Last Updated on November 20, 2025
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If you’ve ever felt like your eczema flares come out of nowhere — even when you’re doing everything “right” — a staph infection might be sabotaging your skin’s ability to heal!
For many people with eczema, Staphylococcus aureus (commonly known as Staph aureus) isn’t just a coincidence…it’s a major driver behind persistent flares, inflammation, and itchiness.
This common skin bacteria doesn’t just live quietly. It can compromise your skin barrier and lead to more intense flare-ups.
And while it might be tempting to write it off as “normal,” the presence of staph on your skin could signal a more serious problem brewing beneath the surface.
But Staph aureus isn’t the only player when it comes to itchy, painful eczema flares. The gut microbiome, environmental toxins, and even air pollution could be creating the perfect storm for eczema.
Joining me to discuss all this and more is listener favorite Dr. Peter Lio, a board-certified dermatologist and leading expert in eczema and inflammatory skin conditions.
Dr. Lio is a Clinical Assistant Professor of Dermatology & Pediatrics at Northwestern University Feinberg School of Medicine. He received his medical degree from Harvard Medical School, completed his internship in Pediatrics at Boston Children’s Hospital, and his Dermatology training at Harvard where he served as Chief Resident in Dermatology. While at Harvard, Dr. Lio received formal training in acupuncture. Dr. Lio has written a textbook on Integrative Dermatology and has published over 100 papers.
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In This Episode:
- The surprising ways Staph aureus disrupts the skin barrier and triggers eczema
- What comes first: eczema or staph aureus infection on skin?
- How staph toxins directly trigger itch and increase inflammation
- 4 triggers of atopic dermatitis (the SAIGE model)
- Why “just moisturizing” doesn’t fix the skin barrier (and what will)
- How environmental triggers like wildfire smoke cause adult-onset eczema
- The little-known role of filaggrin and how inflammation shuts it down
- Topical steroids and biologics: Can they help calm staph and a staph infection?
Quotes
“When there's inflammation in the skin…the body starts shutting down the ability to make filaggrin. You become functionally filaggrin deficient.”
“Normal skin shouldn't really have much Staph aureus, although it can. And this is where things get really confusing. Some people actually do have some Staph aureus on their skin and in their gut, and they're totally healthy.”
Links
Find Dr. Lio online | Twitter | Facebook
Learn to fix your root causes in the “Stop My Eczema Masterclass” HERE
Healthy Skin Show ep. 279: Chemical That Triggers Eczema (Oh My!) w/ Dr. Ian Myles
Healthy Skin Show ep. 107: Symptoms Of A Staph Infection On Your Skin
Healthy Skin Show ep. 328: Client Case Study: Severe Eczema On Feet + Body
Healthy Skin Show ep. 299: What Is Eczema Herpeticum? w/ Dr. Peter Lio
405: Staph aureus + Eczema: Why This Inflammatory Bacteria Is A Problem You Shouldn’t Ignore (Especially When Your Skin Flares) w/ Dr. Peter Lio {FULL TRANSCRIPT}
Jennifer Fugo (00:13.039)
Dr. Lio, it is such an honor to have you back on the Healthy Skin Show. Thanks for being here.
Peter Lio (00:18.264)
Thanks for having me back, it's always a pleasure.
Jennifer Fugo (00:20.759)
So I know one of your favorite topics to talk about, not only is eczema, but specifically things that happen around Staph aureus and staph infection on the skin. I feel like Staph aureus and atopic dermatitis go hand-in-hand. Do you feel like that's a fair way to look at it?
Peter Lio (00:41.826)
Very much. And it's just been this incredible journey of long ago, people realizing that staph could definitely take advantage of the situation, it could be an opportunist, but increasingly, as you say, they're going hand-in-hand and we realize it's probably one of the key drivers of atopic dermatitis, at least in some patients.
Jennifer Fugo (00:58.785)
So is it, so when we say Staph aureus, and I will get into this in a little bit, but I was also kind of thinking like, is there a chicken and an egg scenario, like, what comes first? Is it that you have more staph on your skin? Or is it that the skin barrier gets compromised and then leads to the, like is there one that comes first and then the other, or do you have eczema and then staph overgrowth? What order does it happen in?
Peter Lio (01:27.278)
So yeah, it's probably one of those questions where the answer is just yes, like probably both of those things can happen. And I will say that, in general, normal skin shouldn't really have much Staph aureus, although it can. And this is where things get really confusing. Some people actually do have some Staph aureus on their skin and in their gut, and they're totally healthy.
Jennifer Fugo (01:28.313)
Yeah, they don’t necessarily have a staph aureus infection on skin.
Peter Lio (01:49.962)
Right? It can just be present. So it's out in their environment, it's a very popular bacteria in the world, so it can be there. But we really do see a pretty strong correlation, which as we know, correlation does not mean causation, but a strong correlation with atopic dermatitis. And it really does go up with the more severe the skin is. So the most severe patients, if you swab them, I mean, it's almost a guarantee, especially if there's anything open or oozy, you're almost always going to get Staph aureus. So it's like, for a long time, people are like, well, they're strongly correlated, there's definitely something going on, it's not perfect, but which came first, as you say. And I think, initially, people thought really it was that the skin barrier was damaged, and staph is just out in the world and it found this niche where it could just say, I'm taking over. The defenses are down, the openings are here for me, the skin open barrier, I can just take advantage. And that's what we believed, that's what I learned, 20 years ago plus, that that's how this all worked.
But then Heidi Kong, who's a great dermatologist at the National Institutes for Health, she published this paper in around 2012 where she really turned everything upside down. She showed very, very much the opposite, that it wasn't just taking advantage of an open door, that instead you could actually show Staph aureus increasing on the skin. It would go up in number, and the diversity of the other guys would sort of go down because it became this dominant force. And then you'd see a flare up. And then on the other side, on the backswing, staph would go down first, and then and only then would the skin seem to heal. Now, this is just a model, it wasn't like a perfect thing, but it really changed the discussion.
Jennifer Fugo (03:16.431)
So you wrote this amazing paper called “The Atopic Dermatitis Continuum: An Updated Paradigm for a Common Disorder and a Novel Multipurpose Treatment Option.” So this is like a brand new paper. And I honestly thought, you have this graphic in it that looks like basically this pendulum swinging from side to side with the four demons, which we'll talk about, which are the, you call them interdependent pathological presentations. Yes, I love getting to read all the fancy science speak, and sometimes I understand it, and sometimes it's beyond my understanding. But what I got from this is that you have kind of identified different triggers, correct, for what seems to drive eczema specifically. So before we get into that sort of pendulum swinging with atopic dermatitis and whatnot, what are the key triggers that people who are going like, what is causing my eczema? What's making it worse? What's making me stuck? What would those triggers that you've identified be?
Peter Lio (04:24.533)
Yes, I mean, I think that's the question that many patients are asking, you know, why me, why now, why this week instead of last week? So the answer is probably not one thing, as you can imagine, we kind of pulled these different things. So we kind of say it's SAIGE, S A I G E. The S A is for Staphylococcus aureus, the bacteria can drive it. I is for immune, G is for genetic, E is for environmental. And these four categories can really drive, any of these can do it. And then we kind of have, one of the figures talks about sort of how these might map to things. So the dysbiosis, meaning the microbiome is out of balance, it's out of whack, because there's too much staph.
We also have the idea that there's that uncontrolled inflammation, that even when things look good, we use the term subclinical, meaning clinically, you can't see it. If you come in and like, oh, your skin looks clear, but under the skin, under the microscope, you would still see some uncontrolled inflammation happening. Of course itch, and then dryness, and all these things are kind of playing a role, but of those triggering events, bacteria is a huge one. The immune system is another one. We hear this all the time, people are stressed, people haven't slept well, and then their skin flares up. Or you get sick. A lot of little kids, if they get a cold, you know, they're at daycare, they get a bad head cold, they're fine, they don't even maybe have a high fever, but then all of sudden their skin starts going crazy.
Genetics, w understand, at least play some role in some of the patients, probably some role in everybody, but a bigger role in some of the patients. And then environmental, we've learned in the last few years how powerful the environment has a role on this disease. And in fact the California wildfires really opened a lot of people's eyes, that people who were exposed to wildfire smoke had new onset adult atopic dermatitis. This was shocking, if you would have asked me this five years ago, I would have said no, I don't think that's it, that doesn't make any sense, it doesn't seem right. But it really is one of those things where epidemiology, looking at the numbers, really shaped the understanding of it. So that was a really neat smoking gun, I guess pun intended.
Jennifer Fugo (06:18.361)
So actually, I have a question for you about environment because I think most people, when they hear you say like an environmental trigger, and so wildfires would be out in the environment, or they could think, oh, well, dust mites, and pollen, and these things outside. But could the environment also be what's happening on the internal, like the gut microbiome and those kinds of things, in terms of like an environment? Is that where you would kind of categorize that, or would that be something else? Just curious.
Peter Lio (06:47.859)
Oh, big time, 100%. And I mean, I think one of the things, and you know about this so well and you talk about this so beautifully, but when we eat processed foods, for example, if they have emulsifiers in them, what's an emulsifier? It's just a detergent. It's a fancy name for a detergent. So that goes and damages our gut barrier, which can then secondarily alter our gut microbiome. So all these things are deeply connected. And the person who really put all this together in the last few years, his name is Cezmi Akdis. He's a Swiss allergist and he talks about this epithelial barrier hypothesis model, where our skin barrier, our gut barrier, and our lungs, our respiratory barrier, are all under constant attack from the modern world.
Jennifer Fugo (07:25.103)
Wow.
Peter Lio (07:28.263)
Pollutants, irritants, allergens, food stuff, all this crap, which is very different than we used to be exposed to, is pushing us kind of over the limit. I know people look for all these different things, is it more C-sections, is it antibiotic exposure, and people keep looking, and the answer is probably that there's multiple causes. But these have really emerged as making probably a much larger effect than we had anticipated before.
Jennifer Fugo (07:46.64)
Yeah. You know, it's funny you brought that up about the barriers. I remember, and this was probably the first time, or maybe the second time, I had Dr. Olivia Friedman on the show, who's a good friend of yours. She had also mentioned, from a Chinese medicine perspective, that there's this barrier issue, the internal gut barrier and the skin barrier are kind of looked at very similarly as like, if you start to see a lot of skin barrier dysfunction, you're gonna see a lot within the GI tract as well, as they're thought of as similar within Chinese medicine. So, it's so neat to kind of see the overlap of where we can find the old wisdom and the new wisdom coming in and helping us to find better answers for these types of things.
In terms of genes, is there, is it like, oh, you have an eczema gene, or are we talking about filaggrins more specifically, or is there some other type of, maybe, genes that we don't normally hear about with eczema?
Peter Lio (08:53.367)
There was a minute, maybe like 15 years ago, where we kind of thought, maybe this was going to open it, and you're right, it was with that filaggrin story. People realized there's this gene that encodes for a protein called filaggrin. Filaggrin is really important because it plays a role in our skin barrier, it also plays a role in natural moisturizing factor, it becomes like one of the ways our skin can hold on to moisture naturally. And people thought, maybe this will be it, but it turned out it really didn't seem to explain much of it if you look across the world. Like in some populations, I think it was done in like Northern Europe, in this particular population it was more represented, so people said, wow, there is a correlation here. But then as soon as they went to other populations, like, nah, it's not really that reliable. So it's more, I think, of an example. There probably are a whole bunch of different types of mutations that are not really, they're probably neither necessary nor sufficient. They're not enough to do it on their own, and they don't even have to be there, but they make people susceptible.
I think that's maybe the way we're gonna have to think about this condition, where it's depending, because honestly, if we take a person, somebody who says, you know, I have tough skin, nothing bothers my skin, I've never been irritated by anything, I have no history of eczema, okay. You're like, all right, so you're kind of a non-eczema patient. But if I put something super irritating on their skin every single day, I mean, we can make eczema, right? Eventually I can break it, you know, if we try. And that's the idea. And then there are some people maybe, that are just so sensitive that even things that are in the air or products, like you wash your clothing, maybe you even do a double rinse, but there's still some residual detergent. Now you get a little sweaty or the humidity in the room, it kind of activates that detergent, now you're putting detergent on your skin, harsher cleansers, all these kinds of things that might be enough for some people.
So there's probably a range, and I love the way Dr. Ian Myles, from NIH, used to talk about this idea. If you live near a lake and a whole bunch of fish die, you'd say, oh, what's wrong with these fish? But if most of the fish die, you say, uh oh, what's wrong with this lake? And we're getting to that point where enough people are getting allergy stuff that it's like, well, I don't think it's genetics, and it's happening so fast, it really has to be something in the environment. And it's global, so even across different cultures, and we see that it tends to correlate with urbanization and more modern life.
Jennifer Fugo (10:51.043)
And one thing that was interesting, and you had actually pointed this out in one of the first interviews that I ever had you on for, was this interesting idea that inflammation, which I think a lot of people, they go, okay, I understand inflammation, but then they're not as clear on the cytokine piece of this, and then that gets into more like immunology and whatnot. But in your paper, you actually mentioned that activated T helper cells and their cytokines can interfere with with filaggrin, and you've mentioned that before. So can you just explain that for anybody who has been like, oh my gosh, I need to get the filaggrin gene tested, I have to figure out if I have this gene because I have eczema and I think that's the thing. But I think they miss the fact that there's a role that inflammation plays in kind of dysregulating or disrupting filaggrin that I don't think is discussed enough.
Peter Lio (11:52.3)
It's such a good point. The first time I heard that, I was kind of shocked, but you realize that it is kind of the perfect storm that makes eczema happen. And exactly right, let's say you have normal filaggrin genes, you make normal filaggrin, everything's perfect. It turns out, that in the presence of inflammatory cytokines, when there's inflammation in the skin, for whatever bizarre reason, the body starts shutting down the ability to make it. You become functionally filaggrin deficient.
Jennifer Fugo (12:17.016)
Wow.
Peter Lio (12:20.855)
And it turns out, one of the first ones described was IL-4 and IL-13. Those are ones that seem to directly decrease your filaggrin, which is what one of the newer medicines, dupilumab, the brand name Dupixent, that's actually what it blocks, it blocks those. And that's why a lot of people think, okay, well, it's not only helping itch and inflammation, but it's also helping the skin barrier because those cytokines actually damage our skin barrier. Why that is, I don't fully understand why Mother Nature put it that way. It's weird because again, it makes for a very vicious cycle, as you're trying to boost up your skin barrier when you need it, now it's getting attacked from the inside.
Jennifer Fugo (12:49.623)
Yeah, so on the inside we have the filaggrin, and then on the skin microbiome we've got staph aureus. So you're right, it's interesting that you have this potential internal reaction happening that then, unfortunately, we start to see this decrease in filaggrin that creates kind of almost like a leakier skin barrier. But then that's really helpful and good for staph, which is not good for us. So how does staph take advantage of that situation?
Peter Lio (13:24.535)
So in the worst case, it would cause a real infection. And that could be impetigo, where you get kind of the crusty, yellow stuff that's uncomfortable. It could be cellulitis, where it's now painful, and red, and tender to the touch, you might have a fever. Or, heaven forbid, it could actually then get into your blood and you could have bacteremia or sepsis, where you're sick-sick, and you can die. I mean, it really can be frightening, and thankfully very rare, but staph is a mean, mean actor, we do not play around with it. And that's why it's so scary. I mean, I have an entire clinic full of patients who are walking around with essentially a huge amount of Staph aureus hanging out on their skin, just waiting to cause trouble. And that's why I think there's particular pressure. It's like, we don't want you to have a bad flare-up, we don't want you to wait if you have open sores because if you get infected, and again, thankfully it's fairly rare, but if you do get really infected, we could be in big, big trouble.
Jennifer Fugo (14:14.861)
Yeah, and that was why I liked this graphic that's in the paper. So, one of the things that was interesting is, you talk about colonization, dysbiosis, and staph infection. So how do you differentiate between those, do you consider them to be similar, or different, or different points along the severity of staph? How do you, for somebody who's like, this doesn't make sense, I seem to be fine, and then they always go trying to figure out what the heck they did, what caused it, all of a sudden they had this huge flare up. But like you said, it might not be something you did. It could be a situation with the staph, which is opportunistic, so it takes advantage of opportunities. So how do you differentiate or define colonization, versus dysbiosis, versus staph infection in terms of Staph aureus?
Peter Lio (15:10.317)
I love the question, I think it is a hard one. I don't think we have strict, hard and fast guidelines.
Jennifer Fugo (15:14.509)
Yeah.
Peter Lio (15:16.07)
But I think the idea would be that somebody who really has no symptoms, their skin is clear, they're comfortable, they may or may not have staph on their skin, but many of our atopic dermatitis patients, even when they're clear, they have abnormal microbiome, there's imbalance. And that's kind of that first level. And it's sort of that concept of nature abhors a vacuum. When there's that imbalance, sometimes the bullies come and say, look at this, there's this, it's not a harmonious society here, we're going to come in and take over. And that's often when we see staph starting to take advantage of the situation, just the imbalance.
So those are kind of those early phases. You might not have any symptoms or signs, you're comfortable, but there's something fishy. Then you might start to see some colonization of staph. Now you're swabbing it or doing PCR, however you're testing this, and you're saying, boy, now there is a signal for staph, but maybe you don't have anything clinically yet, so you could still potentially be clear. But then you start to move into the patients where there's something happening, either subclinical inflammation, kind of low level but it's there, to more moderate effect, of course all the way up to a really bad flare-up. And of course, in those really bad flare-ups, many times, I wouldn't say always because I truly do have some patients with severe atopic derm that don't seem to grow staph, but many, many, many times they have a lot of staph and it's abundant, and it's probably playing a direct role at that point too.
So you can see it's a little slippery, but this is why it’s such a complicated condition. I mean, if there were just a simple, easy answer, I think somebody smart would have hit it a while ago, but you know the fact that it's complicated when we have 26 different treatments, and different traditions trying stuff, and we send patients to Dr. Olivia Friedman to do traditional Chinese medicine, and we do nutritional intervention. I mean, it's complicated and I think it is different for each patient to some degree.
Jennifer Fugo (16:47.673)
Yeah. Do you think that, because Staph aureus produces toxins, right? It's alpha-toxin and beta-toxins?
Peter Lio (16:57.325)
Yeah. Uh, there might be a beta, the ones I often talk about are alpha- and delta-toxin.
Jennifer Fugo (17:03.229)
Oh, sorry, alpha- and delta-toxins, okay.
Peter Lio (17:05.707)
Yep. But they're probably all there if we find a list of them. And then there's even one called V-8 protease that seems to directly bind to the nerve endings and drive itch, like literally, you can directly trigger itch. There was a beautiful paper just a couple of years ago showing that.
Jennifer Fugo (17:18.765)
Wow, so do you think that the, so do the toxins, do they also create, like is it almost like a, like going in and like napalming the area? Like do they do a lot of damage to the skin barrier or do they, or is it possible that the toxins maybe have an impact? I know the pH of the skin also, I believe, changes, that we tend to see skin pH increase, which also favors staph. I don't know if those toxins contribute to that, I'm not sure how that process happens, but could they also potentially have an impact on the other bacteria in the microbiome?
Peter Lio (17:57.42)
Absolutely. So, exactly right, so it's like, some of those toxins damage the skin barrier directly, they hurt the cells and literally poison them. And then some of them activate mast cells, so you start releasing histamine and other inflammatory mediators. They can directly activate the immune system more, calling more cells in, which are of course releasing things like IL-4 and IL-13, which further damage the barrier. And then they can directly drive itch, and when we feel itchy, we start scratching, which is also damaging.
Jennifer Fugo (18:22.241)
Oh man, yeah.
Peter Lio (18:30.545)
So it's crazy, but you're right. The other thing they do is they're having an effect on the other bacteria in the skin, and there's this whole concept of quorum sensing. If staph feels like they reach a certain level, then they go crazy with their toxins, if you kind of knock them back down, they stop doing that. And there's a whole technology of you can trick them into thinking that they don't have their quorum sensing stuff, so you can turn that off and make them quiet down.
There's also this kind of concept of biofilms, where they can create this kind of sticky, protective covering that makes them really, really adherent to the skin and difficult for antibiotics to get to, like it actually is like a wall around them. So then there's a whole technology, how can we break these biofilms down, how can we push back? And again, we don't want to do massive damage to the good guys, right? That's the problem with giving somebody super potent antibiotics all the time, or broad spectrum things, because you potentially can cause, it's kind of like shaking up the snow globe. And you hope everything will fall back into place, but sometimes you end up, as you know, in the gut especially, this can make everything even worse, potentially, if you overdo it.
Jennifer Fugo (19:23.95)
So what it sounds like to me, as an outsider, and I'm just thinking like, for patients who are listening to this and they're like, okay, this helps me make more sense of why staph is a problem. A lot of times, and I've heard this, like, well, it's just normal to have staph, like you'll go to the doctor and that's sort of the response. Well, and it kind of sounds like, I'm not saying it's normal and I know that's not what you're saying at all, but it does sound like there's a normalcy around eczema and staph being together. But does it being normal, and I don't know if that's even the right word to use, does that mean that it's okay or we don't necessarily need to worry about it?
Peter Lio (20:09.419)
Yeah, no, I like that. If somebody called me out for saying normal, I might say, okay, fine, it's not normal, but it's common and expected, right? It's abnormal, but it's just, we see this, in this situation, because I think you're right. And I think the answer is that we have a real sense that it's abnormal and it's probably doing bad things even in the lower dosing, but we just don't have a good way to fix it. So I think we just sort of end up being like, all right, well, we see this and you know, there's not that much we can do right now, you're comfortable, certainly some patients can carry on like this for months or years, and then if something gets worse, then that'll kind of force our hand. Which, I think we can all agree, is not optimal. Like it's kind of like waiting for something really bad to happen. It's like, why don't we try to fix it earlier? And I think we're just all desperate for like, what could we do to do something earlier?
Jennifer Fugo (20:55.833)
Yeah, so if you do have, so say a patient comes into your office and they're in a bad state, their skin is really flared up, they're clearly like eczema in a severe state, they're not sleeping, they're severely itchy, they're like gashing at their skin and really miserable. What do you think, I think giving people some just ideas of what they can do, like what are some things they could potentially ask, maybe their doctor, for, like is there a certain type of maybe like antibiotic that might be more helpful than others?
And then I do wanna ask you, not just yet, but I do wanna talk a little bit about why biologic drugs and immunosuppressants, one thing that I've really learned from talking to a lot of dermatologists is that they can also help decrease staph on the skin. I don't understand why that is, but I thought let's start off with what are some things that the patient can do, or ask for, or consider? Because also, too, people are afraid of antibiotics and they think if they use a topical antibiotic it's gonna mess up their gut. So anything you can share around that would be helpful.
Peter Lio (22:11.497)
Sure, thank you. And I think, well, let's start with the easy case. If somebody comes in super severe and clearly infected, there's open sores, there's maybe even pustules, the skin is painful, maybe they even have a low grade fever, well, then it's a slam dunk. It's like, you need antibiotics systemically, either by mouth or by vein, and typically we're going to pick a broad spectrum cephalosporin that's going to really address staph.
If we think that they have MRSA, the methicillin-resistant type, then we might have to pick something different. We'd have to pick clindamycin or we might have to pick a sulfa, which these also have a lot of potential side effects. That's why we don't love using them, because some patients are going to get diarrhea from them, some patients could get, heaven forbid, they could get an allergic reaction to the antibiotic that can be even worse. So you kind of have to walk this tightrope. You don't want to be too much of a cowboy, just saying, oh, let's just throw it at it. But if it's really bad, then there's sort of no choice. It's like, we're concerned about your overall health here, we have to do this. So that's easy.
Jennifer Fugo (23:02.553)
Yeah.
Peter Lio (23:11.777)
The next level down is still pretty easy. If they have maybe an area of impetigo where it's kind of creusted, yellow, oozy, then I think it's pretty straightforward to use mupirocin, the topical antibacterial, that's pretty darn safe, it's very rarely causing trouble. Again, it doesn't mean it's perfectly safe, and you can get resistance to it over time. And that's one of the fears, people are saying we're seeing more and more bacteria that just laugh at it now because we've overused it.
Jennifer Fugo (23:26.638)
Wow.
Peter Lio (23:29.918)
But for an individual patient, that's something we can do. And then the hardest is somebody that just has a flare, but it doesn't really look infected. And I'll tell you this, kind of spoiler alert, is that many times we understand that if you put them on antibiotics, even if it doesn't look infected, many people get better.
Jennifer Fugo (23:41.688)
Wow, interesting.
Peter Lio (23:43.483)
So I think your instinct is right that you can push back. But again, then you sort of get called out by your peers and by other people saying, well, you're kind of abusing antibiotics here. It's not good stewardship, and you're contributing to a potential future where all of a sudden they don't work anymore because we've overused them. So that's the tension. Of course, not to mention the individual side effects for the patient, as we said.
Jennifer Fugo (24:01.263)
Sure.
Peter Lio (24:04.685)
Of diarrhea, allergic reaction, all these things. So we do think that they work for many patients, but these are the trade-offs, so we try to reserve them for when it's more clear. That's why I think we've all been searching for things we can do that are short of that. Now, here's the other weird part of the spectrum, and you kind of asked this initially, about how do the biologics like dupilumab, do they help? They do. They seem to help the microbiome, both on skin and gut, and we think it's indirect here. We think it's just that it helps repair the skin barrier, which then allows for the proper harmony to take place and the bacteria can kind of sort themselves out.
Jennifer Fugo (24:33.057)
Interesting.
Peter Lio (24:34.401)
And then here's the weirdest one of all. The weirdest one of all is that topical steroids, which, we often kind of vilify a little bit and they have their place, but we have to be careful. But even they have been shown to have essentially a bacterial helping effect, a rebalancing effect of the microbiome. I don't want to call it antibacterial, because we don't think they're directly attacking staph, I mean, I'm pretty sure they're not. But when you treat damaged skin with just steroids, the staph goes down. And again, we think it's the same concept as what we saw with dupilumab and other things, it helps cool the inflammation, it breaks that vicious cycle, the barrier can rebound a little bit, and then we can heal.
But obviously, if somebody has infection already, we typically don't want to put steroids on there because that can suppress the immune response, in theory, and make them more susceptible. So again, it's a bit of a tight rope, and sometimes if somebody looks infected, I'll say, why don't we do non-steroidal stuff for a little bit? Let's get this infection under control. We can do things like wet wraps, changing the environment of the skin. We can do things like black tea compresses, which also can change that local environment, probably a little acidic too, so they strengthen the acid mantle potentially. And then once we're a little bit better, then we can then shift if we need to, use our anti-inflammatories again to get things under control.
Jennifer Fugo (25:38.223)
That is so interesting. And it's interesting, there's so many pieces to this we still don't know. We don't understand how they do all these things, but we see that this happens. So, gosh, so wait, I think the one question, I'm thinking, if somebody was listening to this, because I think that's important. So if somebody is using a topical steroid and, say, there's a very flared up area and they don't actually know that they have an infection and it's not getting better, is that a red flag that you need to go see your doctor and look for an infection?
Peter Lio (26:17.089)
Very much. And in fact, it's funny you bring this up, I'll send it to you as soon as it's out, we just submitted a paper for a pediatric emergency journal. You may remember, my wife is a pedes emergency doc.
Jennifer Fugo (26:27.747)
Yes.
Peter Lio (26:30.201)
So we wrote it together, with a great medical student, and it's sort of an approach for pediatric patients who come to the emergency department, which they do, with bad eczema flare-ups. And that's exactly what we said. The first step, when somebody comes in with a bad flare-up, is to make sure, do you think you have an infection? And of course it's not just bacterial, but some patients can have a viral infection, in particular with the herpes virus, and then we call that eczema herpeticum, where you have the widespread, normally what might just be a cold sore for somebody with kind of non-eczema skin, for eczema patients, that cold sore, quote unquote, can become a huge area and make them actually quite sick, and they can get really in trouble.
So the first step on that algorithm is to make sure, do we think there's an infection, could this be playing a role? You have to do the testing to be sure, because you can't always tell by your eye. You should be swabbing, you can do viral PCR, all these kinds of things to make sure. And then if we feel like, okay, there is those things, then it's sort of easy, you're going to treat those, make sure they're better. If there's not those things, then we can do some of the other approaches we were talking about, cooling the inflammation, cooling the itch, healing the skin barrier more directly.
Jennifer Fugo (27:28.696)
Do you think that the flakiness, is that a sign that basically the skin barrier, so flakiness in eczema, where they're just like flaking so much, is it because the skin barrier is so compromised that, is it almost like your body's trying to desperately produce more cells to try to fix the problem but it's not happening, or is it because the skin barrier can't hold moisture in? What exactly causes, do you know what causes that? Do we know the full picture?
Peter Lio (27:57.676)
Yeah, I like the way you put it. Yeah, I think what we see is, we'll see a lot of exfoliation and a lot of buildup when the metabolism of the skin is ramped up. So when there's a lot of inflammation around, there's increased blood flow, there's a whole bunch of inflammatory factors. So the skin is actually going crazy, it's trying to push back and it's actually metabolically superactive, so you end up with lots and lots of layers being formed. And of course, we really see this in psoriasis, we get all the buildup of those layers.
But you can also see it if patients have a terrible allergic reaction to like a medicine, and they turn beet red, they call it erythroderma, their whole skin is beet red. As they're healing, they often will have tons of sloughing and all this exfoliation. And again, it was because, acutely, they had this massive increase in the metabolism of the skin and then it sort of has a big die off, so you see it. But with our eczema patients, it's more of a chronic thing, they're kind of chronically out of whack.
Jennifer Fugo (28:45.379)
Right, right. And then they're like, I don't understand, my skin’s so dry, I'm trying to apply moisturizer, but it just doesn't last, almost, it's like it doesn't work.
Peter Lio (28:56.747)
We always use the bucket with a hole in it analogy. It's like, you could keep filling a bucket, but if it's got holes in it on the bottom, you're never going to be able to carry that water. So we have to heal the holes, we have to fix them. And that's what we got to do with healing the barrier.
Jennifer Fugo (29:05.741)
Yeah. Yeah. My goodness, this is such a fascinating conversation about staph infection, how to treat staph infection, and so much more. I love that you do so much research. Obviously listeners are not gonna know that you have me on your list of, I love it, I get all of your new papers, and I read through all of them and I learn so much, and I'm always like, my gosh, this is so fascinating. And so I saw this one and I was like, we have to talk about this because I think it's really fascinating, the idea that there seems to be, we're not saying it's one for one, this causes that, but there does seem to be this interesting shift back and forth between these organisms like Staph aureus and the severity of atopic dermatitis.
It'll just be fascinating to see where research goes over the next few years and the things that we uncover. And I just thank you so much for, not only your curiosity, because if it weren't for curiosity, right, we wouldn't be here having this conversation and learning new things, but also your willingness to not only share this information, but I've watched you in action in your office with your patients and the level of compassion that you bring to your patients is just like, it's like I would watch your patients just relax. Like, it was like they finally for the first time, because they're all ramped up, it was in between appointments, or this is the first time you're ever seeing them, and they're like, oh my gosh, I feel heard. And there's just something beautiful to see, because I grew up in the medical community, my dad was a doctor, we had a practice. So I understand what it's like for people to be in such terrible suffering, and I think you've brought so much goodness to people's lives trying to help them get out of these very sometimes horrible, desperate situations where their health is just so bad because of their skin, and I just want to appreciate you for that.
Peter Lio (30:57.555)
Well, thank you. I do, I'm grateful to my patients. They keep me on my toes, you know, they say, fix it, figure this out, come on, you know, let's go, I'm miserable. So that's where it all comes from, right? Not being able to give a good answer and saying, I got to figure this out. I want to give you an answer.
Jennifer Fugo (31:02.767)
Yeah, well, thank you so much for joining us today, as always. My gosh, I think you've been on the Healthy Skin Show more than anybody else, and I always look forward to having you back again the next time.
Peter Lio (31:22.679)
Thank you, my friend. Take good care.
Jennifer Fugo (31:24.334)
You too.
