Thanks, so, it's lovely to be here with you and good afternoon for snowy UK. So we're gonna be talking about my favourite subjects, strangles and certainly within the UK how that often can cause panic, on, usually multi, owner, horse yards. So we're just gonna run through what we plan to cover in the next hour.
Gonna give some background to strangles, and then really pick out from a clinical sort of frontline point of view, the relevant bacteriology, what affects what we do in clinical practise, epidemiology and the pathophysio pathophysiology very much from the standpoint of how it changes what we do at the horse side. Then move on to the very thorny subject of diagnosis and different diagnosis tests that we have available, and the problems of false negatives, and to get even false positive results and how best to use our clients . Money, often and how to communicate, the vagaries of strangle diagnosis.
Then move on to treatment of acute cases, and then, and as we'll touch upon in the, early part of the talk, you know, screening for carriers and removing these carrier animals is probably the key to prevent strangles from spreading in the future. And then moving on to some top tips of treatment of carriers, couple of videos there, and then at the end, talk about maybe. More on prevention of how to prevent strangles in the future.
There are a number of slides at the end, which you may not have time for, which are some examples, commercial examples of how, modern technology are helping us as vets, communicate. Hate prevention to owners and if I have to flip through those quickly, I apologise, but hopefully it'll just give you a flavour of what's out there because I'll be very different nationally, quite a lot of them are sponsored by pharmaceutical companies that, sort of picking out what's relevant to you in your, jurisdiction. So starting with background and relevant bacteriology.
I think the key thing is that, this disease is as old as horses themselves. I mean, I picked out this report, by Gordonis Rufus in 1251, but I think in, in, in ancient Egypt, there are also descriptions of, strangles, and I think that really points to how successful that this bacteria is, and I always think about infectious disease as a battle between the pathogen. And us, the hosts stroke immune system, and strep should be respected in that this is a hugely successful disease from the point of view of itself in maintaining itself from one generation to another.
And this is also reflecting the fact that it is probably the most common infectious disease reported worldwide. So a third of, or just under 13% of reported infectious disease, is, from strangles. But generally there is a high morbidity, and we will touch upon that a little bit more because I think that does vary, but generally the high morbidity, but, low but significant complication rate and mortality.
And I think certainly within the UK where people tend to be very sensitive and even within the UK there are very regional differences. Some areas are much more relaxed about strangles than others. I think it's getting that balance of communication to say yes, this will, this disease can be potentially, .
And rarely cause mortality, to get people to act on it and prevent it, but also not to overstress that and actually mortality, certainly in the adult population is relatively rare. If you're dealing with young stock, suddenly mortality rates do go up. Now, the ACBM, produced a consent statement, it's quite old now, issued in 2005, but still the, the core, factual details, within this are still very relevant today and I'm hoping that, this year or early next year, so 2018, early 2019, that the updated consensus statement would be available.
This is the abstract and this is in the Journal of Veterinary Internal Medicine, which is an open access journal now, so if you download the app for JVIM. You'll be able to access this free of charge, and when the new consensus statement is published, like I say, hopefully soon, it is a great resource to keeping up to date with the current thinking on strangles. So this is bacterium, as I've said, Streptococcus ere subspecies equi.
It's worth noting in the name, this was named, quite some years ago, but this is actually, the sister bug to Streptococcus equi subspecies zoo epidemicus, and actually genomically we know that equi is actually, derived from zooethericus, Zoommius which Affects multi-species and multi-organ systems, has a much larger genome, and equi has evolved from that genome and is a very small, relatively speaking, sort of genomic material compared to that. So actually the name is slightly misleading. It actually should maybe perhaps be Streptococcus epidemicus subspecies ere, but, up until now we're still calling it equiere.
That's the talk just gonna refer to it as strep equry. It's a gramme positive aerobic, a chain forming bacteria. You can see this is a slide, a psychological preparation of, a gut or pouch, and it forms these chains down here.
I think hopefully you can see my, pointer. And when we come to how we sample for strangles and try and get it to the laboratory to get us the diagnosis, I think remembering that that this is a fastidious organism. It requires special medium, so tortu medium with a slightly enriched, atmosphere of 5% CO2, and once you take this bacteria, you can see it on the bottom right here living on the, epithelial surface, .
I once you take it outside the horse, it, it spires for very short periods of time. We'll give you some numbers a bit later in the talk, but we've got to think of that when we're trying to get it from horse to the laboratory, and this is on a blood Aga plate at the top. Right, it's a beta hemolytic.
You can see the, hemolysis around the, colonies, Lancefield group C, but so is strep zoo epidemicus and so therefore differentiating these two organisms can be challenging at a laboratory level. So what relevant epidemiology and pathophysiology do we need to know about? So it adheres to the upper respiratory tract epithelium, it translates very quickly within a few hours.
We then get a massive outpouring of neutrophils, so probably . PMNs and these are unable to phagocytose and kill the bacteria, and it is this key, virulence factor that enables abscess formation and survival of the bacteria. Nasal shedding after the initial contact with the bacteria occurs 2 to 3 days after the onset of fever.
So when that translocation occurs in the first few hours of the bacterium hitting the nasal mucosa, upper respiratory mucosa, you get a spike in fever, but the nasal shedding doesn't occur. 2 to 3 days afterwards, and you'll see when we get on to control of the disease, if we can identify in contact horses by measuring temperature when they first bit that temperature, if we isolate that animal, it is before it becomes infectious, so it can be really successful in controlling the spread of the disease. The incubation period, is often cited as 1 to 14 days, and that's very dependent on the, size of the intranasal inoculum, in other words, more bacteria, the shorter that incubation period will be, and also the underlying immunity of that animal, whether the horse has seen strep ry before, how old it is and how immunocompetent the animal is.
One thing I would say is in the majority of my patients, which would be, middle aged, say maybe 5 to 15 years old horses in athletic use, that tends that incubation time tends to be towards the 14 days. And often in the index case we miss that, initial fever, and as you'll see, abscessation doesn't often occur till 3 to 5 days post infection. So you can be talking towards 2021 days before you're starting to, .
See that first case. And then, therefore, when we start looking at how long we should isolate animals to prevent the disease, you can see why maybe 2 weeks is not long enough, and we might be thinking more 21 days, isolation to, safeguard against, strangles, entering a yard. And this disease is spread by direct contact or con con contaminated fomas.
It doesn't spread in an aerosol. And really, as far as the horse can throw a bit of mucus would be as far as it goes, and this should make the disease much easier to contain and some very simple biosecurity tips should stop the spread of the disease, which we'll touch on later in the talk. Epidemiology was an acting Todd in the First World War in the beginning part of the last century.
He observed that 3 quarters of horses develop a solid and enduring immunity after recovery from the disease. And sadly this is something that we've not been able to replicate, with vaccine vaccination as of yet. Older horses would have a residual immunity, and we tend to then see atypical or so-called caral strangles.
So they tend to be much less classical. So you might not see lymph node abscessation, sometimes not even a fever or a very transient short-lived fever. And as you'll see on the next slide, these horses are still shed virulent bacteria and therefore risk to susceptible horses.
So, in, in these older horses sometimes. The clinical cases that you're observing are just the tip of the iceberg. Recovered horses can shed bacteria for up to 6 weeks after the clinical signs have resolved, and then when we start talking about when to screen for carriers, you'll see that we'll offset that sort of normal shedding of bacteria after recovery.
From those old horses distinct to to go on to be long-term carriers is when we intervene to screen for those carriers is a, is a sliding wall of, benefit. So we don't over-diagnose, carriers, and therefore treat more horses as, as, as carriers. On average, 10% of affected horses develop a sub subclinical carrier state.
So you can see on the top right of the slide here, this is the medial compartment, of the guttural pouch, and you can see a glob of pus, and it's usually the retropharyngeal lymph node rupturing in the floor of the compartment here that contaminates the guttural pouch. And therefore, the, organism has entry here and then will switch off in this roughly 10% of horses and therefore remain later within the horse in the clinically normal horse to, to recrudesce and spread, bacterium in a naive population, often months and sometimes even years down the line, and you can just see the guttural pouch, here on the bottom right. This is a, just an example of this endemic silent transmission cycle and these mature horses.
There's some data gathered by Jeremy Simons, back in 2006 2007. And we had 700 horses that were at risk, 450 of those, were sero positive. 87 were co positive, and when we get them diagnosis, I think we'll sort of, confirm that, often culture can be disappointing.
And 114 of those horses ended up being carriers. And if you look on the right hand column here, the variation of carriage rates varied massively. So on some very small yards, you can have up to 100%, and some would be 0%.
So even though we quote the figure of 10% carriers, post, an outbreak, it is very variable from one yard to another. So transmission of infection, as we said, it was direct or indirect, so, we don't see aerosol transmission, it's just the mucus, the discharges, so it's different to the viral diseases such as EHV or, equine influenza. Indirect transmission is really important, especially when, say in the UK or livery yards where you've got high, traffic of people and horses, so we might have 40 horses and 35 owners coming and going at the.
Beginning of the end of each day, and that causes large indirect transmission cycles unless we put good biosecurity measures in place. Water troughs, feeders tack, people are obviously the key things of this indirect transmission, and we'll come on to the survival of requi in the environment and certainly darker, wetter environments such water troughs will extend its . Environmental survival time.
But as I said, this is generally short, but I will just put some numbers on that in the next slide. But the key take home message again, I've stressed this a number of times already, is the main reservoir is carrier horses. If we can identify the horses that are carriers, and either prevent them coming onto a yard or identify them at the end of an outbreak and treat those carriers, we will go a long way to stopping strangles in the future.
And as I said, don't forget to sign the transmission. So, Scott Reese, from, the US published in the Canadian Vet Journal in '09, relatively short, survival of Ere on services and really looking at sort of 1 to 3 days. Professor Andy Durrow from Lippo equine Hospital actually presented some data in Budapest at the ECIM, conference, at the back end of last year, which Challenge this slightly in that er with all these environmental survival studies it depends on the sort of, local environments that you're performing the study under, and I think, Professor Durham showed that there was some seasonal or climatic, changes.
So, rep is, as it says actually in this abstract, very, susceptible to exposure to UV light. To sun, so therefore, in the winter, these survival times are going to be slightly longer, still a matter of days, but certainly longer and dark, wet places that might be even further. So certainly, I think we still need to disinfect the environment if we are in wet and dark conditions.
So clinical signs, I think everyone will be happy with the classical strangles, very high fever, profuse thick nasal discharge, bilateral, swellings on the head. You can see this horse down here is sort of always photographed, the more atypical ones, but this is actually a cranial cervical, lymph node, and you get really black necrosis in this case, but often actually it's just a large abscess with a draining tract, sore throat, difficulty eating, dysphagia. Sometimes we see obviously the lymph nodes compress the airway, hence why the disease got its names, strangles and sometimes these horses might need a track to to allow them to breed, breed, sorry.
In my hands actually, classical strangles is relatively rare, in my population of sort of ridden athletic courses which may have some, previous immunity, atypical strangles is much, much more common, so we get a mild, short term fever, may lose appetite for a brief time, maybe even it's just a serious nasal discharge as, as opposed to more classical, mucopurulent discharge, no abscess formation. These horses are at risk to others, and it's usually maybe the 3rd, 4th, 5th horse in an outbreak that you get the more classical signs, you get a typical horse, a typical horse, and there's a horse that, It may be getting a higher bacterial load, maybe slightly immuno compromise for for one reason or another, and that horse will be the first horse that will present classically. So we just have to be aware that strangles can present like other forms of respiratory disease, infectious respiratory disease, and can be quite hard to differentiate at times.
I think I touched upon the chance of asphyxiation and death due to lymph node enlargement and compressing of the airway. Once again, thankfully, I think this is very rare, but it is, obviously how the disease got its name. It's Beyond the scope of this, discussion to talk very much about bars or metastatic strangles, but suffice to say it does happen, and I, I personally prefer the, terminology metastatic strangles.
This is where we see abscessation, throughout the, the, the body, whether that be the thorax or the abdomen, and usually some weeks, if not a couple of months after the initial, infection, they often present as sort of weight loss cases with intermittent, pyrexia. Purple hemorrhagica, a immune-mediated disease, of which a number of infectious organisms can trigger seem to get the tication of the . And mucous membranes, you tend to get a sort of vasculitis, a sort of head edoema here and eventually edoema down here.
Once again, beyond the scope of this discussion to talk about much further, but it obviously is a potential sequelae, and it usually is once again weeks to months after the initial infection. So getting on to diagnosis of the disease. I think it's really important to know which animals we want to sample, which samples we're gonna take, and therefore which tests we're gonna use on those samples and how we interpret them.
So I think we for bacterial disease are all fairly happy that culture is historically been known as the gold standard for diagnosis. We tend to do these on nasopharyngeal swabs, abscesses, or, get onto gut or pouch in the bar. In a few slides of time, I think often more useful in screening for carers at the end of an outbreak rather than acute diagnosis where you're trying to sample more the nasal pharyngeal area.
I think it's worth mentioning and you'll see on the next slide that a nasal swab, you definitely get lower culture rates. You want a nasopharyngeal swab, so that's up to 30 centimetre swab. It wants to go up the ventral medial meatti of the nose to the nasopharynx so the horse swallows and the gutter pouch will then open on that swallow.
So if there is any proent material in gut or pouch, it should be discharged onto your swab. So it'll sample the biggest, volume. Of mucosa that you can possibly do.
In North America, they're getting very into the nasopharyngeal lavages where you, instil sterile saline up the nose, the back of the nasopharynx then collected at the external naries. I find it a slightly, messier technique, but certainly the, sensitivity of the technique is, is, is, as high as nasopharyngeal swabs. So certainly, I, it's, it's worth considering.
So we've touched the beta hemolytic Group C gramme positive cocky, and the key thing is to differentiate this bug from its sister bug strep zoo and the key thing is, and you'll see on the bottom right, the API, test kits, and it does not ferment lactose, sorbitol, or ribos. As we've sequence more genomes, actually there are a few. Strep zoos, eququi that cannot be differentiated between just on the more standard APIs.
I had a case actually only 3 or 4 weeks ago. A donkey actually that had a uterine infection that came back as equi or genomic, sequencing actually, and using, the specific, PCR. We could differentiate it and actually it was a strep zoo.
So it would always be slightly suspicious of culture results, if it doesn't fit with your clinical picture and using, laboratories that are very used to, dealing with equine samples and therefore, have expertise in differentiating zoo from EI, I think is important. The key thing obviously with culture is we need sufficient live bacteria for a positive and this is a very fragile bacteria once you remove it from the horse. So we need to take our sample up up the areas and like I said to you hopefully to the back of the nasopharynx.
We need to transport it. And hopefully that is 24 hours, but in in a weekend situation or if laboratories are further away or the postal service isn't what we would like it to be, that can be longer, and we need to get it to a strep selective AA. So I think the key with culture is, if you get back a negative, and we'll talk about other tests that we'll run with it, it doesn't rule out strangles.
It is prone to, false negatives. And if the horse looks and, like it has strangles, we've got big, enlarged lymph nodes, maybe. Draining, tracks, then it generally is strangles, and we need to resample.
I think communicating that to the owner, before, and so their expectation is that if we don't get a positive, we haven't ruled out strangles, that we need to might run further tests, and it's often the 2nd, 3 samples that give you a diagnosis. And this is where PCR I think has really helped in recent years and that it's a very sensitive, diagnostic test. It exponentially, amplifies the target DNA fragments.
You start with one copy, and in 35 cycles we get up to 34,000 million copies, so it's hugely sensitive, technique. And like I say, if you get 100 copies of a better diagnostic sample, you'll then obviously got a huge number of copies available. And this is the PCR, on the eMI bride, as, as a positive.
So PCR pros and cons, we don't get false positives to the to the inability of recognising some strep zoos that do ferment ribosal which I touched upon in a couple of slides ago. We have improved sensitivity and also we have a 24 hour turnaround, so culture takes 3 to 5 days, so that's quicker, which in a outbreak scenario can be really really helpful. I think I've got a couple of slides on different PCRs, but I think it is worth pointing out that not all PCR strangles PCRs, repry PCRs are the same.
Currently the gold standard in the UK is the Triplex, PCR developed by the Animal Health Trust in Newmarket, and that has one gene, that, is, Only on strep zoo epidemicus, and 2G is in the strep peque. So therefore, it is, using three different, genetic, DNA fragments, to differentiate, whether we have a strep equi and differentiating from strep 2 epidemicus. The one thing that has been thrown at PCR for many different seasons, especially in strangles, and especially when it comes to carriers, is can you get a pulse, false positive result, because the bacteria have died and you just got DNA lingering around in the upper airway of the horse.
The thing I would say about that is. A mucosal clearance of DNA is highly efficient within the number of hours, especially within the native pharynx. So the chances of getting a false positive are very rare.
Within the gutter pouch, we'll touch upon this more when we look at screening for carriers, it is slightly slower, but within the time frames that we're talking about and sampling, carrier horses, I think it a PCR positive result even with culture negative, because we know that the culture has such a high, you have false negative is that we still should assume that that animal is infectious. And so therefore, I, I'm not a great believer in that last point. And so this is a sort of a little 2x2 table, and I think everyone, if we've got PCR culture positive, that is infected, PCR positive culture negative, which we just discussing is infected.
Now, until recently, we could get COL positive PCR negative because you can have organic day that would interfere with the PCR reaction, from clinical samples, so sometimes you get a false negative on PCR. In the last 3 years within the UK we've had none of those results, from my colleagues at the Adam Health Trust to a point now where we would be happy if finances are limited that you would only run the triplex PCR because we're not seeing any culture positive. PCR negative samples, so we could use PCR alone, and I know in North America and a number of papers, published out of Pennsylvania University, they also are using PCR alone and no longer culture.
The culture negative PCR negative sample, even though we have increased sens sensitivity of PCR, we still need to say that that horse could still be infected, and we might need multiple samples to get a, a positive diagnosis. And certainly if you've got multiple animals, it may be that the second or third animal might come back as PCR positive culture negative, for example, and then give you a diagnosis. So just to emphasise that point, this was a paper published I think, from Sweden back in the equine Veterinary Journal in 2006, so fairly old data, but they sampled horses weekly.
The bottom, 4 horses, sorry, 5 horses down here had, strangles clinical signs, the grey boxes of when those clinical signs were, so you can see horse 14, for example, had clinical signs for 8 weeks. On the first sample, it's culture negative and PCR negative. It was then positive on both for 2 weeks and then for the last, 4 weeks just PCR positive, and actually, the last 2 weeks of signs once again negative from both.
You can see how intermittent these tests can. Just talking about this silent transmission of strangles in these mature horses, these horses had no obvious clinical signs of strangles and yet were PCR positive or culture positive and PCR positive on a number of weeks. So these were direct contacts that we needed to be sampling to.
See where, whether they were, contagious to, to other animals. And when we get on to serology, I think this is where serology can be really helpful in, helping know whether, the disease is circulating in a group of horses that are in contact but aren't showing, clinical signs. I think I've touched upon this, won't dwell on it too much.
I think this is really just saying how, tests have evolved, and now we are actually the Trix PCR I mentioned is a QPCR so it is quantitative, and I think PSPCRs have evolved and got much more sensitive, over, over time. It's moving on to serology, and I'm gonna be focusing very much on the serology run here in the UK, by and developed by the Animal Health Trust, although it's under licence to a number of other labs within the UK and I know actually it has been now, under licence in a number of laboratories around the world. In the ACVM consensus statement in 005, they talk about SEM protein serology in the UK we felt that that, wasn't, sensitive or specific enough and therefore we screened a number of different, antigens, actually I think 56 off memory, and we felt that we needed a combination of two antigens, so protein A and protein C, to get the, an adequate sensitivity and.
Which you can see on the left of the screen, to add to reliably differentiate horses that have seen strangles and who have not. And just when you get the results is, you get an optical density, so an OD number, and really it's just looking at the colour of the well. So 0.0 is clear, translucent, a high number is more yellow, and so the optical density number reflects how yellow, the well is.
So the A antigen is actually a protein set 2 190 antigen and considered negative is less than or equal to 0.2. 0.3, 0.4, this is an S curve, so this is on the vertical part of the curve.
0.3, 0.4 is inconclusive and greater than or equal to 0.5 is considered positive.
When this test was first launched, in about, I think it was 2007, we used the B antigen which had a slightly different cutoffs, but the, reagents for the B antigen got too expensive, and actually the C antigen performed as well as the B antigen, and so we moved on to that, in November 2010, and. From a clinical point of view, it's much easier to use because the cut-offs are exactly the same as the A antigen. I think it's worth emphasising, and I think I'll write it on the next slide, that these antigens are considered together, so this is a duplex elizer, and you are to be.
Negative, you have to be negative on both antigens. To be positive, you only have to be positive on one antigen. So the reason that we introduced the second antigen is there were horses that had seen strangles that were negative to a antigen and therefore would be positive on the C antigen.
So just to say that again, to be negative, you have to be negative on both antigens, to be positive, you only have to be positive on one antigen. So remember we're measuring antibodies, take up to 14 days for those antibodies to be produced and they can stay high for a number of months. So the use in a very acute early stage of outbreak, I think has to be questioned.
So on your index case that's maybe spiked a fever, maybe has just, developed a nasal discharge, that animal, if even if it has seen the disease and has formed it strangles, might be sero negative because it hasn't had time to produce the antibodies. And if that horse has another infectious disease, say, let's say, equine influenza, it may be serro positive due to previous exposure strangles maybe 7 or 8 months ago. So you, in that scenario, if you were going to take a blood, I think you need to communicate that to the owner that the first, result isn't going to be meaningful.
It'll only be a paired sample in 2 weeks' time. When you're using paired trology. It's really important that you're retesting the sample versus sample one.
So there's an inter-assay variation of up to 0.3 optical density. So when you send that second sample and you need to make the lab aware.
And they will take out your first sample and rerun it on the same elizer plate that you run your second sample on. So let's say you had a 0.4 on your A antigen on your first sample, they will take that back out when you send your second sample, and that might now be 0.6 on this Eliza plate.
But the key thing is the comparison between the two, Two tests, and obviously we're comparing A to A when we had B B2B and now with C C to C, so you're comparing like for like. The ge fertiliser has high sensitivity and specificity. It correctly identifies infected horses, it correctly identifies unaffected horses, and as I said, serial conversion is 4 to 14 days.
The M protein, Eliza, you can see weasly sensitive, but, is more foreign to a false positive diagnosis, so specificity is lower at around 77, and there's a nice paper, published in the Pem Journal in 2013 looking at the, different, serology tests. So what appropriate selection of samples and tests depending on the stage in an outbreak that you are in? So in acute case, I think a nasopharyngeal swab or a nasal lava that we touched upon, I think's really helpful, but you may need multiple samples either from the same animal or from different animals.
Serology, as I said, isn't helpful because it doesn't tell you very much in those first few days unless you're then gonna follow it up with a paired sample in 14 days' time. But hopefully you'll have had your diagnosis by that point. Sometimes it's nice to have the belt and braces approached, to have that in your locker to go back in 14 days' time if you've got an outbreak, you're still not quite sure whether you have strangles on the yard.
The classic 3 nasopharyngeal swaps of weekly intervals which came from a UK. A directive by the HBLB, is a process for, picking up intermittent shedding of, bacteria from the guttural pouch. So that isn't appropriate in an acute case, it's appropriate to run a screening for carriers.
As I said, the guttural pouch lavage, I think in that acute case, it's more expensive than, for example, a nasopharyngeal swab, I think should be reserved for carrier detection. Quarantine testing, obviously, single nasopharynge source is not sensitive enough, serology you can use it pre-arrival, or when you're in quarantine. You can use 3 nasopharyngeal swabs to try and detect, carriers, and you can use guttural patch lava.
Exposure, screening, so looking to see whether horses have ever seen the disease, serology is obviously, your, diagnostic, modality of choice, and carry detection, as I said, I think gut or patch lava. And current HBLB advice, so the sort code of conduct within the UK has actually recently in the last couple of years, suggested that we use one nasopharyngeal swab within combination with the guttural patch lavas just to try and pick up the very, very few horses that might be carrying disease within the sinuses rather than guttural patches, but I must stress that is extremely rare. And if I could only do one thing, it'd always be a guttural pouch lava when screening for carriers.
So treatment of acute cases, roughly 20 minutes to go, . I think that depends on the stage and spiratory disease. Most cases, in acute cases don't need any formal treatment, just rest, soft, moist, palatable food.
I think antimicrobials are contraindicated in most acute cases. Firstly, strep ry has never been demonstrated to be resistant to any antimicrobis that you expect to work on Gram-positive cocci. So the antibiotic choice in most cases would be penicillin.
If you give penicillin in an acute case, often it just prolongs, the disease, so you'll cause sort of a temporary re remission, and when you come off the antimicrobials, the horse will get sick again, because you don't get adequate penetration with it to the lymph node and therefore there's still some bacteria present even when finished. I think beyond the scope of today is to talk about antimicrobials and the association with purpoheagica, what I would say on that is that, it remains, unknown and certainly the evidence is equivocal either way. One place I would use antimicrobials is in the really sick horse.
So, say in the horse that, is, maybe gonna need the tracheostomies due to, airway compression, or very sick, . Of its food, or, or an abs or an abscess compressing, on a, structure within the head, and that, then I might use, antibiotics in a more sort of intensive care setting. But the vast majority of, adults, healthy horses before developing infection won't require antimicrobials.
Non-steroidals, I think, I would use much more frequently. So when horses are flat, feeling usually unwell from the fever, I think non-steroidals bring that fever down very well, reduce inflammation around the abscesses, and or swollen lymph nodes, and can make horses feel much better very quickly. And any nonsteroidal nexin, phenyl bustone, meloxicam, to name a few, would be, .
Quite adequate. Controlling in this acute stage, I think is really important, segregating clinical cases and contacts designate the clinical case areas dirty, obviously stop movements on and off the yards, as we mentioned when we talked early in the . A lecture about pathophysiology, we should be taking temperatures every 12 hours, because if we can detect that initial, fever, pyrexia, and add it and promptly segrebrate those cases before they can shed the disease as I said, shedding usually of the bacteria 2 to 3 days after that fever, we will stop the, spread, in the outbreak.
A very high hygiene standards, so, disinfect, hands, clothing, barrier clothing. And then we're gonna screen convalescing cases and they're healthy in contact to see whether we had that silent transmission and or where the carriers were, how the disease got in. And the aim is to move our horses from the dirty area back to the clean area.
So bi security within the outbreak, top left of the screen, I think certainly within the UK when you talk about biosecurity, people have visions of the horrific foot and mouth outbreaks, in, clothing hoofed animals, back in the early part of, this, century, 2001. And these white overalls and sort of the state vets getting involved. And I think for most horse owners, that's what they conjure up when you think biosecurity, and that alienates them very quickly.
I think the key with strangles is it's very easy to kill. You don't need to be dressed in a white suit, with big, signs, like you would, for the more. Contagious, sorry, not more contagious, the more harder to kill, viruses.
So simple, as you can see in the bottom left, waterproof clothing that we're only using when we're handling the infected horses, ideally, and that's separate isolation units, so this would be our dirty area with a simple, sign saying do not enter, and all the, disinfectants that are commercially available will kill strep equy very, very easily. And so therefore, simple biosecurity measures will go a long way to halting the spread of this disease. So this protocol was come up actually I think with a Texan, veterinarian in southern United States and I think it's still the best way to communicate to her is how they should be dealing with these animals.
So if your horse has had clinical signs or you've got positive diagnostics. You're in a dirty in so-called red area, and I would start labelling equipment such as wheelbarrows, forks, brooms with red tape. So it's a visual guide to owners that I'm in the red area.
I can only take in things that are staying within the red area and therefore we don't get fo rights and transmitting from one area to another. Anything in contact and in some outbreaks that's everything else, cause it's very hard sometimes to have an animal that you're absolutely sure has had no contact with other animals on the yard. Those are so-called amber.
We're measuring those temperatures and anything that spikes temperature has been moved from amber to green. Sorry, amber to red, obviously, amber to red. In green, so some outbreaks start with no green horses.
If you had a yard with a very separate barn, perhaps a professional yard which has a commercial livery. The livery has the outbreak, but on the professional yard there's no people or personnel that that go from one yard to the other. They may be green.
If there are no green to start with, obviously, our aim is to get the red and amber group horses back down to green at the end of the at the end of the outbreak with clinical testing. It's a very brief outlines of biosecurity principles, as I said, very short distances for strangles is more than adequate, 10 to 25 metres. But if you can't do that, literally a solid barrier or a solid wood barrier, for example, separating so horses don't have nose to nose contacts, if that's the best that you can do, will be adequate.
And just to compare it to the other viral diseases that spread over much greater distances, separate water supply. Restricting personnel access, quite often they go onto yards and they have a lovely red area, amber area. You'll have personnel that are restricted to those areas, but you'll see a dog running between, those said areas.
So obviously no pets, which can be challenging. Dispose of bedding, and eating food and water, protective clothing and hand hygiene, and disinfect, when finished. So when to screen for carriers?
So moving from the acute scenario where we're getting the outbreak under control, we've now got the outbreak under control, we've had no clinical disease for a number of days to weeks, and then we need to decide when to screen for these carriers. So this is a stylized graph that I made that shows that as horses recover from clinical disease, the number of horses and we've got the number of horses on the Y axis that shed bacteria decreases with time. And as I said, some horses will go on on and shed bacteria for up to 6 weeks.
We want to detect the number of horses that will go on to become long-term carriers, and those are the horses that we want to treat. The HPLB guidelines in the UK have used the phrasing that we should be waiting at least, so you can go longer, at least 28 days after the cessation clinical time, clinical signs. But anyone who's dealt with strangles outbreaks and knows you come under huge pressure from clients to to get on with testing, .
Because obviously the longer they're shut, the longer they can't get out and, go to competitions. After 4 weeks, you won't have any new clinical cases because you've gone past the incubation time and the chance of getting a short-term carrier is relatively low. If you've got a yard where economics are precious, therefore every horse that you're gonna scope is gonna be a financial pressure.
And you're not under the time constraints you are on other yards, waiting till 6 weeks, you will decrease the chances of, of, of, falsely diagnosed a short-term carrier. In my world where actually usually people want to open earlier, I think the, the shortest you can physically go is probably 21 days. Because if you go short, less than 21 days, then you'll have a chance that you will have a clinical case as you're getting on with screening your carriers.
If you went for 21 days, as long as they're aware that you might overdiagnose some horses, so some horses that will resolve their carrier status of their own accord, you will pick up, but that may be something that the owners are willing to do. But in a, in an ideal situation, you should be waiting at least 28 days. And so moving to this disease continuum concept, so we have acute infection.
All horses will be that short term shedder with a decreasing number shedding over time, and as I say, most horses will stop shedding at that 4 to 6 weeks, time, and then it's this long term shedder, these horses that go on to discharge permanent material from the guttural pouches for months to years, and that. Puss usually hardens into some cottage cheese-like material and eventually to the hard chondroids, these pebbles that usually take months if not years to form, and these are the very difficult to, or more difficult to treat long term carriers, so if we can. Detect the horses as they come into that early long term shedder phase, then they're usually much easier to treat that 28 days after clinical signs of an outbreak.
So screening for carriers, we touched upon it in the acute diagnosis, table, we can use 3 nasopharyngeal swabs, and we're looking at, if we just use culture alone, only about 60% being positive, so that's not sensitive enough. So 3 nasopharyngeal solved with culture or PCR or nowadays if you're using the Triple PCR PCR alone, you're looking at about a 90% detection rate. And one gutter patch lavage would equal 3 nasopharyngeal so, sorry, there should be an S, on there.
The alternative is, looking at serology, and I'll give you an example of a an outbreak of where we could use that and how to use it effectively. So this is a 40 horse DIY in every yard, the head of horse developed classical strangles. It was culture positive on nasopharyngeal swab.
The horse was isolated. 30 other horses developed clinical signs, 10, which were designated red, and 10 horses had no clinical signs or fever, and therefore amber and in contact. We have a number of options at the end, so it's 4 weeks since we had the last clinical signs, we could just open the yard.
Obviously, we will have some carriers or probable carriers within that cohort and therefore, eucrescence of the disease in the future is highly likely, so that wouldn't be my option. We could do 3 days of pharyngeal swabs on all the horses in the red and amber groups. It's quite laborious, it's gonna take at least 3.5, 4 weeks, and we're still gonna have to do a guttural pouch lavaage or any positive animals to see where the carriage is in the guttural pouch and to treat.
We could do Gush Pauch Lara and all the horses in the red and amber groups, so, that's certainly possible, but that is quite a lot of work to do and the finance is required to do that. Or we could do serology of all the horses in the amber groups and then gut or patch all the horses in the red groups and the serro positive horses in the amber group. Option is that you could do astrology on all horses in green and amber.
So we opted for option D. So these are all the horses, so even though I've got the serology values, we didn't, I wouldn't actually do this in real life because all the . Red horses, you can assume and you can see from these numbers are sero positive.
So if I had individual owners for each of these horses, I wouldn't ask them to pay for the serology test. I would just say your horse has had clinical signs, we know it's had strangles, and therefore we're going to screen the guttural patch lava. But the Amber Group, we can use serology to decrease the number of horses we're lava.
So out of the . I think it's 10 horses, we've got 2 horses that are on one or other advantage in above 0.5, and then we've got 1 horse in the grey zone.
In the grey zone, it is a personal preference to whether you count that as positive or negative at this stage, because doing a paired astrology when you're already 4 weeks after treatment, I don't think it's going to help. Personally, I would like just to lower the threshold so I would get on and scope that horse, but there would be others that would only scope on the above 0.5.
As I said, don't test the horses in the red zone, in my opinion, would be a waste of money. You're gonna get positive results, and even if you didn't, you're not gonna believe it. You might think it'd be the small number that would be a false negative, so, I would just get on and do gutter pa lava on those horses.
So all the horses that er are negative are now green, so they're moved into the green zone. We have one in the amber, which like I said, we could, either scope or or not, and personally I would, and then we have two that are definitely in the red group. So horses 28, 1022 and 35 were PCR positive in one or both guttural pouches.
They were treated with penicillin and gelatin mix, which I'll show you on the next slide, and then they were retested a week later, which is arbitrary but I find is, The easiest timeframe, I think a day or two is probably too short, and waiting longer than that, you'll get frustrated owners, so usually try and do these on a weekly cycle, so ret a week later, and they were all negative and the yard was then reopened. So how do we treat the carriers? So firstly, how to get into the guttural pouch.
So we need to be at the ventral medial meatus, you want two flat sides, either side, not a Mercedes-Benz, which is more medial meatus, so you want to be nice and ventral. Dorsal dorsal ventral ventral, so the soft palate's down here. We have the guttural pouch ostea of the left guttural pouch here.
Metal biopsy forceps in the dorsal commissure of the gutter pouch, apologise. Just forward it for a little bit. Dorsal commissure of the guttural pouch, we then rotate whichever way opens the gut or pouch, and then sometimes you need to just rotate back as you go through.
It's like a little S bend, and we're in the guttural pouch here, we want the sti hyode to orientate yourselves. The top of the styohyode is dorsal, bottom is ventral. This is the large and medial compartment here and the smaller lateral compartment here.
For as we're running out of time, the rest of the video is, to go in the other guttle pouch, you can go up the same nostril which is technically a bit more difficult, or if you're just learning, I would go up the ipsilateral nasal passageway to make it somewhat easier. Once you're in the gut of pouch, if you were treating a horse, this would be penicillin, but if you're doing a wash, it'd be saline and just use the wash because you can't see anything once you start doing the penicillin with white. And you want to start at the top of the guttural pouch and then you want to instil either sterile saline in the wash or penicillin if you're treating it at the top, and really you're trying to coat as much of the area of the gutural pouch as physically possible.
You can aspirate it, if it's a lavage, you go down to the medial compartment usually, usually where the biggest pool is, and then aspirate from the bottom of the gut or pouch. The retropharyngeal lymph nodes just got bubble on the screen here, it's just above, so I'll be inspecting that and seeing whether we had any little permanent material tracks coming up there. So this is the recipe for guttural pouch carriers, 2 grammes of gelatin, 40 mLs of water, heating dissolve.
You mustn't go above 50 degrees, otherwise you'll denature the penicillin. Ideally you want sodium benzoyl penicillin, trade name in the UK's cristalen. And then cool, and then do this in the practise, and then when you're out in the field, heat the once again, usually 45, 50 degrees, desired fluidity, often if it gets too cold, it will become too thick, and then infuse into the pouch.
If you have chondroids like the top left, you. You need a memorable helical polyp retrieval basket down the biopsy portal and occasionally you'll need surgery to treat those horses, but in my hands, these top two would cure 90, the vast majority of, carriers. I think we've only got 4 minutes left, so we might have to skip a number of slides at the end, but I'll get as far as I can, so moving on to prevention.
I think communicating to owners whether they're high or low risk, I think it's really important. Apologise for slightly garish colours, but essentially to give them an idea that. There are some things that make the risk higher, so maybe hot, and some that are, are, are, you know, preventative strangles, and I think you can read the slide, the very obvious things, but, you know, large contacts, if you don't have isolation going onto your yard, you're not screening for carriers, obviously increase that your chance of developing strangles.
A number of institutions or groups have tried to come up with different sort of client orientated educational material to try and emphasise this. Excel Equine produced a number of years ago in tandem with the Animal Health Trust, the guide to Preventing equine contagious disease, Plan Preventive Protect, which is essentially trying to go through and score the risk factors you saw on the previous, slide. Here's an example, and you can see, general biosecurity practises and then you would go through order in place either intentional or not applicable.
A couple of years ago, an app was developed by, MSD in the UK, but I think they have launched it across other, nations, that went through, to, try and act as a guide of how risky a particular yard was, and, some information of how to, go about getting this from your local rep. But really just questions like this, so I how, isolation of a new hard horse coming onto the yard is, and therefore you have a sort of temperature gauge at at the bottom and this temperature gauge fluctuates as you go through the questioning, i.e.
Red being you're more at risk and green being you're less at risk. So hopefully with a doctor's go, we'll bring that to a conclusion. I'll be happy to answer any questions and I hope you found the last hour interesting.
Many thanks. Thank you very much, Philip. Yeah, really, really interesting talk.
So we've got, a few questions just starting to philtre through. So one was referring to an earlier slide, where you listed the, the, a large variation in the percentage of horses that became carriers. You know, was that potentially due to different stereotypes or, is it not really known why that, why that happens?
It's a great question. We, have and actually partly by, work, probably 10 years ago, we, we have used stereotypes for tracking different, infections either between or during our outbreaks as a research tool. As of yet, we've not.
Isolated the virulence factors that affect how commonly a particular strain will go on to be a carrier and obviously there will be some host factors as well. It is one of the big questions in Strang's research that we have yet to answer adequately, but the typing that we do at the moment is looking at. From an epidemiology point of view, different strains, but it doesn't correlate with virulence in any way, and suddenly the virulent factor that causes courage is unknown.
OK. And then, a question that's probably relating to the UK, is, do you think we should make it notifiable, notifiable? Should it be more stringent reporting to try and control strangles or?
Every, stranglers conference we go to, it usually comes up, I think if I'm right, one of the Scandinavian countries are not off memory. I want to say Sweden, but it might be Finland in country and in the EU that is notifiable, and I think it has been very effective there. The worry certainly within the UK is it will drive the disease underground and within the horse owning population in the UK already it's quite hard to get people to admit that they have strangles, so I think it might be counterproductive and certainly from DFRA, the UK State Veterinary Service have no .
Want to make it notifiable because it has no human health connotations or particularly trade connotations, so they feel it's a cost that the horse owner should bear. And so, so, kind of in that vein then, do you, do you think there's something that we could do as vets to kind of reduce the stigma of a strangles outbreak? You know, as you say, yards don't like admitting they have strangles.
They almost become ostracised. You know, there's always one poor horse that gets blamed for being the carrier, it can be done on a more PR basis to. Yeah, so, exactly, and I think that's why some of the apps I showed you at the end can be really important and desensitising horse owners, and I think.
It it varies where you are between clients, client is you get some are very sensitive and you spend all your time dumbing the disease down and wishing it was called a different name and not strangles, just a mild snotty nose that might, cause something a little bit more serious occasionally. Other communities are totally blase about it, and you see horses with strangles being ridden openly in groups of horses, so it's very dependent on the client base, but I think, either way, communication and tools to help that that communication is absolutely key. Yeah.
Brilliant, thank you very much. Sadly, that's all we've got time for on this equine morning. I want to thank, Ruth Morgan, Debbie Archer, and Philip Ivans for three really great talks this morning.