Description

After birth, the majority of lamb losses occur within the neonatal period.  There are many management and husbandry factors, diseases and disease syndromes that contribute to this picture and improvements can be made on many farms leading to improved welfare and profitability.  In this session we will look at the causes of lamb losses, prevention, treatment and control.  We will use peer reviewed evidence coupled with a pragmatic and practical approach. 
 
Learning objectives:
 

To understand the scale of the problem
To develop an understanding into causes of neonatal lamb diseases
To gain confidence in diagnosis based on signalment, clinical signs and simple tests
To be able to take a practical approach to prevention, treatment and control

Transcription

Good evening and welcome to our farm webinar for February. My name's Rich Daley. I'm the head of sales for the webinar vet and I'm pleased to welcome you all this evening.
We've got a very interesting presentation this evening by Joe Angel, on a practical guide and evidence-based approach to neonatal lamb diseases. A little bit about our speaker for this evening. Joe graduated as a vet from the University of Liverpool in 2008, and since then has combined research with private veterinary practise.
He's currently an associate partner at Wen Veterinary Surgeons in North Wales and an honorary fellow of the University of Liverpool. He holds an MSC in epidemiology from the London School of Hygiene and Tropical Medicine and a PhD on the epidemiology of contagious ovine digital dermatitis from the University of Liverpool. He is currently involved in various research projects on ischemic teat necrosis in cattle, blood gases in neonatal ruminants, and digital dermatitis in cattle, as well as further work on CODD.
So, we, we're delighted to say have Joe with us. If you have any questions throughout the webinar, please do enter them into the Q&A box, and at the end of Joe's presentation, we'll have some time to ask those questions. So please do, get your thinking hats on and, put some questions in there and test Joe and there'll be a prize if anyone manages to stump him along the way.
So without further ado, I'd like to hand over to Joe. Thanks a lot, Joe. Thanks very much.
Well, thanks for having me and welcome to this webinar. This picture is how I imagine lambing to be sunshine, lambs on the ground, and no problems, but obviously that isn't, how it always is. And this talk's supposed to be a bit of a refresher on, neonatal lamb diseases, and also to dig into some of the research and evidence behind, behind that to give you some .
Some base on which, on which to stand. So, without further ado, this is what we're going to quickly look at. It will be a bit of a whistle stop tour through because there's a, there's a lot to cover.
So if you do have questions, do put them in at the end and I will do my best to answer them. We're gonna spend a bit of time just looking at how big the problem is. Obviously husbandry is really important.
Enteric diseases will make up quite a large chunk, and we'll look at some specific diseases and, and finish off with, some trace element, vitamin deficiencies and the congenital malformations. So how big is the problem? Well, there isn't actually a huge amount of data to tell us how many lambs are lost each year, and.
How sort of big the problem is, as a whole, so the. Most recent survey available is one carried out by Habiki Cymry, that's the Welsh version of AHDB beef and lamb, and er they did a questionnaire survey of farmers. The survey's not publicly available, so it's quite difficult to interrogate it properly, but this is some of the data they've presented and we just need to take it at face value.
So, I'm going to consider losses and mortality and morbidity er after the lamb has been born alive. I'm not gonna cover abortion and . Sort of poor conception rates and all that, that, that will be dealt with elsewhere.
I, I'm bothered about the lamb being born. It's born alive. What do we do now and what's going to go wrong now.
So the data from Habiki Cymry suggests that, if you look at that green bit of pie there, about half of lambs lost. Are lost within the first two days. So.
That's a time we can make a big difference, through our advice to farmers, as vets. And obviously if we're dealing with lambs or or use lambing as part of our work, then this is, this is the area we can make a big difference in. You can see there that the other largest chunk is .
Between scanning and lambing, so about a third of lambs are lost there somewhere. These are sort of late abortions, . And And so there's, there's obviously work that can be done and focused on there, but we haven't time to cover that.
Now we will touch on briefly and a few diseases that raise their heads in this bit after the 48 hour period, and there's obviously overlap between diseases that start early and but also occur up to 2 weeks after, after lambing. But by far the biggest area we can make the most difference on is the er first couple of days. Yeah, another study that presents very similar data, so we can sort of perhaps believe the hubby cucumry data more, was, published in 2001, by bins and colleagues, and again, they show.
It was again a questionnaire study, so it's based on farmer reports. They show very similar spread of data that actually a majority of lambs are lost within those first couple of days. So that's where we can make perhaps the biggest difference.
So let's just consider that first period, so the lamb is born, . And we hope that it hits the ground, the U turns around, licks it, it gets up and it suckles, and off we go, and everything's fine. If .
There is, if it's a tight lambing or there's some dystosia then. And prolongation in the, in lambing, then the lamb can suffer from birth stress. This is a a sort of secondary hypoxia due to prolonged lambing, and can result in hypothermia.
And hyperglycemia, such that the lamb just takes longer to get going. If it takes longer to get going, it doesn't suck colostrum. If it doesn't doesn't suck colostrum, it, it's, it's harder for it to maintain its body temperature, and it's also harder for it to .
To, to, to get its energy and, and get started. So, birth stress can just be. A primary cause of morbidity and, and then can knock on and lead to mortality later on as a, as a consequence of not getting up and not sucking colostrum.
These lambs, if we bleed them, often have, metabolic acidosis, and this can cause sort of, short term depression of the lambs. So, that can sort of slow it down as well. So shepherds, shepherds are very well aware of this, and, and I'm sure you are as vets, lambs that, that suffer from dystopia need more attention because they're.
Likely to to be slower to start and slower to suck Colostrum and then that has all the knock on. Consequences. Primary hypothermia can occur as well, .
Risk factors for this, include outdoor lambing flocks. I mean, it's not rocket science, the, outdoor lambing, they're more exposed to the elements. And er particularly if it's wet conditions, lambs don't dry off and they haven't got the wool density there to trap the a layer of air to to maintain body heat.
Primary hypothermia is more for the lambs is more common in lambs born to younger ewes, these ewes just tend to be less attentive mothers, and particularly ewe lambs or yearlinger or . Or shelling ewes tend to produce slightly smaller volumes er of of slightly less good quality colostrum, so the lamb needs to ingest more to get the same energy benefits from that. There's several studies that show associations between, small birth weight lambs and all disease.
So pretty much any disease you look at, if the lamb is under average birth weight, then it tends to be more at risk of developing disease later. So lambs do have brown fat and if they don't. Get up and suck Colostrum, they will metabolise some of that brown fat to provide some of their energy needs, but a small lamb has less brown fat and tends to metabolise that that faster as well.
So average birth weights for lamb, what should it be? Well, it varies definitely from breed to breed. But, most breeds you would expect lambs to be between 4 and 5 kg, .
So slightly under 4 kg is not necessarily abnormal, but the smaller we go, the more at risk they are of, of disease. Obviously, the bigger they get over that as well, but they, it, it increases the risk of dystopia, and then that has knock-on effects in, in in things like . Birth stress or the ewe needing interventions like caesarean section or something, but but certainly, farmers want to be managing their ewes sufficiently that they feed well enough to to produce lambs that are of the right size, that are not too small, not too big, and there's an art to that and they're only going to know if they weigh lambs, and I would encourage.
You to be encouraging farmers to weigh just a sample of lambs, not every lamb born, but a few, a series of lambs. Let's take 50 lambs born within 24 hours or something in in a large flock and and take a good average of those weights in order to say, OK, well we're, we're at, you know, our average is reasonable, or actually we've got quite a spread. Of weights here and we've got some down at 3 kg, some up at 5.5 kgs and .
And you know, maybe some of the problems we're seeing are related to that. . The way it, there's been, there has been work looking at the best way to weigh lambs, .
And the picture there of a suspended scale with a feed bag is actually been shown to be the most reliable way to weigh lambs. So there are plenty of other ways, but that's the way I would recommend. This is a paper by Rob Christley and colleagues published in 2002 and it looked at a a data set from the 190s and.
In this study, they showed, a strong association between low birth weight and, reduced lamb survival. So smaller lambs were much less likely to survive in this study, compared to larger lambs. And they also, showed that those lambs that had less serum immunoglobulin, were also less likely to survive.
So, i.e., those lambs that had sucked less colostrum.
We're less likely to survive. So it's not, again not rocket science, but it's nice to put some data behind what we already know. So to, how to address primary hypothermia, I think most farmers would, in severe conditions, if they could try and house, sheep, but certainly around us, that, that is often a problem, and I quite like the use of these lambing macks if you haven't seen these lambing macks, I don't know if you can make out in this picture this, thin plastic jacket that the lamb is in.
And these can be used mainly to keep the lamb dry, and if a a lamb is dry, it will stay warm. Even in in, in quite cold conditions. It's, it's the wet that seems to affect them more by preventing the wool trapping a layer of warm air there.
You can buy expensive landmarks that are fluorescent and can be reused, . Oh, these, these are very cheap, so a couple of pennies each and . The lambs will eventually wriggle out of them and you'll find them at the edges of the fields later on, but they, they certainly can help, in severe inclement weather.
So Clostrum, we're gonna bang on loads about Clostrum and hopefully you've seen some of the media attention, this, this spring, as we're sort of trying to, as, as an industry, as a sheep industry, trying to encourage farmers to think again about Colostrum and to think more about Colostrum. It's something that's free, it's already there, and, you'll have seen some of the sort of slogans like colostrum is gold, . And and I think Emily Gascoigne calls it the food of life.
So I don't know, whatever you want to hang on to. . When a lamb is born, it, it needs to have approximately 1 litre of colostrum within the 1st 24 hours, .
So You know, if you're sort of breaking that down into feeds, it's sort of 150 to 200 mLs every 4 or 5 hours. Now, obviously the lamb's own eucalostrum is, is best, and it has the highest density of, of antibodies for the lamb. And Often if you were to bleed a sample of lambs on a farm, and again if you're investigating .
The failure of passive transfer on farms, I'd encourage you to bleed a sample of lambs and, and perhaps carry out a zinc sulphate turbidity test or a sodium sulphate tbidity test or if you can persuade them to do total immunoglobulin, those would be, that would be the most accurate. Or you can do total proteins and, and, and, tests like that, then, . You can assess the the passive transfer in blood and you, when you do this you you often find sort of binary distribution, those lambs have had really good passive transfer and those lambs have had virtually no passive transfer.
And this can be quite helpful to show farmers in order to get them focused on, right, which are the lambs that have not sucked, which of the lambs that have not had colostrum. And for many of the diseases we'll keep coming back to colostrum being a key prevention, and, of disease. So, as I said, the lamb's own ewe colostrum is certainly the most suitable, but if for some reason that's not available, the ewe is dead, the.
You had triplets or quads and there's not enough there, not enough volume there for, for all the lambs then . You may be able to source eu colostrum off another you. There is a small risk there of transferring infectious disease like yoni's or Madivina, but that's .
That's a small risk compared to the risk of not getting any antibody or or any energy early on, which, which are much more catastrophic. Cow or goat colostrum can be used. Cow colostrum tends to be lower in density of immunoglobulin compared to eu colostrum.
And occasionally, some, cow colostrum has a factor within it which can cause a, a hemolytic anaemia in lambs. There is, or there used to be an assay. Available to test cow colostrum, which I believe ended up at the SAC.
So if this is something you need to do, then I would suggest you select cows that are free of this asset so you can test the Clostrum prior to use. But I very much sort of. Yeah, if you and if you need to use colostrum, you're going to need to use larger volumes to get reasonable passive transfer.
Goat colostrum can also be suitable, but again, you've got disease risk such as yonis or . My division, which is CAE in in goats, and, those, those pathogens can be transferred through the lostrum. And then I suppose as as a, as a last resort there's there are plenty of commercial lostrums available.
These however all tend to have lower provide lower amounts of energy compared to you or goat colostrum and, and much lower antibody levels despite good marketing, so. My approach would be to really encourage farmers to, to put the effort in and even employ staff in order to get good colostrum into the lambs and then, and to try and source new colostrum from their own farm. If that's not possible, then maybe one of these other things and if necessary going around topping lambs up with commercial clostrum, but as a as a as a sort of backup rather than as the as the primary source of lostrum.
Some farmers have switched and just go straight to using commercial lom to every lamb, but I think what what happens there is, is you actually reduce the. The hunger drive on the lamb, so it, it then sucks less of its own mother's lostrum and you can and overall reduce the amount of immunoglobulin transfer, so they should certainly prioritise the lamb sucking eu colostrum over the commercial colostrum and use the commercial lostrum as as a backup if necessary. So, If as a result of dystosia or primary hypothermia or a secondary hypothermia or or something like this, then there's a failure to suck.
Then this can quickly develop to starvation once the brown fat reserves are exhausted. So what can we do about it? Well, if, as a sort of rule of thumb, if the lamb is holding its head up and there is a suck reflex, then .
You can stomach tube. The lamb, with either use colostrum or if or if if there's nothing else com commercial colostrum, but if it's not holding up the head then. If you try and stomach tube it, it can regurgitate the colostrum.
And and then asphyxiate and as aspirate and asphyxiate. So if you can't hold the head and there's no such reflex then don't do that until it's able, able to do that. .
The idea of getting the lostrum in is that it's got an energy source in which to, to warm itself up and obviously. On which to thrive. So if it's not holding its head, you can inject intraperitone, you can inject glucose, which suggests a 20% glucose solution.
So the commercial glucose that we tend to buy is 40%, so you need to have, half dilute this with an equal volume of recently boiled water to ensure that it's sterile. Then the way you do this is to hold the lamp vertically and then to place your needle at 45 degrees to the lamb, so this is the 45 degree angle here. So, and then inject into the peritoneum and you also go slightly to one side of midline, so you don't interfere with the umbilicus.
Suitable dose of a 20% solution would be about 10 mL per kg, so that'd be about 40 mLs for a 4 kg lamb. And if that is warm, that'll also have the added benefit of, of warming the lamb as well. Once it's then holding its head, you can revert to tubing with, with Clostrum.
Just a note of caution, don't try this in lambs with watery mouth disease. In, in about 30% of lambs with watery mouth disease, there's a dilated right, a right-sided dilation, which is the Abemazin, and you can easily rupture this with the needle. .
Which can result in peritonitis and death later on. So ensure that you've got your diagnosis right first because some which will come on to watery mouth specifically but so you know, a cakectic lamb. And one with watery mouths can can look fairly similar.
So we're gonna move on to some enteric diseases. We'll we'll sort of spend some more time on some of these and others and others we'll just whistle through so don't panic too much. So I'm gonna focus on watery mouth disease because research would suggest that this causes about 25% of all .
All of those, lamb losses in, in the first. Few days of life, so it's certainly a major disease. We'd see it more in housed lowland flocks and perhaps in outdoor lambing, hill flocks, but you can see it outside and you can see it in hill flocks as well.
But as as . As I'm sure a lot of you are dealing with housed indoor flocks, then you'll be all too familiar with this. So what are the clinical signs?
Well, the majority of lambs will present within, 12 to 72 hours of age, so it'll initially just present as dull and unwilling to suck. They'll actually be nomothermics, this is how we know they're not, just a hypothermic lamb, which hasn't sucked. And they develop very quickly this watery mouth, which is just saliva drooling from, from the muzzle.
They sometimes have a profuse lachrymation. And it's frequently accompanied by Amazel timpani. They can scour, but it's unusual, and they can be constipated, so often you can find retained meconium.
So There's not necessarily available a specific diagnostic test for watery mouths, so you need to certainly develop good history taking skills to get some of these information and and then a good clinical exam to pick up the rest of it. So what happens as a result, is death tends to occur within 24 hours of the onset of clinical signs, so from the lambs starting to look dull, and we end up with a terminal hypoglycemia. It's used up all the, it's energy reserves because it's not sucking.
It goes cold and there's a lactic acidemia. So these signs you'll find in any caketic lamb. So you need to have the history and the other clinical signs in order to decide is it watery mouth or is it just the lamb that hasn't fed.
On, as I said, it, it causes about 25% of . Of all land losses, and, from this study, most of the studies on watery mouth disease are now very old, so they're what we've got to go on. But in, in this study from 1986, mortality of affected cases, so of all cases, 83% of them died, so it has a high death rate.
So certainly. We need to focus on prevention and intensive treatment of affected cases in order to to try and bring some of those figures down. And there was this, another study by Collins and colleagues in 1985, which just put put up there and this showed that older lambs that developed watery mouths were much more likely to die compared to to those classic ones within the first couple of days.
So if they're getting to 72 hours old or or or 4 days old, then . The the the mortality goes up compared to those that develop it earlier and we're not quite sure why that is. So what we find at postmortem?
Well, there's not many abnormalities recorded. The Amazin is often distended with gas and saliva, and clots of milk, and there's only been only one postmortem study, looking at this and, and in that study, they found, inflammatory changes throughout the gastrointestinal tract, . And as I said before, about 1/3 of cases had retained meconium in, in that study.
Anne Cropsey they found evident of a bacteremia and we think this is coming on to sort of the cause of, of watery mouth disease and . We'll deal with that a bit more in the next few slides. This is just a photograph of a lamb, it's not dead, it very much looks, looks that way.
This lamb is, is older. It's had watery mouth disease, and as you can see there, as I've indicated, it's got this dilated Amazin which you can detect as a swelling on the right, right hand side. If you were to, and just to sort of remind you going back, if you were to inject this man with glucose into peritone, you'd be at real risk of, of damaging that with your needle and possibly leading to peritonitis.
So the aetiology and pathogenesis, the clinical signs are well, it's been well shown that they're caused by an endotoxemia, so this has been done in various experimental studies, which have been really well done, carefully, and elegantly they're all done predominantly, . So with, with different study designs, they've shown that just the presence of the endotoxin is enough to cause the clinical signs seen. .
So where does this endotoxin come from? Well, it's, it's the shell around, gram-negative bacteria, so we think it's, it's, it's present as a result of mass lysis of, of, . Of gram-negative organisms present in, in the, in the bloodstream.
In one of the studies they took, E. Coli strains and cultured them from watery mouth cases and they showed that these E. Coli strains and the, the, the type 3 of them, .
Were not known to be pathogenic, so they were considered to be a pathogenic E. Coli, and when they re-injected these back into lambs, they were able to cause clinical signs of watery mouth as the bacteria died and released the the LPS, the endotoxin. So that's all been done experimentally.
But what we don't know is, can it be any E. Coli bacteria or is it specifically these three strains or is, and are, you know, if we, these, these three strains are considered a pathogenic, maybe we, we need to consider them as pathogenic now. And certainly there's much more work to be done to decide.
Is it any E. Coli, is it specific E. Coli, and how does it?
What makes lambs more or less likely to develop the disease. So other studies have looked at the Abemazin and and they've they've shown that in watery mouth disease, lambs have a delayed abemasil emptying compared compared to . Lambs without watery mouth disease.
So there is, there tends to be a delay in abomazy emptying in the healthy lamb for the first few hours of life, and the thought behind this is that if it's delayed when they have that first drink of Colostrum, it allows time for the immunoglobulins to be translocated from the small intestine then into the bloodstream and to form. The, the maternally derived antibodies which we like to detect. In watery mouth cases that that delay was increased in in a in a radiographic study that was carried out.
And there's a thought there that maybe for some reason. That, that delay therefore allows these bacteria to translocate from the intestine into the, into the bloodstream via the normal penocytotic mechanisms which are there to, to translocate the immunoglobulins. So I'm just going to put this all together into a picture so to try and sort of understand what sort of the current atopathogenic hypothesis is, and remember this is still a hypothesis.
It's not been proven. There's some good work to understand each little bit of this, but there's, it's, it's not been sort of pulled apart properly yet. So what we think happens, well, this is my crude representation of a gut, and you must forgive me, I'm not an artist, .
But if you can imagine that bacteria enter the lamb very shortly after birth. And then by the normal pena cytotic mechanisms which exist in the gut to translocate immunoglobulin rather than doing that or in association with transligating immunoglobulin, that some of these bacteria are also translocated into the blood. And when they're present in the blood, the immunoglobulin that's been translocated with them, causes.
Lysis of those bacteria and the release of endotoxin and then we, as has been shown very well, the release of endotoxin, causes the clinical signs seen of watery mouth disease, so that's the current, Working hypothesis, risk factors on farms show that lambs, in, In big litters are more likely to get disease, so triplets are more at risk compared to twins or singles, and that may be related to the fact that some that triplets have got more competition. For the same other, and therefore, potentially get less immer colostrum initially than, than than singles or twins. Again, we've got this association with lamb size, this crops up for many diseases, so smaller lambs are more at risk.
Use of poor condition, this may come back to. Colostrum quality again. If they're in poor condition, they'll tend to melt less well and the immunoglobulin concentration of the colostrum will be, will be lower as well.
Time, . That as a risk factor, it tends, we tend to see watery mouths later in the lambing season than than earlier and maybe this is just a build up of bugs in the environment, if they're a pathogenic E. Coli or an accumulation of pathogenic ones that we have yet to discover.
Colostrum. The, the jury's out on colostrum at the moment. We would strongly believe it to be beneficial and certainly in experimental studies, lambs given colostrum don't develop, and sufficient colostrum don't develop watery mouth disease.
But then when this is translocated into field studies, observational studies, that is yet to be borne out, . So in field studies, we don't find colostrum to be that protective. So there may be other factors going on and it may be that if you've got enough bugs that can overwhelm even a lamb that has had plenty of colostrum.
And again it seems to be more common in in-house lambs again, perhaps because you just, it's more, they're more likely to have in sanitary conditions. So treatment, there's only been two, there's been a few, . Reports of things people have tried, kind of case reports, but no proper randomised controlled trials, a couple of the best sort of .
Pseudo trials if you like, . Show that, these two, so Esal in 1986 show treated clinical cases with neomycin and streptomycin given orally and he also used in some other cases, amoxicillin, given by injection. To all cases he .
He didn't feed them milk because of the bloating and he gave glucose electrolyte solution regularly by stomach tube, left the lamb with the ewe and when it started to suck milk of its own, . He allowed that and he had success in 80 out of 90 of those cases. So that gives me some hope for intensive nursing and and treatment of cases, perhaps using that approach.
Scott and Gser in 1996 also tried a treatment approach again, non-randomized, again non-controlled, but they used amoxicillin and clavilanic acid injection. And also flinnexin, melamine, and again, they use an oral rehydration therapy, and that's quite, quite a small study, only 23 cases, but again they had quite good success in 21 out of those 23 cases. So people are trying to address the under these sort of proposed underlying each pathogenic hypothesis.
Try and kill the E. Coli if there's any left, try and treat this lamb which has got an endotoxemia, giving it, . Fluids and don't give it any milk until it's ready for it.
And again, the non-steroidal there by Scott and Guest I think is to try and address some of the other results of an endotoxemia which can be leaky blood vessels. So what can we do to try and prevent it? Well, we come back to pro promoting adequate volumes of good quality colostrum, and I can't emphasise enough farmers putting effort into colostrum will reap massive benefits.
Going forward for, for all, all infectious disease, but certainly, . We would expect that with watery mouths as well. We think these lambs are ingesting bacteria, and we actually think, there's some evidence to suggest that they ingest it within the sort of 1st 15 minutes of life.
So actually the pens where they use lamb are perhaps the most important pens to focus on. A lot of farmers will put a lot of effort into cleaning out these little individual pens afterwards, and I think that should be applauded and encouraged. But they often put less effort into the larger pens where ewes may lamb, and, and ewes may be housed there for 68 weeks, sometimes 3 months before lambing, so they can be a huge buildup of, of faeces and, and general bugs in that environment, and if it's any E.
Coli, . An insanitary lambing pen is likely to, to cause major problems, and maybe some of the source. Of infection for these lambs.
So, we need to try and help farmers practically work out good cleaning and disinfection protocols. One, thing I've been advising farmers is is just there's no studies to support this, but it's, it's just trying to put all this together practically is OK, you've housed your ewes for 8 weeks, we've got a great big build up of bugs now in where you're about to lamb these . Immunologically naive babies onto.
As soon as that first lamb hits the ground, say, you know your lambing date when you're due to start, so you can wait for this first lamb to drop as soon as it drops, empty the shed of sheep back onto the neck, onto the field, muck it out completely, lib the bottom, re-straw, and put the sheep back in, and now they can lamb straight onto, onto a clean bed rather than just topping it up with straw. Let's completely clear it out after that housing period and, and, . And, and, and start, start afresh and, and the ewes can lab straight onto that.
So that's some one approach I've been. Which I think I've had good success with on farms where I've tried it. It's not going to work for everyone, but, it's something I've tried and it's something I could suggest to try and deal with that, that problem is obviously just adding straw and things can can sometimes not, not really improve things.
And then we come back to giving lambs at birth a dollop of antibiotic. There's certainly a lot of pressure to try and stop this now, and that, and trying to reduce antibiotic use is something I would strongly support. But I just wanted to give to you the evidence for where this has come from, .
So again, back in the, in the 80s, in an experimental model, . There were 3 groups of lambs in this study. One group were colostrum deprived at birth, and then, given, glucose and milk powder.
That's an energy source thereafter. About half of that group developed watery mouth disease later on. In the second group, they were all given, Colostrum.
At birth, and none of those lambs developed watery mouth disease. And in the third group, they were colostrum deprived but given an antibiotic instead, and none of those lambs developed watery mouth disease. They were all small groups and it's a small study, but it was, it was robustly done, and, and so this is where the idea of if we're not sure about Clostrum status then give antibiotics at birth, but actually that study.
Showed that antibiotics could prevent watery mouth disease, true, but also it shows that giving colostrum at birth potentially. Has, has the same effect. So, I know it's hard to try and wean farmers off antibiotics once they're on them, and there are different ways to approach this, but, .
Certainly helping farmers understand. Where things have come from can can certainly bring them with you in the decision making process, . And trying to emphasise the other things they could be doing rather than just putting a squirt of antibiotic down, maybe we can put a squirt of something that is much more useful and long lasting, such as colostrum and has all those other benefits we've been talking about, then, maybe you can help, help with that.
Something again to sort of try and help farmers start with this is to say, OK, well, let's not start with the antibiotic, let's start with Colostrum, and if you, if we don't get disease, then we don't need to use the antibiotic, but if, if we get a disease outbreak, then, you know, maybe we need to go in with an antibiotic at, at, at that time. But I think that, you know, there's many farms that will trial that approach and find they don't need to use antibiotics for, for many seasons. Certainly there was a study where they they tried to use metoclopramide.
This was to prevent disease, and this, the approach here was to try and deal with this perceived abemasal stasis, let's try and get the Abemazin moving. But actually in that study, they, they had to halt it because they got a, a large outbreak of watery mouth disease, and it was only when they went in with antibiotics to, to treat it that the outbreak stopped. So I'm not against antibiotics, but I, I think if we're having to use antibiotics, we've failed with the other key tenets of prevention which are.
Improving our hygiene and, improving lom delivery, and our efforts should be put there rather than just, prescribing antibiotics. I do believe that some people have tried using E. Coli vaccines to give and to use, .
There's, there's nothing published on this that I can find, so, I have, and I have no experience using them, but again this would rely, if you're giving E. Coli vaccines to use to try and create suitable antibodies that still relies on the lamb getting sufficient. Colostrum in and sufficiently early in, in time for it to develop a, maternally derived antibodies within its blood.
So we're gonna move on, I'm conscious of time, . I'm just going to briefly pause on lamb dysentery. It's an important cause of death in, in unvaccinated, flocks and, and lambs that that fail to get clostrum.
You probably remember it's caused by Clostridium perfringence type B and is associated with the beta and Epsilon toxins. It tends to occur in these first few days of age, and it often just presents as a sudden death. You do see hemorrhagic diarrhoea in some cases, but often you just find a dead lamb and it's only really on a postmortem when you see those dark red intestines, that you then suspect lamb dysentery, .
It's easily preventable. There are good vaccines which can be given to use, prior to lambing in order to boost, the antibody concentration within the claustrum for the, for the, for this disease. But again, it's reliant on, good passive transfer, and, lambs actually getting the Clostrum in the first place.
Entoxigenic E. Coli or EE, you may be more familiar with this in carves if you, if you do any sort of amount of cattle work. These are E.
Colis that produce the bear, the K99 or F41 antigen, and, . This causes a toxicenic E. Coli, so the, this toxin causes the the gut to release lots of water and you end up with a secretory diarrhoea, this brown watery brown diarrhoea, .
And Again, prevention is through improved hygiene. It spread, . Through the faeces, and through the diarrhoea, and adequate colostrum intake in order to.
Provide lambs with the defences to fight disease. If you get sick lambs, they need fluid therapy, and, possibly oral antibiotics, and we would suggest to isolate them in order to try and reduce that lateral spread. And obviously it's important that you warn farmers of the zoonotic potential as well.
Cryptospidiosis, again, you may be more familiar with this in calves. It works very similarly in the lamb. It causes a villous atrophy in the distal small intestine, and you end up with a malabsorptive diarrhoea and, a secondary fermentation.
So with a malasorptive diarrhoea, the, carbohydrate moves. Quicker through the gut than you would hope and it ends up in the colon where you get a secondary fermentation. And, and the diarrhoea associated with that.
Again, treatment would be supportive oral fluid therapy and prevention and control would come back to hygiene and improving Colostrum. So it's a bit of a theme as you're probably, probably getting. I want to introduce you to drunken lamb syndrome.
We've no idea how widespread this is, but when I questioned farmers about it, a lot of them have seen it, and, it tends to be, it tends to occur on certain farms and not others. It used to, it's also been known as lamb nephrosis, and it's now been recently renamed as lambdi lactic acidosis syndrome. So we tend to get these sporadic outbreaks, and again, farms that have it seem to know about it and those that don't seem to have no clue, .
So we're not quite sure why it occurs on some farms and not others, but start to ask about it and you may start to find it if you've not seen it before. So I'm gonna show you a brief video of a lamb with mild clinical signs of drunken lamb syndrome. I can.
Let's make this work. So there's no sound. I'm just gonna talk over the top of it.
So this lamb is, is dull. I'm trying to film it and it's, it, it's not that excited to run away from me. I wouldn't normally be able to approach a lamb like this.
You'll note it has a wide base stance. And, as it, as it walks about further as we go through the video, you'll note that it's mildly atactic, so as it walks away from the camera, now you'll see it has this swaying gate at the back end. It's got, it's back legs are, are slightly wider apart than you'd expect, and this is where it gets the name, drunken lamb syndrome from.
So there are two sort of clinical pictures. We see drunken lambs in this sort of 7 to 10 day bracket, and that lamb was 10 days of age. And we also see them much later as sort of a month to 2 months of age, and there's these sort of two clinical peaks.
Lambs typically are attaxic as as in the video there, and they can be much more severely attaic than that. They stop sucking and they become recumbent and depressed, . And if lambs are left untreated, there, there is a 100% mortality rate.
If we do clinical biochemistry on these lambs, we find raised kidney parameters, to raised your ear and creatinine. I mean this is linked back to the nephrosis before. We find the metabolic acidosis there with the decreased bicarbonate, and we find the lactic acidosis characterised by de lactate, and I'll talk to you.
Bit more about that as we go through. If you do histopathology on kidneys of affected lambs, this is where the lamb nephrosis, description comes from. There's damage to the renal tubules and as indicated by the red arrows, they you get these hyaline casts within some of the renal tubules.
But what was what was encouraging by looking at these slides is that there's preser preservation of the basement membrane such that maybe if lambs can be treated, the the kidney could recover function. In, in this paper, I carried out some years ago, . We showed that lambs typically have low bicarbonate concentrations in the blood, so the reference range, we don't normally expect lambs to have bicarbonate at at least 21 millimoles per litre, and the lambs, in this study, they're average.
Concentration of bicarbonate was about 10 milli miles per litre, so very low, which is indicative of a metabolic acidosis. And when we then think, OK, well, where's this acid coming from to acidify the blood, we were able to find that it was caused by this acid de lactate. So what is the lactate?
Well, lactic acid. Is that familiar feeling when. You're running for a calving and your legs are burning, but mammals live in an L optical isomer world, so our lactic acid that we produce, is an L lactate, and if you measure, Lactate on a GDV for a dog, for example, then that'll be L lactate that you're measuring there.
Bacteria live in a world, a D optical isomer world, and so they produced lactic acid. So we can infer that this this D lactate is being produced by bacteria somewhere. There is no reference range for lambs, so this, this is actually a reference range for goats.
So the average the lactate concentration in normal goat kid would be very low, close to zero there this very narrow, . Standard deviation, and you can see here that the, the average the lactate in, in this study was, was 10 so very high. So we've produced this sort of working, pathophysiological hypothesis of of what's happening in these drunken lambs.
Again, we think gut pathogens, whatever they are, enter the gut. We can find it postmortem, we can find villous atrophy, which would lead to increased . Got transit so reduced transit time and .
A malabsorption and a secondary bacterial fermentation here in the colon. We, we know this is happening because we can detect the de lactate which has to come from bacteria and the bacteria are in the gut. And then we can extrapolate data from calves where a similar syndrome happens and also in humans, they've had large chunks of the bowel removed.
The delactate causes the neurological signs seen, and also the, the damage to the, to the kidney. So building on that, pathophysiological hypothesis, we can try and, design a treatment, so we know we've got an acidosis, so, we try to treat this by using oral sodium bicarbonate, and, the administration of antibiotics to try and treat what may be underlying. The way I do this is take a old calcium bottle which is 400 mLs, fill, I, and to that I add 35 grammes of sodium bicarbonate.
And then I fill that up with warm tap water and give it a good shake to dissolve it. And then I give 50 mLs of that to lambs as a single oral bolus. When we were experimenting with this, we bled some lambs to see how their biochemical parameters responded.
So you can see here the de lactate starts at around 10 to 12 here, it's very high, and after a single 50 mL bolus. Given orally This is where it is at 12 hours and this is where it is at 24 hours. So this one hasn't dropped as much, but it's on the way down.
And then if we measure the bicarbonate. This is increased and after 24 hours is, is, is approaching the bottom of the normal range, which would be 21 millimoles per litre. So, and you very quickly get a resolution of clinical signs, often within an hour, and the biochemical parameters take longer to catch up.
In our study of 18 cases, which wasn't very many, but we had a 100% cure rate with those. The, the lactate assay is not very readily available in the UK, so we try to find a proxy for, to help you with diagnosis. Measurement of bicarbonate is reasonably well correlated with .
With the lactate shown in this, this graph here, so it can be used as a reasonable proxy taken with the history, signalment and clinical signs to help you guide you with whether, whether you've got . Drunken lamb syndrome or not, you could often measure bicarbonate using a blood gas machine or you can measure it with an, Old school halico or if you it's it's relatively stable in plasma as well, so you could send it to a laboratory by as long as it gets there relatively quickly, you'll get a reasonable approximation from, from a commercial laboratory as well. This graph here is just to show this was a single farm.
We recorded all the lambs born and when the clinical cases appeared, and you can see we've got these two peaks for when lambs are born on this farm over time, so the lambing period over the along the bottom. And then the clinical cases occurred toward the end of lambing. So thinking about prevention, we think maybe it's bugs coming in, where we want to look at hygiene and Clostrum again.
In this study as well, we also showed smaller lambs that were more at risk of disease. So we'll move on. Just consider another major disease, joint till.
This is usually seen in in older lambs at age 2 to 3 weeks, but it can be seen earlier, tend to get a sudden onset lameness, and often there's more than one joint affected, although you can just have single joints affected. There's variable response to treatment, sometimes get better very quickly, others never get better, . We're still not quite sure of the specific cause.
There's been a few studies looking at this, and the bug that comes up the most is, is Streptococcus dyscalactiae. But in this study by Watkins and Sharp, they also found E. Coli as another, is another cause there, and various other bugs were, were isolated, in that study.
In a more recent, study by, Rutherford and colleagues, they specifically focused on strep disco collection, and they were trying to find where is this bug coming from. And, they took thousands and thousands of samples but failed to find it in most of them. They did find it in, some of the vaginal samples, so it's possible that lamb, that there are sort of carrier ewes.
And lambs nosing around the vagina after birth, may, get the, get the infection that way. So maybe they, they're infected through sucking dirty teats, through infected milk, sucking bits of wool, we're not sure, but certainly. Hygiene, and things like that are likely to help.
So, they they followed that up by sampling various lambs with, joint till and then culturing them and then doing culturing the, the streptoscalactiae from there and then assessing the sensitivity. Of those, isolates to various antibiotics. They found in out of the 25 samples they had, the 20 all of those were resistant to tetracycline, so we suggest you don't go in with, with those as a first line approach, and 24 out of the 25 cases were sensitive.
To penicillin, so treatment, you would try penicillin in early cases, but if the refractive, non-responsive, or later chronic cases then euthanasia is probably the best course of action due to the irreversible joint damage. That's already occurred. If you're getting outbreaks, I would definitely encourage you to take sterile joint samples from euthanized lambs to try and establish the bacteria you're dealing with and also to carry out sensitivity testing so, so that you can back up or change your, empirical treatment plan, and it will give you confidence and the farmer confidence moving forward with treating other cases that may develop.
In relation to joint till, we've got naval i also known as Ophallophlebitis. This is an inscending infection leading to abscessation of the navel. This is often found at postmortem in association with joint ill.
There are various sort of consequences that can develop in the lamb as a result of naval ill, such as peritonitis or liver abscessation, and one specific consequence is hepatic necrovasillosis. With ethnerora, which will show up as sort of a milk spot liver where you've got lots of little white spots on the liver, . In association with the Ophallo phlebitis.
Prevention and control can be successfully carried out through the application of strong iodine within 15 minutes of birth. So this is the time we think the navel is being colonised by these bacteria, and I would encourage farmers to actually squirt iodine, not only on the outside of the navel, but on the inside as well. It's a tube and to actually squirt inside the tube.
And reminding farmers that there's sort of two sides to the, to the navel and both are equally capable of transmitting bacteria into the lamb. Again, those lambs need to receive a good amount of lostrum in order to fight any bacteria that that may miss be missed by the iodine. We'll have a quick whistle stop tour through some, some common trace element and vitamin deficiencies.
Iodine deficiency tends to be uncommon, but, we do see cases, where I am in, in North Wales, in practise here. If it's severe and clinical, then you, you actually get a goitre in newborn lambs, and that, that is quite rare. You can see late abortions, .
Associated with iodine deficiency as well, and you may need, postmortem samples there in order to determine whether that's the case. If you're going to do postmortem then try and take, . A chunk of thyroid for histopathology and try and weigh the lambs and weigh the the thyroids, and if, if the, the ratio of the thyroid weight to the live weight is, is greater than 0.4 grammes per kilo of the live weight, then you should be suspicious of iodine deficiency there.
You actually need probably need to weigh about 15 grammes to get a reasonable sample. In order to decide whether there is a flock problem and not just sort of that's a one-off lamb. So we would encourage you to get on farms and try and, and persuade farmers to let you postmortem 15 lambs to see, see if that's, if that's happening.
Treatment and prevention can be quite simple through the iodized oil injections or oral dosing, 8 and 4 weeks prior to lambing. You can give bonuses, but often these are combined with other minerals, that you. May not need, such as copper, so, .
You know, that can be an expensive way to do it. And I've put a dose for treatment of affected lambs there if they're born alive. Hi Joe, just to let you know we've we've just run a couple of minutes over, so if you're at a good place to start to say, that'd be great.
Yeah, I'll wind up now. So, so the rest of these, . Conditions, I'll let you read in the notes.
I've supplied these with some notes and as I did say there was a lot of diseases to go through. So I'm sorry for running over time, but hopefully, there's been some new information there for, for people as well. I'll just skip through to the summary slide at the end, .
Which, basically we want to think about colostrum, lostrum, colostrum and and managing hygiene on these farms as well. Fantastic, thank you very much for that, Joe. As you say, it's a broad topic to cover with many diseases that are obviously prelevant at this time of the year and hopefully, What you've put through cross will give those attending a good food for thought in terms of if they got any issues over the next day, during the lambing season over the next couple of months.
So please do, post any questions you may have into the Q&A box. It's good to see, some of our regulars joining us this evening, especially Mina from over in California. And hope your ankle is mending Mina.
And also, Patrick and, Windalla as well, who was one of our, speakers at VC. So great to see some of you joining us this evening. So please do put a question, in the question box.
And I, we've got a little bit of time, so I can ask Joe that. One of the questions I was gonna ask Joe, was, it was regarding watery mouth, you were suggesting about, Given the lambs, antibiotics, you know, within the 2, initial 2 hours. How does that sort of sit with, obviously, you know, the movement at the moment in terms of resistance to antibiotics if you're using it as a sort of prevention rather than cure, is there that risk that going forward that that a resistance will build up, or have you not seen any evidence of that yet?
Yeah, there's definitely evidence of resistance when we go and look for, look for it and test it, but I think a lot of places aren't, aren't testing for it. So we're strongly advising people to be reducing their antibiotic use on farms. But what I was trying to do was to show where that had come from originally in, in the literature.
but actually there's strong evidence, certainly experimentally, if not in the field, to suggest that actually watery mouth disease can be prevented with colostrum rather than antibiotics, but maybe antibiotics are needed in an outbreak situation. No problem. And so in terms of from the the farmers that you're dealing with, is it a a a big education or point with them to try and change their way of thinking, as you say, to move them away from.
Antibiotics being the answer to everything, to some of these alternative sort of ways of dealing with some of the issues they're facing and yeah are they open to these or how do you find you can work with them to change their round their thinking? Well, I find farmers resistant to change for, for any, for any reason, but I, I certainly. I think that farmers are beginning to reduce antibiotic use and certainly we're seeing that on the farms we're working with, and when I talk to colleagues in other practises, they're seeing that too, and I, and I think it's, it's it's something that's not likely to change overnight, but something we can start to, to see change by degrees.
So certainly encouraging farmers not to start out using antibiotics, but to use. To change their sort of cluster management instead can, be a way of saying, you're not sort of saying you can't use this anymore, but saying, well, let's try this and see how you get on and, and, and if, you know, if there's a disease outbreak, of course we'll, we'll treat them, but, we might be able to prevent them and you may end up not using any antibiotic, which is also gonna be a cost saving when it, when it can cost about 1 pound of lamb in some cases, so. No, that's brilliant.
So no, so I think. You've must have covered all the key points because we don't have any questions. Mina has just put in say excellent lecture.
I wish it was in Wales and not in California. There's hardly, hardly any lovely lambs over here. Well, I think probably Mina.
There you are, Mina. There's an open invitation and we're not too far, the webinar that isn't too far from Joe, so you could combine it with a visit to us as well up in a lovely, Liverpool as well. But no, as Joe says, he's provided the note, kind of provided notes to go with the presentation, so they will be available afterwards once we've got the, webinar recording up on our website.
So thank you very much for joining us. Thank you again to Joe, for giving your time and, putting across such a comprehensive presentation this evening. And we look forward to welcoming you onto a webinar in the future.
So thank you very much and enjoy the rest of your evening. Thank you. Good night.

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