Good evening everyone, and thank you for joining us for tonight's BCVA webinar. My name is Sarah Peterson from the BCPA board, and I'll be chairing the webinar tonight. Our speaker tonight is Colin Mason, and Colin's happy to remain online for questions after his presentation.

So please type any that you may have in the Q&A box during the webinar and I'll save them for the end. If you have any technical difficulties, then please also let us know by using the Q&A box and we'll do our best to assist you. If you can't see the Q&A box, then if you just wiggle your mouse, then the taskbar should become visible at the bottom of the screen.

It's my pleasure tonight to introduce BCVA fellow, a fellow BCVA board member, Colin Mason as our speaker. Colin is a veterinary investigation officer with the SRUC and he's based in Dumfries where his work involves disease investigation and diagnostics for livestock farmers in southwest Scotland and northwest England. Prior to moving north of the border, he worked in farm animal practise in Cheshire.

Tonight, Colin is going to be talking to us about respiratory diseases in adult dairy cows, where infectious diseases mix with management factors. So thanks very much, and over to you Colin. Thanks very much, Sara, and good evening, everybody.

The webinar tonight, was initially given the, the task of talking about infectious disease, which is a, a pretty broad remit. So I was trying to think about how to, to focus that down. So I thought what we would talk about this evening was, a problem that we see a lot of, and we get involved in investigations, very frequently now, on respiratory disease in adult dairy.

Cows, and, the hope is, is that that brings in quite a range of possible infectious diseases, but what I hope to do in this talk is, link that back to, you know, what's genuinely going on in farm, and also what the risk factors are for this and, and as vets, how we might manage this condition. So, what I want to do in this talk is, is mention some of the key infectious disease differentials. I want to talk through some of the pathology that that I see and my colleagues see in our job.

And then relate that to what's being seen on farm by farms, by farmers and vet practitioners. also maybe think about things that we're missing, because I don't have all the answers to this, and also think through what the risk factors are as well, and how we might well control them. So hopefully we can get through that in the next 45, 50 minutes thereabouts.

We'll see how we go. So, Really by means of introduction, for most farm animal practitioners, the, the focus in terms of respiratory disease and pneumonia is on young stock. And as I said at the start, what we've seen in Dumfries, and I think that's mirrored across the country, is increasing numbers of reports about or samples received or cases received of, of adult cow.

Pneumonia. And I think for a lot of vets, this at times comes into the problem case category. Treatment can be difficult, successful cures can be hard to achieve in some cases, and, you know, it, it causes quite a lot of problems for, for farm clients.

So, Really, maybe to go back to the start of this, I've, I've called, or, or this condition, one could name it, acute bacterial pleura pneumonia in dairy cattle. And this is not a new thing. It was first reported, in the UK or, or first discussed in detail in the UK by David Harwood, back in 1994 and 1995, .

And I think what we're looking at now really is, a similar thing. It's just perhaps we see more of this now than, than, than we've seen then. as I said, it can acute disease presentation, pure treatment response, in, in some situations, a high mortality, and the, the pathology very often is, is typical, of a bacterial type aetiology.

And, I maybe start off with, My first infectious disease of the evening, which would be contagious bovine pleurumonia, and I'm very pleased to say I have absolutely no experience of this condition. It's notifiable disease caused by mycoplasma, mycoides, subspecies mycoides, and It's worthwhile mentioning it right at the start, because it is, one of the differentials that, that needs to be perhaps considered in the back of one's mind. And, and, and that was one of the reasons why David and his colleagues first got involved in looking at these, which was to consider, could this be CBPP.

now, thankfully, I think the conditions that we're looking at aren't, but just to go through some of the pathology that One sees with, contagious bovine pleural pneumonia. You, you get what's termed as a pulmonary hepatization. You can see the picture at the bottom of your screen there.

You see thickening of the interlobular septi, sometimes with edoema fluid, sometimes with fibrous tissue. Ultimately, in the chronic cases, you see sequester forming in the lungs, and the condition is at times described as being unilateral, affecting one lung field over the other. So again it's just worthwhile, while bearing this in mind in that as, as, as vets.

We always need to be aware of, of the possibility of notifiable disease, when we're looking at these conditions. Anyway, I want to move on from that, and I thought to start off with, I'd show you some gory pictures, I guess, of, of what we see in the p.m.

Room with some of these, cases. Really just to emphasise some of the challenges, I suppose. In terms of, of what these animals actually have, in terms of pathology and, and why it could be so difficult to treat.

And, and very often when you're looking at these cases, I think it's not, it's not how the animal died, it's more how on earth did it live. And I would emphasise as well that some of these pictures were, were taken from lungs, from animals that had died. Some had been euthanized, so, you know, they were still under treatment, and, you know, at times, farmers were still thinking that they might be able to get a cure from these, .

But the pathology is, is variable depending on, on the severity. But just going through the things that we'll see is a, very often a fibrinous pleurisy, which, can be anything from mild to severe. It can be very active, like in the picture here, and it can also be quite chronic with, fibrous adhesions between the lung and the, and the pleura and the, thoracic wall.

Long consolidation, is a, a, a common feature, and that can form either the antraventral distribution, typical of an airborne pathogen, and occasionally we'll see them with more diffuse distribution associated with, with hematogenous spread from another source, and I'll show you some pictures of that and talk through that in a minute. We will very commonly see variable abscess and micro abscess formation within the lung tissue, and very often we'll see degrees of craicity in terms of severe fibrosis and sometimes marbling of the lung tissue with fibrosis of the interlobular septi as well. Emphysema is a really common finding, and it's a common finding in adult cow postmortems in any event, but it's a really common finding, and I think probably explains some of the, the clinical signs of severe dyspnea that these cows have, when they're affected quite badly.

the Pathology in the trachea can be variable. Sometimes we see nothing at all. Sometimes we see a genuine tracheitis, which could be either acute or chronic, and I'll show you some pictures of that in a minute.

And also We'll see intercurrent disease as well, and probably the most common findings would be concurrent abomaal ulceration, and sometimes as part of, of fresh cow problems, concurrent metritis as well. So, these are the range of things that we'd expect to see, and just going through some, some more lovely pictures of these things, The pleurisy is a, a, a very common feature of this disease. You can see in this one, it's, very acute, with, with evidence of, of severe haemorrhage on the chest wall, and you can see the, the, accumulations of fibrin on the chest wall as well.

So that's a very common finding, . Moving on to, to this set of lungs, a very typical antraventral pattern, like a lot of pneumonias, typical of an airborne pathogen, and you can see the sort of almost blackening of the lung tissue that is seen there, the extent of the affected lung, and the cut surface of that often reveals, either larger or micro abscess formation. This is a, a case that we've seen fairly recently, very acute presentation of this animal, in that she presented with, with really acute respiratory disease.

You can see the size of the lungs first enormous and that they are, they, they're very much enlarged. And yet the antraventral portion again is, is collapsed, consolidated, and, and consistent with an airborne pathogen and the damage that's seen there. And if you look at the same set of lungs from a sort of dorsoventral view, you can see the extent of the emphysema that's caused these lungs to be dramatically expanded, and, and this really explains why this animal was struggling to breathe before it died.

And, and, and again, this animal was, was put to sleep rather than. Actually died of this condition, so it was really suffering. Quite extensive breathing difficulties, with severe emphysema.

A different case, and again, you can see the antraventrial pattern there, but, very, very chronic lung lesions and when you cut into these sort of pale, sort of. Almost grey areas in the antraventrial lung lobes, marked fibrosis was occurring in this case and and collapse of that lung tissue and again within the diaphramatic lobes, severe emphysema caused by dyspnea and, and really the struggle that these animals would have had to, to try and move air through consolidated lung tissue. Moving on to slightly different presentations, one of the things we've got to bear in mind is, is that not all these pneumonias are as a result of an airborne pathogen and some is a sort of hematogenous spread of infection from elsewhere in the body.

So, this is a chronic supative pneumonia and, affecting the diaphragmatic lobe, which an abscess had actually, Invaded into a blood vessel and a fatal haemorrhage had occurred as a result. So, an acute sudden death as a result of fatal haemorrhage, but, but related to chronic abscessation. And occasionally we will see pulmonary thromboembolisms as well, like you can see in this portion of lung too.

If we move to the tracheas, Very often the tracheas, there's not that much to see apart from maybe referred. Nuclear pollent material moving up from the lungs themselves. This particular case showed an acute tracheitis, and this actually was a genuine IBR case when the traquial mucus and material there was, was swabbed.

It tested PCR positive for bovine herpes virus one. And I'll, I'll discuss that in a little bit more detail later on in terms of, of how much involvement there may or may not be, with IBR in these cases. And again, you can see the, the, the emphysema and the, the lung tissue on the right there.

Very often a lot of the Shaquille changes are as a result of Referred mucaus and inflammatory material brought up from the lungs, a failure of the mucociliary elevator and, and associated tracheitis as a result of that. So you can see in this picture, obviously I'm picking the good photographs here, but, actually, forming tracheal abscesses, and you can see the extent of the tracheitis that was there with, with a lot of material being brought up from the lungs. So again, a chronic tracheitis in, in response to lung damage rather than a, a, a primary tracheitis that that may or may not be associated with IBR.

What we've also got to bear in mind with the hematogenous spread conditions is are what is what we're seeing in the lungs and is the clinical signs that these cows are experiencing as a result of damage elsewhere within the body. And you may have seen reports in the literature in the last year or two about o the cleft dermatitis and, how that might link to spread of bacteria. Into the blood system and through and settling out in the lungs causing abscessation or causing endocarditis and as a cause of sudden death.

As a result of that. So that's a possibility. The picture on the right, obviously showing sort of scattergun, millary abscesses through the liver, and this animal also had abscessation throughout the lungs as well.

So, We've got to bear in mind that a primary respiratory presentation may have actually originated somewhere else, within the animal before that time. So, One of the things we did a few years ago, one of the things that I did a few years ago is a few, a series of cases which actually presented at a previous BCVA conference, and it was reviewing, a series of cases that we'd had in through the disease event system in Scotland. And really just what is being seen on farm.

And these were the typical herd histories from 22 farms that had presented cases to us, and, this was some of the common findings from these farms. So, tended to be larger dairy herds, tended to be herds that were purchasing cattle. a range of control programmes, all the herds were, vaccinated for BBD and for IBR, and, variable stages of eradication of, of BVD from the herd.

Just over 50% of herds were permanently housed. And then a split between the remainder that were, were grazing herds in the summer or high yielders were permanently housed. And in nearly half the herds, they were reporting ongoing issues with adult cow pneumonias.

The cases tended to be sporadic. There was no real seasonal trend to it, although we do, and more recently have had some herds that definitely report more cases in the summer months than in the winter months. So this is just a scriptive data, and you could certainly argue that this would be typical of a lot of, of a lot of the large dairy farms in our area of southwest Scotland.

So, although I'm highlighting a specific herd history that we've seen on these farms, you could say, well, this is maybe just the normal pattern that we get on these farms anyway in terms of, of history. If we look at individual case history, and, and looking at the individual cases, when they were submitted, there was not particularly an age trend, in that it could equally affect adult cows, as it could freshly carved heifers. Roughly 50% of cases were occurring within two months of calving.

Some cases were associated with a diet change, and we'll come on to that later on, . Whether that was as they approached drying off, or as they started to move back through the transition phase, to carve back down again. .

These cases presented as sudden onset respiratory disease, even though you can see from the pathology that that, you know, some of these are are far from acute. Some of them are quite chronic, but they tended to present a sudden onset respiratory disease. Cows would be anorexic.

The milk drop was severe and in some cases almost complete in that the, the milk drop was really dramatic, and I've said already, a variable response to treatment with antibiotics and non-steroidal anti-inflammatory drugs. Interestingly enough, a perception that I've had, having seen these cows on farm is sometimes they seem just reluctant to move, and sometimes reluctant to lie down. They stand, they're air hungry and they are struggling to breathe.

and they're in pain as well. They, they grunt and they, they just look like they are really struggling. And when you see, you know, the pathology which I showed first, it's, it's easy to imagine why that might be the case in some of these situations.

Pyrexia is a consistent feature, as is tachypnea and, and severe dyspnea would be the, one of the main clinical findings. Over time, poor room and fill in relation to the anorexia, is a consistent finding. Some animals will have, Reported to have epistaxis and, and halitosis, but that's by no means all of the cases, pain as I've mentioned.

And in general, coughing or a nasal discharge don't seem to be a consistent feature of this. It's not to say that that won't occur or that doesn't occur, but it will be the tachypnea, the dyspnea, that will be the main clinical features of a lot of these cases. It's perhaps interesting to relate this back to what farmers are reporting, and I guess in, in a lot of dairy herds, what we've got to consider is this, is that these cases will be farmer reported to start off with and potentially farmer treated to start off with, through the, the health planning approach and the protocols that are in place on farm.

And it may be that as, as practitioners, we only get to see a proportion of the cases. So it's interesting, I always think when investigating these problems in dairy herds, is, is really get farmers to Define their case, and what are the criteria by which they're saying this is a pneumonia case. And there's a range of criteria that can be used, and it will depend a little bit on the degree of recording in the herds, whether they're using rumination collars, whether they're robot milk cows, etc.

Etc. But the, the range of findings will be reduced feed intake, obviously, milk drop, reduced milking frequency if it's a robot milked herd. Reduced rumination, if they've got the ability to assess that, increased respiratory rate, and the pyrexia.

But I do think it is important to discuss these cases with clients and, and actually really make sure that we are examining these cases as vets to be sure that they are genuinely pneumonia and not something else, because the other differentials. Very much do include pyrexia of another origin. So, septicaemic condition, for example, it's got nothing to do with the actual primary lung pathology and lung disease.

Heat stress may be part of the issue, pain for another reason, may be part of the issue. Acidosis and other similar conditions, may be part of the issue. So there are other things that might mimic this condition, if we consider farmer reported cases only, and I think, you know, there is a real important role as vets to, to actually define these cases as, as genuine pneumonia.

And that maybe brings in another infectious disease that we, we need to think about, and it's certainly a disease that's very common in our area, which is salmonellosis and in particular salmonella Dublin. And when my colleague Katrina Henderson reviewed our data on how salmonella Dublin presents in herds and predominantly dairy herds, this was the graph that came up. We've got different shades of green here.

But what you can see in the darker green is, respiratory disease does feature as one of the main clinical presenting signs in a small percentage of cases in adult dairy cows. And similarly, milk drop does present as, some of the, the presenting clinical signs in a few herds. So this, I guess, would be an example where the clinical signs, particularly in the farmer's eyes, might mimic or be considered to be pneumonia and considered to be respiratory disease, but actually, in truth, it isn't.

And I can now think of Two examples where farms have done a fair amount of workup with their vets looking for a full range of respiratory pathogens, whether they be viral or bacterial. This would perhaps be more with, with cases that were treated and survived in some way. Didn't really come up with a conclusive diagnosis based on, let's say, paired serology or, nasopharyngeal swabs.

And it, you know, was, was named a, a, a, a, a respiratory disease, but was not really a diagnosed respiratory disease. And when we suggested maybe trying serology for salmonella Dublin, And looking at pay strategy for Selma Dublin, it showed really, really nice seric conversions, consistent with the disease presentation, so. Certainly it's something to bear in mind, if you're not nearly a diagnosis and you're not sure, what is going on, you're thinking there may be some involvement with systemic disease, as well as pneumonia.

It could actually be a slightly less typical presentation of salmonellosis. Diagnostic options for salmonella Dublin, there's a range there that's listed in, in this slide. And, and just maybe just to highlight a couple of points, is, is that faecal testing for salmonella, faecal culture of animals, actually has quite a low sensitivity, particularly for the, the septicemic form of the disease, in that the organisms may not be excreted in the faeces or it may be that, you know, the, the faeces that you collect doesn't contain them or it can't be detected.

And if looking at a herd level, bolt tank serology is, is a really useful tool, and the sensitivity, particularly if bulk tank testing is repeated 4 times in the space of a year, is really quite high. And, if there are clinical signs as well in the herd, then the sensitivity is probably better. So if you're wanting a first snapshot to see whether salmon in Dublin might be involved in a range of clinical presentations in the herd, but, but certainly with, signs of respiratory disease, pyrexia of unknown origin, etc.

Etc. Then, then it's worthwhile considering salmonella status for the herd. It's also worth pointing out as well that although Dublin is the main, strain of salmonella that, that we see in the UK and certainly see in Southwest Scotland, we have had other diagnoses that are presented with respiratory signs, and signs of pyrexia and milk drop, etc.

And these include salmonella, and Baka, which we see increasingly commonly now, and we've occasionally seen it with, Group B salmonelli as well, which is the most common one of which is, is salmonella typhoon. So just moving back to the respiratory disease stuff, just trawling through the literature a little bit and just sort of trying to get a feel for how common this might be. And there's a range of evidence out there, like a lot of these things, it's not complete, and I would like to do a lot more work to try and investigate this in a bit more detail.

But, if you take, the first bullet point there, just taking, farmer reported cow deaths, in over 30-month cows, then Just between 2.5 and 3% of these were reported to be due to respiratory disease. Now, again, that's farmer recording, so that may or may not be the true cause of death, but when you look at the number of animals involved, then There is some weight in the evidence there, shall we say.

The next couple of bullet points down, look at, disease surveillance system, studies looking at, the number of diagnoses either of Mannheimer hemolytica associated disease or, Adult cow pneumonia in a range of, of animals seen at postmortem. So again, percentages there, you can see. And then the last couple of bullet points there, show, reported.

Evidence from the states looking either at one particular dairy farm where they reported 7% of all cow deaths on one large dairy farm in 12 months due to respiratory disease. And a slaughterhouse study looking at cows coming through a large slaughterhouse in the USA where they were processing, cold cows, where 10.7% of the cows had severe lung pathology.

So there's a range of evidence out there. I accept it's not incomplete, but it does give us a bit of a guide and, and you could take whatever figure you like from that and estimate that between 2 and 11% of dairy cow deaths on farm, not cull cows, but deaths on farm might be associated with respiratory disease, but, but these are very much estimates, and it will vary from herd to herd. If you look at the UK surveillance data and you look at the UK by the data, and this is now slightly old data, but it still tells a story, and it pulls out the full range of infectious diseases that are involved in this adult cow, respiratory disease presentation.

So you can see the full range of things that have been diagnosed through the surveillance system there, and I don't worry, I'm not going to go through every single one of them. But I will pull out a few, and maybe just mention them in a little bit more detail. Just in terms of some of the key differentials and and things to look out for.

So we've mentioned salmonella, which features very minimally on this graph, but perhaps since that time has come to the fore a little bit more. I, I suppose it's worthwhile mentioning, T. Pyogenes, Tella pyogenes as a cause of chronic supreative pneumonia, because this is one of the bugs that we find in a lot of these PM specimens, .

It probably is the end stage of the process, in terms of, of how the, the pathology is developed and the clinical sciences have developed in these cows over the, the, the weeks or months, or possibly even years. but towards the end, and the end stage of the disease process, it is having a significant clinical effect. It is an organism that will invade devitalized tissue.

So if there's already damage there, it will invade it, and the, the picture of a section of lung there, is actually lung that was initially damaged as a result of, lung worm, and then was, invaded with T pyogenes as a sort of secondary coloniser that caused a lot more damage. So it's an end-stage respiratory pathogen, Occasionally in the reports, it's been associated with aspiration pneumonia, as well, possibly with recumbent cows, but although it's a common diagnosis, we need to really focus on the initiating causes because this is not the whole story. It's worthwhile mentioning IBR, and I'm not gonna go through every one of the clinical signs listed on the left of this slide that relate to IBR.

It's a disease that I think all farm animal practitioners will be aware of and have seen, and it's certainly linked a lot to this condition of adult care respiratory disease, . And yes, some of the clinical signs do very much mimic IBR in terms of the anorexia, the milk drop, the fever, the respiratory disease, in terms of tachynia and dyspnea. But at the same time, if you remember back at the start, ocular nasal discharge, larymation, coughing.

Very often isn't a, a, a primary, sign in a lot of these cases. So, I'll make a, a, a, a controversial statement, but it's a statement that others have made as well, is, is that probably, IBR is overdiagnosed as a cause of adult respiratory disease. It's commonly reported based on the clinical signs, but my question is, is, are these all.

Really IBR. Now that's not to dismiss IBR and bovine herpes virus one completely, because yes, large scale outbreaks do occur, and when you see them in dairy herds, they can be spectacular. They can cause really severe disease and are not subtle at all when they do occur.

So I'm not by any manner or means saying that these don't occur, but they are probably more rare, . My experience of IBR and I think that of others, is probably that when it does occur, it's, it's less of a large outbreak. It's more of, sporadic cases and flare-ups as a result of recrudescence of the virus, and it's picking out the naive cattle, when very often there's a high level of seropositivity, seropositivity in the herd.

I think there has certainly been reports and, and, and experience of IBR infections in herds causing fairly low levels of clinical disease. Clearly animals are ser of converting and it might well cause milk drop, but not causing overt severe respiratory designs in, in quite a lot of dairy herds. There's certainly a high level of IVR vaccine use, and there is an apparent response to vaccine administration, particularly with live virus vaccines.

But one of the thoughts here, and I'm not claiming to be an immunologist, is that this may be due to, to non-specific effects of the live vaccine rather than this being a primary IVR problem. So, there's a lot of debate around IBR. I think my opinion is, is, is that whilst it could be involved and will be involved in some situations, it's by not any means the whole story here.

And it's really important to get an accurate diagnosis because this either proves that it's IBR or it allows you to rule it out with confidence and, and move on to other potential diseases and other risk factors that you need to focus on. And Actually, using the PCR tests that are available for IBR, it's really quite simple to confirm a diagnosis. And similarly, the flip side of that, which I think is equally important, is, is that if you get negative results, you can have confidence in them and say, well, this is not IBR.

So nasopharyngeal swabs from animals will be positive for potentially up to 2 weeks after initial infection by PCR, the PCRs are sensitive, the virus is robust. So if you're collecting guard nasopharyngeal swabs from 2 to 4 animals in the acute stages of the disease presentation, where they're febrile, they have a, a, a serious nasal discharge rather than a mucopro nasal discharge. And if you're sending those swabs into a lab, you use virus transport medium.

Then you're going to get a diagnosis if it's IBR because that discharge will be hooching in virus if it is IBR, and therefore, the flip side of that is if it's not, you can rule it out with some confidence. And that's the best advice that I can give any practitioner when considering IBR is test for it, prove that it is, or prove that it isn't, and then go from there. One of the other, you know, key respiratory viruses that, that is implicated is respiratorial sensitial virus.

And certainly in, in our experience, it's a rarer diagnosis in, in adult care respiratory disease, although it has been reported more commonly in other countries, and it's more, more commonly diagnosed in other. Countries as a cause of this syndrome. So there is a possibility that we're missing this in some of these animals.

Again, PCR testing, either on nasopangal swabs or on postmortem lung tissue would be the test of choice. And this diagnosis has been, this virus has been implicated as a cause based on paired serology and some outbreaks with a, a perceived and good response to, to vaccine use. So, It's something to certainly bear in mind, although again, I'm not necessarily sure it's the, it's the whole story.

Probably worth a quick mention of, of husk, and I don't want to get too involved, in, in a full debate on, on lung worm, but we're talking about infectious disease, and we're talking about adult care respiratory disease, and it is a significant cause if the history is right in terms of a grazing history. Graham David back in the late 90s, reported a, a changed epidemiology with this disease, and I think that has continued, that the Increased levels of housing of our dairy cows, the increased implemented use in our young stock and the decreased vaccine use, all, making the likelihood of some cows being non-immune. And then if they're turned out for shorter periods of time, particularly in the late autumn, then they can be quite susceptible.

So it's always something that's worth bearing in mind if the history's right. And my opinion, certainly in the Southwest of Scotland, is when we get drier autumns, we get more lung work. Because the cows stay out for longer.

If we get wetter autumns, the cows come in sooner and we perhaps see less of the disease as an issue. So, if we go back to the pathology that we had right at the start, and, and rather than the gross pathology, consider the histopathology, and, and what's really going on in these lungs just to help us think through some of the risk factors, and, and some of the potential etiologies, the sort of things that are being seen in these cases, acute supparative bronch pneumonia, as a, a, a genuine primary disease. in a lot of cases, the evidence is there of a combination of chronic change, chronic lung change, indicating long-standing damage to the lung with an acute flare-up of supperative bronchial pneumonia.

It tends to be consistent with the bacterial aetiology, We do see some cases that are reported as acute interstitial pneumonias, or at least areas of the lung have evidence of acute initial pneumonia, which I think is an interesting one, in that the cause of this is not entirely known. If you go to the literature, it might relate to, a dietary cause, particularly 3 methylinol, which is implicated in, in the fog fever presentation. And it's also thought that inflammatory medias mediators from, an area of, of chronic lung damage might, cause these acute intertitial pneumonias in some situations.

So, I, I find that quite interesting. The tracheitis can very often be secondary, and, and secondary to the presence of mucopurulent material that's there, and I've shown you some pictures of that already. And then we have had some cases where, particularly where they've got chronic damage, there is evidence of increased, edoema fluid, sometimes fibrin containing edoema fluid, which is thought potentially to be in association with, an endotoxemia, and it's thought potentially, although hard to prove that the rumen microflora releases of, of endotoxin from ruin microflora might exacerbate the disease process as well.

So, It can link us back sometimes to a dietary cause as well as acute and chronic, mainly bacterial presentations. And we've reviewed a series of cases, and this was a review of 26 postmortem cases, looking at causes, firstly, the, the evidence of viral involvement by the time these animals reach postmortem is pretty limited, with the exception of, of BOHB1 in a very small number of cases. .

This is really a bacterial disease, and these are the range of organisms that have been isolated and no one bacteria seems to predominate. The pasturelli are there, T. Pyogenes, Mycoplasma bovis, salmonella Dublin.

So there is no one organism that, that really predominates for sure. Just picking up and and mention of another infectious disease that's on that list is Mycoplasma bovis, because it's certainly very topical and, has certainly been implicated in some of these adult cow pneumonia outbreaks, and, it certainly is involved in the disease process, but it's maybe worthwhile just thinking about what MOIs does and how it can behave in the lungs, and that we think initially it spreads. And it's picked up either by calves or cows, and through initial colonisation of the tonsils, spread to the upper respiratory tract where it may invade the tissue, with or without disease.

it can invade, erythrocytes, blood mononuclear cells, and that can be a mechanism for evading the immune system and, and some of the the issues that are maybe seen with persistence of this organism. Bacteremia and hematogenous spread can lead to the full range of clinical presentations that one sees with them bovis. And for sure, the respiratory tract and the mammary gland are, are some of the main sites of infection.

A lot of the pathology seen associated with M bovis is, is because of an excessive activation of, of macrophages and neutrophils, and it can evade the immune system and be shed for a period of time. . This is American data in the graph on the bottom right of this slide, which certainly shows that, as her size increases, the chances of, of the bolt tag being positive for mycoplasma bovis goes up.

So it certainly does fit with, with the picture that we see in the large dairies in that, the, the larger they are, if they're buying in cattle, the more likely they are to be M bovis positive. The question really is, is MO is primarily involved with this adult care respiratory disease presentation? Is it involved, in part or fully to explain the clinical signs that we see.

So we know it's part of the pneumonia complex, usually involved with the full range of other bacteria that can be involved, and It can act by itself or with others, with acute and chronic disease presentations. And again, some of the clinical signs and some of the pathology that we see here is that typical picture of, of chronic bacterial pathology, as you can see on the bottom right of the slide with the, the marbling of the lung tissue, which we do see with M. Bovis, and we do sometimes see with these adult count pneumonias as well.

Again, the pathology is, is fairly classical in some of these cases with a sort of caseine necrotic pneumonia, which we do see, and one of the questions really with this is what comes first, the chicken or the egg? Does, does Mbo this infection. Predisposed to secondary pastorella infections, or is it the other way around and, and perhaps this true pyogenes, invade and bovis associated lesions, and, and cause that sort of final terminal pathology that these cows experience.

So we would certainly suggest that it's involved, and potentially in some situations as part of the mix, but it is not the sole single agent cause of this problem. From a disease surveillance point of view, it's always interesting to think of what we're missing, and it's certainly a question that gets raised from an infectious disease point of view with adult care as well, is there, is there something that we're not finding? Is there something that is out there that we're not picking up?

And it's interesting just reviewing the literature ahead of doing this talk, and, and there has been some metagenomic sequencing of calf pneumonia cases that's been done. Looking at nasopharyngeal swabs from these cases and just looking at the full range of viruses that can be found and, it, it picks up, Influenza, the virus, there are bovine rhinitis viruses, bovine respiratory coronavirus, bovine pava viruses, bovine adenoviruses, are all there, to varying degrees in calf pneumonia. I think the challenge that we have is, is making an association between these pathogens and specific disease processes.

And in truth, the role of pathogenesis is not known. And it would be really interesting to do some metagenomic sequencing of some of these adult count pneumonia cases as well, just to see what else is in there. But, at the moment, there is no evidence to think that there is a, a, a new virus out there that is causing this.

It's more likely to be associated with the common things that we expect to see on farms and, and some of the risk factors, which I just want to mention in the last. 5 or 10 minutes of this talk before we wrap up. Now, the risk factors for acute bacterial pneumonia in cows and dairy cows.

This is the list that we came up with based on our own thoughts, on the thoughts of colleagues, practitioners, and. They seem to make common sense, really, so obviously. Sheds, ventilation, overstocking, clearly potentially issues.

Poor ventilation and particularly in collecting yards has been suggested, particularly large collecting yards where cows might spend. Considerable amounts of time, particularly if they're being jammed up by backing gates and things like that. And, and, we've certainly seen that in, in some sheds where they've been new build sheds, the stocking rates have been good, the ventilation of the sheds is excellent.

So actually, you know, the air quality in the shed is pretty good. However, collecting yards, the air quality might be a good degree worse. And if cows are being milked 3 times a day, for example, and they spend Potentially some time in there, so some issues to maybe think about there to try and improve things, biosecurity issues, clearly purchasing, mixing cattle, the opportunities to either bring diseases in or bring susceptible animals in that naive, and how we refine the vaccination protocols around that is really important.

And then the issues around, transition early lactation management, could be factors as well, . Heat stress might form part of the issues in the summer, and, and for some of these herds where they do get flare-ups in the summer, one wonders about that. And then this is the million dollar question, really, and it would be nice to get some really hard answers to this is do previous episodes of calf pneumonia predisposed to this, and Although there's no hard evidence, there's no case control studies been done, I would suggest that looking at the pathology, we have some predisposed cows with some pre-existing lung damage in a lot of these cases that then meet a trigger factor, one of these risk factors that allows the disease process to flare up.

So maybe just picking up some of these, certainly. In your clients herds, if you're experiencing these problems, it's certainly worthwhile reviewing shed ventilation, reviewing stocking densities, and looking to see where that can be improved, whether that is, by, improving the air inlets, opening up ridges to maximise, outlets, and again, the use of fans and how you're managing heat stress in the summer months in permanly house dairy cows. So, These are all good areas to consider, and I would argue it might be well worthwhile focusing on some of these areas, potentially, rather than, you know, worrying about whether it is virus X or virus Y, in some of these cases.

As I've said, collecting yards is certainly something to focus on, and it's, you know, something to focus on for a whole range of reasons. The, the less time cows can spend in collecting yards, the better. And, and you sort of target of cows should spend no more than.

Now a milking way from feed, seems to me a pretty good one. And allowing cows the space within the collecting yards is, is really, really important as well, and improving ventilation in these areas as well, whether that is through fans or, or through opening up, more air inlets just to try and let the air move, really important and something that can be done practically. Does calf pneumonia predispose to adult cow pneumonia?

Subtle levels of lung consolidation, we're fully aware, I think that, we, we underdiagnose the amount of calf pneumonia that is occurring. So there will be calves that leave the calf rearing environment, go through the young stock rearing, that do have areas of lung damage, do have areas of lung consolidation. And that then goes through, to live with that cow for the rest of her life, and, .

We've looked in a few herds to see if we can try and link, the young stock disease with the adult cow disease, look back at the records, for cows that are affected and, and look back at their treatment histories from, their period as a younger animal. And, it all hangs around getting a really good treatment history and a really good treatment records from the young stock, and that sometimes can be challenging on some farms, particularly. If metaphylactic treatments have been used as well.

So, it's a really interesting area. I, I don't have the hard evidence to support it or to back it up, but would suggest that potentially there is a real risk factor there. And in the longer term, these adult cow pneumonia problems, is yet another reason to, to focus in really well and really hard on, on what's going on in the young stock to try and minimise the risks of, of lung damaged calves moving through.

And then the early lactation risks, what risk is there of a diet change as a predisposer for this? There is some evidence coming from the pathology that would suggest that this might be a trigger. In the US, you know, there's a reported link in general terms between subacute relastosis and a higher turnover rate within 60 days of calving.

In the states, they, they do report and pneumonia cases and and cows bleeding out through a ruptured blood vessel. Which we do see in some of these cases. So again, when looking at the nutrition risks, you know, actually defining the pathology is quite important.

Are we looking at an airborne pathogen or are we looking at, millary abscess spread? because of potentially a, a liver abscess that's spread or an endocarditis lesion or something like that. And certainly when we reviewed our cases, there is, roughly a quarter of cases that, that had history of, transition cow disease, which might, again, propose to dispose to really lactation risk, etc.

Etc. So, diet changes may be part of the story, and again, it's, it's, it's looking at, again, how we refine these. I, I think one of the interesting things to do if you are looking at herds, with adult cow pneumonia problems is, is define your case definition.

And then look through the farmer records and see, well, is there any association between time of year? Is there any association between time of, of, of lactation, either in, in early lactation or possibly as cows move towards drying off and experience a diet change through the dry period. So definitely part of the workup that's worthwhile doing.

So, we've got to 10 to 9, so I'm gonna wrap up in a sec. Final thoughts really, conclusions, acute bacterial pneumonia, I, I do believe it is, an increasing emerging problem on dairy farms. I Do not think that there is a single viral cause that can be identified as, as the sole cause.

It would be so simple if it was, but I don't think it is significant to that. There is a range of infectious pathogens that can be involved, as I've highlighted in this talk, and therefore appropriate diagnostics, whether that's PMs on some cases, or, sampling of acute cases, to try and work that through really, really important. I think it's really, really important to review what we know about the risk factors.

We don't necessarily have all the answers, but we have some of the answers that can help you as a practitioner decide. Where, some of the challenges might come within an environment, within a cow's management system that you can perhaps change. And of course, it would be really good to be able to, to look at this and study this in more detail to, to have a more evidence-based approach to it.

Recommendations in terms of, of, of treatments, like, like so many things, the earlier the treatment can be, the better. And when you see some of the pathologies, you can fully understand that. Monitoring treatment response, clearly gonna be important from a welfare perspective, and, you know, considering the prom diagnostics, you know, particularly for something like IBR so that you can either rule it in or rule it out and then and then move on with confidence, really, really important.

OK, just to finish up, I'd, I'd like to acknowledge the help of, of, friends and colleagues, that have helped our thinking over this disease over a good number of years now. So, particularly in our area for, the vet practitioners and the farmers that have been good enough to submit cases, to discuss this and to try and get to the bottom of it. For colleagues within, my workplace, are particularly, Heather Stephenson, Katri Henderson, Sandra Scholes, Fiona Howie, but there are many others, and, and we're fortunate enough to, to receive funding to help us do this work from the Scottish government as well.

And that is, that is me. Thank you. Fantastic.

Thank you very much, Colin. That was a really insightful, and interesting presentation. Just to everybody listening, before we go to questions, and we already have lots of questions coming in for you, Colin.

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So now, over to our questions for you, Colin. So, I'm going to start off with one here that came in fairly early on, whilst you were discussing postmortem findings. And it's regarding tracheal abscesses.

How do you know that they're from the lungs rather than the other way round? So how can you identify, I suppose the origin of the infection? It's actually really difficult, and I, I'll be absolutely honest with you, those, that picture there, was actually taken from a case fairly recently, and I've never really seen it before, up until the last month, and I've actually seen two cases.

Since with it in the last month in two completely different farms. So it, it's, it's a new one on me, I'll be brutally honest, and, really what I've done is, is go to our histopathologists. And, and got their view on it, and we've also cultured the organisms that are in it.

And it seems to be, that, you know, it's the same organisms that we're seeing in the lung. So it was, it was T pyogenes that was the cause. and given the amount of mucopus that there was in the lungs and, and perhaps some of the damage that we were seeing to the tracheal mucosa that was associated with it, the thinking was, is that this was just that material that was.

Sitting there, not moving as well as it should from the that area of the trachea, and, and setting up a localised infection there. But I do take your point. You can't say for sure that this isn't either a hematogenous spread from somewhere else, or you could also suggest that perhaps this is a source infection that's seeding down to the lungs as well.

But our thinking at the moment is it's probably as a result of what's coming up from the lungs or stuff going down the lungs. OK, brilliant. Moving on to the next question that's come in from Mark.

And this was in relation to the early case study that you were discussing early on in the presentation. And he was just wondering whether there was any association between the cases you were seeing and recent oral propylene glycol administration. It was something that we'd asked about, and just in terms of the general history, and, there was nothing mentioned about that.

There was no association with that at all. And, and we'd asked about, you know, concurrent treatments, concurrent management, treatments, routine treatments, and, and that was never brought up, as part of the history. No, I, I can, I can see it as a possibility, but it was never brought up as part of the history.

OK, thank you. Two questions here about RSV. So starting with this first one from Alice, with RSV in adult cattle diagnosed on PM, would you advise herd vaccination or once serial converted, do you feel that cattle remain, retain immunity, and so you wouldn't be recommending herd vaccination?

What are your thoughts? Yeah, and it, it's an interesting one, this, so. Firstly on RSV, I mean.

A lot of the cases that we look at, whether we're looking at, at, at swab samples from, from acute cases or whether we're looking at PM samples, we'll look for the virus, and We'll find it fairly rarely. That said, you know, you could also argue that that some of the, the cows that we're looking at are, you know, fairly chronic in the disease process, therefore, it could have come and gone. So, on the basis of serology, we have seen.

Some examples where animals have converted really nicely, and I guess this is the benefit of, of doing that sort of investigation. It takes time and it's sort of workup that that farmers can get a little bit demoralised with, because you've got to, you know, go back and and resample these cows 4 or 5 weeks later to, to find the pairs. and we've seen.

Two different scenarios with a paired serology, if I'm honest. Very often it will be that scenario you've just described, where you've got cows that will start off as antibody positive, and then they will go to being antibody positive at a higher level, but they've started from a positive baseline. And the assumption, therefore, is, is that the level of herd immunity is, is fairly widespread.

we have had the odd outbreak where, you know, animals have started off being se negative and then moved to. Being genuinely seroposit, and those are more clear cut and more easy to be, you know, a bit more definitive about. You can say, well, they weren't exposed, and now they are, and it's in association with disease.

And it's in these scenarios that vaccination might be worth a go, . But it's like all of these things, it's something that's worthwhile trying, if the circumstances warrant it and you've got the, the, the diagnostic support there to back it up. but it, it doesn't absolutely guarantee a, a, a good outcome.

Some of the feedback that we've had is, is that there has been a good response, but, it's, it's one of these areas where we don't know absolutely for sure. OK, and possibly on a case by case, case by case basis, yeah. OK.

So another question, RSP and PI3 within this question. Is there a minimum number of samples that you would take to confirm the diagnosis? The, the listener says that sometimes it's difficult to convince the farmers, if they don't have very severe cases, especially in large herds.

So what really would be your, your minimum? So, yeah, for adult cows, really, you need a minimum of 6, probably ideally, probably double that to be really sure, but a minimum of 6 would be what I would say, and you do need pairs, and I, I accept entirely that getting those pairs can be a real pain. and I think the problem we have with adult cows is that, A lot of these dairy herds, these cows have been exposed anyway, you know, there, there's a lot of serial positivity, you could pick PI 3.

IBR, RSV, all these different pathogens, and, you know, generally speaking, there's, there's a lot of seropositivity out there. So, in that scenario. You need more samples, to actually, you know, prove a significant rise, from the pairs, so.

Simple answer question should be a minimum of 6. OK, brilliant. It seems to be 6 for, for lots of things, I find when we're doing, we're doing testing.

A question then about sticking with PI 3, because that was mentioned in the last question. You didn't mention this as initiating cause of disease. Do you think this is a significant, initiating factor?

It could be, the simple answer is I don't know, I didn't mention it, and it is a fair point. It's not something that we've picked up, and equally on any serological testing, it's not something that we've significantly picked up. Certainly, you'll find animals that are antibody positive again, but is that just background immunity or, or, or what is going on?

So, I, I've never had the evidence to suggest that, you know, this is a significant cause. It's certainly there and the cows have been exposed, but it's been hard to be sure that this is a, you know, a significant part of the, of the disease process and, and probably again, you know, looking at pathology and, and thinking about the risk factors, there's probably more to be gained by focusing on some of these other areas. OK, brilliant.

And we'll just have one question about monitoring before we move to our final question on treatment. In terms of monitoring bulk milk salmonella, is there an advantage in, in vaccinated herds, or does it, does it, blur the response? It blurs the response, and perhaps I should have said that, so it's a good point well made, in that, vaccinated herds will be antibody positive, and we have.

Well, I suppose we have less, less experience of handling these samples from vaccinated herds, because, because generally speaking, the, the, the samples that we're looking at will be, you know, in herds that are not vaccinated. But the assumption is, is, is that they will be antibody positive. I guess you've got to bear in mind also that in, in herds that are purchasing cattle, there may be vaccinated cows that form part of the, of the pool.

So, there, there can be some, some. Areas of interpretation that need to be thought about fairly carefully there, but it is a very useful tool in, in herds that don't vaccinate and, and don't buy in. And do you have an approximate cost, sorry, to, to put this but approximate cost for that testing?

Well, it's cheap. So a single bowl of milk can't be a, can't give you a precise course, but it's, it's between a fiver and a tenner. So it's not, it's not big money.

And, and that's a really good way of dipping your toe in the water just to see, is there exposure there. So it's a fairly good starter for 10, just to see what's going on. And, and as I said in my presentation, if you repeat sample on a quarterly basis, then that increases the sensitivity of that testing quite markedly, or similarly, if you've got clinical disease.

Then, it's more likely to be positive. Great. OK, so last question, I'm gonna amalgamate the last two questions because they're both, relating to treatment.

How important do you feel it is to identify and treat the specific organism, especially in the case of bacteria, versus just treating suspected bacterial pneumonia with broad spectrum antibiotics? OK, so, I suppose there's two things there, . The main organisms that we're seeing, you could see the ones that are listed.

So we're talking mainly about the, the pastorlace, as, as the ones that are main to the for T pyogenes, and then probably to a lesser extent, M. Bovis, salmonella, other organisms as well. So, Initial treatments, Really getting in early is the most critical thing, .

Sensitivities of the pastorelli, which will be our main causes, don't tend to cause much in the way of problems, but I would always say it's worthwhile monitoring these sorts of things. So, I think the most important thing for a farmer or a practitioner, is, is to treat early, and, and to, you know, treat as per farm protocol. so whether that's just simple, you know, oxy tetracycline for, for these cases to start off with, will work particularly well.

but also is to review antibiotic sensitivities for anything that we're isolating, so that you can refine that as necessary, but. When you see some of the pathology that you get, and, and that's why I showed it, is, is, is that, you know, sometimes these can be pretty advanced with bacteria that are, are well, hidden away within the lung, they're within abscesses. They are going to be hard to get to with antibiotics.

So, Not delayed treatment is the critical thing to start off with. Brilliant. And that, brings us to the end of our questions.

So I just want to thank you, Colin, once again for your presentation this evening. We're getting great comments coming in, thanking you and saying it's very, very interesting talk. But also thanks to everybody that's attended tonight's webinar.

We've had over 200 of you online tonight, which is an absolute record for our webinars, so thanks very much. And we really do hope that, you'll join us for our next webinars, which are on Tuesday, the 21st of July. So, two weeks' time, we've got Philip Skis from, the Morden Research Institute, who'll be taking us through liver and roommen flute control in cattle and sheep.

And then on the 11th of August, we're going back to beef with, weaning the beef calf with Joe Henry. And obviously these are all still free for BCVA members, and we point you towards the webinar vet, website to sign up for these, or contact us at the BCVA office as well. So, just want to say thanks again, Colin, absolutely fantastic, presentation, really enjoyable.

And also to everybody listening, we'll see you next time, but until then, good night and stay safe.