Good, good morning to everybody. Well, it's good evening or good afternoon, and here it's very early early in the morning, and I'm delighted to share with you one of the, my most favourite topics with regards to dermatology. I love talking about cats.
I really like treating cats and I'm looking forward to sharing the next hour with you, with regards to the diagnosis and management of the allergic cat. The International Committee on allergic diseases of Animals has developed some very sophisticated guidelines for the treatment of atopic dermatitis in dogs, and these are derived from evidence that is based on a very large body of randomised and controlled and trials and systematic reviews. But the issue with cats is that the evidence that we have is really limited.
To a much more limited or smaller body of scientific knowledge. And really, when you look at what's published about cats and you go and actually communicate with other dermatologists who are treating cats, much of the, guidelines that we're utilising and the methods that we're employing are based on uncontrolled clinical trials or consensus among authors. And so, Really, what we, what I've done this morning or, or this afternoon or this evening is to try and use the framework, if you like, of the guidelines that have been published in dogs to help you design, a very structured way of, logically approaching the, both the diagnosis, but also the management of the cats that you see, with pruridic dermatitis, with, itchy skin.
And so what we're going to do is we're going to make an assumption that the cats that we're talking about this morning are cats where we have excluded parasitic causes. So for the cats that you're seeing that are either over grooming or present with crusting or milid dermatitis or alopeciic skin, we're going to Assume for the purposes of this discussion that the ectoparasite causes through things like I guess mites, which I think can be very regionally different in terms of their prevalence, have been excluded by basically skin scrapings and or trichograms. And if you have a bias in your area for disease entities such as Noa Iris or Kyla Tella or feline dematocosis that we've removed that from the diagnostic possibilities by using or implementing either achaocides or in a carocidal trial.
The other issue with, I guess, the database in cats that I tend to include, particularly if I'm working in Asia or Australasia, is that thematophytosis in cats in at least this region of the world in the southern hemisphere, can also often present quite atypically with a pruridic manifestation. So my standard database for a cat that I'm seeing on a referral basis is independent of the reaction. Pattern is a skin scraping to rule out an ectop parasite and at least some screening for dermatophytosis, either using the old traditional woods lamp evaluation.
And if I've got a reasonable index of suspicion for dermatophytosis, removing or plucking hair for either an in-house dermatophyte test medium fungal culture or sending that sample to a laboratory. So on that premise that we've excluded those diseases, the way we're going to tackle today is we're going to use the framework of these guidelines to think about. How we manage acute flares of feline allergy, how we manage the chronic skin lesions of feline allergy.
So in other words, the cat that has a long standing history of requiring recurrent intervention with all manner of, different, therapeutic interventions for chronic skin disease and potentially how we can use interventions to prevent disease relapse. So let's get going. So when I see a cat that comes to me on referral, what I'm thinking about once we've established that the initial database has been handled with regards to ectop parasites and the possibility of dermatophytes, what I'm thinking about with the cat that's had a short history of over grooming or my dermatitis or alopeciic skin disease, what I'm thinking about is, what are my flare factors?
What are the triggers that I need to think about? And those flare factors can be, they seem reasonably basic, but they're very important to consider in a quite structured manner. So in this region of the world, the flare factors that I think about are basically fleas, concurrently often presenting with bacterial overgrowth.
I think that Malaysia otitis is really Undiagnosed as a flare factor in, allergic cats. And then the second thing I think about after I've identified those three trigger factors is how can I then improve the skin and the coat hygiene in cats. And as in where in dogs, we can regularly use shampoo bathing to help us with that particular category in cats, that's not over.
Practical. And then the third thing I'm thinking about is how can I reduce the pruritus and resolve the skin lesions. So that's what's kind of running through my mind as I'm seeing the cat with what I presume to be a short-term history of pruritus, when I've got, you know, maybe 1015 minutes to allocate to that cat in The confines of that particular consultation.
So, do I have fleas as a flare factor? Do I have infection? And is that infection taking place as a bacterial overgrowth?
And how do I need to address that? Does this cat have malay otitis, and how am I going to resolve the pruritus? So let's spend the next, say, 5 or 10 minutes, looking at that.
So, basically, I guess with these flare factors, if we look at the first flare factor of fleas in relation to cats and pruritus, what I guess we recognise in dogs is that there's a very typical reaction pattern that we see in the canine with regards to the distribution and The lesions of flea allergy dermatitis. And all of us recognise that the typical flea allergy presentation is, you know, often acutely papular eruption, more chronically, a range of secondary skin lesions associated with self trauma in a very typical dorsal lumbar tail-based distribution in the dog. And what's interesting in the cat is cats don't follow nearly such prescriptive rules in relation to clinical presentation.
And if you look at the reaction patterns that we recognise in cats, so cats that present with mil dermatitis, cats that present with over grooming, presenting in a very symmetrical, non-inflammatory, alopeciic manner, cats with osinophilic granuloma, cats with head and neck. So-called sort of facial puritus. Really, when you look at the statistical split in terms of a large cohort, and this is a particular piece of work that was published by Stephan Hobi, in 2011, looking at a large multi-center study of cats presenting to European referral practises.
The take home message from this is, it doesn't really matter whether you've got an EGC lesion over grooming associated with Alopecia or millery dermatitis, really, statistically, any of those cats can really have flea allergy dermatitis. So we need to, I guess, move away from the concept that every cat with FAD has a millary eruption, because sometimes, just a single EGC lesion or a cat that presents potentially with non-inflammatory alopecia can be associated with flea bite hyper. Sensitivity.
And then distribution wise, if you look at that drawing up on the right hand side of the slide, you can see that the, the areas that are coloured represent from orange and yellow being the highest areas of lesion representation down to the blue, which is the least. These cats do typify the dog in the dorsal tail, base, and ventral in Englandal distribution. But very interestingly, from my Perspective, I think, is that the head is just as represented with FAD and the cat, which is in quite significant contrast to that that we're seeing with dogs in our practise.
So take our message from this really is that there isn't any specific reaction pattern per se, and that the head and neck, or rather the head per se in the cat can often be involved with flea allergy. And you and I know it's difficult to often Convince owners, particularly those that are cynical about the role of fleas in, skin disease, because definitive evidence can be challenging. Cats that are pruritic will often ingest fleas.
We recognise now that there are these exquisitely allergic cats, and that flea allergies are a dose dependent allergy, contingent really on the dose of the antigen, contingent on, the sensitivity of the host, and it's the Magnitude of the allergy and the amount of antigen that's injected by the fleas during feeding, and that will vary, I guess, the threshold for that will vary depending on the individual patient. And what we need to focus on is not so much necessarily the implementation of good flea control, because I think the recognition is that most of our owners already doing some form of flea control. The key to this is to select.
Products that rapidly reduce flea feeding. Because if you can, independent of flea kill, if you can actually reduce the amount of salivary exchange, then you are reducing antigen access, less saliva gets injected, and therefore, theoretically less allergen or less antigens, injected, and your patient has a reduction in clinical signs. And if you look at the data on The products that most rapidly reduce flea feeding, we're really still seeing, a marked superiority with the three products that are represented on this screen.
So I use, often a combination of spinostat and n and pyrimine cats, for what I call a flea therapeutic trial. And in cats that are very difficult to peel, then I'll use the I doxicarb, which is the Actavil product. And what I'm doing is using that, not As a maintenance programme long term, I'm using this as a tool to assess a response to a therapeutic trial.
So I'm saying, as a diagnostic tool, in the absence of detecting fleas on my patient, I'm overusing, if you like, an extra label dosaging for a short period of time. Sometimes one product, my go to product is usually the spinosad, but in a high flea burden situation with a very Allergic cat, I will combine that with oral night and pyrim. And I'm doing that for a 4 to 6 week period to assess's response to therapy.
So I look at these cats generally in, a, a month, and then if I've got some degree of improvement with my patient, then I'll extend that therapeutic trial, generally for another, 2 to 4 weeks. And so, I guess the question I often get, is, are the newer products, the Iazolines useful and And I think that a foxelana, which is the next guard, which is not yet available for cats, but Floreana is here, in Australia for cats. I don't think that they're, to be frank, that their reduction in flea feeding, it's not that these products aren't highly efficacious.
At 8 to 12 hours, they're all equal, but it's the reduction in flea feeding that we're looking for in the first sort of 30 minutes to an hour of flea contact. I don't think these products, are as good. And so, I guess, just moving forward in the in the interest of time over the graph, there's a nice example of a cat with clear demarcation associated with a distribution pattern that is the caudal part of the cat with very little to see apart from clear, you know, alopecia with hair coat thinning, a cat that would fit into the reaction pattern that we recognise.
As being the so-called non-inflammatory alopeciic pattern. You know, 25 years ago, when I went to vet school, we were taught that these cats all had hormonal disorders and they needed over it. What we now recognise is that the vast majority of these cats actually have organic triggers for skin disease, and they are indeed just another reaction pattern that we're seeing as a Manifestation of, you know, often allergic skin disease.
Here's the cat, 4 weeks into the therapeutic trial, and you can see, even though the hair coat's not perfect, that there's substantive improvement. And this is in the absence of being able to detect fleas on flea combing, or indeed being able to find anything that lesionly represented, anything akin to a flea bite. So, and here's another cat with a nice example of an eosinophilic granuloma complex, no other lesions apart from the caudal thigh, and the lesion associated with the, the lip, and the response to therapy after a flea therapeutic trial.
So take home message here is that fleas can be a trigger factor in cats associated with any reaction pattern, in a distribution that is consistent with what I've described, akin to the diagram, that we need to be aware that fleas can still be a trigger in cats that are taking routine flea control with products such as fipronil, imidoloprid, slamectin, not because these products are not, effi. But because in cats that have an exquisite level of hypersensitivity, it is the reduction in flea feeding that is being compromised by using a product that just simply takes slightly longer to affect a 100% kill. So there's been sufficient feeding happen and exchange of salivary antigen for these cats to still exhibit clinical signs.
And most owners respond quite nicely to that explanation if you're able to give it. Second flare factor that's really overlooked, and this I think is really important to emphasise is that we consistently see, pyoderma as a complication of allergic skin disease in dogs, and we're all very confident that we can recognise pyoderma and we treat pyoderma very effectively, I think, in, dogs, but we often seem to overlook the concept of bacterial overgrowth being a feature that we need to address in cats. And that's because, and if you look at Linda, Vogel nests work in this area with her colleague, Dr.
Yu. If you, if the cats, the clinical Lesions are just very non-specific, and they're also very poorly distinguishable from those associated with the underlying primary disease. So what I mean by this is that cats with, you know, crusting, cats with, papular eruption, erythema, those are things that can well represent, primary allergic symptoms.
And unlike in dogs, some of the specific pustular and epidermal colorette and hyperpigmentation that we see in, in, in dogs just doesn't happen in cats. And so, typically a lesion like this in, you know, a cat with an underlying allergic skin disease, how you would basically approach this cat is, after you've examined the cat and applied your original database, you go through your flare factors. Could fleas be a flare factor with this distribution, potentially, yes.
Is infection playing a role in this cat? Absolutely, because you can see that there's a moist, exudative type. A crust on this cat's face.
So take a slide, use a glass slide to collect an impression smear of this exudate, stain it with diff quick, look at it in-house in the clinic, make a decision on the spot as to whether this patient actually, will require some form of antimicrobial therapy, whether that be topical, which is not often that useful in this particular area of involvement, or whether it needs systemic. Antimicrobial therapy. And this cat also had perineal lesions, ventral interdigital, dorsal interdigital lesions.
And here's the cytology from this cat. It's demonstrating that we're seeing these tetrames associated with bacterial cocci, and we have bacterial overgrowth. This cat needs antibiotics.
And you can see a complete response to antimicrobial therapy, in this particular cat, independent of any other, intervention that we actually, resorted to. Second infection that we need to consider is that cats with allergic skin disease are absolutely predisposed, particularly to Malaysia otitis externa. Malacizia dermatitis is slightly less common in the cat than it is in the dog, but it is a common complication of cats with feline A to P.
These cats present very typically. They itch, they have head shaking and scratching. They have brown to black seruminous exudate in the external ear canal, but you also need to be aware that malaysia can produce overgrowth on the skin as well.
So, once again, it's about applying some very structured rules. Here's another cat with an extremely pure skin disease. So you just start at the beginning.
Do I have a mite, scrape the cat, scream with a Woods lamp, eliminate the ectop parasite, eliminate dermatophytosis. Then you start looking at your flare factors. Could fleas be a flare factor for this cat?
Absolutely. Does this cat have infection? Absolutely.
Cytology, very simple. Either use a tape strip, use an impression smear if the skin is, greasy or moist, look inside the cat's external ear canal. Evaluate whether there's any black, brown, abnormal ceruminous debris, make us prep of that exudate, stain it for bacteria and yeast, and also, you know, look for ectop parasites along the lines of either Demodex or Oodexy in the ears.
And all this can be done in-house, with a good microscope, relatively little equipment, and it makes the Good science and it makes for good economics, because these are things that you should be charging for because they are changing the nature of the way that you manage the case. So here's the rest of this scaly cat. Here's a cat typically with that ceruminous debris that you see inside the, concave pinner and external ear canal, and there's the malaysia, numbers typically lower than in the external ear canal of the dog.
Just briefly to show you that the rex and the sphinx are predisposed to a more generalised form of malaysia that seems to be inherent to that particular breed, much higher numbers of malaysia, the typical pericia associated with the brown exudative material in the proximal claw, these cats generally have a more generalised brown ceruminous exudate on the skin. There's the claws again, once again, high numbers of malacisia. So the take home message with infection is look for it.
And psychologically, if it's there on an impression smear with the cocky on the left, I quite like using erfovisin, which is the convenina product. Some veterinarians are not overly enamoured and prefer to use things like labulox or cephalexin. Cats are inherently more difficult to peel.
That's your decision as a clinician, somewhat biassed by Probably your regional availability of different medications. But my rule in cats is that generally I use cephalosporins if I see cockoid organisms. And if I see rod-shaped organisms cytologically, particularly in the ear, I'll often culture, but my go to fluoroquinolone for cats in that circumstance is marbafloxacin, which is A really nice fluoroquinolone because it avoids the issues with the retinal toxicity that we see with refluxes and take home message is that itraconazole is the absolute go to drug in my opinion, for cats.
The dose rates are there. It's a once a day dosing. It's a, that particular azole is very effective.
And of course for otitis, we're just using the topical. Myconazole clotrimazole combinations. So those are things that we're often doing in conjunction in a, in a patient, say, with a flea therapeutic trial.
So if I've got a cat that I perceive has got fleas as a flare factor and infection as a flare factor, then I'll run those two in alignment. I might have that. Cat on Spinose, perhaps with Capstar, and I might have them on a convenient injection that they would return in 2 weeks to see one of my technicians or a veterinary nurse to get the second injection, and then I would review the cat at week 4 to see the progress on the flea therapeutic trial.
But I think that you speed Things up if you can try and run these things together rather than doing sort of one thing at a time. And I think that it's generally we see much higher levels of client compliance, but also positive responses from owners if we can rapidly improve the status of some of these cats. Now, bathing dogs, bathing cats isn't realistic.
I think that there's a lot of attention paid, as there should be on bathing dogs with acute pruritus in cats. I think that, owners are able to, wipe cats, and I think that if you're in a position where we definitely do have pollen or dust involved in our atopic cats, and we will get To that in the latter part of this seminar in relation to where that fits in in my schema of diagnostic workup. But I do find that if you get owners to just take a normal face flannel in tap water, warm tap water, wring it out and it's damp, that most cats respond very nicely to that strategy where the majority of them are not that amenable to bathing.
So what about reducing itch in a cat that's presented with acute pruritus? Really, we're confined to a much fewer therapeutic modalities of intervention compared to dogs. There's really nice efficacy for or good evidence rather for efficacy of hydrocortisone epinate or cordovans in, dogs.
And there's also limited but good evidence for the intervention. With this product in cats, and I like this product in cats, but I would suggest that you do not spray it on cats. I like using it, applied with a cotton wool ball, because cats seem much more, much calmer than, than when you apply it in that manner than when you spray it.
And I really like it for, prearicular area and, and the pinna, and I'll often use it more corally in cats, particularly with lesions on the trunk and tail base because The sometimes the odour of this product, puts some cats off. So typical lesions where we might use it are, say, for instance, this cat with flea allergy that I showed you earlier, it's useful in eosinophilic plaque lesions once the secondary pyoderma is controlled. So, topical corticosteroids, at least those that are not in ointments or creams that are too, too tenacious and too sticky for cats because they tend to groom them off, I think are quite useful.
I'm an oral prednisolone fan. I use tonnes of liquid, paediatric prednisolone, which is about, it's 5 milligrammes per mal. Ready Pred just happens to be the brand I use.
It is tasteless. It goes very nicely into food. It means that owners are, generally much more likely to comply because they're not battling with having To give a cat pills.
I don't use any long-acting injectable, corticosteroids in cats. And I think most of the cats, where we're using short-term, dosaging, we need to use the 2 milligramme per kilogramme and not be shy with corticosteroids because, they're much more efficacious at slightly higher dose rates for inflammation than the dog, and we need to treat those cats until they're in remission. And if you combine short courses of corticosteroids while you're managing your flare factors, what you'll find is that the corticosteroid courses need to be much shorter.
So I use these just to get cats into remission. I taper them out fairly quickly, and I'm using those drugs to get sufficient traction with reducing pruritus, which I think is in the best interests of both the, the cat and the owner. Limited evidence for Apaquil.
Most people are still asking about whether Apaquils are valuing cats. I don't think it is. I've used it in about 1015 allergic cats where other therapeutics have not been an option.
And my impression is that it's quite poor with its efficacy, and if it's going to work, it's really, seems that you've got to use it at higher dosages in the dog. Than in the dog. So at 1 milligramme per kilogramme, we've got no prospective studies yet.
It's not registered. We don't know about its pharmacokinetics, and we really don't know about its safety. And so it's for me, it's a last resort in a camp where simply nothing else has worked.
So, in summary, I guess the first sort of half of this webinar was to try and encompass the things that we do when we've got a cat, we're seeing a cat for the first time, in our practise. The history is perhaps relatively short and we need to explain to an owner that there are trigger factors associated with itchy skin in. Cats that basically all appear clinically to be very similar.
So in other words, a cat that presents to you tomorrow, or, perhaps next week with my dermatitis in your practise, what I would do is I would scrape it and rule out dermatophytosis. If that, if those are diseases that really have very little regional relevance for you in your geographic region. The way I would approach that cat would be thinking in exactly the structure that I've, helped you, with this morning.
Are fleas a trigger factor for that cat is a therapeutic trial with a rapidly acting, flea product that reduces flea feeding warranted. Could this cat have infection in either the form of bacterial pyderma or malaitsia overgrowth in either The skin or the ear, or both. And how am I going to address that in conjunction with reducing and obviating the lesions and the clinical signs of pruritus, because we have to intervene.
And it's not realistic just to send cats out on antibiotics and flea therapeutic trials and expect an owner to manage with this cat, for several weeks before things start. To settle down. Like, I'm a pragmatist.
I work all day in the clinic. I see cases, I guess, constantly, so I'm very aware of owner, needs and, and, and responses in relation to not obviating clinical signs. So I use a lot of steroids in cats at moderate, what I consider to be appropriate dose rates, and I intervene early, and I go hard, and I Keep those clinical, I guess, courses of steroids reasonably short.
So I would see a cat like this on maybe 10 to 14 days of induction, or maybe 10 days of induction, and then tapering out to have that cat off steroids by the end of week 4. On the premise that if we've got a flea allergy that's causing the problem with a secondary pyoderma, then that cat will be markedly better, basically, over that time frame. Now, so, what about I guess the chronic feline allergic cat?
So this is a cat, right, in a different framework, a different genre. This is, these are the cats that, you know, the record is as thick as your thumbnail, I guess. It's been in and out perhaps of your practise for the last 2 or 3 years on intermittent Depimentro, intermittent prednisolone courses, it's the cat that You know, you hide at the back and hope your associate sees it, because it's generally attached to an owner that's not happy, or it's a cat where people have been vet shopping and they've been to 2 or 3 different, veterinarians seeking advice for what is essentially a chronic and recurrent problem.
There, More challenging. I get that. And they're the cats that, I mean, I guess that most of the dermatologists or people who are seeing dermatology as a second opinion tend to see.
And of course, compliance, in cats with chronic allergic management, that's what cats think too, basically, when it comes to, I guess, long-term disease. So how do I approach these? The bottom line is, is the flare factors are the same.
OK, so that list looks exactly the same as the one that we shared with the acute cat. Fleas infection are the first things that I think about. But then what I add on to my list of flare factors in the cat with chronic disease, is I think about the the other things that are, are highly relevant for the cat.
And I think Is it possible that food is an allergen in this particular instance? And has this cat got an environmental airborne allergen to either dust or pollen, or could there be psychogenic factors in conjunction with any one of those organic trigger factors causing an issue for this cat? Then I think about how I'm gonna fix it.
And I guess that's a combination of strategies to support the skin and reduce pruritus. And I guess that's how I want to sort of spend our time in the, the last part of this webinar, looking at how we do that. We've talked about fleas and infection.
Let's talk about the rest. So we've talked about those two. So, food.
How do we work out clinically whether food's playing a role? Now this is where if you look at Hobie's work, the distribution helps us a little bit. Any reaction pattern can be a food allergy, but the head and neck distribution sneaks slightly ahead.
Look at the numbers on the right hand side of that screen. Look at the diagram on the left. We've got face and I guess neck as being overrepresented with regards to food allergens, but what we've also got to remember is that these cats.
Also can have, you know, other distribution, like the ventral abdomen is also often involved in food allergy as well. And the take home message is you can still have any reaction pattern in a cat that potentially, presents with food allergy. They're indistinguishable from cats with environmental allergies, I can tell you that.
And there's a perfect example of a, you know, nasty self trauma on the face of a Devon, Rex cat of mine that was purely food allergic. So face. And neck.
There's another on the left-hand side there in that Siamese, but it's not diagnostic. So what I'm saying is we can't assume that cats with head and neck pruritis all have food allergy because they're indistinguishable from atopic dermatitis, but it's slightly ahead of the pack on the clinical presentation. What else helps us?
The bottom line is, not much. In dogs, most of the dogs that we see, or 50% of the dogs we see are less than 12 months of age. In cats, they can be basically anywhere.
Vogelnest work said 3 months to 9 years. Hobie basically says that most of them, many of them are young, but about a quarter of them are actually older than 6, and perhaps the Abyssinians at risk. So an 8 year old Abyssinian that presents to you tomorrow with face and neck pruritus is absolutely a candidate for food allergy.
That cat does not need to be, you know, 12 or 18 months of age. They're non-seasonal. Here's a nice example of a cat, the cat I showed you before, that's after a 12 week.
Diet trials simply of horse meat and resolving infection. What about other clinical signs? Sometimes these cats have gastrointestinal signs, but the bottom line is, is 80% of them don't.
So a cat with a perfect gastrointestinal tract doesn't mean it's not got food allergy, but if you have gastrointestinal signs, it's about more, doubly more likely to have food allergy versus ATP. Oitis externa seems to be more common in the cats with ATP. Once again, take home message, they look the same.
So how do we make a diagnosis? It's an elimination diet. It's possibly one of the most challenging things to do in a cat.
We know that probably the gold standard is a novel source of meat protein, here in Australia, they're the three go to. I know that's going to be very much influenced by your regional bias, but horse meat, donkey meat, crocodile meat, and marsupials in the form of kangaroo, if that's not. If that's not feasible, then probably the commercial hydrolyzer, and I would say updating that slide, given that now as of about a month ago here, the feline royal cannon and allergenic, which is the hydrolyzate poultry feather diet, in my opinion, very much supersedes those other two hydrolyzants.
And that's because if you look at once again at Vogelnest work on food allergy, About 25% of her cats that presented in her study of confirmed food allergy cats had been fed ZD prior to presenting but were allergic to chickens. So this is this unenviable situation where the hydrolysis of the poultry molecule isn't sufficiently, sophisticated to render these cats or render the diet rather non-allergenic. So what I'm saying is in a that's had a diet trial on a commercial diet previously.
These are good diets. They're good diets to go to in the first instance, but if you are in a situation where you are convinced that food is playing a role, or could be playing a role, a second diet trial utilising a novel source of meat protein that's regionally relevant for your geographic area is indicated. Needs to be 8 weeks.
In a cat that doesn't respond to a flea trial or a diet trial in the absence of infection, then potentially that cat has A to P. And that is a clinical diagnosis. None of the reaction patterns is diagnostic.
Have a look at the distribution pattern here, they almost look exactly identical to the cats of food allergy and the reaction patterns in terms of whether they're presenting with EGC lesions, milary dermatitis are roughly the same. These are cats that we skin test. And serum test, and we do both.
And one of the, I guess, issues with intradermal allergy testing in cats is that we believe and we've published work in this to support this last year, is that the allergen concentrations for testing cats are too low. So many people are very dubious and dermatologists quite cynical about the value of intradermal allergy testing, but we've done some threshold testing here that we published in veterinary dermatology late last year, that indicates that the cats that we're testing. Really need to be tested at much higher allergen concentrations than at the dog.
So it's worthwhile talking to your local veterinary dermatologist or dermatology referral centre about what strength of allergen they're actually using to allergy test cats because bottom line is, most of these pollens need to be tested at between 6 and 8000. We use fluoro. To identify positive reactions.
This is me testing a cat, positive reactions, inject the fluorocene, read the reactions under the woods lamp. And what we can clarify with that is that many of these cats actually are producing very strong reactions to pollen, and to dust mite, and these are good candidates for immunotherapy. The last factor that we need to think about is psychogenic factors.
These are cats that often develop stereotypic components to over grooming. These may not be necessarily cats that are exclusively psychogenic, but the psychogenic factors are playing a role. And I think these are cats where you've either identified food or identified either pollen or dust in the framework of The trigger factors, but cats typically for me, where I would flag a psychogenic factor, possibly being involved, is a cat that's not responding to conventional antipyretic therapy.
So the standard dosage of either prednisolone or cyclosporin, isn't, either working or at least partially working. That's why I look for it. These are often cats that are in that breed group.
They're oriental cats. They're often indoor cats that are coming from multi-cat households with other behavioural problems. And that's where I'll look for, I guess, flags in my history that might accelerate my, intervention with psychogenic drugs.
It's very, very important that when we see these cats that look like they are psychogenic, that we evaluate them using This very structured approach that I've shared with you this morning. Many of these cats have organic causes of pruritus, and psychogenic factors are overdiagnosed. Here's a perfect example of a dust mite allergic abyssinian that came to see me that didn't respond to clomipramine, that was basically perfect on 6 months of immunotherapy for dust mite.
So we need to be aware that it's just another reaction pattern. So in summary, we are going to look for in these chronic cats. Fleas as a flare factor, infection as a flare factor, food as a flare factor, remembering the limitations of commercial hydrolyzants, environmental allergens, remembering the limitations of intradermal allergy testing, possibly.
The diagnosis if we're not testing the appropriate concentrations, remembering that psychogenic factors are possibly things that we should consider when our standard anti-therapeutic dosages of, you know, prednisolone, cyclosporin, etc. Don't appear to be helping. So, how are we going to manage these cats?
Bathing, hard work. We're going to wipe these cats, perhaps on a daily basis, if they're a topic to remove dust. There's really very little evidence that fatty acids are of value for inflammation.
They help their hair coat. Do I use them in cats? Only if cats find them palatable or owners find them, find them, I guess, not difficult to use.
Because cats are much less, I guess, amenable to dietary intervention with fatty acids than dogs. So I use them, but I think they're low yield as monotherapy, and they're not, I guess, integral to my management regime unless the cat will consume them. I like the poor product because it seems to have high levels of palatability.
In dogs, there's good evidence to support or limited evidence to support that these interventions with topical fatty acids help with barrier function. There's a lot of good evidence in humans, but in cats, this particular product is the only product available here. It has a really a pungent smell associated with the melaleuca in the product.
Cats don't particularly like it, and I'm not a huge fan of it, but some dermatologists use it. What about reducing pruritus? Glucocorticoids we've talked about, I think that there's good evidence to support the use of topical glucocorticoids in dogs, there's evidence to support the proactive intervention with the application of cordovans on two consecutive days.
Each week. So in other words, identifying areas that are likely to relapse and using it in this proactive manner. It's not been published in CATS, but I do use it as long as in that manner, as long as we're not treating areas that are predisposed to cutaneous atrophy.
We've talked about using prednisolone at appropriate doses for induction. We taper out the clinical dose and where I, this is the only place where I'll use antihistamines in cats that are amenable to pilling in a steroid-sparing manner. I'm not a fan of antihistamines in cats.
I don't think they're useful as monotherapy, but occasionally something like cetirazine or hydroxyzine in a cat will help with Steroid sparing, where we would also in that in that, in that circumstance, add fatty acids. In terms of cyclosporin, great drug, some limitations, useful for long-term control, higher dose rate than in the dog. Remembering that it takes a much longer lag time before this drug gains traction in terms of puritus, so it's not in the management strategy for the acute cat.
It can sometimes be of value in the more Chronic cat, it will take 4 to 6 weeks to achieve complete remission. And then, in my hands, I find that tapering out cyclosporin in allergic cats, is more effective than in the dog, and it's because of its longer acting modality, often these cats can be reduced to twice a week. We know that we have to be careful with cats with gastrointestinal signs and gingival hyperplasia.
Cats will occasionally vomit cyclosporin. Most of you are aware of the risk of the either the recrudescence or the risks with active toxoplasmosis in naive cats. And the way we try and reduce that risk is by measuring trough levels in cats and reducing the dosage, on the basis that the cat must achieve no more than a 600 nanogram per mL concentration as a trough level.
Gingival hyperplasia that was reversed in a cat on cyclosporin. And I've talked briefly about trough levels and avoiding things like raw meat and viscera. Remembering too that if you freeze meat and then thaw it or cook meat for cats, particularly if you're doing, I guess, you know, restricted or, or, or, modified diets for cats, that's important to remember for toxoplasmosis.
We've talked briefly about an antihistamines, I think They're low efficacy. The two I do use for cats in a steroid sparing capacity are hydroxyzine and tirazine. I think almost all the other antihistamines are ineffective.
I think that if you're going to use antihistamines, they must be administered prophylactically along generally with corticosteroids at low dosages in our chronic maintenance plans for cats with chronic skin disease. As far as tricyclic antidepressants are concerned, they have a specific focused targeted role in those cats where we perceive that psychogenic factors are playing a role in conjunction with probably other therapeutics that you're using and other strategies that you're using to manage these cats, and those drugs, particularly paroxetine, I think, can be of value. So, I guess, really in the cat, the strategies for management are confined to glucocorticoids, both topically, orally, and cyclosporin, with a lesser role for antihistamines and tricycloids.
So let's just finish briefly with a touching on allergen-specific immunotherapy. Allergen-specific immunotherapy, there is no studies, we've got almost all our information is, it is anecdotal. It is the only intervention, though, that has the potential to modify the long-term outcome.
The success rates that are reported in the literature vary all over the place, but there is really no single standard protocol that's been assessed, no injection volume or standardisation of concentration. But what we're doing is, we do a lot of immunotherapy in, in cats. And my perception, which is, I guess, my anecdotal bias, is that these are guests, these are cats that often do very well on immunotherapy.
What we do is rush immunotherapy, so the induction of the immunotherapy is done over the course of the. And I presented some numbers last year at the World Congress on I think 28 cats that we did rush immunotherapy with. We see very few adverse reactions.
We think it markedly increases on a compliance because of the reduced burden of the injections at the beginning of immunotherapy. We test our cats at a higher concentration of allergens, and we Also serum test these cats at the same time that we're intradermal testing using the Allerce test. We had 28 cats looking at the maintenance dose between 10 to 20,000 PNU generally on a four-weekly basis.
The rush immunotherapy is done very safely, and I guess outcomes in those cats is often very positive. Sublingual immunotherapy, that there's some evidence that it's safe and effective for dogs and cats that are really objecting to subcutaneous injections. We have done sublingual immunotherapy, and there are some once again anecdotal reports of benefits have been observed.
It's palatable, it's a small volume, it's well tolerated, but the, I guess the downside is that sublingual immunotherapy has Be administered once or twice a day. So if you're interested in immunotherapy for cats, you really need to be talking to the local person that you have, either in a dermatology referral capacity or, or a dermatologist to see whether they're in a position to intradermal test with or without fluorocene, looking potentially at if you've not got a referral centre close. As to whether serum testing with the LEP test is available to you.
And then theoretically, just looking at different published regimes on immunotherapy, which are really very straightforward. I think it's useful. I think we should be doing it because I think it reduces the drug reliance long term and in some of these cats, it's highly successful.
So in summary, success rates 60 to 75%, allergen selection from two tests in this practise, rush immunotherapy to improve compliance, 6 to 12 months before we see clinical benefit, remembering that these cats are going to require antipyretic. Regimes using some of the strategies that we've discussed today, and barrier function strategies. And then generally in our practise, what we'll do is switch to slit or sublingual immunotherapy if the subcutaneous therapy has been of limited benefit.
So, we're all, we're nearly done. If we're going to put this all together, the next time you see a cat that is either over grooming with milid dermatitis, eosinophilic granuloma complex lesions, face and neck pruritus, the first thing we do, rule out mites, think about ringworm, get it off the list. Think about the flare factors.
Do I have fleas in a cat that's exquisitely allergic? Do I need to Change my flea control to something that rapidly reduces flea feeding. Do I have infection?
Get out my microscope, get out my slides, my sticky tape, ear swabs, do cytology, look under the microscope, a administer antimicrobial therapy, and potentially the next set of flare factors is, do I have a diet playing a role? And in the absence of any improvement, On a diet trial, then theoretically, am, am I looking at a cat that's a topic. Acutely, we can manage pruritus with leukocorticoids, chronically, we're looking at longer term strategies with cats on steroid sparing regimes with antihistamines or cyclosporin.
And then we've got to think about, I guess, you know, are we going to help these cats by wiping them to remove allergens and applying topical. Or lipids and supplementing them with fatty acids. And ultimately, I guess, the role of allergy testing and immunotherapy in those cats, where none of those other strategies is, is gaining sufficient traction because those cats are a topic, and we need to basically look at whether immunotherapy is another tool that might help those cats with more longer term disease.
And we're there. Thank you very much. Slightly over time, but time for questions.
Man, that was absolutely fantastic and I promised an amazing start to our 2018 virtual congress and you have not disappointed. Thank you so much for your time. My pleasure.
Folks, we unfortunately, as Mandy said, have run over time. So at this stage, we are not going to be able to take any questions because of the fact that we are, going to unfortunately then run late in the whole programme. So what, no, that's OK.
Don't worry. What we are going to do is, we are going to take just a 5 minute comfort break. So, we will be looking please to start, at the top of the hour, again with our next speaker, Andrew Carter, who's going to be talking about otitis cases.
So, Mandy, once again, thank you very much for your time. And we look forward to hearing from you again.