Hello and welcome to this webinar on neurological disorders of the goat. Don't lose your head. My name's Ben Dustin.
I'm the president of the Goat Veterinary Society. I'm a vet in practise. I work up in Cumbria, for Tarn Farm vets, Paragon Veterinary Group.
So over the next 45 minutes or so, we're going to have a look at the current UK goat industry, the population figures to date, and how that's made up. Then we're going to have a quick look at how we might approach our goat patients, including a basic clinical examination, clinical parameters, before focusing more a bit specifically at the neurological examination, reflexes, the wheres, hows and whys of what we do next. Then we're going to try and break up the various neurological disorders and diseases, and I find it's generally easier to look at these by the age of the goat that they affect.
So we'll start off by looking at neonatal diseases and disorders, then we'll have a look at the growing kids and finally adults. Tetanus fits into probably all three, so we're looking at that separately at the end. The UK goat population currently stands at about 110,000 goats.
That's actually an increase over the last two years, since the population fell, during the pandemic. We're now starting to get back up to the levels, pre-pandemic. The latest stats that we have available are from October 2023.
The next lot of information will be published towards the back end of this year. It is worth bearing in mind though that this is likely to be an underestimation, and that's because a lot of goats are kept in very small numbers by smallholders and sort of backyard enterprises, and they're not always registered with the relevant authorities and probably don't complete the annual sheep and goat inventory as required by animal health. The UK goat sector is comprised of three main industries if you like.
So that 110,000 goat population is made up by the dairy goat, the meat goat, and the fibre goat. Around about 55,000 dairy goat population currently within the UK. With an average unit size of around 600, the largest can be anything over 5000.
The main breeds involved include salons, Tockenbergs, and alpines and various crosses of the three main breeds. True meat producing goats total around about 16,000, probably a little over that now actually, and primary breeds include burro, and some dairy surplus. There is actually an increasing trend to sort of Billy kid dairy cross meat which is killed out around about 9 months of age for the gourmet goat markets.
Fibre goat production has dramatically decreased over the recent decades. Probably less than 3000 fibre goats remaining in the UK, and true commercial units are pretty scarce nowadays. The main breeds involved are Angora and Kashmir.
The remaining of the population to make up the 110,000 are those kept within the sort of pedigree show smallholder sectors of the industry. How do we deal with goats? What's the fascination and what do we need to be aware of when we're dealing with these patients?
Well, goats are gregarious, they're playful, they're inquisitive, they're into everything and really sociable creatures. They crave stimulation and enrichment, and it's really important that the environments in which we keep them have enrichment provided, otherwise the animals can become quite bored and their behaviours can deteriorate and their welfare is compromised. They're exceptional climbers and the ability to climb or have things to climb upon or hide behind or underneath are really important elements of their environment enrichment.
If you haven't had much to do with goats in the past, it's worth bearing in mind that they are incredibly vocal animals. They will vocalise for a majority of reasons, including sort of pain, discomfort, feed, excitement, thirst, eastre behaviour. And if you're not aware or you have animal goatkeepers who aren't familiar with goats, it's worth bearing in mind and letting them know how vocal goats can be.
And sometimes the sort of the screams and yelps and various calls that they can make can sound quite human, so it can be quite off-putting if you're not expecting it. Goats are browsers. They're not grazers, and this has meant they've adopted a sort of a heads up approach to feeding.
They tend to scan the horizon as they eat, but this has had an evolutionary impact both on their immune function and systems, but also on their development and escape mechanisms as prey species. They've often earned the reputation of being pretty fussy or wasteful. I probably prefer the word selective.
They certainly know what they want. They certainly know what they don't want, and they're also very attuned to the fact that if they pull out a whole load of forage or leave an element of concentrate, if that isn't removed and just simply put back in front of them for a 2nd, 3rd, 4th time. They will simply ignore it.
They're also very fastidious about clean water. Water supply is really important for goats as it is in all ruminant species, but goats will not drink or will very rarely go and drink dirty water. They will rather, they would rather dehydrate themselves than drink dirty water.
So clean water provision is really important. You can condition school goats in a similar fashion to how you might expect versus other small ruminants like sheep, but they do keep a lot of their visceral fat or abdominal fat within the abdominal cavity, so it's not immediately apparent in the subcutaneous tissue, which means it's worthwhile if your body condition score. Taking it from multiple sites, so we tend to use the lumber scoring system as well as the pectoral scoring system, and there's some great diagrams and atlas of illustrations on how to do this in some of the GOAT reference textbooks which I'll highlight at the end of this presentation.
Goats are unlike sheep. They don't appreciate physical restraint, and they certainly don't like being turned upside down and made to sit on their on their haunches. It's best actually if you need to examine individual animals to restrain them individually with a neck collar and an experienced handler at the front end just resting an arm or a hand underneath the chin, and they'll often stand quite placidly and allow you to examine them if you stand like that.
The why, how and where of the clinical examination of the goat becomes really important. History is a good place to start, and it's really important to get an idea of the signalment, a history of the actual unit, what it's aiming to do. Do we have dairy goats?
Are they retired dairy goats? Are they a meat enterprise? Are they pet small holders?
Because this will have an impact on the type of management and environment and husbandry practises that you're going to see on this unit. All of these things will have a bearing on the likelihood of disease or the prevalence of certain disease risks, and it starts to guide you down the routes to find out what could be going on with the clinical patient in front of you. Don't forget to ask about historic disease status as well as what's going on currently.
And as I mentioned on the previous slide about the immune response of the goats being slightly different because of the fact that they are evolutionary browsers, it's worth knowing what their immune status or vaccination status is for certain key diseases, and Clostridial disease would be a big one which we'll come on to talk about in a lot more detail later in this presentation. Where we're gonna do this examination is also important. The area should be light, or at least have means of artificial lighting and also the ability to be made dark, which we'll come on to in the next slide on neurological examination.
Underfoot it should be non-slippery. We don't want the goats fearful that they're going to slip over. Equally, you don't want to be sliding over on your backside if the goat decides it wants to head off at high speed in a different direction.
It should be dry. We should also keep the goat patient in sight and sound of other goats, and that's because being a prey species, they can be quite anxious, fearful, and the behaviours of which they're going to then portray to you will be different if you've got them in isolation versus if they're in sight and sound of other goats. It will keep that coat calmer for investigation and examination as you go forward.
I've touched on restraint in the previous slide, but this is where having an experienced handler can be really useful. Somebody with a reassuring hand that the goat is familiar with underneath the chin, supporting the neck collar as in the bottom left photograph on the screen now can make all the difference in how that goat is going to stand for you, what that goat will allow you to do, pick up each foot individually, literally run your hand from top to bottom, nose to tail. In a manner which is then repeatable, consistent, and this will mean that your clinical examination is both simple, easy to do, time effective, and most likely to give you the most meaningful results out of your clinical examination.
Just briefly, by means of a quick reminder, here we have a table which I've adapted from the Diseases of the Goat textbook by Matthews, the 2009 edition, which gives you the common clinical parameters of the goat. There are some kid and adult differences which are worth bearing in mind when you come to your clinical examination. The bottom right hand image is a reminder that the pupil of the goat has a horizontal slit which can be quite useful actually to bear in mind when you're doing a neurological neurological examination as to the direction of the pupil dilation and the angle of the globe within the eye socket.
We're going to look in a little bit more detail now at the specifics of a neurological examination of the goat, and first and foremost, be aware of the goat patient in front of you, its consciousness, its alertness, and its behaviours. And right from the outset, these sort of behaviours and display of neurological presentations give you a guide as to what areas of the central nervous system may be impacted for. Since the fore and midbrain part of the brain stem, they are generally responsible for mental state, most behaviours and sensory functions, whereas the cerebellum is what's generally coordinating and governing fine motor control coordination.
So straight away a snap judgement call can be made about where we might be seeing a neurological disorder taking effect. It's also worth noting that anything which impairs the vision or hearing of this prey species is likely to lead to sort of the induction of fear-induced behaviours. So the types of behaviours you see displayed could be being directly influenced by a lack of vision or a lack of hearing, and that needs to come into your thinking when you're looking at the neurological examination in front of you.
Reflexes are a really useful way of determining what sort of central nervous system impacts that you're having, but it is worth bearing in mind that for in order, in order for a reflex pathway to work, all elements of that arc must be intact. So for example. Is the lack of a menace reflex in a case of Listeriosis because of facial nerve paralysis caused by Listeria, or is it simply the fact it can't see in an eye because of a previous existing injury or another reason why vision might be missing?
Also worth noting that in goats, the pupil, when you're doing the pupillary light reflex rarely constricts fully fully, so you might find this horizontal slot doesn't decrease to what you might expect in other species where you've got that circular pupil to look at. Goats do respond to noise. And the thing to bear in mind is with their stoic nature nature sometimes that response to a sharp noise could be a little bit delayed.
It's worth using quite a high pitched noise to try and get their attention. If the goat can hear, it should be looking straight at you. It should respond by turning its head towards you.
Gag and suck reflexes can be quite easily elicited by palpation of the larynx and should induce a simple swallow, which it could be easy to see. When it comes to examination of the goat's gait and posture, it's worth trying to work out whether the animal is ataxic or weak. Ataxia actually means a lack of order which results in sort of irregular, unpredictable movements which can be exaggerated by forcing certain behaviours or movements.
For example, if you force the goat to circle or force it backwards, you might get a more. Exaggerated atay response where the movements become quite stilted, irregular, they might stumble. Weakness is generally a consistent manifestation of a neurological disorder.
So if you were to lift a leg, for example, it's like to make that worse. You're not going to get a sort of a stumbling or unpredictable response. You'll often see the contralateral leg sort of tremoring away.
It's a consistent weakness that you find. You can try and elicit and exacerbate a situation by doing these challenging movements. I've just suggested circling or making the goat move move backwards.
You can also lift legs, as I've said, the wheelbarrow test which you might be familiar with when looking in neurological examinations with sheep. It's also helpful sometimes to blindfold the goat, and that can be quite good for accentuating abnormalities which might be affecting the brain or inner ear, so-called vestibular syndrome. You would generally blindfold one eye and then the other and then both together and see what kind of response you can get.
When the goat is actually recumbent, there are certain reflexes which are going to be more useful than others. The patella reflex is actually quite a helpful and reliable reflex in the recumbent goat. I don't tend to rely too heavily on some of the sort of.
Responses to noxious stimuli, so sort of into digital space pinching, because the goat is quite naturally placid and quite stoic, it can be quite a delay for the goat to actually remove its limb away from that noxious stimuli. Now that's then difficult to interpret. Is that because of an impact of a neurological disorder, or is that just the goat's natural sort of stoic nature coming forward?
There are also differences when we consider neonates. It's worth bearing in mind, for example, that the menace reflex is actually a learned response, so that might be entirely absent until the goat is around 7 days old. And neonates will also quite likely have a sort of mild wide-based stance and often show some mild hypermetria which could be entirely normal.
And as the goat kid grows a little older, grows into its limbs effectively as around 7, 10 days old, those kinds of behaviours then start to start to disappear. Always, as with our previous slide on clinical examination, we need to have a consistent repeatable approach so that things don't get missed. It needs to be simple, and the more you do something in a consistent and repeatable manner, the more time effective it becomes and the more useful what you see becomes in terms of interpretation and giving you a useful indicator as to where you might be needing to look for these neurological diseases and disorders.
OK, so having considered how we would do our clinical examination and then a little bit more of a focused look at the neurological examination, we're gonna move forward now and start to have a look at some of the specifics of the neurological and diseases disorders that we might encounter at various life stages of the goat. First up, we're going to look at meningitis of the neonate, which in goats is most commonly bacterial. E.
Coli is usually the islet, but lots of other different bacteria can be involved, things like Truerella as well as rarely things like clostridial diseases as well. Typically these cause encephalitis and meningitis following a septicaemic or hematogenous event usually from the umbilicus and often concomitant to failure of passive transfer. So these goat kids have a lack of immunoglobulin within the system and are much more susceptible to disease.
Clinical signs can depend to an extent on what areas the brain are affected, though with bacterial meningitis, it's normally a relatively generalised infection across the brain, rarely extending into the spinal cord actually. But where specific brain abscesses do set up, then the neurological impact can be a little bit more specific. Generally, however, we're looking at depression, we're looking at ataxia, some teeth grinding, blindness, and also things like head pressing and potentially sort of circling movements which can be impacted by the location of these brain abscesses as mentioned.
To diagnose these cases, we're really looking at the signalment, the type of spectrum of clinical signs that we're seeing, and we can also do cerebrospinal fluid analysis and send that away for culture and sensitivity, which might actually enable us to be a little bit more specific with our treatment. The response to treatment can also be informative in terms of the diagnosis. If we're going to have any success at all with the treatment of these cases, we have to be on these early.
These are neonates after all. They have very few reserves of either fat, energy source, and also immunoglobulins, particularly, as I've mentioned, the fact that these are often concomitantly suffering from a failure of passive transfer. The antibiotic choice needs to be broad spectrum, generally have gramme negative cover as well, and the ability to cross the blood brain barrier.
So for example, you might want to start off these cases with intravenous trimethoprine sulphur, potentiated sulfonamides. You might also want to Include some intravenous crystalline penicillin if available and probably likely to want to put these on to long term intramuscular penicillin type drugs with broad spectrum potentiated amoxicillin, for example, to create a 7 day minimum course. Supportive therapies are gonna be really important, so nonsteroidals to help reduce, brain swelling, edoema, reduce the pyrexia, which is often apparent.
And then we're going to have to try and nurse and support these patients heavily, and particularly if these have meningitis as a result of a septicaemic event, they're almost certainly going to need intravenous fluid therapy, usually with a, with a crystalloid type solution like heart. Might need to be quite a high rate initially anything up to 40 mL per kg per hour, but keep an eye on these kids on that kind of fluid rate. We don't want to start sending them over into pulmonary edoema if we correct too much of the fluid loss too quickly.
They need to be eating and drinking and taking in some energy, so if they are completely inappetent at the start of your therapy, you will have to use some kind of tube feeding system. But as soon as a weak suck reflex is back, then you can try and encourage them to take little and often milk feeds to try and support recovery. The prognosis seems to be about fifty-fifty, if you can get these goat kids responding to intravenous antibiotics quickly and treatment starts soon enough.
Next we're having a look at copper deficiency and congenital sway back. So this is actually a copper deficiency within the pregnant doe itself, and this leads to spinal cord demyelination in the foetus, the unborn foetus, from around 4 months onwards of gestation. The clinical signs are obviously present in the kid from birth and it becomes a progressive ascending paralysis of the hind limbs first, some generalised ataxia and muscle in coordination.
Diagnosis can be quite tricky because it's not useful really to take serum samples of the kid itself. You could do some liver biopsies of the dose to give you an indication of the copper status within the group, which may then signpost you towards considering copper deficiency and sway back in the kids, but ultimately analysis of the kid's liver is probably the most useful confirmatory diagnosis, which is usually at postmortem. Treatment, I'm afraid in congenital sway back is pretty poor, pretty poor prognosis.
Control really centres and prevention really centres around adequate supplementation of the adults, so the dose, their ration throughout gestation, really important to make sure sufficient copper is there. Now copper is an interesting mineral in goats from the point of view that both goats can get toxicity and deficiency syndromes. Where I'm from originally in the southwest of the UK and the.
At Somerset levels we have very high levels of copper antagonists and high levels of molybdenum in the soil, which means a lot of our goats, the forages and the soils that we graze upon or take the forages from are effectively deficient in copper because of the high level of antagonism of the copper, so the copper is made unavailable to the goats when they eat it. In other parts of the country, the reverse is true, so copper is freely available and they are much closer than or much more at risk of copper toxicosis. So whenever you're looking at copper control and supplementation within a goat herd, it's really important to understand your local farm conditions, the forages, the soil analysis, and the copper content, but importantly also.
The antagonists within those products as well, and being able to try and then have a gauge of what's going on inside the goats will be useful and guide you in terms of whether supplementation is necessary or not. The most meaningful way of getting an idea of whether supplementation is necessary within the adult goat, as I've said, is through liver biopsies. So my apologies for the slightly gruesome picture on the bottom left of the slide for this next condition.
Thank you very much to my colleague David Harward for the image. This, I'm afraid, is neurological disease caused by a budding injury. I'm sure many of you will be aware that the disbudding of goat kids in the UK is a vet-only procedure.
But unfortunately there are fewer and fewer vets who are prepared or happy to do budding, which is leading to an increase in these type of injuries and reports or sort of complaints put against vets to the Veterinary defence Society. Essentially this thermal injury is being caused directly to the brain through prolonged contact of the disbudding iron with the skull. So anything more than 23 seconds at a time when the goat skull is so thin in these neonatal kids, bearing in mind these kids are only 345 days of age when they're being disbudded, can lead to this type of thermal injury.
And clinical signs and the neurological deficits encephalitis are usually apparent within 24 to 48 hours, rarely up to up to 3 days later, and they are invariably fatal, essentially that the brain tissue is destroyed. You can often get a sterile suprative infection that sets in after this event as well. For anybody who'd like a little bit more information on disbudding itself, I have produced a webinar for the webinar vet back in 2020 that is available in the Webinar vet library, and there are also several articles that I've co-written in practise, which would be a good place to start if you need more.
On disbudding. I should just also point out that at the Goat Veterinary Society, we'll be conducting some disbudding, CPD opportunities over the next 18 months or so. So keep an eye on the Goat Veterinary Society website if you'd like further information or further training on the disbudding of Goat kids.
A bit of an odd one to finish off our neonatal neurological disease roundup, and we're looking at floppy kid syndrome. Essentially this seems to be a metabolic acidosis, but without any diarrhoea, and the kids don't really seem dehydrated. The kids involved are often 3 to 14 days old, and we're not entirely sure of the specific aetiology of this.
There are obvious risk factors. It's strangely enough the biggest sort of fittest in the group or the litter which seems to be affected, and intensive milk feeding systems seem to be one of the biggest known risk factors. There is some thought that it could be linked to some bacterial overgrowth within the rumen, typically E.
Coli, Clostridium species, that kind of thing, but by no means is that a factor in every case. The clinical signs, well, these kids are born healthy. They usually have good passive transfer, and then at a period over 34 days old, we start to see this muscle weakness.
The goat kids almost appear drunk. They appear kind of intoxicated. The tongue can often be seen to be paralysed.
It tends Loll from one side of the mouth and these kids start head pressing against walls looking as if they are pretty drunk and got a got a pretty severe headache and instead of forcing their heads against the walls for a sort of a sense of relief. They often have a degree of ruminal bloat. And it's, it's difficult really to understand quite what's going on.
There's a decent paper which I've put a reference to at the bottom of this slide which is got a lot more information if you want to do some further reading, but in terms of treatment. It can be useful to use a half to 1 teaspoon of baking soda dissolved in a glass of water, which you'll give to these goat kids orally, 2 or 3 times over a 3 to 6 hour period. We're talking about 10 to 20 mL, so not huge amounts, and that's basically designed to try and combat the metabolic acidosis going on inside the kid.
It's quite often a good idea to provide some antibiotics, generally broad spectrum. If the animal is quite severely affected, you might want to start with intravenous potentiated sulfonamides. If the kid remains standing, doesn't become recumbent, then you might want to just go with potentiated amoxicillins intramuscularly.
For a 3 to 5 day course, in all cases, it seems to improve the outcomes of treatment if you withhold milk feeding for at least 24 to 48 hours. As I said, one of the largest risk factors with this particular condition seems to be intensive milk feeding systems. So if you have an outbreak in a group of kids, taking them off ad lib.
Feeding systems of milk is usually worthwhile. Restrict that milk to feeds given by hand and certainly for those clinically affected, no milk for 24, 48 hours. So we're just giving them oral electrolyte solutions and then reintroduce milk after that sort of 48 hour period and see how things go from there.
So we're going to have a look now at some of the neurological diseases and conditions which affect growing kids and certainly one of the most commonly talked about or widely known about would be cerebral cortical necrosis CCN. This is essentially a disturbance to B1 vitamin metabolism inside the rumen and it's usually precipitated by dietary disturbances which alter dramatically the rumen microbiome. It basically prevents the ruin microbiome from creating enough vitamin B1 and allows the growth of other types of bacteria within the microbiome which produce a large amount of thiaminase enzymes which actually then further degrade or break down thiamine B1 within the rumen so there's even less available, so you get an exacerbated thiamine deficiency as a result.
This essentially leads to a degenerative brain tissue condition and that's because there's a link between sodium accumulation and thiamine within brain tissue cells. So this allows sodium to accumulate within brain tissue cells, which allows water to move into these brain cells, get cellular brain swelling and then brain cell death as a result of this increased swelling. Clinical signs, well, as I've mentioned, it's more common in, in growing kids, young adults, but older animals, mature goats are also affected if the right dietary conditions or dietary disturbances predominate.
Typically it's quite an acute onset, a matter of hours, rarely extending into days because the dietary disturbance is often quite a shock event and it leads to quite a rapid alteration to that room in microbiome as we've already discussed. The goats become depressed, they often stop eating, they'll often have this typical sort of star gazing appearance where they will appear to disappear looking off into the distance and actually often blindness is reported. The goats will become recumbent.
They'll collapse, and they'll have this sort of classic epitanosis arched back almost swan necking rigid neck stance, and without treatment, quite aggressive early treatment, these goats will die. This condition is diagnosed primarily on, on clinical signs and the history of a diet change, and potentially via response to treatment. And what we're looking for here is the response to intravenous, vitamin B1 treatment.
As I've said already, it needs to be quite a rapid, a committed treatment response. We're trying to get B1 in probably every couple of hours over that 1st 24 hour period. Then we're putting it onto sort of two daily injections for 2 to 4 days and plenty of supportive therapy.
So these animals will benefit from. Treatments which will reduce brain swelling, potentially steroids if, if not in kid or non-steroidals will be useful if they're struggling to eat or drink, and the provision of oral fluids will also be important. Hopefully if this now works, there's a video on the top left which actually shows a goat recovering from CCN.
So this goat had been sick for around 48 hours. We've been treating it intensively on day one with intravenous B1. On day two it had further injection of B1, and this is day 3, and the goat has managed to stand up still pretty wobbly.
And still see the wide base stance, we've got a little bit of sight back, it seems to respond to the handler coming in front of it. So, this was actually a successful treatment outcome. Perhaps more unusually, we're going to look at CAE, Capri arthritis encephalitis next.
Now we're probably all familiar with CAE where we consider the other types of syndromes that this viral infection is classically associated with, particularly sort of swollen joints, perhaps the mastitis type syndrome. But it is also a cause, of, encephalitis. Just a quick recap on the virus that it is a lentivirus, part of the family retroviridae, it is, transmitted primarily via ingestion, of the, the vireons, in lostrum.
Or milk, but it can also be spread aerosolically as well, whether that be through, through, through milk aerosols within the parlour, even infected blood, via injection guns, and also transplanally. The virus essentially enters through the reticular endothelial system and then makes its way towards its target tissues which include things like the synovial membranes, also lung tissue, and, and other as you might expect. I've already mentioned the other varied clinical presentations, things like the joint swellings and mastitis, but when it comes to the encephalitis, it's actually a leukoencephalomyelitis, and this is most classically associated with kids, so growing kids, hence why it features in this sort of life stage of our neurological disorders and diseases, diseases.
The kids are typically 1 to 6 months old, but true of the lentiviruses generally this is a slow developing condition. It starts off as some in coordination, progressing towards parasis and paralysis. Blindness is frequently reported, but you can get this this nystagmus being evident as well, the sort of flicking tracking of the globe from left to right.
Which can be quite disconcerting when you're looking at it for your neurological examination. Classically, with these CAE encephalitis syndromes, the head is carried in an abnormal fashion, so it's often slightly tilted and off to one side, not so much that the goat will lean or travel to one side, but the head carriage is not in a normal position, not in an upright position. It's sort of held off to one side slightly.
Diagnosing this is usually based on clinical signs and a herd history of infection with Capri arthritis encephalitis virus. Serology can be done and sometimes in in these growing kids, we don't actually have an antibody response elicited yet despite clinical signs, so that's why we talk about a herd history of CAE being prevalent and being important. Unfortunately there isn't a treatment for CAE we don't have yet a commercially available vaccine.
So control really focuses around prevention and these sort of test and cull policies. The SRUC run a CAE eradication scheme, and if you want further information on that, it's definitely worthwhile visiting the SRUC's website and. Also, if you're trying to tackle a CAE problem within a goat herd, please bear in mind the close and interspecies relationship between sheep and goats and the sheep Madivina, lentivirus, and Cara arthritis encephalitis virus in goats.
We do get cross species jumping and the conditions can affect both species. We're considering adult neurological diseases and disorders now, and next up we have Listeriosis. Listeriosis is incredibly common, caused by in goats, primarily Listeria monocytogenes, which is a ubiquitous gramme positive bacteria and classically, as we all know, associated with soil contamination, particularly of silages and forages which we then feed to our goats.
So husbandry practises here in dietary management become incredibly important. A reminder that Listeriosis is a zoonotic or presents a zoonotic risk classically from Listeria associated abortions and abortent materials, but also, you know, you could find that these cases of Listeriosis could be shedding Listeria bacteria within their milk if you're consuming unpasteurized products from the farm and also any of their excretions during clinical phases will also be infectious. Classically, we find that Listeriosis is usually initiated by some kind of stressful insult.
Now that could be diet, it could be weather, some kind of environmental or husbandry change, but often these Listeriosis cases require that stressful initiator to enable the bacteria to really take hold. The encephalitic form usually occurs because of bacterial ingress through abrasions in the oral mucosa. So goats being browsers often will tackle things like brambles, nettles, thistles, which will often lead to micro abrasions within the oral mucosa.
Now if they're then eating. Forages soil with soil contamination within them. These bacteria, the Listeria bacteria have an easy access point across that mucosal barrier which allows them entry to the nerve endings within the mouth, and this bacteria can then travel ascendingly up the cranial nerves and then create focal mic.
Abscesses within the brain stem classically. Now the clinical picture, the clinical signs that you then see are often dependent on where these focal micro abscesses set up and also the response to treatment and what kind of senses or reflexes you get back or return are often impacted on where these micro abscesses are setting up. Clinical signs then include things like depression, anorexia, they're often actually unable to eat as a result of various facial paralysis or cranial nerve impacts because of the bacterial ingress.
These goats tend to be quite incoordinated. They tend to circle, lean to one direction. The circling and the leading to one direction is often repeatedly one direction, and that can have an impact and direct you to where the likely lesion is within the brain stem.
Facial paralysis I've mentioned often manifesting as a dropped ear or autotosis, or drooping eyelids. You can often find one side of the mouth starts to loll, the tongue can protrude, and they often struggle to swallow or masticate because of the cranial nerve deficits. Often death actually results because they are unable to swallow or drink, and often these goats become recumbent.
Diagnosis of Listeriosis or encephalitic Listeriosis is usually based on clinical signs. It's quite a classic and typical presentation. You can do culture and sensitivity of cerebral spinal fluid if you've taken some, that might help to direct treatment, but essentially prognosis is realistically guarded, and that's often because of the extent of the damage and.
So the prevalence of these micro abscesses within the brain stem. If we are going to be successful, we need rapid high dose intravenous antibiotics, classically things like tramethoprim, sulphur, which will cross the blood-brain barrier really quickly and then follow that on with intramuscular antibiotics for an extended course, typically 7 days. You could use potentiated amoxicillins for that extended course after you've finished a 3 day course of your potentiated sulfonamides.
Supportive therapies to try and reduce brain swelling, reduce pyrexia are really important and encourage intakes. Fluids are really important. I mentioned already that often death is a result of dehydration because the coats can't swallow.
So being able to either give oral hydration, maybe even intravenous fluids to your goats in the initial phases is important to make sure they continue to get what they need. It's often necessary to provide some bicarbonate or electrolytes within your oral rehydration therapy because the goats are unable to swallow, they tend to hyper salivate or appear as if they're hyper salivating. In actual fact, they're unable to swallow the saliva they're producing.
So without being able to swallow the saliva, they don't get their own natural ruminal buffering impact from the saliva that they produce. Treatment, prevention, control, we really need to remove the potential sources of the Listeria bacteria prevention, we need to remove any uneaten silage within 24 hours. So Listeria is very able to replicate rapidly when spores are present in the forage once it's exposed to air.
So anything not eaten within 24, 48 hours needs to be removed to prevent the risk. Of exposure, do everything you can producing your forages to reduce the risk of soil contamination and wherever possible, try and prevent any stressful insult which might initiate disease. So find control of diet, little that you can do about weather, but having a good approach to husbandry and environment can help reduce risk factors.
Hopefully we'll have a video here if this works on the right hand side, and this is of a goat. Who is recovering from Listeriosis and still has a bit of a tongue lol. If you look closely to the goat's right hand eye when it turns its head back around, you'll also still see the slight droop the ptosis to that eyelid and the slightly more pronounced third eyelid position on that right hand eye as well.
You can see there's a little bit of movement of the tongue there and and some swallowing. So this is a recovering Listeriosis case. Enterotoxemia is classically a disease of the older or adult adult goat and is associated with Clostridium perfringensy D in goats.
This is an anaerobic gramme positive spore forming bacteria which produces really potent exotoxins, and it's the exotoxins themselves which cause most of the damage and clinical signs. Clostridium Clostridium itself is a commensal found within the intestine, and it is shared in in faeces. Pathologic infection though occurs when these commensal normal levels, low levels of commensal bacteria are allowed to rapidly multiply out of control, usually following some kind of stressful insult.
So that might again be a dietary change. It might also. The environmental or weather alterations, something happens, some kind of stressful insult which, as I say, allows these low level commensal bacteria to rapidly multiply and then leech basically high levels of exotoxins into the system.
Clinical signs, well, we get various syndromes in enterotoxemia. We find these per acute cases which are essentially found dead. The disease kills them so quickly they're often not visible in the clinical phase.
The disease overwhelms them before we can even notice that they're sick. In older goats we tend to find more of an acute pattern of disease where we get this sudden sudden onset depression, very high temperatures, pyrexia, inappetence, and quite marked signs of abdominal discomfort colic. The goats will kick out at their abdomen, will often lie down and thrash, and then get back up.
They quickly developed this very watery hemorrhagic diarrhoea shown here on the bottom left hand side of the images, and you'll often find that intestinal casts, so mucosal lining of the intestine, are shared and that's the bottom right picture there. The disease progresses rapidly with dehydration, head pressing, quite marked ataxia. Blindness is sometimes reported, and these goats tend to sort of collapse, convulse and without very rapid aggressive intravenous therapy die.
Diagnosis, if you happen to see any clinical signs, diagnosis is often based on the clinical signs and the recent history of a diet change, turn out to lush pasture, some kind of stressful event, accidental concentrate overload, for example, these type of things. Postmortem can be helpful in confirming the diagnosis and you can actually demonstrate the presence of the exotoxins via PCR. Treatment right from the outset, you have to recognise that treatment success is poor, limited, particularly when you have a comatose goat on your hands or you have a goat with profuse hemorrhagic diarrhoea.
These are both extremely poor prognostic indicators. If we're going to attempt treatment, then it's going to be pretty aggressive. It's intravenous antibiotics as soon as possible, things which will cross the blood brain barrier again, so potentiated sulfonamides.
It is not uncommon to need to use concomitant potentiated penicillins at the same time to try and hit both the enteric and blood brain barrier. And bacteria. Support supportive therapies are going to be really important, so non-steroidals and intravenous fluids to try and replace what is being lost will be necessary.
Sometimes gut active astringents, activated charcoals, things like that can be useful, supportive measures. Quite a few anecdotal reports of B1 supplementation being helpful. The mechanism for that is not entirely.
Understood, but it might go some way to trying to reset the ruminal microbiome and try and enable basically the healthy bacteria in inverted commas to recolonize and reset within the microbiome to try and outcompete some of the Clostridia, which is basically overwhelming the goat with exotoxin formation. Vaccination is clearly the mainstay of prevention and control, and although we're not going to discuss it in too much detail within this presentation, there are other presentations within the webinar vet library, which I've done on herd health planning which talk about the Clostridial vaccination. Programmes and approaches in much more detail.
Essentially there is a very useful sort of 5 in 1 clostridial vaccination which covers specifically Clostridium perfringence type D, which really should be the mainstay of your prevention and control programmes, the aim being to reduce severity and prevalence of disease. Quickly, hopefully there should be a video which works on the top left hand picture here, which is a goat recovering from enterotoxinia, one of the few cases I've had which we've been able to turn around, you will see in this video when it starts to play. The sort of very unsteady nature of the goat in recovery, the obvious pain that this goat still remains in, the profuse diarrhoea and faecal staining on the rear end, and then it steps forward and tries to drink.
Mhm The next series of slides relate to metabolic disorders which can all have a neurological component to them. I'm sure most of you will be familiar to dealing with metabolic disorders in other ruminant species, so I'm not going to go into too much detail about the whys, where's, and how's, but a very quick overview, our first one being hypocalcemia, so low blood calcium levels. It's actually reasonably uncommon in goats, typically occurs in late pregnancy, often before the goat actually kids.
And can be precipitated by stress, so moving within the herd and flock or different fields, things like that. Clinical signs presenting as reduced appetite. Often these goats become really lethargic and quite unsteady in their gait.
Then they can obviously develop recumbency, bloat and constipation, and failures to treat will usually lead to mental depression and death as ruminal bloat kicks in and actually impairs respiration. Diagnosis typically based on clinical signs, stage of gestation, and often the response to treatment. It can be quite difficult to differentiate between the main metabolic disorders associated with this stage of pregnancy.
The hypocalcemia milkpheia, meek fever, hypomagnemia, so staggers, and also hypoglycemia, so called ketosis or twin lamb twin kid disease. So frequently treatment will offer all three products really, so calcium, magnesium, and some form of glucose supplementation. Specifically for hypocalcemia, we're looking at a very slow intravenous injection of ideally the 20% calcium brogluconate.
In the UK, the 20% small rubinant version has been discontinued, so we're often forced to use the 40% cattle product, and we would simply halve the dose rate given. Remember to give something, subcutaneously as well, just to force a slightly longer, slower release form of treatment. Moving straight along to hypomagnemia, so tephy or grass staggers, again, a a common metabolic disorder which I'm sure you're all familiar with and basically is low blood magnesium levels within the body.
Relatively rare in goats because goats tend to be browsers rather than grazers, which means they're often going to be able to eat a variety of forages and plant materials which contain variable amounts of magnesium within them and aren't going to be so affected by our dairy cattle are by a lush grass ward low in magnesium or high GI transit rates. Common to our other ruminant species though, goats don't store or can't store levels of magnesium for use within the body, so they must eat daily magnesium to remain within normal biochemical limits. Clinical signs as we'd expect with our other ruminant species, classically hyper excitability.
We often see some muscle tremors, in coordination and twitching, particularly the facial muscles. That seems to be quite a quite an apparent feature in goat grass staggers, particularly the muzzle tends to twitch. It almost appears like they're nibbling, then they become recumbent and they can convulse and rapidly progress to death.
Diagnosis on clinical signs, feeding history, you can take, bloods to demonstrate low serum magnesium concentrations. If unfortunately the goat dies before you get a treatment response, you can confirm your diagnosis or your suspicion of diagnosis, by sample. The aqueous humour of the eye for up to 48 hours after death.
Be sure to take the aqueous humour and not the vitreous humour, the vitreous humour has a different, magnesium concentration within it and won't be useful in terms of the deficiency reading. Treatment handle these cases very gently. Sudden and rash handling can precipitate a sort of catastrophic fatal convulsion.
You can't inject the magnesium sulphate directly IV. However, in very severe cases, you can mix some of your magnesium with some calcium products and inject that intravenously and then put the remainder of your dose under the skin. As I've said already, goats generally, if they're allowed to browse, are much less likely to be affected, but where you have intensively farmed goats who are housed all day, don't have access to browse, then perhaps the provision of things like salt licks can go some way to helping prevent prevent hypomagnemia.
Finally, on our common metabolic disorders, hypoglycemia, so-called pregnancy toxaemia or twin lamb twin kid, and sometimes lactation or ketosis if this disease syndrome presents after kidding. Classically, we encounter this disorder again like hyperagg and hypocalcemia prior to kidding actually happening. It does seem to be a problem of intensively farmed goats or overfed read that as being over fat pets, typically those carrying multiple foetuses.
Essentially, the diet has a lack of energy either because Of lack of actual energy constituents within it or because there's a lack of appetite in late gestation and the goats just physically aren't able to eat enough of the diet to get enough energy to maintain what they need. Rationing does not supply sufficient energy, means then that the goat is forced into utilising its own body fat stores. Now this body fat metabolism of trying to create glucose er leads to feeding into the reb cycle which can easily be overwhelmed, leading to ketone body production.
The brain becomes affected by the hypoglycemia and hyperketonemia, and that leads to an encephalopathy with clinical signs usually manifest as lethargy, rapid weight loss, blindness, head pressing seems to be quite a feature. Of hypoglycemia in goats, they can press quite firmly into the corners of buildings and then they often tend to stumble forward, slip into a coma, and if you're not quick with some intravenous glucose, will die. Diagnosed by clinical signs and the state of gestation, as with the other metabolic disorders, you can take blood samples to demonstrate elevated levels of blood ketones, particularly, BHB, blood beta hydroxybutyrate.
Treatment usually if the animal is still standing and able to swallow oral treatment with propylene glycol and B vitamin complexes to entice the goat to eat can be sufficient. If the goat becomes comatose or recumbent, we're often going to need to give intravenous glucose doses, often in combination with things like calcium and magnesium, because, as I've said before, often these syndromes are indistinguishable from each other in the pre-kidding phase. If we are in the pre-kidding phase and the goat remains refractory to intravenous glucose therapy, then we're going to induce parturition.
Let's get those kids out of the goat because once the energy demands are less, we can try and support the goat, once the kids have been taken away, and see if we can get some response and recovery from that point. We're moving on to consider scray now, an example of a prion disease, a transmissible spongiform encephalopathy TSE. Other diseases within the group include BSE of cattle and also chronic wasting disease, CWD of deer.
Scrapey is a notifiable disease, so if you suspect scray within a goat or sheep for that matter, then you are legally obliged to report that to the authorities. It's a disease which has been known about for hundreds of years, but actually the first naturally occurring goat infection was only confirmed in the UK back in 1975. The disease occurs as.
As far as we understand it, because of an abnormal form of a naturally occurring prion protein, so PRP, and we end up with a disease associated form which is PRPSC, which can accumulate within brain tissue, and it's the accumulation of this protein within brain which leads to cellular vaculation, so holes within brain tissue and associated cellular pathology. Most natural infections are spread laterally, but it's quite rare. Usually you get sporadic cases er cropping up, but once you get scray within more intensive goats rearing systems, transmission rates can actually be quite high.
New infections typically occur via ingestion of infected materials, things like placenta and uterine fluids, and the prion proteins, it's important to note, are extremely resistant within the environment, so very stringent control, cleansing, and disinfection policies are in place for any affected premises often. Once a herd has become affected, total herd depopulation may result, and that holding may remain under a restriction notice, so no goats or sheep allowed on that farm for many, many years after total depopulation. If you want more information on PRP, C and D protocols, there's plenty of information on the DEFRA website, which is worth a read.
Scraping unfortunately is 100% fatal. There is no cure. There is no treatment, and as I've mentioned before, it's notifiable.
So this is a question or a situation where you report the suspicion of disease, the animal may be culled if that suspicion is upheld by the government and testing then is performed to determine whether or not this is scrappy or not. Scraping can affect both sexes. Usually goats are 3 to 5 years old, very rarely, again, largely dependent on infectious load.
Younger animals are affected down to say 9 months of age, but usually this is a disease of adult 3 to 5 year old. The clinical signs of scrape tend to fall into different characteristic changes within the animal. So temperament changes are described in around about 80% of cases, and these temperament changes often appear as sort of a dull, vacant stare.
The facial expressions of the animals are often altered, so they can appear more depressed. Oftenal tooth grind, which is associated with pain, and they sort of lip lick, a sort of a nibbling reflex. Temperament can also be affected in terms of behaviour where the goats can appear more aggressive, more likely to stand their ground or charge.
The appearance of the goats can alter quite dramatically in around about 50% of cases. You get some associated hair loss as a result of nibbling, but you also get increased lying behaviours, so the goats often appear to be lying down more than you would expect. They'll often dissociate from the rest of the herd, and they can also develop sort of head tremors.
Skin irritation is noticed in around about 75% of cases. Unlike sheep, prurituss seems to be less of a common finding, but you certainly do get an increase in grooming and rubbing, and that then philtres through to sort of hair loss around the tail head, top of the head. You do get this sort of scratch, nibble reflex, and you often find the skin becomes a little bit more crusty and you can find secondary infection as a result of that.
Weight loss is described in over 75% of goat cases. Usually, this is because the affected animals have a, have a difficulty, in swallowing because of the brain stem, accumulations of prime protein. Appetite is often unaffected until quite late on, so it seems to be the difficulty in swallowing, which is the cause of weight loss more than anything else.
Nervous signs described in 30% of cases, but you'll notice that throughout the previous categories I've just described, there are elements of nervous signs in each of those, but when we think about predominant or yeah, predominant nervous signs, we're talking about things like progressive ataxia, you get quite a lot of stumbling, a head tremor, and often sort of this. Not quite hyper excitability, but an excessive response to external stimuli of sight and sound, so a high pitched sound can elicit a much more profound effect, a sort of a startled stumbling, backing away response, much more exaggerated than you would expect, and aggression, as I've already mentioned as well. Diagnosis is based on clinical signs and a herd history and really the exclusion of other differentials.
There is no antemortem test for scrape currently, so most of the confirmatory diagnostics are via postmortem, and I've said before, as notifiable you would be reporting these cases and if approved by government, these would be slaughtered and sent for histology, confirmation, and sometimes immuno histochemistry as well. There is a lot of ongoing research into the genetic susceptibilities and genotype resistance of goats to scrapy. We're trying to emulate the success of the scray resistance breeding programme in sheep, and there seems to be a lot of Positive headway in in the last 5 to 6 years.
And there's a fair bit of information available online, specifically relating to genotype resistance, to scraping goats. And I'll put a couple of references in the back for you. Finally, we're going to briefly consider tetanus as a neurological disease, which doesn't quite fit into our life stage system.
We can see tetanus cases throughout the lifespan of our goats, neonatal, growing, and adult. Tetanus, as you'll know, is caused by the Clostridium bacteria, Clostridium tetini, again, Gram-posit, anaerobic spore forming, but it is ubiquitous, this bacteria found in animal faeces and soil, so our risk factors are ever present. Essentially, the bacteria proliferates at any site of entry, so it's usually a sort of a skin puncture wound, maybe the point of tooth loss, or oral mucosal abrasion, a puncture wound on skin from fencing or poor pen architecture.
And what you get is this proliferation and release of neurotoxin which can then infect the peripheral nerves and transport it up to the spinal cord where we get the sustained triggering of motor neuron response which leads to these clinical signs of tetany, this rigidity and continued firing of neurons. Clinical signs can be quite variable, but often a reluctance to move one of the early reported signs and this limb rigidity. The ears are often kept in a high carriage position, unable to be drooped or dropped.
The necks. Extended. The third eyelid often becomes quite prominent.
Constipation and a raised tailhead becomes quite an obvious feature. And once the animal becomes recumbent, convulsions quickly follow, and without rapid intervention, the goat will die. No live animal diagnostics currently, so essentially the diagnosis based on clinical signs, which thankfully are relatively characteristic.
Treatment would be early and aggressive intravenous antibiotics, classically something which again would would cross the blood brain barrier, potentiated sulfonamides, often in combination with potentiated penicillins would be useful. If you have access to tetanusitoxin, that can be particularly useful. Then we're looking at nursing and supportive treatment with nonsteroidals, making sure we can prevent ruminal bloat, perhaps the placing of a trocar, and if we're in the stage where the goat is recumbent and convulsing, sedatives and specific anti-convulsants may be necessary.
Prevention and control centres around the use of vaccination systems. As I've mentioned already previously in other webinars, we talk about Clostridial vaccination programmes in herd health planning available on the webinar vet library, but the vaccine is available, effective, cheap, and should be the mainstay of your control and vaccination programmes. So to summarise, I'd like to thank you all very much for listening to this webinar today, and just to reiterate some of the salient points, goats being incredibly inquisitive and gregarious, they need quite careful consideration with regard to restraint and handling, and that philtres through.
Into your approach to your clinical and neurological examinations. Don't forget the specifics of certain reflexes and techniques, how we can use certain enforcements, blindfolding, for example, to extrapolate the data we need from our neurological examinations. We then started to look at the common neurological disorders of the near date, before looking at growing kids, and then finally adult neurological diseases, including the notifiable disease, scray and finished off by looking at testus.
As promised, here is a list of many of the references I've used and cited within this webinar. I'd like to draw your attention to a couple, please, the reference books by David Harwood and Karen Muller, Goat Medicine and Surgery 2018, and John Matthews' Diseases of the Goat. 4th edition.
2016 within these there are some really useful colour photographs and Atlas illustrations of things like the body body condition scoring mechanisms and lots more information regarding many of the neurological conditions we've discussed in this webinar. I'd like to thank you all again for inviting me to speak to the webinar vet and also to register my thanks to my GBS colleagues, particularly David Harwood for many of the pictures that I've used within it, to Bryony Kendall, Judith, and John Matthews, and also to Nick Perkins for encouraging me to get out on the goat farm both as a student and subsequently as a qualified vet. I'd also like to thank clients of mine, the McPhes, for some of the brilliant images, and wonderful case discussions that we've had relating to many of the neurological conditions that we've discussed tonight.
Thank you.