Good evening, everybody, and welcome to this Wednesday night webinar. My name is Bruce Stevenson, and I am the host of, and chair for this evening's session. First and foremost, a huge big thank you to our sponsors, Protein.
If it wasn't for them, we wouldn't be able to bring you this webinar. So huge big thanks protection. We really do appreciate it.
Little bit of housekeeping for you before I introduce our wonderful speaker. If you have any questions for us, just move your mouse over the screen. Little control bar pops up at the bottom.
Q&A box, click on it, and those questions will come through to us. And hopefully, we will have enough time at the end. If we don't, we will get back to you on those, I promise you.
So tonight's speaker is Victoria Robinson, and she graduated from the University of Edinburgh in 2008 and spent several years in mixed and companion animal practise and completed a rotating internship at the University of Liverpool. She started her residency with Hilary Jackson and Peter Forsyth at the dermatology referral Service in Glasgow in 2017 and became a European specialist in 2020. Tory then rejoined the University of Edinburgh in 2022 as a senior lecturer in veterinary dermatology.
Outside of work, Tori enjoys yoga, Pilates, running, stand-up paddle boarding, as well as being kept really busy by her dog, Lucy. Tori, welcome to the webinar vet, and it's over to you. Thank you so much for having me, Bruce, and thanks again to Protex and for sponsoring tonight's webinar.
So what I normally do at the start of any talk is I'll just declare what my conflicts of interest are. So in the past I've received funding, lecture fees or travel from Siva, Dera Ilanco, ICF, Berece, Nextmun Pet Savers, Verbe and Zoeas, and tonight's webinar is sponsored by Protein. I might actually start just putting in the people that I haven't received funding from.
So my job tonight is to try and keep you awake at 8 p.m. On a Wednesday night, talking about something that I see every single day in the clinic and something that's really important to me.
So what's the outline for tonight's webinar? So we're gonna have a little bit of a discussion about what atopic dermatitis actually is, the clinical signs and breed specific patterns of disease, diagnostics. Therapeutics in induction and maintenance and some case examples.
And I'm gonna point out that this dog at the bottom will feature with in quite a few of the images tonight. This is Lucy, who is my ethically sourced French bulldog who obviously has atopic dermatitis. Why else would a dermatologist re home her, and she's also had two hemilaminectomies in true French bulldog style.
So why does KI atopic dermatitis matter so much to us, especially as dermatologists and as vets. So it affects 10 to 15% of dogs in the UK and if you think about the level of dogs that are coming into your practise on a day to day basis, it's actually a phenomenal number that we're seeing. Most of our patients have got lifelong disease.
We know that canine atopic dermatitis massively affects both the quality of life for the pet, but also for the owner. It affects sleep quality, it affects fatigue and behaviour, and that's particularly noticed in the human side, but we certainly notice huge similarities in our patients. And 25% of companion animal consults are of dermatological disease in the first instance.
That's what they're normally coming in for, let alone the 10 to 15% that we actually have atopic dermatitis. The other thing is that humans with atopic dermatitis also report pain associated with the disease. It's not just itch, and I think that's something that we may be under recognise.
So what is atopic dermatitis? So I've just popped this slide in, so this is Richard Halliwell and the AAA Group's definition of atopic dermatitis, which was updated in 2006, which basically said that this was a genetically predisposed inflammatory and poetic allergic skin disease with characteristic clinical features associated with IgE antibodies, most commonly associated against environmental allergens. However, we're now coming away a little bit from the allergic component, and I'll explain a bit more about that in a in a short while, and we're really now focusing on this being a genetically inherited chronic, recurrent, non-infectious inflammatory potic skin disease, which I appreciate is still a massive mouthful, but it's getting to that point that this is something that's genetic.
We cannot fix it, but we can absolutely manage it. And it's recurrent, it's not infectious, it's not contagious, but we may see it in several pets in the same household. So what's causing atopic dermatitis?
So, genetics, environment and lifestyle are really driving a lot of this, so 50% of the reason why canine patients develop atopic dermatitis is actually associated with their genes. In terms of the environment, we know that a rural setting, woodland walks, and living with other dogs actually is protective against atopic dermatitis, but being allowed to sit on the on the upholstery, being in an urban environment and high levels of smoke appears to predispose to atopic dermatitis. We know the epidermal barrier is abnormal in patients with atopic dermatitis.
We don't know if this is primary or secondary. It doesn't necessarily matter that much, . And and the grand concept of things and I'm gonna talk a little bit more about the barrier shortly.
We have allergen penetration through this. Dysfunctional epidermal barrier and the allergen penetration of is things like food proteins, environmental components so that can be pollen such as grass tree weeds, it can be house dust mites, it can be moulds, and then fleas are also playing a role in some of our patients as well. We've got abnormalities in both the innate and the adaptive immune system, and all of this drives changes within the microbiome, and it's even possible that the microbiome at the beginning is also having an effect on the epigenetics, and this is them playing a role with epiderm barrier and allergen penetration.
So this is just sort of showing that this really is a wheel of disease. So what's important about the epidermal barrier, so we always use the analogy of a brick wall with the keratinocytes being the bricks and the mortar in between them, being this lipid layer. So we know that in dogs that have got atopic dermatitis that their keratinocytes are actually abnormal.
They don't seem to be able to make connections between one another in comparison to dogs without atopic dermatitis. And that's usually when you're growing them in the lab. And we think that's mainly associated with abnormalities in the tight junctions, because we've noticed changes in the .
The level of expression of occlusions, a zon occlusions and lodons in the tight junction. The lipid layer, we've got abnormalities both in the organisation of the lipid layer with decreases in both free fatty acids and in the ceramides, and the nonlesional skin is also affected and there's worsening after exposure to allergens. The surface lipid layer has largely been ignored, but actually there's been some recent studies looking at the surface lipid layer, which is basically what's being released by the sebaceous glands onto the stratum cornea, and there's abnormalities in that in dogs with Westies with atopic dermatitis in comparison to weties without atopic dermatitis.
So it's not even just the mortar that's in the epidermal barrier, but it's also what's being released. Flagran, we've got increased expression in some dogs with atopic dermatitis, and we've also got increased levels of enzymes associated with breakdown of flagran, but we don't know if this is the chicken or the egg in this situation, so we don't know if the change in expression is the barrier trying to replace itself and replenish the damage that's there. Or whether or not that was the primary problem and certainly in humans flagran genetic abnormalities plays a role in a percentage of humans, but not in all with atopic dermatitis, and certainly some of the initial studies that looked at it in dogs were promising and then repeat studies actually didn't show a difference so we're we're still not really sure with what's going on there.
Antimicrobial peptides, so there's increased production, but decreased secretion of AMPs in patients with atopic dermatitis. And then other studies have shown the similar levels of antimicrobial peptides in patients with atopic dermatitis versus healthy controls or unaffected controls. But then there's decreased antimicrobial efficacy when it is released.
So again, we've got abnormalities. We've got an increased pH in our patients with atopic dermatitis. Transepidermal water loss is something that we use to measure the amount of water extruded from the skin.
So as we all know, dogs don't sweat, OK, so they lose heat by panting. Now, I know with my dog, if she has been lying in a position for a prolonged period of time, her axillae are quite damp, which, you know, that's one of her main sites for her atopic dermatitis, and so it just shows me, yes, she is losing water from those areas. There's quite a lot of variation between studies, and it could be associated with the equipment being used, where in the world the patients are, breeds of the patients affected.
So the measurements with tool at the moment, there's a there's definitely a couple of of differences with those. We also know that if we treat a secondary infection associated with atopic dermatitis, we see a decrease in chill and that we know that lesion or atopic skin has reduced hydration. So there's a huge amount of abnormalities just within the skin barrier in the first instance.
So dermalase is a new product, relatively new product that's been brought out by Protexin. So it contains biosphine, which is a yolipid extract, and dermoid, which is hyaluronic acid based extract, and anybody that's really into their skincare from their own point of view will know how useful hyaluronic acid is at retaining moisture in the skin. It helps with plump plumpness, it helps with like early wrinkles as well.
So basically it's gonna help support the dermis and improve hydration. So if lesion of skin and patients with atopic dermatitis has got reduced hydration, then surely this has got to be beneficial. This finger lip is a hyaluronic acid and glycaminoglycans are all shown to increase hylagran expression.
So again it's going back to if this is abnormal or is altered, potentially it's helping the epidermal barrier repair. There's been two papers looking, the first one looking at one of the compounds in the dermals and then the other one looking at topical treatment with the dermal products. So the first one's by Serato E which was in 2016.
So this was looking at an in vitro model of canine skin. And it showed that by adding the sphingolipid compound to the skin, there was increased production of ceramides. And ceramides are really important.
In the lipid barrier, as I sort of mentioned before, ceramides and free fatty acids are decrease in patients with the atopic dermatitis. The second paper by Rosanna Marcella's group looked at using the Dermalese product on dogs with atopic dermatitis. They had two groups, they had a control group and they had a treatment group and in both groups they exposed them to house dust mites and actually what they found is that.
The Dogs that had been pre-treated with the dermales had a reduced cadisi, so that's the lesion score that we use in comparison to the untreated group at week 1 only, and then a significant reduction in PAs at week 8. So this is just two images from that study. So I've just included the figure that looks at the pits scores so you can see the significant difference in the PAs between week 0 and week 8.
There's a bit of alteration with the prior, the timing of the of the episodes of scoring, but if you actually just look at the two clinical images, we've got one image of the treatment group and one of the control group, and that's at the end of the study. So you can see there's a significant difference in actually the lesion development there. So back to our wheel about what atopic dermatitis is.
So we've already said that the epidermal barrier is dysfunctional, we end up with environmental or food or insect allergens coming through, they're picked up by Langerhan cells and the epidermis. And if these Langerhan cells are in an environment where there is inflammation. Then they're much more likely to go to the draining lymph node and set up a TH2 response.
So just added in this image just to try and give a bit of an idea of the 3D. Component to atopic dermatitis is actually happening in our patient's skin. We've got abnormalities in both the innate and adaptive immune system and in patients with atopic dermatitis.
So briefly mention the Langhan cells and the dermodendritic cells. We know that the Lagaha cells, if the keratinocytes are producing what's known as type 2 alarmins, these are cytokines such as IL 25, IL 33, and TSLP that the Langhan cells are much more likely to take the allergen. To the draining lymph node, and some of the things that can activate these keratinocytes to release these type 2 alarmins are things like proteases, and proteases are really commonly produced by things like house dust mites and by some of our pollens and our moulds.
So it's just being aware all of this is playing a role in driving this. Inflammatory pruritic chronic skin disease. Traditionally we've gone with mast cells are cross linking with IGE and that's an IGE mediated form of type one hypersensitivity, but also mast cells can release just because of proteases and that's not via IGE.
We're not just looking at a change with TH2 which is producing more IGE between class switching with IL 4 and IL 13. But also sad normalities in TH1, TH17, TH22, and I'm sure every time I read an immunology paper they've discovered more cytokines and another TH. So don't be surprised if the TH17 and TH22 are new to you tonight.
They're honestly finding new things all of the time, which is wonderful, from our understanding of the pathogenesis because then we can start to look at more targets to try and manage this disease. I've just included a little diagram from Bradley in 2016, which was a study looking at the cytokines produced in skin and 6 hours post challenge 24 and 48 hours just to try to get an idea of what cytokines are there again so we can have a little look at targets. So you can now see by our definition that was updated in 2006 where we sort of said look you know this is associated with IGE.
Most commonly against environmental allergens, how we're really now changing the narrative on that in terms of the level of inflammation and all of the other changes that we're seeing. So what are the most common clinical signs and what's Favro's criteria, it's something that you might hear us talking about. So most vets in practise will recognise patients with atopic dermatitis, and Favro's criteria is something that you can use.
So it's a list here which. Everybody will recognise you and the majority of patients we'll see will develop signs between 6 months and 3 years of age. It's not very common that we see patients developing disease after that point.
It does happen, but it's not as common. If you use a set of these criteria, you're gonna get if you get 5 positive criteria, you're gonna get a sensitivity about of 77% with a specificity of 83%. So basically what that means in practise is you're gonna get 1 out of 6 wrong.
So not every dog is gonna read the textbook and and we're all aware of that. We see differences in breed predisposition and presentation. So sharpies, we tend to see them really affected on the face and on the hind limbs.
Golden retrievers, the axilla, the ventral abdomen, they've often got pedoporritis. This is a breed that we also see echithosis in and actually we see some golden retrievers with echithosis, some with atopic dermatitis, some with both. Westies.
Before, you know, showing favro's criteria where they've got a non-fed dorsal lumbar area, Westies, always want to prove that they're not gonna follow it, and they often do have an affected dorsal lumbar area. We're also seeing a completely different face of atopic dermatitis, you know, we're not seeing lots of staffies or certainly we're not seeing it in the clinic, lots of staffies, lots of boxers, lots of Westies. We are seeing the Frenchy hugs, the cavapo cockapoo, this mix is is just presenting with a huge amount of atopic dermatitis, and then British and American bulldogs.
So what are we gonna do when we see an itchy dog in practise? So this is obviously gonna depend on whether or not you've got a 10, well, 7 minute, 10 minute, 1520 minutes, 30 minute consult time. You know, there's a wide variation in the in the length of time you're gonna have for consult whether or not you're in charity practise and doing open consults or what your time limit is.
You really want to try and get history and clinical exam from a client, want to try and get some diagnostics, treat the secondary infections in any parasites. Reassess them at that stage. And then we're gonna look at reactive versus proactive therapy, so it's just a little bit of an algorithm of things that you can go through.
So when we see cases in the clinic, what are the most important things we want to get from the client. So from a history point of view, we want to know when. So has this been going on for days, weeks, months?
What time of year did it start? Was there anything that the owners noticed that maybe triggered it? So something might be getting the Christmas decorations done, putting the heating on, having redecorations done at home, taking them for a walk in a different place.
Where? So what's the lesion localization? Where was it when it started?
What? What did it look like when it started and were there any changes? Did they notice the patient itching before the patient became erythematist?
Did they notice spots of blood? Did they notice staining of the fur? Did they notice development of alopecia?
So it's all just trying to find out what did it look like, and everybody's got a phone on them, everybody takes 12 million pictures of their pets. So it's really useful if actually they come in with like a little photo diary of what's happening. What's the progression?
So has it waxed and waned, has it steadily got worse? What treatments have they used and always ask about home remedies because honestly, most people's brothers, cousins, aunts, uncles, groomers, friends will have told them what to use, rather than what we're gonna give them in the clinic. It's really important to know about it parasite control for all of the pets in the household, and actually it's also really important to know what sort of animals are in the household.
The last thing you want to do is find fleas in a patient, send them home with an environmental spray and discover that they've got a fish tank that's 20 ft in their house. That happened to me years ago, so that's what I'm saying. You want to ask about the environment, not only the environment that they live in, but do they go anywhere else, so people may have second homes, they may go to the caravan, they may live by the beach, they may live in a rural environment, urban, they may have moved from different areas.
So I always sort of say to clients, I'm not being nosy, it's just really important that I get this information. We want to know about zoonosis and contagion. Just be aware that some clients may show you things that you're not wanting to see.
And we want to ask about travel history. Certainly it's becoming more and more pertinent to ask that question. Not always in association with atopic dermatitis, but actually in terms of other things that they're carrying or potentially therapeutics that we're gonna use that would be contraindicated in other diseases.
Once we've got a history, gonna try and get a a decent clinical exam or doing your clinical exam while we're doing a history depending on how long you've got. You want a general and a dermatological clinical exam and include autoscopy, you'd be surprised how often ears don't look that bad and then you actually have a little look down them, and it turns out the winners have been using these finger wipes and that's why the vertical canal looks really nice and normal, and then you try and look in the horizontal canal and it's full of discharge. You want to get an idea about what's lesional versus nonlesional and have an idea about your primary or your secondary lesions.
And I've just included a little table at the bottom because it can sometimes help us with our sampling technique or where we're gonna want to take, you know, hair plucks from, etc. We always want to rule out anything that looks similar to our patients, OK? And this is all obviously gonna depend on what you find on clinical exam and not on history.
So if you have a one year old French bulldog that comes in with facial, oral facial pedal axilla pruritus, and it looks very obviously like an atopic dermatitis case, there's some other things that you're probably not gonna look at. But some of these other patients here at the bottom can, you know, can be mistaken as atopic patients. Rotorua its parasites, so demodex near trabecula depending on where you where you're practising sarcotes can certainly be an issue in the predilection sites for that are almost identical to the areas of of atopic dermatitis.
Want to rule out any secondary infections and then instead included there's a bit of a rose gallery down here at the bottom. But these are things that you can sometimes see in the summer that can be confused as a as a. As development of atopic dermatitis or as a breakout.
So this little poo at the far end has got Xenophilic folliculitis culitis for folliculosis. We've got a bulldog puppy here with crusting, and this is actually, this is the youngest patient I've ever diagnosed pemphigus foliacious in. And then this is another puppy, and this is a puppy with what we call puppy strangles.
So most patients with atopic dermatitis don't present with any lesions on their face, but we can see these in the summer. PFUV does trigger it, and not all dogs have got facial lesions, or maybe have lesions just purely on the trunk. And ease inophilic folliculitis ronchiosis, we really see that in the spring and summer months and it's thought to be associated with insect bites or spider bites.
Want you to add in this photo, this is one of Tim's with lots of neo trabecula autumnalus so these little orange harvest mites or triggers which again depending where you work, you maybe see them a lot or you or you won't at all so certainly in Edinburgh. We see a lot of these in Glasgow, I rarely saw them. So what things are you gonna do as part of your rule out?
So you're gonna do diagnostics. So I think one of the biggest things that I can say about this is this can be scheduled. If you've got a 10 minute consult and you've done a history and you've done a clinical exam, do not feel bad about saying hi, so, you know, this is what I think's going on.
I need to get a load of samples, can you bring? Dolly in on Tuesday at 10 a.m.
Or just, just make your life easy. The vast majority of patients, this hasn't just happened in the last 5 minutes. They can wait for the diagnostics to be done when you've got time and you can schedule it.
Use your highly trained nursing team. My first job, there were 3 nurses who were just absolutely astounding at doing cytology and. I think between us we really got into our into our dermatology and I'm I'm so appreciative to them as well.
And so using your nurses if they're keen to look at derm samples I think is a is a really really good use of everybody. Place the microscope in a readily accessible area, it does not need to be upstairs in the cupboard in a box with a dust sheet on it. It also doesn't need to be somewhere where it's used by everybody and covered in everything, including dust and oil and muck.
So make sure you keep it clean, make sure you service it and value it. It's a really good bit of kit, you know, a decent microscope's not gonna cost to practise more than 1000 pounds to 1200 pounds, and actually, Given the number of derm cases you'll see daily in companion animal practise, and that's just derm cases, that's not cases that you're gonna want to take a haematology and do a blood smear or look at an FNA or look at a sample from a joint. These are really, really useful pieces of kit to actually have in the practise.
So samples, how can we take them, so cytology, you can either do that direct, so taking the sample directly from the patient, using things like an impression smear, or you can do indirect cytology, that's where you're using something like a Q-tip into the ears, onto the lip folds, tail folds are really good, facial folds are really good for cotton buds. Tape is very malleable, so we use sellotape in our clinic, I've worked in other clinics where we use Scotch tape. I've tried using the supermarket versions that they do not work, so, you know, get a decent tape.
It's really malleable, you can put it into different areas that actually onto lips. Knocking the side of a bit of crust off with your slide and then applying tape to the skin of the of the bit of crust that you've removed is is really useful. And then I've just sort of demonstrated how I tend to loop the tape to stain it and hopefully you guys can see there's a little loop on the end.
Sometimes I do a bridge in the middle of a slide, but actually I find it just create as much mess and I find this is a little bit more useful. Staining when you're doing your staining for cytology again, stiff quick set up, it's not overly expensive, even if you don't get the alcohol as the fixative and you just get ethanol, which is a lot cheaper, and it shouldn't be more than like 120 pounds plus fat for a difficult quick set and that's gonna last you a decent length of time in clinic. So when you've got tape, you don't want to use the first stain, you can air dry the sample .
Usually I just sort of wafted it as I'm going from the patient to the stain. You can heat fix with a lighter if it's quite oily. You need to do 5 to 10 dips per stain, and then you know in between the stains just blot it onto the cotton wheel so you're not contaminating one stain with the next one.
And if you're really short in time, literally put a drop, you you you put a drop of the basophilic stain onto the slide, or you can just quickly dip your sample into into the basophilic stain. One other little tip, if you're FNAing things like lipomas and I know this completely goes against the logic. Once it's fixed, leave it in the alcohol for, you know, the the first step for a prolonged period of time it it preserves the cellular quality and it's a much easier to look at them, and it's always gone against what I thought would work, but it it works really nicely.
And this is usually what our kits will look like at the end of the day and actually that's probably a good day. I think my nurses would say that that can be a lot messier than than that. So what are you gonna look at on cytology, so I've got an image here of loads of intracellular cocky and neutrophils, so hopefully you can appreciate the shape of the neutrophil and we've got loads of cocky sitting in here.
And then this one, and this one's just a patient with malaseia overgrowths, so we've got these lovely little snowshoes or peanuts or Russian dolls, just whatever way you you fancy calling it. And then this is a sample from a disgusting ear, so these are rods with neutrophils. Tychograms incredibly useful, this is a patient with dermatocosis, so hopefully you can see all of the demodex on this slide.
I even after 15 years of being a vet and. 8 years now of really being in dermatology practise, I get so excited when I find Anna Dexter scopies, and certainly, especially nowadays because we don't since we've got Isoyolines, we don't see it very often. This is a patient that came in to see me and they'd been a long term atopic patient and was no longer under control and treatment, and the owner said that, you know, there's lots of hair loss on the patient and this is actually a dog with dermatophytosis, which I wasn't expecting and I was so pleased that I'd done a trichogram and actually found that level of dermatophytes.
Skin scrapes, skin scrapes, you're gonna find a different. Sets of things than a trichogram. So trichogram you can look at the entire length of the hair, you can assess if it's an antigen or tilon, you can look at a bulb for Demodex, you can look at this the length of the hair for things like eggs or dermatophytes or macro melanosomes and then you can look at the tip to see if the patient is traumatised.
The hair or not. Skin scrapes are purely for mites. OK.
So, this is a patient with Modemodex, and this is one with scabies that, we saw during the pandemic, which is a really lovely case. And one of the things I always sort of say is students are often asking about what's the difference between a superficial and a deep skin scrape, and I say, it doesn't matter, you're just gonna scrape the patient. But it's always worthwhile remembering where things are, so.
Kelly Tella, they are crawling and they are cutaneous.arcoptes, they've got suckers, they're in the superficial epidermis, and then Demodex are deep. They're living in the hair follicle.
So trying to remember that the letters are all the same, is just like it's a good way of remembering where things are actually gonna be. So once you've got your cytology findings, what are you gonna do? You're gonna treat any secondary infections that you see.
You're gonna consider the pet and the owner and that's really important because I think we all have patients where we know topical therapy is absolutely not gonna happen. And we all have owners that we know have got incredibly hectic lives. They live in a flat, they have a massive dog, they don't have a shower, they have a, you know, orthopaedic issues or mobility issues where they're not gonna be able to lift a patient into a tub to do a shampoo.
So it's always really important just to ask what can they manage at home. I hate giving clients something home that they cannot use or looking at a patient and knowing I'd really like to give an X, but there's absolutely no way that pet's gonna tolerate it. You want to treat any identified X parasites.
I've put in here it parasite treatment trial, question mark. I think we kind of need to be a little bit more aware of what we're doing with X parasites and whether or not we need to be blanket treating everything all of the time, or whether or not we just need to be thinking a little bit more about what we're doing with these with these treatments. I've just put in some papers there at the bottom that are open access articles that are really useful for guidelines for systemic antimicrobials, and there's two papers by Beal that was in the vet rec in 2013, which actually is now 10 years ago, which is quite horrifying.
There's really lovely images in there about superficial and deep infections and when to use more antibiotic and as well as the antibiotic. Doses that you can use because actually some of the ones in the formulary are appropriate for other conditions but not necessarily for skin disease. Little clinical consensus about malashesia dermatitis, I think that's a 68 page document, but for most vets and practise the 1st 3 pages, which are the summary is really what you're gonna want to have a quick look at.
And then Dan Morris and the rest of the group there including Scott Wise are just looking recommendations for dealing with MRSP infections, which I think we can all say that we've seen more of. With our cytology findings, we might be using systemics, we might be using topicals. I can honestly say I do not prescribe systemic antimicrobials to many patients at all.
Maybe once or twice a week, if that, I'll prescribe systemic therapy. Most of our patients are topicals. Anybody that is used to getting referral letters from me knows how much I like chlorhexidine containing products, .
So there's a whole variety of these, so we've got various different shampoos, different concentrations of chlorhexidine in here, so we've got 2%, a 3%, 4%. We've got CLX wipes, we've got Dixie pio wipes, these are again chlorhexidine contained products. Hypochloric acid, .
This is fusidic acid, this one's with betamethasone. Quite often I'll just use fusidin or flyins, which is the human product, because I don't want the steroid because it's gonna negatively impact the ability to resolve the infection. But there are also other indications where actually betamethasone is really useful.
I just popped in here. You know, I'm very aware, I think we all are about the cost of living crisis and actually these products can be expensive, some of these do not need a prescription, and owners can purchase them online without one, and the vast majority of time clients are very grateful of that information. But something else that we can do is you can use sort of 10 to 20 mLs of thin household bleach in a one litre sprayer bottle that you would get like, you know, spraying roses outside.
Fresh warm water, and so basically making a 0.5 to 0.05% solution and you make up a new solution of that daily.
So things like vein, like Renison, like solosan, these are stable products, so that's why they can be used and left open for a period of time. If you're just, if you're cost conscious, this is actually really nice, it's a same concentration that's used in humans with eczema. So once we've seen our atopic patient in the clinic, we've treated the infection, we've managed it to parasites, if we need to manage them, we know what our baseline itch actually is.
We may have had to use some antipyretic anti-inflammatory treatment while we've been treating this secondary infection, which is, which is really abiosis of the microbiome, but we may need to give something else here, you know, especially the patients are really itchy. We don't necessarily need to give something for the entire time, but maybe a short course of therapy at the beginning can be helpful. Want to repeat the itch score, so you can either do that by PAS, which is, you know, actually in a bit of paper or verbal, and then if patients have got .
Perennial clinical signs, the clinical signs all year round in an elimination diet is really useful. Elimination diet only when required, and the reason I'm sort of putting this in here just now is actually, if a patient has only got summer itch, actually there's no use in doing an elimination diet because you may see a response to diet in August, September time and you put them back in their old food and there's no change, and actually that's because they were sensitised to a pollen in the environment and actually food wasn't playing a role in their disease. So generally we're looking for additional clinical signs like increased defecation, soft stool, flatulence, rumbly tummies, etc.
You want a suitably hydrolysed diet, you want a decent duration, and you want to give them some rescue therapy. So usually we'll start patients with sort of like a 3 or 4 week course of prednisolone or Olocitinib, or you can use Lomab as well if owners can't tablet otherwise . Elimination diets very useful in dogs presenting in the summer that are itching, especially if they're young dogs.
So if they're less than one, absolutely do an elimination diet. Those that have got GI signs, those I've got all year round, but if it's the first time they're coming in, don't go too algorithmic with it because actually you don't yet know what the pattern of disease actually is. I've just popped on some papers that are really useful, so these cats in BMC vet research got lots of information about elimination diets in there.
And Rebecca Rishi's paper is just looking at things that are in these elimination diets that we don't think we're gonna be in there. And then last paper from Petra and Terry, just looking at two different hydrolyzed poultry based diets in patients with chicken allergy, and it's basically why it's really important to know from a dietary history, what foods the patient's been on because even if it's extensively hydrolyzed. A percentage of those patients can still react to the diet.
So what we're gonna do with our induction reactive therapy, so I sort of alluded before that we're gonna use some treatment just try and get the patient into remission. So it kind of depends on where the patient actually is. So if they've got severe, moderate, mild or normal signs, and this is .
A letter, an open access letter to vet erm from Terry Olivery and Frannie Banovich, basically sort of showing the breadth of targeting, and it's usually based on what's done in the human side. So in humans, huge amount of information and and a lot of therapeutics is associated with the epidermal barrier, and then looking at induction and reactive therapy. And our patients were maybe not as hot in the epidermal barrier as we need to be.
And part of that is associated with the levels of studies that have been done, the discrepancies in studies. But actually getting our patients itch free and reducing the inflammation is vitally important, so I've just put in some of the treatments that we'll really use. I'm a big fan of both Pred and methylpred or Apaquel so oppocitinib.
Once their patients are Into induction and we've got that inflammation, the chronic change. Under control, we're then gonna put them on to proactive therapy and that can really depend on what the patient's history is, what the the the lesions normally look like, what their progression is, and we've got a whole host of different options that we can use. We can also look at allergen avoidance and immunotherapy, and I'm gonna talk a little bit more about that.
Systemic treatments can be used, we've got topicals in there and and barrier support again as I was saying before, I think it's something we're not as good at looking at in the veterinary side in comparison to the human side. Part of that is associated with the fact that our patients are really hairy, the vast majority of humans, I say the vast majority of humans aren't as hairy as some of our patients. So one question we get asked a lot about is why would you do intradermal testing versus allergen serology.
And I've just got an image here on the left of a patient with an intradermal test that's got some lovely positives and also a patient we've taken blood from. So what's preference? So we know from studies that have been done that actually choosing the allergens, whether or not you do an intradermal or you do serology doesn't affect the response to immunotherapy as long as you've listened to the history.
So if you've got a really good history and you know where your patient is living, you know you've got, you know, appropriate positive results on testing because you can test any patient and they can have positive results. That doesn't mean to say that they have atopic dermatitis. Atopic dermatitis is a diagnosis of exclusion, and we should only be doing allergy testing if we're planning on doing immunotherapy.
So we've got a couple of the pros and cons on on this on this table that I've popped on there and certainly for most people allergen serology can be done really easily in the clinic. There's a variation between the tests, that's not something I'm. Go into tonight and you've got to get the the time for results and interpretation, as I said, requires practise with serology, but you need to know what's actually relevant to your patient, what's in the environment that your patient is in, what's potentially cross reacting versus what's co-sensitizing.
So as I said, when to test only if the patient and the client can consider allergens specific immunotherapy. Lots of pets have allergy tests done and then nothing is done with that information and actually, you know, it's really a waste of money at that stage. Formulations we've got various different ones intralymphatic, sublingual, subcutaneous, all with different protocols, over the next few years, I suspect as dermatologists across the world have more and more conversations.
I think protocols with these immunotherapies will change and when to test, you need to test the patient when they're symptomatic, so basically you really want to do it. Either when they're showing signs or within 4 to 6 weeks of showing signs or having a flare, you always put a caveat with that. So if I've got a patient that's got seasonal itch and I want to test it in August, I make the owner aware that actually I might have missed some of the tree pollens which will have started January, February time, and if I do it in August, I might miss some moulds that'll be later on in the year.
She's just letting owners know. That there are changes with that. Withdrawal times is another question we get asked about quite a lot and I just popped this paper on just for people to note down and be aware that that paper exists and again it's an open access paper so it's just really easy for you to have a quick look at and know what your withdrawal times need to be.
As I said, how did you choose the allergens to put in your immunotherapy, so history, know the knowledge of the environment, you can't really avoid a lot of allergens, and the number of allergens is really important, so a a vial of immunotherapy only takes so much PNU. So basically a lot of them might be 20,000 PNU per mL. Or a different number.
Now that basically means that whatever the PNU is, you divide it, so the protein nitrogen units, you divide it by the number of allergens you're putting in. So if you want to put in 20 allergens into a vial, the level of concentration of each of those allergens is actually gonna be really small in comparison to you putting 4 in. So it's just being aware of that's potentially why you're not getting a positive response to immunotherapy because you're putting too many things in.
Immunotherapy with other drugs, there's a quite a bit of discussion about this recently in the literature, and I think the biggest thing is actually you've just got to get your patients comfortable. We need to be aware that we've got time taken to them being effective, so we're always saying with patients it's gonna be 3 to 6 months before you're gonna start seeing an improvement, and we're looking for improvement in the next year. Patients we usually break that down into 1/3, so 1/3 of patients are purely controlled by immunotherapy, 1/3 of patients are on immunotherapy plus other therapeutics, but we're able to actually decrease the doses of the therapeutics and other patients without immunotherapy, we weren't able to maintain them, but with immunotherapy actually the rest of their regime works.
We can look at other treatments at the same time like Loyvetmab, Olacitinib, topical glucorticoids, skin battery support are really just combinations of all of this. We want to regularly reassess our atopic dermatitis patients. I think it's really easy for us to get them under control on occasions and send them off and we don't see them back.
And these are just some images of some of the adverse effects that we can see. So patient here has got calcinosis cutus this is on the caudal ventral abdomen, and this was a patient that was on steroids for an immune mediated disease and then started to get what I suspect was pyderma. And then started using different steroids containing products to try and improve clinical signs and actually end up developing calcinoscuti.
This is another patient with calcinosocutis that was on long term prednisolone for management of atopic dermatitis, and then this is patient with gingival hyperplasia associated with cyclosporinus and this is one of the pictures from my supervisor for my residency, which is Hilary Jackson. So I popped in a couple of case examples just to try and finish off. I'm acutely aware of the time, so we've got Jack, he's a 3 year old Westie, he's got perennial itch.
She's itchy all year round, but he's got. It definitely worsens during the summer and the owner knows he's got so much worse after they've walked in a cut barley field. So we've got an image of the dorsal aspect of the paw, we've got a frontal, we've got a draining lesion on this dorsal aspect between digits 3 and 4, and then on the underside, probably got a bit of that barley field still in there, the post moderately erythematous.
So in terms of investigations, we take Q-tip to the top of this, and this is our cytology. So we've got lovely pi granulomatous inflammation, so we've got a macrophage over here, a very hungry and full neutralil with loads of extracellular cocky, and some more in this one and plenty of extracellular cocky as well. Take a sample from the underside of the paw, you'll sometimes see these this is this is pollen and fungal spores, so don't be surprised by them at this time of year, and I took a hair plot and there was loads of demodex, so.
Jack had piogranulomatous inflammation with cocco bacteria, the fungal and mould spores in the palmer aspect, and Demodex and the trichogram, and actually looking that original photo of him, it would have been really easy with that history to have gone, this is a foreign body, and actually that's that's why I ended up seeing him was it was suspicion of a foreign body that wasn't improving. So what did they do with Jack? So he had systemic antimicrobials the secondary deep yerma he had on the on the paws.
Use topical antiseptics said before, massive fan of chlorhexidine. I use an isoxazole, I do prefer fluorolina for patients with Demodex, and that's pretty much because it's got, it's, it's 3 months, it's a long acting isoxazoline. It's also majority fecally excreted, which I feel from an environmental point of view is quite useful.
Gave him analgesia, you know, certainly that pause was incredibly painful, and then followed up with management of the underlying atopic dermatitis. So with Jack, we did an elimination diet. And we put him on immunotherapy and on long term lowy vetab so side to point and actually his atopic dermatitis was really well managed with that regime, but it would have been very easy to have mistaken him at that time of year.
This is another patient, Bruce Bruce is a 2 year old Sharpei. He's got severe facial, ventral neck, limb, and pedal puritus. He's also got recurrent otitis and he is no longer responding to oliinis.
And actually like the vast majority of Sharpies I see he didn't like to be touched, and there are definitely some lovely Sharpies out there. I've met some of them but unfortunately quite a lot of the other ones I've seen are really grumpy. It's important parts of the history with Bruce, he's got mild perennial itch, but he definitely worsens in the summer.
He previously had an elimination diet in the winter, which showed no change and again it goes back to what I was saying before about elimination diet. Doing that in the summer months can be really problematic if the patient has got a seasonal component with pollens cause it can, the allergen level can be so high, it's actually really difficult to assess any response. He goes on lots of different walks, he goes into lots of different areas, so there's nowhere specific that he's actually walked in terms of knowing that he gets walked through a certain type of woodland so if.
Alder and Beach come up on intradermal tests they're definitely going to be significant, you know, he gets walks walked in so many different places. He's not in any parasite control and having a discussion about whether or not the owners can manage topicals when he doesn't like being touched is in another story. So with Bruce, I just got him in and examined him under sedation, so he had diffuse alopecia in the face, he had moderately stenotic ears, this was the pinna and hopefully you can all appreciate the explorations and erythema and crust at the base of the ear.
He had moderate erythema, the axi in the paws and alopecia and the ventral neck, the forelimbs and the abdomen. I described sharp ears as letterboxes. They've got a very narrow opening, and then once you get through that, the rest of the ear can be a lot wider, especially with some of the sharpes that got really hyperplastic skin on the concave pinna.
So investigations, the cytology from the ears, the face, and the paws. I did a trichogram and a skin scrape. I did an intradermal test because I was sedating him.
I knew he'd already had an elimination diet. I knew he flared in the summer. I was seeing him in the summer, and I couldn't examine him otherwise so basically went with.
You know, 12 birds, one stone situation. I did biochemistry, haematology and urinalysis on him as well because he wasn't responding tolocitinib any longer, and patients that are on long term olocitinib really need to be keeping an eye on their biochem and on the urine a couple of times in a year. So we just did everything while he was asleep.
So we had lots of malashesia and cocky in the ears. We had a huge amount of maesthesia in the paws, and the trichogram and the skin scrape were unremarkable. So with Bruce, he had a decent dose of systemic prednisolone, so probably giving him a meg per kg for sort of 2 or 3 weeks.
SID reduced 3 weeks, some analgesia, so big fan of paracetamol. The owners could actually use topicals on Bruce at home. He was a great dog at home.
He just hated being in the vet practise because he hated being in a vet practise, the reason we did intradermal testing was purely so the owners could use sublingual immunotherapy. They weren't aware that that was an option to them. So they previously not wanted to do testing at their primary vet because the primary vet was only aware of injectable forms and their owners and primary vets felt that was just a crazy idea for Bruce.
He was never going to come into the practise, at least for the first couple of injections to get him stable before the owners could do them at home. So we ordered some sublingual immunotherapy for him. Long term Oitti if he actually managed to go back onto, you know, before it wasn't working, it wasn't working because he had a huge amount of secondary infection and actually the time we were able to reduce the dose of oplacitinib, a daily dose for him.
He's on sublingual immunotherapy, we did long term regular ear cleaning with a glucocorticoid cleaner and certainly a lecture about ears and management and atopic dermatitis itself would, would be an hour. And he was on long term chlorhexidine products to treat the secondary infections, and these are just some pictures from his mom, and she sent me these because she was just so happy with his response to treatment. This is him when he first came in, this was him after a few months at home, not with us.
This was his ventral abdomen. And this was his neck. So in summary, K9 atopid dermatitis is a lifelong pruritic inflammatory skin disease.
It's not something we're gonna be able to cure, but we can manage it and we've got a huge amount of tools in our arsenal. We need to be really methodical with our workup before doing reactive and proactive therapy. Don't try and deal with everything at once.
You can schedule a lot of things, OK? You know, trying to extend consult times if you're in a position where you can do a 30 minute consult with somebody. Priced appropriately for a 30 minute consult, then absolutely schedule for that, do all of your tests at that point and have that discussion.
Cytology is key, it's really important to find out what you're actually treating, it's really important to do trichograms and skin scrapes. Remember your flare factors, so these are things like food and environment and parasites. Careful management, communication, continuity are so, so important for these, for these cases, handouts are really, really useful, but continuity with the same vet or the same two vets, if possible in practise really helps with these clients, especially when you're seeing them so regularly.
And if you're not sure about what you're doing, so if in doubt seek someone out, there is always gonna be somebody on the end of a phone, end of an email. End of a website that can give you advice on treating these patients. And if anybody is itching to learn more, I'm so sorry I couldn't stop myself with a pun.
WAVD have got a whole load of free webinars, not just in atopic dermatitis, but an autoimmune disease, not just in companion animal, but also in large animal and exotics. BVDSG, a British Vets erm Study Group, meets twice a year and . And has 3 days of dermatology, ESVD and for any of the vet nurses that are watching, the Merit Awards through the ven dermatology group with John Redmond is really useful and is certainly something to have a little look at.
So with that I'd like to say thank you very much to protection for . Sponsoring tonight's webinar and I'll hand over. Tory, that was absolutely amazing.
Thank you so much. It really was so insightful. And maybe some of the, the old ideas that have been around for a while, were flushed out and, and woken up on this.
So thank you. Big thank you to you for your time. No, thank you so much for having me.
And also, a big thank you to our sponsors, Protein. We really do appreciate you sponsoring these to bring the fantastic speaker like Tory to all of our members here on the webinar vet. So just a little bit of housekeeping.
There've been a couple of questions about, oh, can you go back on that slide? Can we get this? This is all being recorded and it will be up on the website within the next 24 or 48 hours.
You can then go and have a look at it. You can stop it, you can pause it, you And rewind it. Unfortunately, tonight, we cannot go back to those slides.
But do go and have a look at the recording, and then you can get, the names and references of all of those fantastic articles. I know there's some of those that I certainly would love to read. Tori, it was very interesting, to me.
I, I've been a vet for 30+ years. I'm not gonna tell you how many. And to see the changes in the species.
And, yeah, I had to smile at the end with Grumpy Bruce there. Yeah, that, that, was a bit close to home. I'm so sorry, Bruce.
No, we've all had those sharpes that come in and your heart hits your boots before you even start because a lot of them, as you say, just don't like to be touched, especially in the clinic. But it's interesting how those breeds are changing. Yeah, absolutely.
I think, you know, fashion certainly plays a role. And what people perceive as the animals that they want to have and you know, at the moment the cockapoos and cava poos, you know, they're being purported to be hypoallergenic, which is really just for the clients in terms of shedding and actually they're not hypoallergenic at all, but so many of those patients have got atopic dermatitis and they have malathhesia hypersensitivity associated with that. So it's just it's really interesting like I qualified 15 years ago.
There was loads and loads of staff, loads of boxers, loads of Westies, and really I've noticed a change, especially in the last 4 or 5 years, and I probably think in another 1012 years we'll be seeing more of these sort of doodle crosses and other dogs coming through and it'll be interesting to see what happens with the patients with atopic dermatitis, does that face change again? Does the presentation. Are the areas completely different, you know, we get so used to seeing if it's X, Y, and Z, it's this.
But actually, are we going to find that that's not the case with some of these new breeds coming through or cross breeds coming through. Yeah, I mean, Westies were always a walking skin condition until, proved otherwise. And, unfortunately, Frenchy's as gorgeous as they are, they just have a shopping list of problems, and skin is just one of those.
Exactly, skin is skin is just one of them. Exactly. So we got another question for you, which says, which glucocorticoid cleaner do you recommend?
In terms of ear cleaners, so not so much about recommending, it's about actually adding things and so just a nice if it's an ear that's quite syromolytic, so things like epiotic . Serum oral, clean oral can be really quite useful. I use quite a lot of epiotic in the clinic.
And then popping some steroids afterwards down the ear, so hydrocortisone stinate, so cortivans can be used down the ear after you've cleaned it, so leave it like a good half an hour before you pop that in there. You can also spike bottles with dexamethasone, there's lots of different concentrations that you can do that with. Make sure the owners are aware it's off licence, make sure they're wearing gloves when they use it, make sure they invert the product before they put it in the ear.
There's some really nice videos from Deccra available about how to get owners to clean ears. I say to owners, there's lots of ways to clean ears and there's one right way. I'm a little bit militant about it.
And and you know, I mean, I make no apology for it now. I think I've kind of been doing this for a wee while now where I I know when they're cleaning the ears properly and when they're not, and actually sending them the link to those videos is great. It's really, really useful to put clients to a resource that they can use easily, so.
If you're really busy in the clinic, either and you're in a position where you've got nurses that are doing consults and they can show clients how to use products, Amazing. If you're not in that position, because actually we know how busy first opinion clinics are, especially at the moment, then actually videos where people can look at something on YouTube, super easy. Absolutely.
And, and we all know that clients will often say yes in the consult room, you know, yes, I understand, yes, I know how to do it. And then go away and tell the receptionist that they have no idea what you're talking about. But a link to a, a video is absolutely fantastic.
Another question that's come through is, all the, the sort of derm products that contain antibiotics, whether they're ear washes or, or, you know, topicals and that, is this a concern to you, especially with all the antibiotic stewardship? So I think it depends on whether or not we're talking about antiseptics versus antimicrobials, so. Most, you know, shampoos, mousses, wipes, solutions, sprays in the UK and Europe are almost all chlorhexidine or hypochlorose based in the states that's different, you know, we have ketoconazole containing products there, that's a different kettle of fish, but in terms from a European point of view, what we have at the moment.
Although we recognise that there are genes associated with resistance, so like the quack genes that are associated with chlorhexidine resistance, we don't have demonstratable clinical resistance. And so it's certainly something that we're acutely aware of and certainly for me, once a patient is stable and I've treated the secondary infection, I'll start changing the topicals. So I'll get them off an antimicrobial or reduce the frequency of the antimicrobial shampoo, put them on something that's balancing or soothing or super moisturising.
Just again, just getting that focus, getting the epidermal barrier better. And then I'll see them back, you know, I might see them after 2 to 3 months and then just reassess the skin and if we're still in a position where there's no secondary microbial overgrowth there, then I can get rid of the chlorhexidine or the hypochlorous acid containing product. And test them on something else.
And I think it's it's being cognizant of that, you know, we're aware of the mess that we've got ourselves into with antimicrobials. We need to be cognizant and we don't do the same with antiseptics. So, topical products by and large, they're at very high concentrations, way higher than what we're gonna get in terms of an MIC or a biofilm production.
So almost always when you're using a topical product, as long as the ear, you know, especially with ears, if the ear is clean, if it's not inflamed, you're gonna have good success with, with most topicals. But the biggest thing with ears is getting them open, getting them clean. Yeah, that's a whole other conversation.
Yeah. Well, I, I, I know Dawn is listening. Dawn, you got to book Tory in to do that ear cleaning and ear maintenance because I think that would be Well, I'm gonna be really weak.
So an eye opener, an ear opener. So that's great. Tori, we're running out of time, but I do have one more question that I'd like to pose to you.
That wonderful diluted bleach solution that you were talking about for treating the skins. One of our attendees wants to know how often would you apply that? Oh, that's a good point.
I put in daily. So make a new every day and use it daily until the patient's in remission. So.
Yeah, once, once a day, new solution each day. I've not had anybody have their sofa or their carpet bleached, but I tend to say stay in a room that you don't really care about until the patients, just so it's one less thing that I have to worry about getting a complaint about I don't want somebody having a bleached bright blue sofa. Fantastic.
Tori, I really look forward to having you back. You have been a wonderful speaker with great information to us. So thank you so much to you for your time tonight.
Thank you so much, folks. To Dawn my controller in the background, as always, a big thank you for making things run nice and smoothly. And from myself, Bruce Stevenson, it's good night.
