. How do I say that then?

That's it, chronitis. I still can't say it. I think that is a very good question, and nobody really knows, but it's got to be anatomical, I think that.

When we looked at, it's basically assuming it's the same as in Texel tups, which I think it probably is in Belgian blue calves that tend to get it, it's to do with a a a narrow trachea, which increases the it's basically a bron a brachycephalic airway issue, I think. Like a pug, but in but in cattle or sheep. So I think what happens is you've got turbulent airflow because of a narrow trachea.

You've got your vocal folds, your two pointy out bitts that that are of the aytinoids sort of meet in the middle sometimes, every so often, when you're making noise or just breathing or whatever, which causes ulceration of the . Epithelium, which obviously then lets bacteria in, and then you know, inflammation and swelling in the last place you want any swelling, so I think . I think it's just anatomical.

I think that's the, the long and short of it. I don't think it's anything to do with the recurrent laryngeal nerve like in er racehorses. I think it's just an anatomical aberration in Texel tups and Belgian blue .

Cattle. The only other thing that can occasionally cause laryngochondritis is systemic, is shipping, sometimes you see it in shipping fever, where you just see focal ulceration of the sticky out bits of the, larynx. But I think that's a different pathogenesis.

I think that's just bacterial sepsis, and and arterial blockage and, you know, tissue epithelial loss because of, ischemic necrosis. Are you with me? But I think laryngeal chondritis, as in that picture, can I get that picture back up on I'm just I think it basically is anatomical.

Do you think that's fair. Brilliant, thank you very much. Two questions the same here, then we'll answer them, two in one.

What's the best way to sample bone marrow practically on farm? Just you go to the store, get your thought, I didn't, I didn't list the . It is sort of kit tool kit that you need for doing a PM because it's, you know, you can look it up in so many different places.

But I should have probably said that a saw, you need a saw, and you basically cut, go into the the easiest way is to go into the sternum, once you've removed all your organs and put them on your table and examined them, go into the sternum, go to the zify sternum, make two parallel saw cuts in the ziffy sternum, so that you can. See into the sternibrae, and then a couple of vertical ones until you can see the sternnabrae and then put a put a sort of sliver of sternum into formalin. Fantastic, thanks.

And how much formalin would you, would you put them in? What ratio? Possibly can, however much you use, it won't be enough.

So a lot. Like, I have three pot sizes, one is 250 mLs. I never use anything less than 250 mLs because it's just not, there's nothing that you can, you know, sometimes the tiny ones are a waste of time.

250 mL, 500 mLs in a litre, and a bucket. So, you know, the smallest pot you should ever use is 250 mLs, I think. So for, for any amount of thing you probably want a pot that's 500 mLs, to be honest.

OK, excellent, thank you. A question here from Josh, can multiplex PCR be used instead of histopath for primary respiratory disease, or is it better to use both together? I think that that is a a a really good question.

And the answer is histopath in my opinion, personally to be histopath first and anything else second. And the reason is histopathology will tell you whether the virus has been and gone. If you're using a multiplex PCR .

You want to know, let's say it, it, you want to know, am I likely to find this virus or not? Because they're expensive. Multiplex PCR is, is expensive.

The histopathology will tell you if you've got, epithelial necrosis, which is an acute lesion. In which case you probably will find the virus, or whatever the pathogen might be that you're looking for, or if you've got bronchiolitis fibrosa oblitaros, which is an old lesion, which means that the virus has been and gone. So if you do histopathology first.

It'll tell you whether or not you're likely to find the virus by PCR, right? Also, if you do histopathology first, it will tell you, and then you say you do histopathology first, and it, and it tells you that you've got, old airway damage plus bacterial superinfection, and you find a multiplex PCR that's positive for Manheime hemolytica. You probably know that that man Jaime Humanita is a secondary, right?

If you, on the other hand, do histopathology and it tells you that this is a fulminating fibrino supparative bronchop pneumonia with no old viral airway damage and you find a PCR positive for Manheime hemolytica, you know that Manheimie helytica is probably a primary pathogen. Bear with me. I, I don't see the point in only doing a PCR.

Without the histopath, for me it's meaningless. OK. Brilliant.

Thank you very much. Question, I'll combine two questions. We've got a lot of questions already coming in.

We'll keep going through them. So, with the, with the calf Abemazms, in a pre-weaned baby calf, what should the content actually look like? And also, how Common at ulcers, because, questions come in saying they wouldn't really expect ulcers in, in pre-wean baby cards.

So, what should it look like and how common are ulcers? Well, I'd say the, the milk should be clotted, for one thing. There should be a sort of cheesy like clot with a bit of curds and whey, whatever the curd is and whatever the way is.

And the, the, the, amasal content should be apart from the milk clot liquid, . And the mucosa should be just a a sort of Probably either a beige colour or a pink colour, and any other colour is abnormal. The lesions are always very, very striking though, if they're abnormal.

Normally you won't be looking at amaze and thinking, is it abnormal or isn't it? It normally screams at you that those, you know, that emphysema, the purple, the horrible, if you're thinking, is it normal or isn't it, it probably is normal. Bear with me.

The other thing not to misinterpret is often abemasons can go pretty purple as postmortem change, and if they're only purple, that doesn't matter. If they're purple, emphysematous, hemorrhagic, then that, then that probably is significant. I don't know whether that helps.

And I agree with whoever said that you wouldn't expect abomasal ulcers to be common in, I don't know about baby calves, whether you mean baby calves, whether you mean dairy calves or suckler calves, but. Suckler carves up to 6 months old. A basal ulcers are not that uncommon in them for reasons that I don't understand.

OK, brilliant. Whilst we're on the subject of of Abermasal disorders, questioning from Mike here, how significant are Clostridium so deli and or sarcinia in calf abamasal disorders? Well, probably, probably quite significant, but they, they're only opportunistic still, I think.

I think there's still something going wrong with. The Abemaal mucosa for them to proliferate, you know, I've had runs of Abemasal problems. I either ulcers or emphysematous, abemazitis, or torsions or just horrible Abemaza in dairy calves, and the guys have given the.

Cows, Covexing to cover the sourellii, when they've been dry for a long, you know, for for enough cows, where they calve down and you would think they would get. Colostral protection against Sordellii in the convex in 10, and it's made bugger all difference, and the only thing that's ever made any difference is the clawtet in the milk. And then that leads you on to beat them with a big stick and say you must improve your hygiene.

So I personally think that Sourelli and sarcina are probably significant, but there is an underlying cause that enables them to proliferate, which is usually too much starch. In the Abemazin, or not enough, or the osmolarity being wrong or there not enough, acid or something's going wrong in the feeding, or, sorry, I, I should say, or suckler cars out of grass getting too much creep or getting intermittent creep, even worse. So I think something is still going wrong underlyingly with the Amazin.

So the milk feeding regime, that means temperature. Concentration, you know, how much water, how much milk is it stirred, is it mixed, whether the calves are being fed it twice a day or 3 times a day, is it the same person? Do they sing a song?

I'll sing a song later, you know, is, is it, is it, . You know, what is going wrong with it, because people will tell you lies when you ask them, do you feed the calves at the same time every day? Oh yes, do you milk mix the milk properly at the same?

Oh yes, oh yes, oh yes. Unless you go, unless you accidentally go one day when they don't know you're coming, they will tell you what you want they think you want here. Isn't that right, Sarah?

Yeah, I, I would agree. Yes, I, I, well, it's just like when the doctor asks you how much alcohol you drink, isn't it? You tell them what they want to hear and not actually what you do.

. So, that actually, your comments on sort of, feeding, leads on nicely to a comment here, which I hope makes sense to you, and it's from Mark. And he says, Ben, remember the M bovis esophageal feeder injuries. Oh yes, that must be from Mark, yes, -huh.

So just so I don't know whether you have a comment on those or how they, how MO is related to that particular case. So that was a good way of spreading, that was a case of . Middle ear disease in calves, which was spread by stomach tube, it had my.

Plasma bovis, whilst we thought being spread from calf to calf with a stomach tube, and, it managed to get, so the stomach tube introduced mycoplasma bovis from one calf to calf to calf, and then the, the, the mycoplasma bovis, we thought, established colonisation of the pharynx, and then it went up the Eustachian tubes of some other calves, didn't it, and led to middle ear disease. And . So I think when we changed or cleaned the other nasal feeding to the esophageal feeding tube, it the problem went away.

And then you can find the letter in the vet record. If you look. Brilliant.

We may be circle out that to everybody, because Mark's just popped up with an, another comment here, and it's that word I can't pronounce again, saying it also, cause laryngeal I still can't say it, chondritis. He, he was saying that, you found in that case that it, it caused that too. OK.

Brilliant. Right. I, I think that we, we've got 3 more questions, but I think we will just try and, and push on and get them answered, as we're only just a little bit over time, and we normally run a little bit over.

So just, a very quick one here about aqueous humour. Is it a valuable sample to collect at postmortem for anything other than the magnesium levels? Yes.

BHP in dairy cows. It's quite useful for calcium. Sometimes you can just get a, a, a fresh cow dropped dead, and that can be calcium with arrhythmias, milk fever, I should say, with arrhythm arrhythmias and whatnot.

So that can be or if you've got a cow that hasn't, or a cow with toxic mastitis, say, a fresh cow, so calcium is quite useful. BHB is quite useful, magnesium, as you say, and sometimes if you're looking at a kidney that you're not sure is this kidney pathological or not, if you take aqueous humour urea, and it's normal, then obviously the kidney is not pathological. And it's, and it's a good cheap way of saying, do I want to do histopath on this kidney, which looks a bit weird.

It's a good screening test to save some money. Are you with me, because of aqueous humour, . Ua only costs, you know, 5 or 6 quid, whereas, histopathology is more like 50.

Bear with me. So that would be my 4 that I have only ever send away. BHP, calcium, magnesium, urea.

And also, also. There is a lot of debate about. The actual, how low does the aqueous humour, stroke, vitreous humour have to be to make a happy diagnosis of grass staggers.

And the reference, there are some who say, now I couldn't comment, but there are some who say that the reference ranges given by the labs are too low, and it's very, very difficult to get a cow low enough to be absolutely certain that it staggers. So I think there is a bit of a grey area, sometimes if you get it sort of. Below the serum reference range, then some people say that's possibly good enough if everything else is .

Suggestive of staggers. And by the way, with staggers, you don't see anything at all on the postmortem, nothing whatsoever. Apart from arrhythmia.

Good, good tips there, thank you. With the signs of mycoplasma, pneumonia calcified lesions, how would you reassure yourself that they're not TB other than with age? Well, I mean, look, I think the answer is look in the lymph nodes.

Normally and if it's mycoplasma obies. No, what am I trying to say? My mycobacterium bovis, then there'll be calcified Caseus lymph nodes, whereas with mycoplasma bovis, it doesn't really go into the lymph nodes.

It stays in the lungs and looks, it looks granulomatous and, you know, calcified Caseus. But having said that, we, we're very lucky up here, we have no TB whatsoever, so it never enters my head really. Well, it does briefly, but then it goes out again, you know.

So I don't, I'm maybe not the best person to ask that question, but if I had to say I'd probably go for the lymph nodes. OK, thank you very much. And the last but one question here, just about, when you dissect the heart, why don't you cut it in a transverse view to look at the ventricles and their size, diameter to compare them first?

Is it useless in calves? Are you better to cut them the way that you showed? What, what's your thoughts?

Well, I just think the percentage call and the likely diagnoses are going to be endocarditis, myocardial abscessation. Stroke, myocardial necrosis with hisophilo somna, etc. And a ventricular septal defect and or the trunkcus arteriosis, that sort of thing.

And if you cut the heart transversely, you've missed your chance of finding most of those things, I think, because you, you don't know where you are then. You can't put your finger through from one ventricle into the other. And, you know, you, you, I, I just.

You can always measure the, you can always measure the diameter of the ventricul ventricular walls later, you know, from once, once, once you cut through them. It's not as though as though, I don't think you need to measure the size of the chambers ever. So I, I just think.

In terms of what the likely diagnosis is gonna be, you're better off for Wi Fi I think anyway, you're better off doing it the way that I sort of suggested. Yeah, that's, that's, that's fair enough and and clearly explained, thank you. So this is our last question, and it is, what is the craziest thing you have seen whilst doing a PM?

Well there are 21 is, I once saw a cow which had swallowed a knife, and it had caused basically a a a reticul reticuloperitonitis. It had somehow managed to swallow a knife which had ended up in its reticulum. Sort of point forward towards the heart.

Actually, I've got 3, can I have 3? You can have 3. Point forward towards the heart and then with a reticular contraction, it, went into the heart, killed the thing dead, stone dead, and I managed to pull the, the knife out of the heart and send it back to the farmer, and it turned out that they'd had some campers on the field having a picnic.

And they, I think they ended up admitting that they left a, a cake cutting knife, on their, picnic blanket, which the cow had managed to eat, amazing, it managed to get it down it's. Anyway, it did. That's number one.

The other one I had was a, a, a cow that had been brought in from. It was a cow that had been brought in from France and it was they got it cheap because it had had a . A a lesion on its brisket, right, so it couldn't serve cows properly.

So they got it for cheap, but it was quite a nice cow. And they, anyway, got to put on a rollover crush to have this lesion dealt with, which was fine. They did that the first time.

The second time they did it, they it rolled off, came off this rollover crush, 30 seconds later, dropped down dead. So anyway, it, it came in and it had a wire, a nail in its . Reticulum that had penetrated from its reticulum into its heart and managed to poke and poke and poke its heart and probably give it a a ventricular arrhythmia and make it drop down dead.

Now, the funny thing was, the fellow had to claim, he said, was it a French nail or an English nail? And I said I couldn't really, I couldn't really honestly say, oh well that's good, he said, because I'm going to claim for it on my . I, I, I want it to be a French nail, so I can claim off the bloke who sold it to me in France because it was a pre-existing condition, and I want him to give me my money back because it was always going to die of this nail having been in it, but I'm going to claim on my own English insurance to say that it was an English nail and that it had accidentally eaten this nail for reasons I couldn't because it had strayed away from its, you know, enclosure and managed to eat a nail.

So, so, his, his own insurance is an English nail, so I think he got, he got, paid out twice for that bull, so he went and bought another one. Anyway, point is that often, you, if you, with these rollover crushes, if you've got, they could often jar, make a make a a a reticular peritonitis happen when it wouldn't have otherwise happened, do you know what I mean, because it's poking through and then you sort of shift everything in the abdomen and it kind of shifts everything in position and jolts forward and goes into the . Heart, with me, and can kill him, kill him quick.

And then the third one is a, is a, a, a fat bullet that had swallowed one of these helium balloons, somehow that people, you know, let go 100 of them and, you know, happy birthday, Frank or something, and this thing had managed to swallow a helium balloon which had gone down. It had swallowed its sort of balloon first and then string last. I, I, I, you might have seen, I, I.

Gave the story to the veterinary time. So the, the string of the balloon was still lodged in its oesophagus, nearly, nearly all the way to the top, which was anchoring the balloon in place in its cardia so that it couldn't erectate properly and the the balloon was like a ping pong ball on a snorkel. Do you know what I mean?

So it couldn't get rid of its gas. So it blew up, and, and that was the end of it. But you could see when, I, you know, you cut into it, you could, I found the string in the oesophagus and I thought, what the hell is that?

And folded it down into the room and where the rest of the balloon was lay with me. So there's another reason why I shouldn't release these balloons and Chinese lanterns and all these, all these sorts of things. No.

Another horrible example. Yes. OK.

Brilliant. Right. I think that, that does bring us to the end of our, our questions tonight.

And I want to thank you again, Ben, for that really, really interesting presentation and for answering so many questions tonight as well. We've had some great comments in. Thank you so much, for putting the webinar on.

It's really helped, confirm PM process and really good presentation. So thank you again, Ben, and also to everybody that has attended tonight's, live webinar. We have got a couple of webinars coming up again before the end of the year.

The 10th of November is the next one when we have, fracture repair in practise. With Mike Kirby of Synergy Farm Health. Again, going to promise to be a really nice interactive, session.

So please keep an eye out on your emails from the BCVA office for, details on that webinar. And then we'll have one again on the 8th of December on retention and recruitment with John Remnant from University of Nottingham. You'll see there we've also got lots of online CPD to keep you, .

Busy over the coming months as well. So again, please contact the office for further details on those. So, before I sign off tonight, I just want to say thanks again, Ben, really, really great evening, from you again.

Never failed to deliver. And, also, again, thanks everyone for, for joining us this evening. We hope to see you next time in November.

But in the meantime, please take care and stay safe and good night.