Thank you, Bruce. That's fantastic. And, hello everybody.
It's, a great topic. Certainly we see lots of pioderma, whenever dealing with animals in small animal practise. And there are some new things that are very relevant and important to, to help understand this.
So the talk will focus on those, as well as just an overview of what we need to know to recognise pioderma and manage it as effectively as possible, in practise. So just a very quick recap on how it presents. It's superficial is the most common form of pyoderma that we see, but also deep pyederma, which is nowadays a little bit more problematic.
So both versions are common, but superficial definitely more so. And they're secondary diseases, so they occur secondary secondarily most often to allergies, especially atopic dermatitis, is the big bulk of patients that we see with problematic pyederma. But they'll also occur due to physical defects and lots of our brachycephalic breeds with all their skin folds.
We see a lot of issues with now. And then less commonly, but certainly importantly to systemic immune suppression of any cause as well. But including our treatments for lots of skin disease with glucocorticoids and the new Aperquil as well.
OK. Endocrine disease, occasionally we'll see, hyperthyroidism, hypoadrenal corticism. We know a lot about these diseases.
They're well talked about and understood. They, they occur sporadically. We certainly don't see them anywhere near as commonly as allergies, and they're important to obviously recognise, but as far as the yoma presenting, there aren't often any clear clues between them.
And then Which, which are, are now and again, one or two in, probably a career rather than a year to see these, they're really not very common, some of the other causes. So, looking at dogs and cats, dogs are very susceptible, and they're the species we think of when we talk about yoma, and partly that's related to the skin structure. And, there's theories.
We don't have a complete understanding, but the paucity of lipids, so they don't have quite as tight a seal on the surface of the skin, potentially low pH. And more exposed openings of the hair follicles are involved in the susceptibility of dogs. And certainly, that there's a high prevalence of atopic dermatitis is one of the big underlying causes.
And we know part of the pathogenesis of that disease now is some defects, further defects in the skin barrier above what general dogs will have as well. Now cats we might not think of as often with pyoderma, but they certainly are commonly affected. And we looked at our population of of cats presenting to dermatology referral in Australia over about a 15 year period, and there were 52 cats that we were able to, to put together in a study, and it was reasonably common.
So we had a, a, Underlying diseases, again, most often atopic dermatitis. And recurrent disease was a real problem at times, in that, quite a lot of these cats continue to have their atopic dermatitis, which is not always that easy to manage. So recurring pyerma was a problem in some of those cats as well.
OK, so that's an overview of, of when we see pyoderma. So, what are the recent problems or what are the difficulties with managing pyoderma? Partly the diagnosis, because there are so many variable presentations, and particularly in dogs, but also in cats, you can't look at the skin and often know whether there's pyoderma present or not.
The newer problem also is in treatment, in that we, we not only need to focus on clearing the infection, we have to, and we have new antibiotic resistance that's becoming, a question and a concern in relation to that. But of course, we need to manage the underlying disease as well. And atopic dermatitis, as I mentioned, is, is a difficult disease and not one that we can fix, and one that we're going to have to manage pretty much for the patient's life once it's there.
So now let's go a little bit more into the detail of how we recognise these pyoderma cases. Firstly, I like to always look at the history. There's always clues, or often clues in the history that help fine-tune what's going on and, and increase our suspicion for, the primary and secondary causes that are important.
So what clues do we find in the history of dogs presenting with pyederma? Well, they just have to be a dog and they're prone to pyerma, and they pretty much just have to have any skin disease and they're prone to pyoma. So, just being a dog and presenting with skin disease, you have to think pyerma, is this part of what's going on.
In cats, it's a little more refined. They were looking at our cats from the Australian group with 52 cats with pyoderma, there were two peaks of occurrence, and that was young cats with allergies in the first few years of life. And then aged cats, which didn't necessarily have a history of ongoing problems.
So those two groups were a little bit overrepresented in, in the presentation of pyoderma and cats. Puratus In allergic, cats and dogs will often be quite severe when there's pyoderma. But it can be absent when there's, when there's not allergies.
So the pruritus will vary from absent and you've just got lesions to very severe. And the more problematic ones, the ones that we have grief with, are, are often the severely pruridic ones. Another historical clue is poor responsiveness or loss of responsiveness to glucocorticoid therapies, and that always rings an alarm bell in my mind that all infections are on the cards, and pyderma being one of the more common ones is certainly right up there.
And similarly, recent illness, immunosuppressive drug therapies, anything that's reducing the host's immune system, and their ability to, to, suppress normal surface bacteria from creating infections are more prone to pyoderma. Now, clinical clues. So what do we see that help tell us that pyoderma is there clinically?
And the presentations, and we'll start with superficial pyoderma, the presentations that are more straightforward and the more often pyoderma, certainly in dogs are when we've got pustules. And other than pemphigus foliaceous, which is, a A rare disease and will again occur very sporadically and tend to have bigger pustules. There really are very few other diseases that present with with pustules in dogs.
Cats don't tend to have pustules very often at all, so we don't have that clue from them. Papules are another big clue for pyoderma, but they have a broader range of differentials that can cause them. And so, any of the parasitic diseases, mites, flea bites, sometimes allergies alone can present with papules.
But seeing a papular dermatitis in a dog definitely raises the profile of pyoderma and creates the question of pyoderma when we're talking about cats as well. Epidermal colorettes are often pioderma when we're talking about dogs, and, and, we see them as great big expanding lesions or quite small lesions. So a circular lesion with a rim of scale is often, suggestive of pioderma.
So they're the easier lesions in my mind to potentially link to pyoderma. Alopecia is very common and very variable. When it's well demarcated, pioderma is high up on the list of differentials, and that's in dogs and in cats.
And, and pyderma has to be excluded when you're seeing these lesions. Then there's a whole range of non-specific lesions, which, all options are open. So erythema, erosion, scaling, crusting, thickened lianide, hyperpigmented skin.
Pyoderma is one of the causes of all of those lesions. So, there are no particular clues when patients present with those lesions as the predominant findings. There are some regional forms of pyderma that, that, are helpful clues to know that these regions tend to be affected.
And that's around the lip margins. German shepherds in particular will get a mucocutaneous pyderma around their lips and even involving the nasal planum that mimics autoimmune diseases. So Always be alert for pyderma in those locations.
Perianal, perivolval areas, you can get all of the same lesions we've just talked about, but focused in those areas. I always worry about pyoderma as, as potentially being there. Not always being there, but potentially with those presentations.
And even some of the really nasty, rosy presentations, you'll get a significant pyerma that's really contributing a lot to the clinical signs and the patient discomfort, in those presentations. Pressure points, elbows, Hockhock areas in larger dogs, those sort of pressure areas are prone to pyoderma. We've got dog skin that's already a little bit more prone, and then you've got some repeated pressure and, and trauma at those sites, means pyoderma is frequent in those areas.
One of the forms that's a little bit challenging in dogs is this funny moth eaten alopecia that I presume is, a mild, rumbling bacterial folliculitis in the openings of the hair follicles, and they're almost like tiny little epidermal colorettes around the follicles, but they'll present to you, sometimes not even pruridic at all, but the owners will bring them in with their patchy hair code and say, Look, if you stand here at this angle, you see all these little bits of hair missing. So that's often a presentation of a mild form of bacterial folliculitis in dogs. Cats, cats have their osinophilic granuloma lesions that are part of, the spectrum of what generally what we see with allergies in cats.
And some of these lesions will have significant bacterial pyerma and osinophilic plaques like these in the pictures on the belly, often ventral abdomen, sometimes axillary areas, can have a very significant bacterial pyoderma component. And we'll talk about diagnosis in a moment and using impression smears. These lesions are very easy to sample with a glass slide impression to know whether you've just got lots of eosinophils, or whether you've got lots of bacteria intracellular there as a pioderma, component to these.
Similarly, lick lesions, lick granuloma lesions on dogs, some of these have a very significant bacterial pyoderma component. That means, we're really prone to, we need to treat this, this part of the, problem, the secondary infection to expect them to get improved. Not all lick lesions and not alleenophilic granuloma lesions have pyoderma, but a reasonable number of them do.
So always screening for surface pyoderma with our surface cytology, as I'll go on to, is very important. Now, the deep pioderma is less problematic to recognise. We, we recognise presentations more readily in both dogs and cats, and they have this irregularly nodular weeping, appearance.
And there are some regions of the body that are more prone, feet, definitely in dogs and around the muzzle of the, some breeds, the chin area, and certainly in cats. One of the complications of chinnane presentations in cats. So, you cannot distinguish this presentation from far less common, diseases that will present like this, any of the nodular causes.
Demodex sometimes in dogs, and less commonly now, we've got the new drugs that are working well, but it's always a consideration in dogs. And weird deep fungal infections and my abacteria and naria occasionally we'll do this presentation. But deep bacterial pyoderma is certainly the most common one that we see.
Here's a couple of pictures again to exemplify that. So bull terrier, with this deep pyodermal lesions. It's a regularly nodular.
You give these a gentle squeeze, and there'll be some blood that and and parent material that you can easily express out of some of these areas. You can see the interdigital areas in of, this dog. And German Shepherd pydermas, they have, potentially an immunosuppression that that makes their pyoderma much worse than some other breeds, so they'll get these really deep, nasty oozing pydermas as well.
OK. There's one presentation that we see very rarely in dogs, but it's an important one to sort of be aware of, because it, it can be life-threatening. And this is a pseudomonas deep pyoderma.
It occurs as a very painful, papula presentation, usually on the dorsum following, shampoo. I immediately, within 24 hours or so of following. A shampoo, often a whirlpool shampoo, and it seems as if we get pseudomonas down into the hair follicles and they set up this nasty, nodular deep dermatitis.
So it's a version of deep pyoderma that looks different to the standard presentations of. Myoderma. And these dogs are very unwell, pyorexic, very uncomfortable with their lesions.
So just to be aware of that, if you see this presentation, you, we often need to culture them with a deep tissue biopsy, and histopath to confirm what's going on. And they, they can definitely, be fatal if not treated aggressively. Another form we see in our sunny Australia, where we're all basking away at the moment, is solar deep pyoma.
And, they have quite a classical presentation. They'll, they'll sunbaking dogs with a bald, sparsely haired tummies will certainly get areas that are affected. But even this, this dog on the upper right here with the, Reasonably thin, but previously complete hair coat there, they can get a nasty solar induced bacterial folliculitis that, is ultimately related to excess sun exposure and, and damage to the skin there.
So that's an important one to recognise in sun areas. OK, so that's pretty much the historical clues that we'll see. Any dog, the young cats, the older cats, Loss of responsiveness to steroids and or on immunosuppressive treatment or unwell of any sort, that's all the historical bells that will be suggesting pyoderma.
The spectrum of clinical signs, lots of them to choose from. So, but when you've got pustules, certainly, and when you've got papules or epidermal colorettes or well demarcated alopecia, they're particular clues for pyoderma, but pretty much any spectrum of lesions, are consistent with pyoderma. So we need more than just those things to make a diagnosis.
We definitely need to do some testing. And the mainstay of diagnosing pyoderma accurately is cytology. And you cannot accurately, recognise and pyoderma, at least quickly without having good cytology skills.
And adhesive tape impressions are suitable to all lesions and are certainly my favourite go to test to know whether we're dealing with pyoderma. When you've got the moist lesions, so erosions, or if you gently rupture a pustule and then push a glass slide directly onto it, or you've got exudate coming out of these deep nodular ones, then you can do a direct glass slide impression. But they're poorly, the glass slides are poorly adherent for intact skin.
So the adhesive tape, definitely has advantages, for the dry lesions, and it's still quite useful for the moist lesions as well. So, multiple coccoid bacteria with typical lesions is supportive of there being a role for pyoderma. And the important thing to remember and, and to take home, take home message, one of the important take home messages when we're dealing about cytology is, although bacterial flora are present on normal skin and they are there, you expect expect them to be there.
They are very sparse when we're talking about looking on an oil immersion field at a tiny little section of skin. So normally, we don't see bacteria on our, on, on our cytology unless we've got an increased number, present. And you need to see them inside inflammatory cells, which are either neutrophils most often, and sometimes also macrophages, to confirm that we've got active pyoderma.
So without that intracellular location of the bacteria, it can be an increased number, but not necessarily infection. At least that's what we, conform to at the moment, and as much as we understand the difference between overgrowth of bacteria and infection. So, there's a little picture, and we'll go through some of this right now, but, these are, once you get used to the appearance of them, degenerate neutrophils as they appear on the skin surface.
And this purple cobwebby material, you need to get comfortable with being inflammatory cells on the skin surface, and almost always that will be neutrophils. And they'll stain with a diff stain, which we'll talk about in a second, and purply, and then the bacteria, are usually cockeyes, so they're paired, often in dogs. They can be more singular sometimes in cats, but paired, and they're very blue and round.
So they do look discreet and, and you shouldn't have to say, Oh, maybe they're bacteria. You have to be able to look down there and convince yourself, yes, these are, definitely bacteria for them to be relevant. So this is how I do the tape impressions.
I use a piece of sticky tape onto lesion or skin and I might do all the feet with one sample. I'll do consistent lesions. So if I've got lots of papular areas, I'll just do them on one sample from multiple areas.
If I've got different lesions, like canification in some areas, I might do that separately. And I'll push the sticky tape onto the, skin until it loses its adhesiveness. So a number of times on there.
Then I'll curl it, stick it onto the end of the glass slide and curl it into a little offset cylinder, so you've got an edge ready to uncurl once you've stained it. And I find this the easiest way, to stain them, evenly and, and, and just practically to get it done quickly without as much mess. I use the red stain as well as the blue stain.
So we do 6 dips into the red and 6 dips into the blue, wash it off onto a gentle stream of running water, then grab your little corner and uncurl it and use a tissue to smear across the surface. So you're spreading it out. It's a nice flat surface.
And it's very. Evenly a fixed to the slide underneath. So, it gives you a very even plane to examine, under the microscope, which is easy.
And it adheres a lot better than I find than just putting a few drops of blue stain, under the, the tape, which is another alternate way of staining them. No fixative. Don't use the fixative because it dissolves the glue on the tape and gives you a fuzzy appearance and you lose some clarity with them.
Glass slide impression, pretty straightforward, push it firmly onto your lesions and do your full diff quick stain as you would for ears and and other asrate lesions. So this is what you see on the tape impressions. This is low power view with usually a 4 times lens, is your low magnification, and you have a lot of scattered keratinocytes.
So they're just these little angular shards like keratinocytes, which I used to think were rolled up keratinocytes. I've now been told by Peter Hill, who's a wonderful wealth of knowledge that, these are probably follicular, keratinocytes that come out of the follicles rather than off the surface of the skin. But regardless, you see a lot of these cigar shaped dark blue shards across normal skin, and then you have also a background of paler flat keratinocytes.
Go, what we're looking for when we're looking for pyoderma is clusters of inflammatory cells. So this is a normal looking, appearance, tape prep with no particular areas of great interest. If I'm going to look closer under oil, I'll go to a clustered area.
When I'm, when I'm seeing any granular areas like this that are suggestive of neutrophil clusters, they're the spots that I get very central under the under the lens and increased power up to oil. You can put your oil directly onto the sticky tape surface. So these are more dramatic ones.
So these might be taken from the edge of these alopeciic areas where you've got crusting, and you've often got lots of these clumped keratinocytes with a rim of neutrophils around the edges that are this purple granular material. So the keratinocytes tend to be a pale blue to a mid blue. Your inflammatory cells tend to be purple, and when we get up to oil, your bacteria tend to be a deep blue.
So lots of neutrophilic material here, to look at, lots of clusters of keratinocytes with rims of neutrophils around. So again, this is the picture I showed before. So you don't always, you have to get your imaginoscope on a little bit.
This is part of a multi, lobed nucleus. So here's one that's more intact, your neutrophils that have multiple lobes to them, and the nucleus is the part that stains really well, and you don't often see much of the cytoplasm on tape preps, where everything's just a little A bit less clear than on a glass slide. So that's one that's intact.
Here are ones that are degenerate. The nuclear material tends to hang together, string together, so it doesn't want to pull apart. So you get this cobwebby appearance of lots of neutrophils.
And here's your intracellular bacterial cocci hanging around, these, nuclear material. Here, we've got some intracellula in this neutrophil. And then we've got a whole lot just colonising.
So just hanging out on the surface of the keratinocytes. This is not normal. This is way more bacteria than you should see on normal skin.
So at the very least, if you've got no inflammation, we need to be cleaning this skin, bathing and or antiseptics to reduce the population of bacteria, because the chances of active infection, pyoderma, are much greater when the numbers, of bacteria have increased. Deep pyoderma is a little bit more challenging on cytology in that we sometimes don't find as many bacteria. They tend to be much easier to find on superficial pyoderma.
And, and the neutrophils are hagocitic cells, so they're gobbling them up and dealing with them in deep pyoderma, and we don't tend to have as many of them to find. And this is a fair. Fairly obvious one where we've got lots that are intracellular.
But many you might just find a couple, on one field here and there, and you have to scan around a lot, but you'll keep finding them in low numbers repeatedly in many samples. There are some samples of deep pyoderma where I don't find any bacteria, and you can't be sure it's deep pyoderma, but if It looks clinically like that, your options are to biopsy, to know for sure what's going on, or to do a clinical treatment trial and see if they respond to treatment. Cytology is helpful with deep pyoderma, but, but it is less sensitive with, with clearly confirming a bacterial origin of deep pyoderma in my experience.
Than superficial pyderma is. So, diagnosis of pyoderma is dependent on skin cytology in many presentations, and mostly it's straightforward, but sometimes it's not diagnostic. Sometimes your neutrophils are absent, so immunosuppression, if they're on, if they've got hypodrenal corticism or they've been on lots of steroid therapy, you might not see many neutrophils at this level, on the surface of the skin.
So, you don't get your good cytology, clues to confirm it. It's also tricky when you've got a moist site and you've had some bacterial overgrowth, so you've got increased numbers on the skin surface, and there's a few neutrophils around because there's some skin trauma. Are they just there for repair?
Is there active pyderma? It's not always clear cut. So the more moist and, injured the skin is, and the more likely we're going to have neutrophils there for repair.
If you haven't got clear intracellular bacteria in large numbers and obvious repeated numbers, but you've got lots of colonising, it's sometimes not so straightforward, do we have infection or do we just have overgrowth. Deeper lesions are harder also to get good cytological confirmation on, and papules and raised plaques and lichenified type of plaques or raised erythemic plaques are sometimes sparse bacteria. So, there are times when you might not get cytological evidence of pyoderma, even when it's present.
So the second way we can diagnose pyoderma is resolution of lesions with appropriate antimicrobial monotherapy trials. So you cannot assess response to antibiotics and steroids at the same time. You really do not know which part of your treatment has worked.
So if we're doing a treatment trial as a way of confirming pyoderma, it is important that it's solely antimicrobials. And I'll talk about that a little bit more as we go into treatment. Now histopathology biopsies, are they helpful?
They may be helpful, and they'll be helpful when it's deep pyderma, definitely, and they'll, papular lesions potentially. But you, you have less help with superficial lesions, and you may not get as clear cut an answer on histopathology. So skin surface cytology.
Certainly in my experience, he's more reliable for diagnosing pyoderma than histopath is. If you are taking biopsies of superficial lesions, it's very important not to do any skin preparation before you collect your sample. You want the surface scale, you want to see what's in there.
You don't rub all that off, or you may well have lost your evidence of pioderma. That's there. OK.
So, That's your history clues, your physical exam clues, how we diagnose it. Now, a little bit about the understanding of pyoderma and what's changed recently. So the common causal bacteria, most of this information is what we know in dogs, and there's a little bit extrapolated into cats, but there's, more species involved in cats and, and, so the bulk of this is all about dogs.
Staphylococcus pseudointermedius is the main causal bacteria. It's normal on the skin surface, hangs out in moist sites around the mouth perianal nais. There are some virulence factors involved, and we know that staph suit intermediacy is really, adapted to living on dog skin and also found on a number of animals including cats.
Occasionally Staph aureus, which is the major human pathogen, much more adapted to human skin, and occasionally leferi, schleferi, in dogs or simulons in cats have been shown as causal bacteria. Then there's a range of other normal bacteria that live on the skin. So staphsu intermediate is not the only bacteria that lives on the surface of the skin.
There's all these others, gramme positives and gramme negatives, a whole range of things that hang out there in low numbers. They're not as adapted to multiply, they're not as able to cause disease as staphs at intermedius is. Similarly, there's transient, so pseudomonas, Proteus, coronobbacteria, just because we culture these organisms off the surface of the skin means nothing.
And I'll talk about that a little bit more in a moment. The major pathogen is staph, and that's why we're looking for paired cocci, and when we're doing our cytology to try and confirm pyoderma. Now staphs in intermediates historically we were very lucky for a long time and there was predictable antibiotic sensitivity for decades, and we had about 98% of isolets that were sensitive to our beta lactam, so cephalexins and amoxiclos, etc.
Then along came methicillin resistance, and this has been talked about in relation to Staph aureus in people for some time, but is now exploded in staff suit intermediates for, for dogs primarily. And what's special about MRSP and MRSA, is that they have acquired this small mobile gene called MCA, and it's transferred readily among staph species. And it alters the penicillin binding protein, so it means that our beta lactam antibiotics cannot work against these bacteria anymore.
And it's a bit scary how this has . Presented and, and quickly multiplied around the world. It was first reported in France in the mid 1980s.
The first disease was in the USA, reported in the USA in 1999. And then an alarming increase in MRSP islets since 2007. So in the last 1011 years around the world.
And there's clonal spread of five main islets worldwide, and very rapid spread. So there's different islets that tend to be more prevalent in different locations, and, that has relevance as far as their antimicrobial resistance profiles. And what's tricky with MRSP and more so than MRSAs in people, is that there's a concurrent transfer of, of resistance to a wide range of antibiotics at the same time.
So not only are they resistant to the belactam drugs, but they're resistant to many of our antibiotics. And that's not something that's happened with MRSA, as such a widespread change. So, as well as the beta lactams, the macrolides, the fluoroquinolones, tetracyclines, trimethoprim sulphur, and chlorophenacol often have resistance, resistance to them as well.
And again, it varies a little bit with what's around the world. Some of the, many of, sorry, of the American islets can be sensitive to chlorophenol, but certainly what we're finding in Australia is not, in Sydney part of Australia is that very few of them are. So, MRSP has become one of the most important pathogens in small animal medicine, and that makes sense.
This is a difficult bacteria to deal with once it has established infection. And we are lucky that the bulk of our skin infections are surface infections. So we don't necessarily need, and more and more we move away from using systemic antibiotics in this situation.
But when they invade deeply into deep pyderma or other body organs, they can be particularly challenging to manage. So where have we seen MRSP infections? Mainly in dogs.
They're also reported in cats, and there are a couple rarely reported in horses. We see them as yoma, superficial and deep, otitis. Where luckily we, lots of topicals usually do the tricks, so we still have some good treatment options, but also surgical wound infections, where they start to become quite scary.
They've been reported in urinary tract infections. And as a cause of septicemia, when they're definitely life-threatening. Now, MRSP is not particularly more pathogenic than, than our standard staph suit intermediates.
That's not methicillin resistant. It's not more likely that this, these bacteria will cause infection. They're just harder to treat when they do.
So that's a good thing. They're not more pathogenic than other staph species. So, Yes, that's what I've just said, Sorry, catching up on what I meant there.
So, yeah, so, so we don't have to worry about them, you know, particularly being, super pathogenic strains, but, but, we certainly need to think wisely about how to treat them. And so treatment has become more complex. A common disease, canine bacterial pyoderma, a little bit tricky to recognise at times, requires good cytology to know that it's there.
And now we have to, we used to be able to say, right, now we've got pyoderma, treatment is straightforward, well, now it's not so straightforward. We not only have to treat the primary disease to help prevent recurrence of pyoderma and with atopic dermatitis, one of the big players, which is a difficult lifelong disease, that in itself is challenging. But we also have the question of are there multi-drug resistant bacteria involved in this patient's pyderma?
And the likelihood of that will be influenced by a number of factors, including your locality and how prevalent MRSP is in the area that you're working. So the optimal approach to acute bacterial pyoderma is now, Altered, and step one is we need accurate recognition and early diagnosis of pyoderma. We, we can't be quite as blase about pyoderma anymore.
We also need careful monitoring of response to therapy for every patient, and if they don't respond, we need to consider. Many factors, but one of them can be that there's resistant, resistant species involved. And culture and sensitivity testing is therefore important for some patients, and we're gonna talk about this now, but not all patients.
So, how do we pick? Bacterial pyoderma due to MRSP. Sadly, they don't look any different.
The lesions do not vary dependent on what the causal bacterial strain is. So there is no clinical clues that you can get. They look the same.
So culture is required. However, it's really important to remember that culture has, lots of potential pitfalls. Normal.
Skin bacteria, all of them can be readily cultured. So you'll get all sorts of things, including MRSP that are just being residents on the surface of the skin and not causing a problem. So just cause they're there doesn't mean there's infection due to MRSP.
So your cytology is absolutely essential and you need to see evidence of intracellular bacteria consistently, in conjunction with culturing a pure, usually when you have pyoderma, it's usually due to one causal species. So Often when you're culturing from there, you'll get a pure growth of that particular species. So if you get a pure growth of a staph in intermedius, that's methicillin resistant, and you have lesions that are consistent, and your cytology shows neutrophils and cocci, intracellular from the skin surface, then you've got enough to say, yes, we have a diagnosis of MRSP.
But any of those steps missing, then you don't. So confirmation requires culture and your cytology concurrently, and that's such a second really important take home message is, don't just look at the culture results, you have to look at the whole picture together, including, most importantly, the cytology. So, you can't clinically suspect them.
When might you suspect them based on the history? And these, the history clues are the main ones that make me think about, could this, could this patient have methasone resistant staph, that it's the history clues that helped me and wave that flag. So if there's poor response to empirical therapy, assuming you've got The right dose, you've got good compliance, you've, chosen the right drugs, etc.
Etc. So, so look at, relook at how the treatment went and what was used and was it all appropriate? Was the dose worked out accurately, all of those things.
Factors that may result in poor response to therapy, so patient factors, occasionally very severe lesions, so animals with really severe pyoderma, may not respond well to treatment or very active primary disease, but that doesn't happen very often. Mostly you can treat the pyoderma irrespective of the underlying disease. Sometimes with concurrent immunosuppression, but if you've got, if you've got active immunosuppression, including concurrent glucocorticoid and or a therapy while you're treating with antibiotics, you often get poor response.
So you have to remove those factors or, consider those factors if you can't remove them as reasons why you might have poor response, rather than initially thinking oh it's resistant bacteria. Occasionally environmental factors, high humidity and temperature, particularly if it's right in skin folds and there's a really humid time of year, then your antisystemic antibiotics may not be able to be very effective. And of course, owner compliance factors and whether they're able to get the medications in and do it reliably as we need them to.
And sometimes our own factors, busy days, mistakes happen, just relook at doses and durations and formulations and make sure everything was right when it was prescribed the first time around. Poorly responsive nodular lesions are difficult, you must exclude other differentials that may mimic deep pyoderma, so we need to biopsy them. There's lots of things there, you can't look at a nodular lesion and know what's going on.
So you, you have to have histopathology. To confirm that it's pioderma, and you also need a tissue biopsy that you culture from which we'll talk about in a second. So you need histopath and a sterile sample for culture, to diagnose MRSP deep pyoderma.
And you cannot rely on the culture results alone. So if you grab a piece of skin and culture, you might again have MRSP. And I've had one case of this recently where, where the dog was sent in to deal with a deep pyoderma due to MRSP because it was cultured from a tissue biopsy.
No histopath was done, and we found it actually had cysts. It had no deep pyoderma, and it was just a transient off the inside, presumably of the, the surface of the hair follicles that was involved where there was, MRSP present. So culture alone doesn't confirm cause.
There have been some guidelines put together, when to suspect bacterial pyoderma due to MRSP so that paper's there, it does, it, it's got a lot of material in there, but it does give you a good background of what to, to bring into practise and what to use. What they recommend for when bacterial culture is, is, indicated is consistent lesions and bacterial cocci with neutrophils on your cytology. Without question that has to be there, but then if you're in an area where there's greater risk of MRSP, if there's poor response to appropriate systemic treatment, The greater risk of MRSP is when you've had infections in that patient or another patient in the same household before, and possibly when it's recurrent pyoderma in that patient and they've had lots of antibiotics in the past, but that again is influenced by, by your locality risk and whether MRSP is very prevalent in your area.
Poor response to appropriate systemic treatment, so there's some guidelines there, I won't read through all the details, but it's all there, poor, poor response by a certain time, so it's giving you a bit more of an indication of, of when to say, OK, this is not responding like it should be doing. So that's helpful to have some more solid guidelines of what is poor response to treatment. Now the locality risk, there is a lot of variation, there's less than 10 MRSP is less than 10% of staff isolates in many countries, but in parts of the US, 40% or so, and in parts of Japan, even up to 7%.
So it can be very high in some areas. Approximately 12% from recent studies in Australia, so still, getting fairly scary. So 1 in 81 in 10 animals with pyoderma may have MRSP.
So how to culture is an important question. So we need to see them on cytology. If you've got intact pustules, you can use a sterile needle to pop the pustule and then use a culture swab just to collect up the, the, pustule contents.
But often you don't have pustules, so we just use a dry swab, rubbed over the surface, no cleaning or anything first, but over the surface of where your cytology is telling you there's nice population of intracellular cocci. And there's, not rods and other colonising bacteria as well. If they're very moist areas, you might get some other colonising bacteria on your cytology.
You don't want a culture from those zones. Go away to the edges of lesions, you want dry areas to culture from. Rub that swab over the surface of affected skin for up about 5 seconds.
And I might do a few areas for 5 seconds and then pop it straight into your transport medium. Deeper lesions, you need to puncture. So if they're papula, they're a little bit tricky.
You can like a pustule, pop them a bit with a needle, and then you just swab over the surface, and you'll get a little bit of blood, but that's fine. Maybe you've got a high yield that way. You can do FNAs from intact nodules, but largely the best way for deeper lesions is a biopsy.
And here you do do a surface skin prep, your sterile, collection of your sample, and you should chop off the top of the epidermis, so your little section, because there are, if you've got deep pyderma, there'll be deeper down in the hair follicles and the middermis. So you want to chop off the very surface epidermis, from your sample before you pop it in a pot. Put it on some sterile saline and a little pot sterile pot to, keep it in the fridge and send it to the lab for culture.
They'll crunch it up with a mortar sterile mortar and pestle and and culture from it. So in culture swabs into transport media, your tissue biopsies straight into the fridge, it's important to try and prevent the growth of contaminants that could have been, sampled as well. So refrigerate them, get them to the lab as quickly as possible, and they should be processed, within 24 hours.
And refrigeration important, OK. How to interpret them, you must again look back at your cytology, and remember, that, that it's, you will grow all sorts of things from the skin surface. Why are they called methicillin resistant staff?
When you look at your susceptibility testing, they've often got an oxacillin disc, and that's a more stable antibiotic equivalent to methicillin, which is the reference point. So you'll see, you won't see methicillin usually on your susceptibility list you'll see oxacillin there. So staph resistant to oxacillin are called methicillin resistant.
The disc diffusion method is the usual way that's used. It's semi-quantitative method of, of, identifying them. And it's not quite as accurate as, as the micro dilution techniques, which are becoming more popular, but are more expensive to run.
So many labs are not using them as yet. They will report a minimum inhibitory concentrate. Of antibiotic that inhibits growth, rather than, having a guide of, on the susceptibility disc diffusion, the closer they grow to the little disc of antibiotic, the more likely they're going to be resistant.
And there are guidelines of how close they can grow, before they're called as a resistant species. So regardless of which method the labs use, they need to be a good lab and they need to stick to standards and and there are internationally recognised standards that are used. It is very important that the labs don't just report.
COAG positive stuff, which I used to do a fair bit in Australia, but it's now all changed. We need to know COAG positive, separate from COAG negative, and we need to know if it's Staphorus as one of the COAG positives, not just, it is a COAG positive staff. The COAG negative stuffs sometimes will be pathogenic, but you do get them from as normal flora on the skin as well, and low numbers cultured are more likely to be normal contaminants rather than causes of infection.
And quite a few of these COAG negative staffs have very resistant profiles. So you can culture them, they look nasty because they're very resistant to lots of things, but they're actually just a few of them hanging out there that grew readily on the plate. So it doesn't mean causal, and you have to question getting a culture back of a COAG negative staff, is this real, a real result.
Staphhorius is important to recognise due to public health implications and different break points, so different ways of measuring on your plate, whether they're resistant or sensitive, based on the different species. So it's no good if that lab just calls it a COAG positive staff. You don't know which breakpoint to use for them.
So bottom line, the results are a guide to treatment, and the clinical response does not always reflect what we find on those lab results. So they're not the be all and end all, which is what we tend to rely on them for. They're another guide as to what's more likely to help us.
Very quickly, I'll just, sorry to go a bit longer. I'll go through 5 minutes, the last 5 minutes on treatment, and we'll have 5 minutes or so left for some questions. Treatment is, there's not a lot of options.
So topical therapy is by far the most recommended treatment now when we're talking about bacterial pyoderma. And it's optimal, probably it's at least helpful for all cases of superficial pyoderma. And it's particularly helpful when we've got MRSP, because often we have less limited systemic options and we don't want to increase the chances of losing, the ability to use those options, particularly if these organisms then invade and we get a deep infection.
So topical therapy is best, and they help reduce the selection for resistant species. The more we start chasing them, bacteria with different antibiotics, the more likely we run out of antibiotics to use. And in particular, topical therapy is very much indicated for localised or mild lesions.
There's really no indication or very few indications to use systemic when we've got localised or mild disease. And also, very important role to help limit recurrence of infections while addressing the underlying disease. And that's our atopic patients, having in play an ongoing preventative topical treatment plan trying to stop these infections recurring is very important.
There's a range of products and formulations, the Leon ones having more residual action are probably more helpful. So there's a range of solutions and lotions and creams and gels and ointments. The rinse off ones, the shampoos, clean, which is really good, mechanical cleaning is a good thing, but they have less residual action, so a combination of both of them is generally what's going to be more effective.
So far, good quality trials are relatively scarce, and the optimal products or protocols are, are not all that clear. However, chlorhexidine is the mainstay of treatment. It's been widely used in human and veterinary medicine for a very long time, but luckily, our staff, including MRSP, tend to be still very susceptible to it, although there is a little bit of resistance in some other bacterial species staff generally are still very susceptible.
And there's high quality evidence of efficacy against broad staph species with a 1 to 4% concentration. And they have shown though, that 3 to 4% is more rapidly bactericidal. So twice weekly, 4% Clwhex shampoo to do the cleaning and the removing of the surface debris, and then a daily 4% Clwh solution.
So that's a solution, not the suds up scrub one, but just the plain ChE solution. Daily. So that combination, twice a week shampoo, daily Clohex solution for 4 weeks was as effective as systemic antibiotics with dealing with pyoma.
So that should be our go to for pyerma whenever possible. We've just talked about that bit. Iodine is an option.
I use that on the periocular area because it's not, not a place where we can use Clawhex because of the problems with, ulceration. It is less effective than Clawh in human studies and can cause more skin irritation, but the 0.5% solution only, not sure why there's a question mark there, that shouldn't be a question mark.
It's definitely that. It is safe to use on that periocular area, so that's my preferred option in that site, and probably also periolval, perianal, mucosal areas that are a little bit more sensitive to the clawh. Other things that have been looked at, silver compounds might be helpful, and flamazine's another thing that we can use certainly on wounds and perianal, very ulcerated areas.
It, it's tolerated well. There's some low quality evidence, not as good as our Clorhex evidence, that it can be helpful, but there's not good studies to really know. Medical grade honey's been looked at, nice and messy, nice idea, but low quality evidence.
To support and some evidence to suggest it doesn't work. So the jury's out with that one. Benzoyl peroxide's another option, that can be used, and there's some evidence to support that too.
But largely at this point in time, Clorhex is still the mainstay. Bleach has been looked at and it's been used in low concentrations, and that's something that might be helpful preventatively more than necessarily for treatment, and a couple of other options. So, based on studies to date, the current recommendations are a combination of full body Clawhex shampoo and your daily Clawex solution as a treatment for pyoderma.
And sometimes your Claw he shampoos and and solutions will irritate some dogs, and particularly more, thin thin, skin in soft areas. So if that's the case, I don't use the Claw he shampoos. I tend to go to, other shampoos that are a little bit less, drying and irritating.
Topical antibiotics we can use, but we need to ideally avoid using these because they're one of the few, two of the few options that work for MRSA's in people. And if we have our people applying these to their animals and having exposure to them through their animals, it's more likely their own staph flora will become resistant to these useful antibiotics. So I generally recommend not to use them.
Systemic therapy, there's not much we can use. And you do need to do culture if you're going to consider systemics, and when we've got deep pyoderma, it's absolutely essential to be culturing them. Important points to remember, all staff are resistant to methicillin and resistant to all beta lactam.
So that's all of them. Sometimes you get a report back saying, Sivahein's OK, but the others aren't, that's just cannot be, so if they're methasone resistant, all of the Beleactams are out. And sometimes we get, some systemic options that, that are, useful.
Usually there's co-resistance to clindamycin and all the macrolides, erythromycin and the fluoroquinolones. Occasionally we'll get tetracyclin or, trimethoprine sulfonamide being effective. And there's a little bit of data about differences around the world there.
So that's pretty much it, what I wanted to cover. Occasionally we have to reach in severe life-threatening infections for other antibiotics such as Amacain or rifampicin. There is no place for those in surface pyoderma.
We shouldn't even be considering, them at all when we've got superficial disease. And it's only life-threatening disease. They both come with significant risks associated with them.
And there are some new, new options that aren't available for use really in veterinary patients. So, careful consideration of antimicrobial therapies is important when we're optimising response. Duration of therapy is important.
The optimal duration is actually not really clarified, but at the moment, we're saying 3 to 6 weeks is often required for complete resolution and prevention of rapid recurrences. And 7 days after resolution of superficial pyodermal lesions is a guide, and 14 days after deep pyoderma. So we still need to do some work in this area.
For a long time, we've said 3 weeks minimum for superficial pyoderma. We actually don't know what the, the proper minimum time should be. And then management of the underlying disease is certainly really important as well.
. OK, I think I'm gonna stop at that point cause there's, the rest is just a little bit about, general treatment and there might be time for some questions as well. Linda, thank you so much for that, very informative treatment, options as well as the, more importantly, diagnostic options. Certainly food for thought, and very well presented.
Thank you very much. You're very welcome. Folks, that's it for this session.
We have reached our time limit, unfortunately, so we can't take this any further now. For those of you that are joining us for the next session, it will be starting at 4 o'clock on the various channels depending on what you've chosen. And thank you for being with us.
And once again to our presenters, Mandy Burrows, Andrew Carter, and Linda Fogelnest for absolutely inspiring. Presentations. Remember, all of these sessions are being recorded and in the next couple of days, they will be up on the website for delegates to go and review and have another look at it.
So from me, Bruce Stevenson and my controller in the background, Chris, we'll see you on the next session. Thank you and goodbye.