Podcasts about Staphylococcus

David Jernigan 0:15Hello! Dr. Deb 0:16Hi there, sorry for all the confusion. David Jernigan 0:19Oh, no worries, you gotta love it, right? Dr. Deb 0:21Oh, I can’t hear you. David Jernigan 0:23No way, let’s see, my mic must be turned off? Dr. Deb 0:27Hang on, I think it’s me. Let’s see…Okay, let’s try now. David Jernigan 0:40Okay, can you hear me? Dr. Deb 0:42Yep, I can hear you now. David Jernigan 0:43Excellent, excellent. And, how are you today? Dr. Deb 0:48I am good, thank you. How about yourself? David Jernigan 0:50I’m good. Well, it’s good to finally meet you and get this thing rolling. Dr. Deb 0:56Yes, yes, I’m so sorry about that. David Jernigan 0:58That’s alright, that’s alright.So… Dr. Deb 1:01Yeah, go ahead. David Jernigan 1:03So, tell me about yourself before we get going. Dr. Deb 1:06Yeah, so I am a nurse practitioner. I’m also a naturopath. I have a practice here in Wisconsin. I’ve been treating Lyme for about 20 years, so I’m really excited to have this conversation and learn what you’re doing, because it’s so exciting and new. David Jernigan 1:21Well, thank you. Dr. Deb 1:22Yeah, so we treat a lot of chronic illness patients, do some anti-aging regenerative things as well, so… David Jernigan 1:30Yeah, I went to your website and saw you guys are killing it, looks like. Dr. Deb 1:35Yeah. David Jernigan 1:35Got a lot of good staff, it looks like. Dr. Deb 1:37Yeah, we’ve got great staff, great patients, busy practice. We have 5 practitioners, so we have about 15,000 patients in our practice right now. David Jernigan 1:46Well, excellent. Yeah. Excellent. Yeah, yeah.So, I’m excited for this discussion. Dr. Deb 1:53Good, me too. So I pre-recorded our intro, so we can just kind of dive right in, and I’ll just ask you to kind of introduce yourself a little bit, tell us a little bit about yourself, and, and then we can just dive right into it. David Jernigan 2:08All right. I’m Dr. David Jernigan, and I own the Biologic Center for Optimum Health in… Franklin, Tennessee, and I’ve been in practice for over 30 years. I shook Willie Bergdurfer’s hand, if anybody knows who that is. It’s kind of infamous now with some of the revelations that have happened about Lyme being a bioweapon and weaponized. But, you know, I’ve been doing this, probably longer than almost anybody that’s still in the business in the natural realm. It chose me. I did not choose Lyme. Matter of fact, there were many times in my career that I was like. You know, cancer’s easier because of the fact that everybody agrees, you know, what we’re dealing with. And in the 90s, it was a whole different reality, where nobody actually understood that you could have Lyme disease and not be coming from New England.You know, so I had actually the first documented case of a Lyme disease, CDC positive.Patient that had never left the state of Kansas before. So they couldn’t say that it wasn’t in Kansas, and so she had actually been, pregnant with… twin boys, and they were born CDC-positive as well, and so it is transmitted across the placenta we know.So, I, you know, the history of how I did all this was, in the 90s, probably 1996, probably, somewhere in there, 97. With this woman, you know, I… if you go into Robin’s pathology books from back then. Which we all used, medical doctors and everybody else studying. you know, there was basically a paragraph about Lyme disease, and on the national board tests, as you recall, it was probably like, what causes, or what is, bullseye rash associated with? And you’d had to guess Lyme disease, of course. Dr. Deb 4:07Female. David Jernigan 4:08But that was, you know, considered to be more a New England illness, and you would never see it anywhere else. But here was this woman. I knew… nothing about Lyme beyond what we had gotten taught in college, which was, like I say, next to nothing. And she would not let me stop feeding me information. I mean, you gotta remember, the internet wasn’t even hardly in existence in those years. I mean, it was brand new. It was supposed to be this information highway, and So I started purchasing, like a lot of doctors do even now, they start purchasing every kind of new supplement that’s supposed to work for bacteria. There was no product in those days that actually was Lyme-specific. I mean, nobody was really dealing with it naturally. It was always a pharmaceutical situation. Dr. Deb 5:04And a very short course at that. David Jernigan 5:06Yeah, 2 weeks of doxy and you’re cured, whether your symptoms are gone or not, which… she’d had the 2 weeks of doxy, and her symptoms and her son’s symptoms were not gone. And so, I absolutely just purchased everything I could find. Nothing would work. I mean, I could name names of products, and you would recognize them, because they’re still out there today. Dr. Deb 5:28Which is. David Jernigan 5:30Kind of a… A sad thing that natural medicine is still riding on these things that have the most marketing. Dr. Deb 5:37As opposed to sometimes the things that actually have the documented research. David Jernigan 5:42Behind it, and I am a doctor of chiropractic medicine, and I specialized all these years in chronic, incurable illnesses of all types. That may sound odd to a lot of people, but doctors of chiropractic medicine are trained just like a GP typically would be. The medical schools, as I understand it, got together, decades ago and said, wow, if all we did was… Crank out general practitioners for the next 10 years, we wouldn’t have still enough general practitioners to supply the demand. Dr. Deb 6:17Right. Everybody in medicine, in medical schools, wanted to be a specialist, because that’s where the money was, and it was… David Jernigan 6:24Easier, kind of, also, to… you know, just focus on one part of the body, and specialize in that. Dr. Deb 6:31Expert in that one area. David Jernigan 6:32So we all now have the same training. We all go through pre-med. We got a bachelor’s degree, I got my bachelor’s degree in nutrition, and through, Park University in Parkville, Missouri. And so, you know, when I ran out of options to purchase, I just used a technology that I developed, which was an advancement upon other technologies, but I called it bioresonance scanning. And I coined the term back in the 90s. It was a way to kind ofKind of like a sensitive test, you know, like you might. Dr. Deb 7:09I wouldn’t. David Jernigan 7:09Of applied kinesiology, then clinical kinesiology, then chiro plus kinesiology, then, you know, you can just keep going with all the advancements that were made. Well, this was an advancement upon those things, so… I developed… I was the first in… in… my known world of doctors to develop a way to detect adjunctively, obviously we can’t say it’s a primary diagnosis. Adjunctively detect the presence of a given specimen. So we could say, thus saith my test. It’s highly likely you have Borrelia burgdurferi. And, but I had to have the specimen on hand to be able to match what I call frequency matching to the specimen. Brand new concept in those days. And so I was able to detect whether or not my treatments were successful or not. This is something even now that’s really difficult for doctors, because antibody tests, even the most advanced ones, it’s still an antibody test. It’s still an immune response to an infection.And accurately, you know, some doctors will slam those tests, saying, well. That doesn’t mean you actually have the infection, that just means your body has seen it before, which is a correct statement, kind of. So being able to detect the presence, and even where in the body these infections are was a way huge advancement in the 90s, for sure it’s kind of funny, I think about a conference I went to, and cuz… I’m kind of jumping ahead. Because I ended up developing my own formula, just for this woman and her children, and it worked. And I was like, wow! Their symptoms were gone, all the blood tests came back negative. In those days, we were using the iGenX. Western blot, eventually. And the, what was called a Lyme urine antigen test. I don’t know if you remember that, because it… Only decades later did I meet, the owner of iGenX, Nick Harris. Dr. Deb 9:17Person. And I was like, whatever happened to the Luwat test? Because I took it off the market after a while. He said, honestly, we lost the antigen and couldn’t find it again. Oh, no. David Jernigan 9:27And so… but that was a brilliant test. It was the actual gold standard in those days. Again, the world… it can’t be understated how different the world was in the 90s. Dr. Deb 9:40Yeah. David Jernigan 9:41Towards natural medicine, even. Dr. Deb 9:44Oh, yeah. We think… we think it’s bad now, but, like, when I started, too, I started in the early 2000s, like, we were all hiding under the radar, like, you didn’t market, we would have never been on social media, we didn’t run ads, we didn’t do any. David Jernigan 10:00Right. Dr. Deb 10:01Because the medical boards were coming for us. David Jernigan 10:04Came after me. Dr. Deb 10:05Because I had the word Lime on my page, my website. David Jernigan 10:10You know, not saying that I treat Lyme. Dr. Deb 10:13Hmm? David Jernigan 10:13Yes Dr. Deb 10:15Just talking about mind. David Jernigan 10:16And it’s funny, because, once I had this formula, it was something… and I trained in Germany, in anthroposophical medicine, and they’ve been trained in herbal… making herbal extracts, making homeopathic remedies in the anthroposophical methodology, and I trained with the Hahnemann versions of homeopathy, which is just slightly different. Yeah. And, so I was well-versed with making some of my own formulas by that time. And so, it was really something that I wrote on the bottle, you know, and I had to call it something, so I called it Borreligin, which is still in existence, and it’s still a phenomenal herbal remedy right now. And to my knowledge, it’s the only frequency-matched herbal formula. Maybe still out there. Because unless you knew how to do my testing, the bioresonent scanning, there was no way to actually do frequency matching. Matter of fact, as a really famous herbalist attacked me online, saying, oh, none of these herbs will kill anything. And I’m like, that wasn’t what I was saying. I was saying, back in those days, I was saying, well, if… what would the body need to address these infections?You know, not, like, what’s gonna kill the infections for the body. Dr. Deb 11:38Right. David Jernigan 11:39Right? So it was a phenomenal way, but the LUAT test was amazing because what you’d do is you would give your treatment, like an MD would give an antibiotic for a week, ahead of time. Trying to increase the number of dead spirochetes showing up in your urine one day out of 3 days urine catch. So you’d wake up in the morning, you’d collect your urine 3 days in a row, and any one of those being positive is a positive. But it was a brilliant test because it wasn’t an antibody test. They were literally counting the number of dead pieces of Lyme bacteria in your urine. I mean, it was pretty irrefutable. So I had a grand slam on the… the Western blot on patients, and I’d also have a grand slam on the LUAT, and their medical doctors would say, oh, that doctor in the lab are probably in cahoots change some lab. Dr. Deb 12:38Of course. David Jernigan 12:39That come in. And I still see that today. You know, it’s like, oh my gosh, the better the tests are getting. There’s still a bias if you do your own research. Well, if you happen to be a doctor who loves research. And you’re a clinician, so you actually treat patients who’s gonna write the research study? Well, of course, the doctor who did the study, well, he’s biased, and I’m like, I still can’t influence lab tests. Well, lab tests aren’t everything. People scream over the internet at me. It’s like, well, a negative lab test doesn’t mean anything. I was like… I get that with the old Western blot testing. Dr. Deb 13:16Right. David Jernigan 13:16The more sensitive tests, which are very close to 100%, Sensitivity, and 100% specificity. So, meaning, like, they can… if you have the infection, they’re gonna find it. Dr. Deb 13:30They’ll find it, yeah. David Jernigan 13:31And if they… if you have the infection, they’re going to be able to tell you exactly 100% correctly what kind of infection it is. Back in those days, you couldn’t, you could just count the dead pieces, which was… Dr. Deb 13:43Yeah. David Jernigan 13:43Significant, but It’s funny, because when medicine does that, you know, mainstream medicine that’s backed by all the nice foundations who donate millions of dollars towards the research. Their negative tests are significant, but if you fund your own, Yours isn’t that significant. Dr. Deb 14:04Right, or what if we call something a seronegative autoimmune disease, like lupus or rheumatoid arthritis, because none of the tests are positive, but you have all the symptoms. Here, let me give you this $100,000 a year drug. David Jernigan 14:19Yeah. Dr. Deb 14:19And instead of looking for what might actually be causing the symptoms. That’s all okay, but what we do is not okay. David Jernigan 14:27Right. Yeah, it’s a double standard, and it’s getting better. I want to do… tell the world it is getting better. Some of the dinosaurs are retiring. Dr. Deb 14:36No. David Jernigan 14:37Way for people who are… Are more open-minded to new ideas. But, getting back to that woman, she… that formula that I made just for her and her son, I… She went online. Dr. Deb 14:54Which, I had never been on a news group. David Jernigan 14:58Not even sure I knew what one was, you know? Imagine, I’m kind of that dinosaur that… Cell phones were, like, these really big things with a big antenna sticking out of it, and… Dr. Deb 15:09Nope. David Jernigan 15:10So I thought I was pretty hot stuff, just that I actually had a computer software program that was running my front desk. And even then, it was an Apple IIe computer. Dr. Deb 15:21Right. David Jernigan 15:22Probably be pretty valuable right now if I’d kept it, but… Dr. Deb 15:25Mmm… David Jernigan 15:26It being an antique. But, suddenly people were calling my clinic, because the lady with the twin boys that was well was telling people on these research, I mean, these Lyme disease forums and boards online. And, I started going, oh my gosh, you know, as a doctor, it’s one thing to treat a person in your clinic, it’s a different thing to have your clinic name on the label. Like, we all do, Even now, and you’re supposed to write everything that’s on the label, and… all these guidelines, and I’m like, wow, I need to split this off. I mean, I def… I definitely want to help people, and this is… I was pretty excited about the results we were getting. Pre-treat… Pre-treatment and post-treatment. And, so… that’s where I developed, my nutraceutical business in the 90s called Journey Good Nutraceuticals. My advice to anybody thinking about doing the same thing, don’t put your last name on it. Dr. Deb 16:25– David Jernigan 16:25You know, because anytime negative anything comes out, there goes the Jernigan name, you know, the herbal, you know, there’s just all these, and especially nowadays, with all the bots that are just designed to slam natural medicine. Dr. Deb 16:38Yeah. David Jernigan 16:39And that is out there in a… and just ugly people. Dr. Deb 16:42Or should we just say, people with a different opinion? How’s that? David Jernigan 16:46Yeah. That are being less than supportive. Dr. Deb 16:49But. David Jernigan 16:51It was amazing, because by 1999, I presented my research, my first research, I’d never done research. This is what I would… I would say to a lot of people who go, my doctor did… I don’t know, my doctor doesn’t know what you’re doing, my doctor… I was like going, you know, most doctors don’t do research. They don’t publish anything. Their opinion is their opinion, but they don’t back it up in peer review, right? And so that’s what I always tried to do, was back it up in peer review and publish. And so, in 1999, I presented at the International Tick-Borne Diseases Conference in New York City. I’m telling you, it was like the country boy going to the city, you know, I got my… I got my suit on, and I looked all right, and my booth was wonderful, and all these different things, and it was just a big wake-up call.Because what we had demonstrated… let’s get back to the… and this was what I demonstrated with that first study. was that… A positive LUAC test, that Lyme urine antigen test for my Gen X, was a score of 32. Meaning, one of those 3 mornings urine had 32 pieces in the amount of urine they checked of deadline bacteria spirochetes. Okay? Okay. With antibiotic challenges, a highly positive was a score of 45. Dr. Deb 18:19Wow when I would give one dropper 3 times a day for a week. David Jernigan 18:24Ahead of time, and then do the person’s LUAT test, We were getting scores 100, 200… And at that point, we only had a couple, but we had a couple that were greater than 400. Yeah, dead pieces, where the lab just quits counting. They just said, somewhere over 400, right? Dr. Deb 18:45Yeah. David Jernigan 18:46Which, when the medical system at the conference, you know, I was the only natural doctor in the world that was… had any kind of proof of anything naturally that could outperform antibiotics. Can you imagine? Dr. Deb 18:59Yeah. And… David Jernigan 19:01They were just, oh my gosh, incredulous. They’re like, I’ve given the most… one guy came up to me, and to my face, and he goes, I’ve given the most aggressive antibiotic protocols And I’ve only seen one patient over 100. I was like, that makes this pretty significant, doesn’t it? But, it didn’t just, like, make us take off, because guess what? In Lyme world, if a pharmaceutical antibiotic made you feel horrible. That meant it was working. Dr. Deb 19:28That’s right. We used to, back in the day, if you didn’t herx. And had that horrible die-off reaction, for those of you who don’t know what a herx is, but if we didn’t make you herx, we weren’t doing our job right. David Jernigan 19:40You’re looking for your patients to feel horrible, and sometimes to the level of committing suicide. Dr. Deb 19:46Yes. David Jernigan 19:47So bad. Dr. Deb 19:48Yes. David Jernigan 19:49And I was the first doctor, I think, in the world to start screaming and hollering and saying, stop using the worsening of your patient’s symptoms as a guide to good treatment, because they’re… I wasn’t seeing it with my formulas. Because I was doing a comprehensive program of care. I think I was also one of the first doctors to say, we need to detoxify these people as we’re doing this. And you would sit there and say, well, sure you were. I was like, well, remember, there wasn’t a lot of communication. There wasn’t anybody on the internet saying, do this, do that. And, It was, it was interesting in those days. It was, how do you… How do you help the world heal from these things? That they don’t know they have. So later, I actually had a beautiful booth at a health… a big health expo in Texas, I remember, and I was like, you know, you spend a lot of money on the booth, and… Dr. Deb 20:43Yup. David Jernigan 20:43And you’re thinking about it because you’re funding the whole thing, you say, wow, if I only sell one case, I’ll at least cover my cost. Dr. Deb 20:51Yep. Yeah, you’re great. David Jernigan 20:52And I had this beautiful banner of, like, a blown-up tick’s mouth under microscope. You know those beautiful pictures of, like, all the barbs sticking out, and how they anchor themselves in your skin, and… And, thousand people walking by my booth, and they’re just like, keep walking, because they didn’t know they had Lyme. There was, like, and they had MS, maybe, but they don’t have Lyme, and so they just would keep walking. Nobody even knew. Why would I go to a conference in Texas? And I’m trying to say, no, guys, it’s everywhere. Dr. Deb 21:24Yeah. David Jernigan 21:24And… and everybody, you know, yes, you probably have this, you know, kind of thing. If you’re… if you… are chronically ill, almost, of any kind of way. You know, kind of trying to tell people this was… Again, in Robin’s pathology textbooks, one of the few things that it did tell you about Lyme was that it was called the Great… the New Great Imitator. Because it would imitate up to 200 or more different illnesses. So, it’s been an interesting journey, of… educating people, writing articles, but it was interesting, the lady who I first fixed, Laboratory verified, everything like that, symptoms went away, all that kind of fun stuff. Her children were fine, they’ve been fine for years now. When she went on the newsboards in the Lyme disease support groups, It created a war. Oh my goodness, it was like, how dare you? And, say that something natural might actually help, right? Dr. Deb 22:30Right, exactly. David Jernigan 22:32And, I even had… A… one of those first calls to… with a marketing company at one point, way a long time ago. And the lady got on the phone, the owner of the marketing company goes, I would have blood on my hands if I actually took your clinic on. Yeah, you can’t treat Lyme disease, and… Even the big, big associations that are out there are still largely that way. I mean, they’re getting better, but it’s just like… you know, a lot of the times, it’s herbs are good. Herbs will help. Good, you know, but they’re safe. So, it’s still a challenge to… to… present in mainstream Lyme communities, even. Because there’s this… Fear of doing anything outside of antibiotics. Dr. Deb 23:32Yeah, so let me ask you this. From your perspective. Why do you think so many chronic infections exist these days, like Lyme and the co-infections, Babesia, Bartonella, mold illness? And we talked a little bit about herbs and why they, antibiotics and things like that fail, but let’s talk a little bit about that. David Jernigan 23:53So, it’s fascinating. When I trained in Germany, they said that we, as humanity, has moved away from what they called the inflammatory diseases. You know, in the old days, it was. Lots of high fevers, purulent, pus-generating bacterial infections. And I said, as a society, we have… Dr. Deb 24:14Have shifted from those to what they call cold sclerotic diseases, which are your… David Jernigan 24:21Cancers, your diabetes, your atherosclerosis, your… and they said, we’re starting to see what used to only be geriatric diseases in our children. That’s how bad it’s gotten. We have suppressed fevers, we don’t… we don’t respect the wisdom of the human body. So, you know, the doctors say, step aside, body, I will fix this infection for you with this antibiotic. And so, what we’ve done with the, overuse of antibiotics, and this isn’t me just talking from a natural perspective, this is… Right, it’s everybody around the world is acknowledging. I’ll show you… I could show you a, a presentation, if we can do a screen-sharing situation. Yeah. About the antibiotic situation in the world, because it’s really concerning. But what I would say, and kind of like an advancement forward, is we are seeing mutated bacteria. You know, they talked about… do you remember when they found the Iceman, you know, the… You know, the prehistoric guy that’s… In the eyes, and he had Lyme bacteria. I was like, he had spirochetes, maybe. Dr. Deb 25:33Yeah. David Jernigan 25:33That isn’t a modified, mutated version. That’s just maybe the… Lyme… you know, Borrelia… call it Borrelia something, you know, it’s a spirochete, but what we’re dealing with today. Even under strep or staph, as you know, you know, Pseudomonas aeruginosa, you name it, whatever kind of infection a person has is not the same bacteria that your grandparents dealt with. Dr. Deb 26:01That’s right. David Jernigan 26:32It’s a much mutated, stronger, more resistant to treatment type of thing. So, I think that’s one reason. I think the, It’s great that we’re seeing, you know, Secretary Robert F. Kennedy Jr. bringing awareness to things that Like it or not, yeah, seed oils do create inflammation, and everyone in the natural realm, as you know. Has been trying to say this for probably how long? Dr. Deb 26:35Yeah, 25, 30 years. 20 years each. David Jernigan 26:48Yes. You know, thank goodness for people like Sally Fallon and her beautiful book, Nourishing Traditions, that started you know, Dr. Bernard Jensen’s books way back in the day, Dr. Christopher’s books way back in the day. Dr. Deb 26:48Damn. David Jernigan 26:49You know, all of them were way ahead of their time, saying, by the way, your margarine is only missing one ingredient from being axle grease. Dr. Deb 26:58Yeah. David Jernigan 26:58I think that was Dr. Jensen saying that at one point, probably 50, 60 years ago, I don’t know. Dr. Deb 27:03Yep. David Jernigan 27:04So, we’ve created this monster. We, we live in a very controlled environment, you know, of 72, 74 degrees at all times, we don’t sweat, we don’t have to work that hard, typically. You know, most of us aren’t out there like our ancestors were, so that’s making us more and more… Move towards the cold sclerotic diseases, of which even Lyme disease is, you know, which… Yes, it has inflammation, yes, but as a presentation, it’s very often associated with some of these Cold sclerotic diseases of mankind that we see now. Dr. Deb 27:46You have it. David Jernigan 27:47Yeah. Dr. Deb 27:48So, tell me, what is phage therapy? David Jernigan 27:52Well, may I show you a cool video? Dr. Deb 27:55Yeah, I’d love that. David Jernigan 27:56I did not make this video, this is just one of my favorites, because it’s from the National Institute of Health. Let’s see if I can just… Click the share screen thing. And get that to pop up. That’s not what I’m looking for, but it’s gonna be soon. Let’s go here… Alright, can you see that? Dr. Deb 28:18Yeah. David Jernigan 28:19Okay. Modern medicine faces a serious problem. Thanks in part to overuse and misuse of antibiotics, many bacteria are gaining resistance to our most common cures. Researchers are probing possible alternatives to antibiotics, including phages. So, bacteriophages, or we like to call them phages for short, are naturally occurring viruses that infect and kill bacteria. The basic structure consists of a head, a sheath, and tail fibers. The tail fibers are what mediate attachment to the bacterial cell. The DNA stored in the head will then travel down the sheath and be injected inside the cell. Once inside the cell, the phage will hijack the cellular machinery to make many copies of itself. Lastly, the newly assembled phages burst forth from the bacterium, which resets their phage life cycle and kills the bacterium in the process. Someday, healthcare providers may be able to treat MRSA and other stubborn bacterial infections using a mixture of phages, or a phage cocktail process would be first to identify what the pathogen is that’s causing the infection. So the bacterium is isolated and is characterized. And then there’s a need to select a phage in a process known as screening of phage that are either present in a repository or in a so-called phage library. That allows for many of the phages to be evaluated for effectiveness against that isolated I don’t know, bacterium. Phages were first discovered over 100 years ago by a French-Canadian named Felice Derrell. They initially gained popularity in Eastern Europe, however, Western countries largely abandoned phages in favor of antibiotics, which were better understood and easier to produce in large quantities. Now, with bacteria like these gaining resistance to antibiotics, phage research is gaining momentum in the United States once again. NIAID recently partnered with other government agencies to host a phage workshop, where researchers from NIH, FTA, the commercial sector, and academia gathered to discuss recent progress. NIH… So… That is… That is what phage therapy in… is. in what I call conventional phage. Let’s see, how do I get out of the share screen? Hope you already don’t see it. Dr. Deb 30:58Yep, at the top, there should just be a button. David Jernigan 31:00I don’t. Dr. Deb 31:00Stop sharing, yeah. David Jernigan 31:01So… Conventional phage therapy, as you just saw, is a lot like what it is that we’re doing, only the difference is they’re taking wild phages from the environment. They’re finding phages anywhere there’s, like, a lot of bacteria. And then they isolate those phages, and like he said, the gentleman at the very end said we put them in a library, and so there are banks of phages that they can actually now use, and One of the largest banks that I know of has about 700 different bacteriophages, or phages. In their bank that they can pull from. Dr. Deb 31:43Wow. Do you want to take a guess? David Jernigan 31:46How many bacteriophages they’ve identified are in the human gut, on average? Dr. Deb 31:52Oh my god, there’s gotta be more… David Jernigan 31:53Kinds, different kinds of phages, how many? Dr. Deb 31:56There’s gotta be millions. David Jernigan 31:57Well… In population, there’s… humongous numbers, numbers probably well beyond the trillions, okay? Hundreds of trillions, quadrillions, maybe, even. But in the gut, a recent peer-reviewed journal article said that there were 32,242 different types of bacteriophages that live naturally in your intestines, your gut. Dr. Deb 32:25Boom. David Jernigan 32:2632,000. Okay, so… If you read any article on phage therapy that’s in peer review, almost every single one in the very first paragraph, they use the same sentence. They go, Phages are ubiquitous in nature. They’re ubiquitous in nature. So my brain, when I find… when all this finally clicked together, and when we clicked together 5 years into my research, I could not get it to work for 5 years. I just kept going. But that sentence really got me going. I was, like, going, you know. If you look at what ubiquitous means, it says if Phages were the size of grains of sand. Like sand on the beach. They would completely cover the earth and be 50 miles deep. How crazy is that? Dr. Deb 33:24Wow. David Jernigan 33:25That’s how many phages are on the planet. There’s so many… they outnumber every species collectively on the planet. So, it’s an impossibility in my mind. I went, huh, it’s an impossibility that… You catching a, a sterile Bacteria, it’s almost an impossibility. Since the beginning of time, phages have been needing to use a reproductive host. And it’s very specific, so every kind of bacteria has its own kind of phage it uses as a reproductive host. Because phages are… and this is a clarification I want to make for people. just like in the old days, we were talking about the 90s, I talked to a veterinarian that had gotten in trouble with the veterinary board in her state. Dr. Deb 34:14Back in the old days. David Jernigan 34:16Because she gave dogs probiotics. And the board thought she was giving the dogs an infection so that she could treat them and make money off of the subsequent infection. Dr. Deb 34:28Oh my god. David Jernigan 34:29Nobody actually had heard of good, friendly bacteria in the veterinary world, I guess she said she had gotten in trouble, and she had to defend herself, that, no, I’m giving friendly, benevolent, beneficial bacteria. Okay, to these animals, and getting good results.So, phages… Are friendly, benevolent, beneficial viruses. That live in your body, but they only will infect a certain type of bacteria. So… What that means is if you have staff.Aureus, you know, Staphylococcus aureus bacteria. That bacteria has its own kind of phage that infects it called a staph aureus phage. E. coli has an E. coli phage. Each type of E. coli has its own phage, so Borrelia burgdurferi has its own Borrelia burgdurferi type of phage, whereas Borrelia miyamotoi alright? Or any of the other Borrelia species, or the Bartonella species, or the… you just keep going, and Moses has its own type of phage that only will infect that type of bacteria. So that’s… You know, when you realize, wow, why are we going to the environment Was my thought. Dr. Deb 35:54Yeah. David Jernigan 34:55Trying to find wild phages and put them into your body, and hopefully they go and do what you want them to do. What if we could trigger the phages themselves that live in your body to, instead of just farming that bacteria that it uses as a host, because what I mean by farming is the phages will only kill 40% of that population of bacteria a day. Dr. Deb 36:20Wow. David Jernigan 36:20And then they send out a signal to all the other phages saying, stop killing! Dr. Deb 36:24It’s like. David Jernigan 36:2560% of the bacteria population left to be breeding stock. It’s kind of like the farmer, the rancher, who… he doesn’t send his whole herd to the butcher. Dr. Deb 36:35Right. David Jernigan 36:36Just to, you know, he keeps his breeding stock. He sends the rest, right? So, the phages will kill 40% of the population every day, just in their reproduction process. Because once there’s so many, as you saw in the video, once the phage lands on top of the bacteria, injects its genetic material into the bacteria, that bacteria genetic engine starts cranking out up to 5,200 phages per bacteria. Dr. Deb 37:06I don’t know who counted all those… David Jernigan 37:08Inside of a bacteria, but some scientists peer-reviewed it and put it out there. that ruptures, and it literally looks like a grenade goes off inside of the bacteria. I wish I’d remembered to bring that video of a phage killing a bacteria, but it just goes, oof. And it’s just a cloud of dust. So, you’re breaking apart a lot of those different toxins and things. So… That’s… That was the impetus to me creating what I did. That and the fact that I looked it up, and I found out that phages will sometimes go… Crazy. I don’t know how to say it. Wiping out 100% of their host. And it could be a trigger, like change in the body’s pH levels, it could be electromagnetically done, you know, like, there’s been documentation of… I think it was, 50 Hz, electricity. Triggering one kind of phage to go… Crazy and annihilate its host population. There’s other ways, but I was, like, going, none of those fit me, you know? It’s not like I’m gonna shock somebody with a… Jumper cable or something to try to get phages to… to do that kind of thing. But the fact that it could be done, they can be triggered, they can switch and suddenly go crazy against their population. But what happens when they kill 100% of their host? The phages themselves die within 4 days. Dr. Deb 38:45Hmm. Because they can’t keep reproducing. David Jernigan 38:47There’s nothing to reproduce them, yeah. Dr. Deb 38:49Yeah. Especially… unless they’re a polyvalent phage, that means a phage that can segue and use. David Jernigan 38:54One or two other kinds of bacteria. To, as a reproductive host. But a lot of phages, if not the majority, are monovalent, which means they have one host that they like to use. And so… Borrelia, so… my study that I ended up doing, and I published the results in 2021, And it’s a small study, but it’s right in there at the high end, believe it or not, of phage research. Most phage research is less than 30 people. In the study. But, we did 26 people.And after one month of doing the phage induction that I invented, which only… Appears to only, induce or stimulate the types of phages that will do the job in your body. I don’t care what kind of phage it is. I don’t care if it’s a Borrelia phage, it may be a polyvalent phage that normally doesn’t use the Borrelia burgdurferi as its number one. Host, but it can. To go and kill that infection. And the fascinating thing is, there was a brand new test that came out at the same time I came out with the idea, literally the same weekend they presented. Dr. Deb 40:1511. David Jernigan 40:15ILADS conference in Boston in 2019. It was called the Felix Borrelia phage Test. So the Felix Borrelia phage test. Because Borrelia are often intracellular, right, they’re buried down in the tissue, they’re not often in the blood that much. And therefore, doing a blood test isn’t really that accurate. But you remember how there’s, like, potentially as many as 5,200 phages of that type erupt from each bacteria when it breaks apart. It’s way easier to detect those phages, because they’re now circulating, those 52, as you saw in the video. 5,200 different phages are now seeking out another Borrelia that they can infect. And so, while they’re out in circulation, that’s easy to find in the bloodstream. So, 77% of the people, so 20 out of 26, were tested after a 2-week period. After only a 4-day round of treatment. Because according to my testing, remember, I can actually test adjunctively to see if I can find any signatures for those kinds of bacteria. And I couldn’t after 4 days, so we discontinued treatment and waited Beyond the 4 days that would allow the phages themselves to die, so we waited about a week and a half.And redid the test. And 77%, so that 20 out of 26 of the people, were completely negative. Dr. Deb 41:50Wow. David Jernigan 41:52Which, you go, well, it’s just a blood test. Well, no, we actually had people that were getting better, like, they’d never gotten better before. We had one woman who was wheelchair-bound, and in two weeks was able to walk, and even ultimately wanted to work for my clinic. I’m just, like, going… Dr. Deb 42:07I didn’t want to write about all that. I wanted to write about the phages. I was like… David Jernigan 42:12article, I probably should have put some of those stories, because, Critics would say, well, you got rid of the infection, maybe, but… Did you fix the Lyme disease? Well, that’s… there’s two factors here that every doctor needs to understand. There’s the infection in chronic illness, there’s the infection, and then there’s the damage that’s been done. Because sometimes I have these people that would come in and say, well, Dr. Jernigan, it didn’t work for me, I’m still in the wheelchair. And I’m like, no, it worked. Repeat lab test over months says it’s gone, it’s gone, it’s gone. It’s like, we would follow, and 88% of the people we followed long-term were still negative, which is amazing to me. Dr. Deb 42:56And then they have to repair the damage. David Jernigan 42:59It’s the damages why you still have your symptoms. And that’s where the doctor has to get busy, right? Dr. Deb 43:06Right David Jernigan 43:06They were told erroneously by their doctor that originally treated them that they’d be well, they’d get out of the wheelchair, if he could actually kill all these infections. Dr. Deb 43:15It’s not true. David Jernigan 43:16Unless it’s caught early. So I love the analogy, and I’ve said it a thousand times.that Lyme disease and chronic infections are much like having termites in the wood of your house. If you find the termites early, then yeah, killing the infection, life goes back to normal, the storm comes and your house doesn’t fall down. But if it’s 20 years later. Killing the termites is still a grand idea. Right. But you have the damage in the wood that needs to be repaired as well. All the systems… when I talk about damage to the wood, I mean, like. All the bioregulatory aspects of the body, how it regulates itself, all the biochemical pathways, the metabolic pathways we all know about, getting the toxins that have been lodged in there for many years, stopping the inflammatory things that have been running crazy. Dealing with all those cytokines that are just running rampant through the body, creating this whole MCAS situation. Which are largely… Dr. Deb 44:21Coming from your body’s own immune cells called macrophages, which are not even… David Jernigan 44:26It’s not… a virus at all, it’s part of the immune system, it’s like a Pac-Man, and research shows that especially in spirochetes. There is no toxin. Now, I wrote 4 books. I think I wrote the very first book on the natural treatment of people with Lyme disease back in the 90s. Why did I write that? Not because I wanted to be famous, it’s a tiny book, actually, the first one was.I was just trying to help people get out of this idea that you will be well when you kill all the bugs. I was saying, it’s… you need to be doing this. If you can’t come to my clinic, at least do this. Try to find somebody that will do this for you. And that ultimately led to a bigger book.as I kept learning more, and I was like, going, well, okay, now at least do this amount of stuff. And you need to make sure your doctor is handling this, this, this, and this. And so, the third book was, like, 500 and something pages long. And then the fourth book was 500 and something pages long, and now they’re all obsolete with the whole phage thing, because this just rewrites everything. Dr. Deb 45:34Yeah. David Jernigan 45:34It’s pretty fascinating. Dr. Deb 45:37Do you think the war on bugs, mentality created more chronic illness than it solved? David Jernigan 45:44Because of the tools that doctors had to use, yes. We’re a minority, we’re still a minority, you and I. Dr. Deb 45:54Yep. Our doctoring… David Jernigan 45:56Methods I never had, and you’d never… maybe you did, but I’d never had the ability to grab a prescription pad and write out a prescription. I had to figure out, how do I get… and this was… and still my guiding thing, is like, how do I identify, number one, everything that can be found that’s gone wrong in the human body. And what do I need to provide that body? Like, the body is the carpenter. That has to do the repair, has to regenerate, has to do everything, has to get… everything fixed right? We can’t fix anything. If you have a paper cut, there isn’t a doctor on the planet that can make that go away. Dr. Deb 46:38Right. David Jernigan 46:39Of their own power, much less chronic illnesses. So, all the treatments are like the screws, saws, hammers, you know the carpenter must be able to use. So a lot of the time, doctors are just throwing an entire Home Depot on top of the carpenter. In the form of, like, bags of supplements, you know, hundreds of supplements, I’ve seen patients walk in my door with two suitcasefuls. And they were taking 70 bottles, 65 to 70 bottles of supplements, and I’d be just like, wow, your carpenter who’s been working for 24 hours a day, 7 days a week. He’s exhausted. There’s chaos everywhere, you don’t know where to. Dr. Deb 47:22Starting. David Jernigan 47:22He goes, you want me to do what with all this stuff? Dr. Deb 47:25Yep, I’ve seen the same thing. People… thousands, you know, several thousand dollars a month on supplements, and not any better. But they’re afraid to give up their supplements, too, because they don’t want to go backwards, either, and… there’s got to be a better way on both sides, the conventional side and the alternative side, although you and I don’t say it’s alternative, that’s the way medicine should be, but… David Jernigan 47:48Right. Dr. Deb 47:49We have to have a good balance on both sides. David Jernigan 47:52And I will say, too, in defense of doctors using a lot of supplements, I do use a lot of supplements. Dr. Deb 47:57Yeah, I do too. David Jernigan 47:58but I want to synergize what I’m giving the patient so that the carpenter isn’t overwhelmed and can actually get the job done. Like, everything has to work harmoniously together, so it’s not that… It’s not the number of supplements, and why would you need a lot of supplements? Well, because every system in your body is Messed up. My kind of clientele for 30 years. Our clientele, yours and mine. Dr. Deb 48:25Yeah. David Jernigan 48:26They have been sick, For decades, many of them. Dr. Deb 48:31Yeah. David Jernigan 48:31And if they went into a hospital, they honestly need every department. They need endocrinology, they need their kidney doctor, they need their… They’re a cardiologists, they need a neurologist, they need a rheumatologist. I mean, because none of those doctors are gonna deal with everything. They’re just gonna deal with one piece of the puzzle. And if they did get the benefit of all the different departments they need, yeah, they’d go out with a garbage bag full of stuff, too. Dr. Deb 48:57Hey, wood. David Jernigan 48:58Only, they’re not synergized. They don’t work together. You’re creating this chemistry set of who knows how much poison. And I want to tell your listeners, and I mean, you probably say this to your patients as well. There is a law of pharmacy that I learned eons ago, and it applies to natural medicine, too. Dr. Deb 49:21Yep. David Jernigan 49:22But the law says every drug’s primary side effect Is its primary action. So, if you listen to TV, you can see this on commercials. I love… I love listening to these commercials, because I’m like, wow. let’s… let’s… I don’t want to say I’ve named Brandon. I don’t know if that’s…Inappropriate to name a name brand, but let’s just say you have a pharmaceutical that is for sleep. After they show you this beautiful scene of the person restfully sleeping and everything like that, they tell you the truth. It’s like, this may cause sleepiness… I mean, sleeplessness. Dr. Deb 50:04Yeah. David Jernigan 50:04Found insomnia. Dr. Deb 50:06And headaches, and diarrhea. David Jernigan 50:08All the other things, and if it’s an antidepressant, what does the commercial do after it finishes showing you little bunny foo-foo, jumping through a green, happy people? They tell you, this may create depression, severe depression, and suicidal tendencies, which is the ultimate depression. So, I want everyone to understand you need to figure out what your doctor’s tools are that they’re asking you to take, and they’re wanting you to take it forever, generally in mainstream medicine, right? In the hospitals and everything. They don’t say, hey, your heart has this condition, take this medicine for 3 months, after which time you can get off. Dr. Deb 50:48Yep. David Jernigan 50:49not fixing it, right? So… That, on a timeline, there is a point, if it was truly even fixing anything. That you… it’s done what it should do, and you should get off, even if it’s a natural product. It’s just like. Dr. Deb 51:03Right David Jernigan 51:03It’s done what it should do, and you should get off, but instead. you go through the tree… the correction and out the other side, and that’s where it starts manifesting a lot of the same problems that it had. So, anti-inflammatories, painkillers, imagine the number one side effects are pain inflammation. So, the doctor says, well. If you say, hey, I’m having more pain, what does he do? He ups the dosage. And if he… if that doesn’t work, if you’re still in a lot of pain, which he would be, he changes it to a more powerful thing, right? But it starts the cycle all over again. So when you ask me, it’s like, why are we having so much chronic illness? It’s because of the whole philosophy. is the treatment philosophy of mainstream medicine that despises what you and I do. Because we’re… our philosophy from the start is the biggest thing. It’s like… We’re striving for cure. That dirty four-letter word, cure, we’re not even supposed to use it. And yet, if you look it up in Stedman’s Medical Dictionary, it just means a restoration of health. Remission. Everyone’s like, oh, I’m in remission. I’m like, remission is a drug term. It’s a medical term. Again, look it up in a medical dictionary. It is a pharmaceutical term for a temporary pause Or a reduction of your symptom, but because it’s just… symptom suppression, it will come back. It’s… remission is great, I suppose, in… At the end of, like, where you’ve exhausted everything, because I can’t fix everything, I don’t know about you. Dr. Deb 52:41No, I can’t either, yeah. David Jernigan 52:43you know, on my phone consults, I try to always remind people, as much as I get excited about my technologies gosh, I see so much opportunity to fix you. I always try to go, please understand, I’m gonna tell you what most doctors may not tell you on a phone consultation. I can’t fix everything. Dr. Deb 53:03Yeah. David Jernigan 53:03For all of my tricks, I can’t fix everything. Not tricks, but you know, all my technologies, and all my inventions. Phages, too. They are a tool. You know, antibiotics. I think I wrote a blog one time, it should be on my website somewhere, that says, Antibiotics do not… fix… neurological disease, or… I don’t know, something like that. You know, you’re using the wrong tool. I mean, it does what it does. Dr. Deb 53:32Yeah, you’re using a hammer to do what a screwdriver needs to. David Jernigan 53:35Yeah, you know, it’s like it’s… And yet, you can probably tell her… that you’ve had patients, too, that they go, Dr. Jernigan. My throat was so sore, and as soon as I swallowed that antibiotic. I felt better, and I’m, like, going… How long did it take? Oh, it was immediate! I was like, dude, the gel cap didn’t even have time to dissolve, I mean… Dr. Deb 53:58SIBO. David Jernigan 54:00But, it’s not going to repair the tissues that were all raw. kind of stuff. So, I mean, that ulceration of your throat that’s happening, the inflammation, there’s no anti-inflammatory effect of these things. So, I digress a little bit, but phages, too… I wrote an article that’s on the website, that’s setting healthy expectations for phages, because they want… we can see some amazing things happen, things that in my 30 years, I wish I had all my career to do over again, now having this tool. It’s just that much fun. I… when doctors around the country now are starting to use our inducent formulas, there’s, 13 of them now, formulas. For different broad-spectrum illness presentations. I tell them all the same thing, I was like, you are gonna have so much fun. Dr. Deb 54:53That’s exciting. Women. David Jernigan 54:54Winning is fun, you know? I was like. You know, mainstream medicine may never accept this, I don’t know. I feel a real huge burden, though, to do my best to follow a, very scientific methodology. I’ve published as much as I can publish at this time by myself. I never took money from the… the sources that are out there, because what do they do? They always come… money comes with strings. Dr. Deb 55:22Yes, it does. David Jernigan 55:23I don’t trust… I don’t trust… I mean, if you listen to the, roundtable that Our Secretary Robert F. Kennedy Jr. Dr. Deb 55:35Yeah. David Jernigan 55:36On Lyme disease last week the first couple of speakers were, like, pretty legit. I mean, all of them were legit, but I mean, they were, like, senators and congressmen or something like that, I think. And then you have… RFK Jr. himself, who’s legit. Yeah they were fessing up to the fact that, yes, they were suppressing anything to do with Lyme. Dr. Deb 56:00Yeah. David Jernigan 56:00Our… our highest levels of, marbled halls and pillars and… of medicine were doing everything the way I thought they were. They were suppressing me. I was like, how can you ignore the best formulas ever, and still, I think Borreligen, and now, induced native phage therapy are still, I believe, I don’t… I’ve never seen it, I could be wrong. The only natural things that have been documented in a medical methodology. Dr. Deb 56:34Hmm in the natural realm. I mean, all the herbs that we talk about. David Jernigan 56:39You know, there’s one that was really famous for a while, and it said, we gave… so many patients. This product, and other nutritional supplements. And at the end, X number of them were… dramatically better. That’s not research. Dr. Deb 56:57Right. That’s observation. David Jernigan 56:59The trick there was we gave this one thing, and then we gave high-dose proteolytic enzymes, we gave high dose this, we gave high dose that, but at the end of the study, we’re going to point back at the thing we’re trying to sell you as being what did it. Dr. Deb 57:12Which is what we do in all research, pretty much. David Jernigan 57:15Well… Dr. Deb 57:16tried to… David Jernigan 57:17Good guys, I hope. Dr. Deb 57:18Do the way we want, right? In… in conventional… David Jernigan 57:22Yeah. Dr. Deb 57:22Fantastic David Jernigan 57:23Very often, yeah, in conventional medicine, definitely. Yeah. And, it’s kind of scary, isn’t it, how many pharmaceuticals are slamming us with, because they’re… Dr. Deb 57:33Okay. David Jernigan 57:34There’s a new one on TV every day, and there’s. Dr. Deb 57:36Every day, yes. David Jernigan 57:37It’s like, who comes up with these names? They’re just horrible. Dr. Deb 57:40Yeah, you can’t pronounce them. David Jernigan 57:41I want to be a marketing company and come up with some Zimbabwehika, or something that actually they go with, and I’m like, I just made a million bucks coming up with it. I’ll be glad when that’s not on the TV anymore, which… Oh, me too. Me too. Dr. Deb 57:54Dr. Jaredgen, this was really wonderful. What do you want to leave our listeners with? David Jernigan 58:00Well, you know, everyone’s calling for a new treatment. Dr. Deb 58:05Yeah. You bet. David Jernigan 58:08I have done everything I can do to get it out there, scientifically, in peer review, so that if you want to look up my name. Dr. Deb 58:16I published an open access journal so that you didn’t have to buy the articles. Like, PubMed, you have to be a member. If you want to look at a lot of the research, you have to buy the articles. David Jernigan 58:26I’ve done everything open access so that people had access to the information. I honestly created induced native phage therapy to fix my own wife. I mean, I… I was… I used to think I could actually fix almost anything. Gave me enough time. And, I could not fix her. You know, the first 10 years, she was bedridden. Dr. Deb 58:49Wow. David Jernigan 58:50People go, oh, it’s easy for you, Dr. Jernigan, you’re a doctor. Dr. Deb 58:54Oh yeah, right? Yeah. David Jernigan 58:56Oh my gosh, how many tears have been shed, and how much heartache, and how much of this and that. I mean, 90% of our marriage, she was in, bed, just missing Christmas. All the horror stories you hear in the Lime world, that was her, and I could not get her completely well. And, she’s a very discerning woman. I say that in all my podcasts, because it’s. Dr. Deb 59:19Just… David Jernigan 59:16Amazing. It’s like, every husband, I think, should want a wife that’s… Always, right? Not that you surrender your own opinion, but it’s like, it’s… it was literally, I don’t know what, 6 months before the ILADS conference in Boston in 2029… in 2019 that She said, are you going to the ILADS conference this year? And I’m like, I’ve been going for, like, 15, 20 years, however long it’s been going on, and I was like, I’m not gonna go to this one. And, 3 days before the conference, she says, I think you should go. And I go, okay. Like I say, she’s generally right. And that… I bought a Scientific American magazine at the newsstand in the Nashville airport. Started reading a story about phages in that that copped that edition of the Scientific American, and It was a good article, but it wasn’t super meaty, you know. very deep on those, but I just was stimulated. Something about being at elevation. Dr. Deb 1:00:02Yeah. Your own mountains, I don’t know, I get all inspired. David Jernigan 1:00:25And I wrote in the margins and highlighted this and that until it was, like, ultimately, I spent the entire conference hammering this out. And it worked. And it’s been working, it’s just amazing. It’s… We’re over 200 different infections that we’ve… we’ve clinically or laboratory-wise documented. There’s a new test for my GenX called the CEPCR Lyme Panel. like, culture. 64 different types of infections, and I believe right now the latest count is something like 10 for 10 were completely negative. Dr. Deb 1:01:03Wow. David Jernigan 1:01:03These chronically infected people. And so, that hadn’t been published anywhere. So, in my published article, remember I was talking about that 20 out of the 26 were tested as negative for the infection? That doesn’t mean they’re cured, okay? Remember, they’re chronically damaged. That’s how we need to look at it. Dr. Deb 1:01:23funny David Jernigan 1:01:24damaged. You’re not just chronically infected. And, but with 30-day treatment.24 out of the 26 were tested as negative. Dr. Deb Muth 1:01:34That’s amazing. David Jernigan 1:01:35So 92% of the people were negative.Okay? The chances of that happening, when you run it through statistical analysis.The chances… when you compare the results to the sensitivity percentages, you know, the 100% specificity and 92% sensitivity of the…Of the lab testIt’s a 4.5 nonillion to 1 chance that it was a fluke. Isn’t that amazing? Now, nearly… I’m not even sure how many zeros that is, but it’s a lot. Dr. Deb Muth 1:02:08That’s is awesome. David Jernigan 1:02:09Like, if I just said, well, it’s a one in a million chance it was a fluke.Okay.So, lab tests don’t lie. You’re not done, necessarily, just because you got rid of the infections. Now that formula for Lyme has grown to be 90-plusmicrobes targeted in the one formula. So, we figured out we can actually target individually, but collectively, almost like an antibiotic that’s laser-guided to only go after the bad guys that we targeted.So, all the Borrelia types are targeted, all the Babesias, for,the Bartonellas, the anaplasmosis, you name it, mycoplasma types are all targeted in that one formula, because I said.Took my collective 30 years of experience and 15,000 patients.that I would typically see as co-infections and put them into that one formula, so…When we get these tests coming back that are testing for 64, it’s because of that.So, there’s a lot of coolnesses that I could actually keep going and going. Dr. Deb Muth 1:03:15That’s exciting. David Jernigan 1:03:15I love this topic, but I thank you for letting me come on. Dr. Deb Muth 1:03:18Thank you for joining us. How can people find you? David Jernigan 1:03:22Two ways. There’s the Phagen Corp company that is now manufacturing my formulas.That is P-H-A-G-E-N-C-O-R-P dot com. Practitioners can go there, and there’s a practitioner side of the website that’s very beefy with science, and… and all the formulas that were used, what’s inside of all the formulas, meaning what microbes are targeted by each one. Like, there’s a GI formula, there’s a UTI formula, there’s a SIRS formula, there’s a Lyme formula, there’s a central nervous system type infection formula, there’s… And we can keep going, you know, SIBO, SIFO formula, mold formula… I mean, we’ve discovered so many things that I could just keep going for hours, and… Dr. Deb Muth 1:04:05Yeah. David Jernigan 1:04:06About the discoveries, from where it started in its humble beginnings, To now, so… There’s another way, if you wanted to see our clinic website, is Biologics, with an X, so B-I-O-L-O-G-I-X, Center, C-E-N-T-E-R dot com. And, if somebody thinks they want to be a patient and experience this at our clinic, typically we don’t take just Easy stuff. All we see is chronic.Chronic cases from all over the world. Something like 96% of our patients come from other states and countries. And typically, I’ve been close to 90% for my whole career.About 30-something percent come from other countries in that, so… we’ve gotten really good and learned a lot in having to deal with what nobody else knows what to do with. But if you do want to do that, you can contact us. And, if you… If you don’t get the answers from my patient care staff, then I do free consultations. With the people that are thinking about, whether we can help them or not. Dr. Deb Muth 1:05:13Well, that’s excellent. For those of you who are driving or don’t have any way of writing things down, don’t worry about it, we’ve got you. We will have all of his contact information in our show notes, so you will be able to reach out to him. Thank you again for joining me. This has been an amazing conversation. David Jernigan 1:05:30Thank you, I appreciate you having me on. It was a lot of fun. The post Episode 252 – Induced Native Phage Therapy (INPT) & advanced natural therapies first appeared on Let's Talk Wellness Now.

Osteomyelitis in children is common enough to miss and serious enough to matter. In this episode of PEM Currents, we review a practical, evidence-based approach to pediatric acute hematogenous osteomyelitis, focusing on diagnostic strategy, imaging decisions including FAST MRI, and modern antibiotic management. Topics include age-based microbiology, empiric and pathogen-directed antibiotic selection with dosing, criteria for early transition to oral therapy, and indications for orthopedic and infectious diseases consultation. Special considerations such as MRSA, Kingella kingae, daycare clustering, and shortened treatment durations are discussed with an emphasis on safe, high-value care. Learning Objectives After listening to this episode, learners will be able to: Identify the key clinical, laboratory, and imaging findings that support the diagnosis of acute hematogenous osteomyelitis in children, including indications for FAST MRI and contrast-enhanced MRI. Select and dose appropriate empiric and pathogen-directed antibiotic regimens for pediatric osteomyelitis based on patient age, illness severity, and local MRSA prevalence, and determine when early transition to oral therapy is appropriate. Determine when consultation with orthopedics and infectious diseases is indicated, and recognize clinical features that warrant prolonged therapy or more conservative management. References Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2021 guideline on diagnosis and management of acute hematogenous osteomyelitis in pediatrics. J Pediatric Infect Dis Soc. 2021;10(8):801-844. doi:10.1093/jpids/piab027 Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2023 guideline on diagnosis and management of acute bacterial arthritis in pediatrics. J Pediatric Infect Dis Soc. 2024;13(1):1-59. doi:10.1093/jpids/piad089 Stephan AM, Platt S, Levine DA, et al. A novel risk score to guide the evaluation of acute hematogenous osteomyelitis in children. Pediatrics. 2024;153(1):e2023063153. doi:10.1542/peds.2023-063153 Alhinai Z, Elahi M, Park S, et al. Prediction of adverse outcomes in pediatric acute hematogenous osteomyelitis. Clin Infect Dis. 2020;71(9):e454-e464. doi:10.1093/cid/ciaa211 Burns JD, Upasani VV, Bastrom TP, et al. Age and C-reactive protein associated with improved tissue pathogen identification in children with blood culture-negative osteomyelitis: results from the CORTICES multicenter database. J Pediatr Orthop. 2023;43(8):e603-e607. doi:10.1097/BPO.0000000000002448 Peltola H, Pääkkönen M. Acute osteomyelitis in children. N Engl J Med. 2014;370(4):352-360. doi:10.1056/NEJMra1213956 Transcript This transcript was provided via use of the Descript AI application Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I'm your host, Brad Sobolewski, and today we're covering osteomyelitis in children. We're going to talk about diagnosis and imaging, and then spend most of our time where practice variation still exists: antibiotic selection, dosing, duration, and the evidence supporting early transition to oral therapy. We'll also talk about when to involve orthopedics, infectious diseases, and whether daycare outbreaks of osteomyelitis are actually a thing. So what do I mean by pediatric osteomyelitis? In children, osteomyelitis is most commonly acute hematogenous osteomyelitis. That means bacteria seed the bone via the bloodstream. The metaphysis of long bones is particularly vulnerable due to vascular anatomy that favors bacterial deposition. Age matters. In neonates, transphyseal vessels allow infection to cross into joints, increasing the risk of concomitant septic arthritis. In older children, those vessels involute, and infection tends to remain metaphyseal and confined to bone rather than spreading into the joint. For children three months of age and older, empiric therapy must primarily cover Staphylococcus aureus, which remains the dominant pathogen. Other common organisms include group A streptococcus and Streptococcus pneumoniae. In children six to 36 months of age, especially those in daycare, Kingella kingae is an important and often underrecognized pathogen. Kingella infections are typically milder, may present with lower inflammatory markers, and frequently yield negative routine cultures. Kingella is usually susceptible to beta-lactams like cefazolin, but is consistently resistant to vancomycin and often resistant to clindamycin and antistaphylococcal penicillins. This has direct implications for empiric antibiotic selection. Common clinical features of osteomyelitis include fever, localized bone pain, refusal to bear weight, and pain with movement of an adjacent joint. Fever may be absent early, particularly with less virulent organisms like Kingella. A normal white blood cell count does not exclude osteomyelitis. Only about one-third of children present with leukocytosis. CRP and ESR are generally more useful, particularly CRP for monitoring response to therapy. No single CRP cutoff reliably diagnoses or excludes osteomyelitis in children. While CRP is elevated in most cases of acute hematogenous osteomyelitis, the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America note that high-quality data defining diagnostic thresholds are limited. A CRP above 20 milligrams per liter is commonly used to support clinical suspicion, with pooled sensitivity estimates around 80 to 85 percent, but no definitive value mandates the diagnosis. Lower values do not exclude disease, particularly in young children, as CRP is normal in up to 40 percent of Kingella kingae infections. CRP values tend to be higher in Staphylococcus aureus infections, especially MRSA, and higher levels are associated with complications such as abscess, bacteremia, and thrombosis, though specific cutoffs are not absolute. In summary, CRP is most useful for monitoring treatment response. It typically peaks two to four days after therapy initiation and declines rapidly with effective treatment, with a 50 percent reduction within four days seen in the majority of uncomplicated cases. Blood cultures should be obtained in all children with suspected osteomyelitis, ideally before starting antibiotics when feasible. In children, blood cultures alone can sometimes identify the pathogen. Plain radiographs are still recommended early, not because they're sensitive for acute osteomyelitis, but because they help exclude fracture, malignancy, or foreign body and establish a baseline. MRI with and without contrast is the preferred advanced imaging modality. MRI confirms the diagnosis, defines the extent of disease, and identifies complications such as subperiosteal abscess, physeal involvement, and concomitant septic arthritis. MRI findings can also guide the need for surgical consultation. Many pediatric centers now use FAST MRI protocols for suspected osteomyelitis, particularly from the emergency department. FAST MRI uses a limited sequence set, typically fluid-sensitive sequences like STIR or T2 with fat suppression, without contrast. These studies significantly reduce scan time, often avoid the need for sedation, and retain high sensitivity for bone marrow edema and soft tissue inflammation. FAST MRI is particularly useful when the clinical question is binary: is there osteomyelitis or not? It's most appropriate in stable children without high concern for abscess, multifocal disease, or surgical complications. If FAST MRI is positive, a full contrast-enhanced MRI may still be needed to delineate abscesses, growth plate involvement, or adjacent septic arthritis. If FAST MRI is negative but clinical suspicion remains high, further imaging may still be necessary. The Pediatric Infectious Diseases Society and the Infectious Diseases Society of America recommend empiric antibiotic selection based on regional MRSA prevalence, patient age, and illness severity, with definitive therapy guided by culture results and susceptibilities. Empiric therapy should never be delayed in an ill-appearing or septic child. In well-appearing, stable children, antibiotics may be briefly delayed to obtain imaging or tissue sampling, but this requires close inpatient observation. For children three months and older with non–life-threatening disease, empiric therapy hinges on local MRSA rates. In regions with low community-acquired MRSA prevalence, generally under 10 percent, reasonable empiric options include cefazolin, oxacillin, or nafcillin. When MRSA prevalence exceeds 10 to 20 percent, empiric therapy should include an MRSA-active agent. Clindamycin is appropriate when local resistance rates are low, while vancomycin is preferred when clindamycin resistance is common or the child has had significant healthcare exposure. For children with severe disease or sepsis, vancomycin is generally preferred regardless of local MRSA prevalence. Some experts recommend combining vancomycin with oxacillin or nafcillin to ensure optimal coverage for MSSA, group A streptococcus, and MRSA. In toxin-mediated or high-inoculum infections, the addition of clindamycin may be beneficial due to protein synthesis inhibition. Typical IV dosing includes cefazolin 100 to 150 milligrams per kilogram per day divided every eight hours; oxacillin or nafcillin 150 to 200 milligrams per kilogram per day divided every six hours; clindamycin 30 to 40 milligrams per kilogram per day divided every six to eight hours; and vancomycin 15 milligrams per kilogram every six hours for serious infections, with appropriate monitoring. Ceftaroline or daptomycin may be considered in select MRSA cases when first-line agents are unsuitable. For methicillin-susceptible Staphylococcus aureus, first-generation cephalosporins or antistaphylococcal penicillins remain the preferred parenteral agents. For oral therapy, high-dose cephalexin, 75 to 100 milligrams per kilogram per day divided every six hours, is preferred. Clindamycin is an alternative when beta-lactams cannot be used. For clindamycin-susceptible MRSA, clindamycin is the preferred IV and oral agent due to excellent bioavailability and bone penetration, and it avoids the renal toxicity associated with vancomycin. For clindamycin-resistant MRSA, vancomycin or ceftaroline are preferred IV agents. Oral options are limited, and linezolid is generally the preferred oral agent when transition is possible. Daptomycin may be used parenterally in children older than one year without pulmonary involvement, typically with infectious diseases and pharmacy input. Beta-lactams remain the drugs of choice for Kingella kingae, Streptococcus pyogenes, and Streptococcus pneumoniae. Vancomycin has no activity against Kingella, and clindamycin is often ineffective. For Salmonella osteomyelitis, typically seen in children with sickle cell disease, third-generation cephalosporins or fluoroquinolones are used. In underimmunized children under four years, consider Haemophilus influenzae type b, with therapy guided by beta-lactamase production. Doxycycline has not been prospectively studied in pediatric acute hematogenous osteomyelitis. There are theoretical concerns about reduced activity in infected bone and risks related to prolonged therapy. While short courses are safe for certain infections, the longer durations required for osteomyelitis increase the risk of adverse effects. Doxycycline should be considered only when no other active oral option is available, typically in older children, and with infectious diseases consultation. It is not appropriate for routine treatment. Many hospitals automatically consult orthopedics when children are admitted with osteomyelitis, and this is appropriate. Early orthopedic consultation should be viewed as team-based care, not failure of medical management. Consult orthopedics when MRI shows abscess or extensive disease, there is concern for septic arthritis, the child fails to improve within 48 to 72 hours, imaging suggests devitalized bone or growth plate involvement, there is a pathologic fracture, the patient is a neonate, or diagnostic bone sampling or operative drainage is being considered. Routine surgical debridement is not required for uncomplicated cases. Infectious diseases consultation is also often automatic and supported by guidelines. ID is particularly valuable for antibiotic selection, dosing, IV-to-oral transition, duration decisions, bacteremia management, adverse reactions, and salvage regimens. Even in straightforward cases, ID involvement often facilitates shorter IV courses and earlier oral transition. Osteomyelitis is generally not contagious, and clustering is uncommon for Staphylococcus aureus. Kingella kingae is the key exception. It colonizes the oropharynx of young children and spreads via close contact. Clusters of invasive Kingelladisease have been documented in daycare settings. Suspicion should be higher in children six to 36 months from the same daycare, with recent viral illness, mild systemic symptoms, refusal to bear weight, modest CRP elevation, and negative routine cultures unless PCR testing is used. Public health intervention is not typically required, but awareness is critical. There is no minimum required duration of IV therapy for uncomplicated acute hematogenous osteomyelitis. Transition to oral therapy should be based on clinical improvement plus CRP decline. Many children meet criteria within two to six days. Oral antibiotics must be dosed higher than standard outpatient regimens to ensure adequate bone penetration. Common regimens include high-dose cephalexin, clindamycin, or linezolid in select cases. The oral agent should mirror the IV agent that produced clinical improvement. Total duration is typically three to four weeks, and in many cases 15 to 20 days is sufficient. MRSA infections or complicated cases usually require four to six weeks. Early oral transition yields outcomes comparable to prolonged IV therapy with fewer complications. Most treatment-related complications occur during parenteral therapy, largely due to catheter-related issues. Take-home points: osteomyelitis in children is a clinical diagnosis supported by labs and MRI. Empiric antibiotics should be guided by age, illness severity, and local MRSA prevalence. Early transition to high-dose oral therapy is safe and effective when clinical response and CRP support it. Orthopedics and infectious diseases consultation improve care and reduce variation. FAST MRI is changing how we diagnose osteomyelitis. Daycare clustering is uncommon except with Kingella kingae. That's all for this episode. If there are other topics you'd like us to cover, let me know. If you have the time, leave a review on your favorite podcast platform. It helps more people find the show and learn from it. For PEM Currents, this has been Brad Sobolewski. See you next time.    

Dr. Don and Professor Ben talk about the risks of wearing "new" (to you) clothes without washing first. Dr. Don - not risky

Dr. Don and Professor Ben talk about the risks of holding raw chicken at room temperature "all day" before cooking. Dr. Don - risky ☣️ Professor Ben - risky ☣️ Staphylococcosis in Poultry - Poultry - Merck Veterinary Manual Evaluation of the Prevalence of Staphylococcus aureus in Chicken Fillets and Its Bio-Control Using Different Seaweed Extracts - PMC

A resistência bacteriana não é exclusividade dos Gram-negativos. Entre Staphylococcus, Streptococcus e Enterococcus, há um universo de mecanismos e desafios terapêuticos que continuam moldando a prática clínica.Neste episódio, o infectologista Carlos Kiffer e William Dunke revisitam os principais agentes Gram-positivos de relevância clínica, explorando o que mudou, o que preocupa e como a resistência segue evoluindo nos hospitais e na comunidade.Do alerta de Alexander Fleming, em 1945, aos cenários atuais de MRSA, pneumococos com sensibilidade reduzida e VRE, o episódio mostra como cada decisão terapêutica é parte da história — ainda em escrita — da resistência bacteriana.▶️ Assista e fortaleça seu raciocínio clínico frente às infecções por Gram-positivos.FLEMING, A. Penicillin Nobel Lecture, 1945. NobelPrize.org, 1945. Disponível em: https://www.nobelprize.org/prizes/medicine/1945/fleming/lecture/.LOWY, F. D. Staphylococcus aureus infections. New England Journal of Medicine, v. 339, n. 8, p. 520–532, 1998. doi:10.1056/NEJM199808203390806.WEINSTEIN, R. A.; HUSKINS, W. C. The changing epidemiology of Staphylococcus aureus. Clinical Infectious Diseases, v. 42, supl. 1, p. S40–S44, 2006. doi:10.1086/491709.BRASIL. MINISTÉRIO DA SAÚDE. Boletim Epidemiológico – Resistência Antimicrobiana em Staphylococcus, Streptococcus e Enterococcus. Brasília: MS, 2024. Disponível em: https://www.gov.br/saude/.LASSEN/INSTITUTO ADOLFO LUTZ. Monitoramento de resistência em pneumococos invasivos: Relatório SERAE 2024. São Paulo: Instituto Adolfo Lutz, 2024.ARAUJO, M. R.; RIBEIRO, V. B.; GALES, A. C. Vancomycin-resistant Enterococci in Brazil: epidemiology, clinical impact and control strategies. Brazilian Journal of Infectious Diseases, v. 27, n. 2, p. 91–102, 2023. doi:10.1016/j.bjid.2023.02.004.

Dr. Don and Professor Ben talk about the risks of making rare roast beef. Dr. Don - not risky

No InfectoXpert, direto de São Paulo, recebemos o Dr. Fabrizio Motta para uma aula completa sobre pneumonia grave na pediatria — um tema essencial para infectologistas, intensivistas e profissionais que atendem crianças em hospitais gerais, onde a complexidade do cuidado pediátrico frequentemente recai sobre as equipes de infectologia.O episódio aborda:• Epidemiologia da pneumonia infantil, mortalidade global e impacto da sazonalidade viral.• Diferenças etiológicas por faixa etária: recém-nascido, lactente, pré-escolar, escolar e adolescente.• Mudanças no comportamento do Streptococcus pneumoniae após a introdução da vacina pneumocócica.• Importância dos sorotipos, dos padrões de resistência e da interpretação dos valores de MIC.• Diagnóstico clínico, papel da radiografia, ultrassom, biomarcadores e leitura crítica de culturas.• Racional de antibióticos na pediatria: doses adequadas, PK/PD, hiperfiltração, distribuição e quando ajustar esquemas.• Condutas para pneumonia comunitária, pneumonia grave, manejo de Staphylococcus aureus (incluindo MRSA) e uso de terapia endovenosa.• Duração do tratamento, evidências para cursos curtos e impacto da disbiose.• Situações especiais: sepse comunitária, suspeita de atípicos e interpretação dos painéis moleculares.No final do episódio, discutimos também o uso de doses altas de amoxicilina, critérios de escolha entre ceftriaxona, ampicilina, piperacilina-tazobactam e estratégias práticas para acertar na primeira prescrição.Se você trabalha com pediatria, infectologia ou emergência, este conteúdo é indispensável. Em breve, novidades sobre a nova Pós-Graduação em Pediatria em parceria com o InfectoXpert.

Dr. Don and Professor Ben talk about the risks of eating hand sliced Prosciutto ham stored at room temperature for months. Dr. Don - not risky

Hello to you listening in Sayville, New York!Coming to you from Whidbey Island, Washington this is Stories From Women Who Walk with 60 Seconds for Motivate Your Monday and your host, Diane Wyzga.The other day I was talking with my longtime friends, colleagues and brainstormers, Tania and Leanne, about times when we set out to achieve X but an unintended, better-than-expected Y happened. You know what I mean: the mystery of unintended consequences that turns out to be amazing!Here's one: The Scottish biologist Alexander Fleming  was working on a project on Staphylococcus bacteria at St. Mary's Hospital in London. He took off on vacation leaving behind an uncovered petri dish of bacteria. When he returned he saw a blue-green mold (like what you might find growing on bread exposed to moisture) growing on the dish and that the Staph bacteria were being killed in the area of the mold. Fleming - knowing a good thing when he saw one - identified the mold as the fungus penicillin notatum, and Shazaam! developed penicillin as an antibiotic. Fleming's unintended discovery of penicillin revolutionized the treatment of infections.Click HERE to learn more about the Discovery and Development of Penicillin 1928-1945Now, as to the moldy bread in your kitchen. Yes, penicillin is an antibiotic produced by a fungus called Penicillium notatum. Yes, this fungus is commonly found on moldy bread. Yes, when the fungus grows on bread, it releases penicillin into the surrounding environment.Let me caution you! Not all moldy bread contains penicillin. Moreover, eating moldy bread is a very big “No! No!” as it can contain harmful substances. Having said that think twice before you toss out what might be an unintended answer to a problem.  Question: When did you set out to achieve X but an unintended Y turned out to be what you were looking for?  What happened next?You're always welcome: "Come for the stories - Stay for the magic!" Speaking of magic, I hope you'll subscribe, share a 5-star rating and nice review on your social media or podcast channel of choice, bring your friends and rellies, and join us! You will have wonderful company as we continue to walk our lives together. Be sure to stop by my Quarter Moon Story Arts website, check out the Communication Services, arrange a no-obligation Discovery Call, and stay current with me as "Wyzga on Words" on Substack.Stories From Women Who Walk Production TeamPodcaster: Diane F Wyzga & Quarter Moon Story ArtsMusic: Mer's Waltz from Crossing the Waters by Steve Schuch & Night Heron MusicALL content and image © 2019 to Present Quarter Moon Story Arts. All rights reserved.  If you found this podcast episode helpful, please consider sharing and attributing it to Diane Wyzga of Stories From Women Who Walk podcast with a link back to the original source.

It's World AMR Awareness Week (WAAW) and we have prepared a special episode in light of that. In this week's Communicable, Navaneeth Narayanan and Thomas Tängdén host Aula Abbara (London, UK), Guido Granata (Rome, Italy) and Tuomas Aro (Helsinki, Finland) to discuss the phenomenon of AMR in conflict and crisis zones. They elaborate on how difficult conditions and austere environments amplify the spread of AMR, drawing on findings from the ongoing conflicts in Ukraine, Gaza, Syria and other regions. Other topics covered include adapting antimicrobial stewardship and infection prevention and control (IPC) practices as well as the need for genuine political will and international collaboration to end conflicts and their exacerbation on AMR.This episode follows the webinar “Beyond the frontlines” organised by ESCMID's AMR Action Subcommittee for WAAW 2025, featuring the same guests, and is available on ESCMID Media. This Communicable episode was peer reviewed by Arjana Zerja of Mother Theresa University Hospital Centre, Tirana, Albania.  Related ESCMID and Communicable mediaESCMID Media, Part 1: Beyond the frontlines - tackling AMR in conflict and crisis zones, webinar Communicable episode 11: Nightmare series, part 2 – how to deal with carbapenemase producers Communicable episode 16: Climate change and infections – effects on clinical practice & sustainabilityResourcesTrainee Association of ESCIMD (TAE) Doctors without Borders (Médecins sans Frontières), Antibiogo, https://www.antibiogo.org/Doctors without Borders (Médecins sans Frontières), Mini-lab, https://fondation.msf.fr/en/projects/mini-lab Further ReadingAbbara A, et al. Unravelling the linkages between conflict and antimicrobial resistance. NPJ Antimicrob Resist. 2025. DOI: 10.1038/s44259-025-00099-yAbbara A, et al. A summary and appraisal of existing evidence of antimicrobial resistance in the Syrian conflict. Int J Infect Dis. 2018. DOI: 10.1016/j.ijid.2018.06.010Abu-Shomar R, et al. Multidrug-resistant Pseudomonas isolated from water at primary health care centers in Gaza, Palestine: a cross-sectional study. IJID Reg. 2025. DOI: 10.1016/j.ijregi.2025.100671Aldbis A, et al. The lived experience of patients with conflict associated injuries whose wounds are affected by antimicrobial resistant organisms: a qualitative study from northwest Syria. Confl Health. 2023. DOI: 10.1186/s13031-023-00501-4Aro T, et al. War on antimicrobial resistance: high carriage rates of multidrug-resistant bacteria among war-injured Ukrainian refugees. Clin Microbiol Infect. 2025. DOI: 10.1016/j.cmi.2025.07.010  Bazzi W, et al. Heavy Metal Toxicity in Armed Conflicts Potentiates AMR in A. baumannii by Selecting for Antibiotic and Heavy Metal Co-resistance Mechanisms. Front Microbiol. 2020. DOI: 10.3389/fmicb.2020.00068 Dewachi O. War Biology and Antimicrobial Resistance: The Case of Gaza, AMR Insights, 2024.Granata G, et al. The impact of armed conflict on the development and global spread of antibiotic resistance: a systematic review. Clin Microbiol Infect. 2024. DOI: 10.1016/j.cmi.2024.03.029 Huang XZ, et al. Molecular analysis of imipenem-resistant Acinetobacter baumannii isolated from US service members wounded in Iraq, 2003-2008. Epidemiol Infect. 2012. DOI: 10.1017/S0950268811002871Hujer KM, et al. Analysis of antibiotic resistance genes in multidrug-resistant Acinetobacter sp. isolates from military and civilian patients treated at the Walter Reed Army Medical Center. Antimicrob Agents Chemother. 2006. DOI: 10.1128/AAC.00778-06Karah N, et al. Teleclinical Microbiology: An Innovative Approach to Providing Web-Enabled Diagnostic Laboratory Services in Syria. Am J Clin Pathol. 2022. DOI: 10.1093/ajcp/aqab160Keen EF 3rd, et al. Evaluation of potential environmental contamination sources for the presence of multidrug-resistant bacteria linked to wound infections in combat casualties. Infect Control Hosp Epidemiol. 2012. DOI: 10.1086/667382Murray CK, et al. Recovery of multidrug-resistant bacteria from combat personnel evacuated from Iraq and Afghanistan at a single military treatment facility. Mil Med. 2009. DOI: 10.7205/milmed-d-03-8008Petersen K, et al. Diversity and clinical impact of Acinetobacter baumannii colonization and infection at a military medical center. J Clin Microbiol. 2011. DOI: 10.1128/JCM.00766-10Scott P, et al. An outbreak of multidrug-resistant Acinetobacter baumannii-calcoaceticus complex infection in the US military health care system associated with military operations in Iraq. Clin Infect Dis. 2007. DOI: 10.1086/518170Sensenig RA, et al. Longitudinal characterization of Acinetobacter baumannii-calcoaceticus complex, Klebsiella pneumoniae, and methicillin-resistant Staphylococcus aureus colonizing and infecting combat casualties. Am J Infect Control. 2012. DOI: 10.1016/j.ajic.2011.03.025World Health Organization. Fourth WHO Global Evidence Review on Health and Migration stresses that equitable access to and appropriate use of antibiotics for refugees and migrants is essential to tackling Antimicrobial Resistance, News, 2022.

Episode 205: Atopic Dermatitis Kara Willbanks (medical student) explains the definition, pathophysiology, and treatment of eczema. Dr. Arreaza adds some input about bleach baths and topical steroids. Written by Kara Willbanks, MSIV, American University of the Caribbean. Comments and edits by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.October is the Eczema Awareness Month!What Is Atopic Dermatitis? Atopic dermatitis, a form of eczema, is a chronic, relapsing inflammatory skin disorder that often begins in childhood but can affect people of all ages. Other eczematous dermatoses include seborrheic dermatitis, contact dermatitis, juvenile plantar dermatosis, and stasis dermatitis. Atopic dermatitis is one of the most common skin conditions in the developed world, typically affecting up to 20% of children and 5-10% of adults. Patients usually present with severe pruritus (itchiness) and dry, inflamed patches of skin. Common sites include the face and extensor surfaces in infants, and flexural areas — like the elbows and knees — in older children and adults. Atopic dermatitis is often associated with other allergic conditions like asthma and allergic rhinitis — what we call the “atopic triad.” These conditions should also be considered when diagnosing someone with atopic dermatitis. PathophysiologyAtopic dermatitis is believed to occur due to a combination of genetic, immune, and environmental factors. A major component is a defective skin barrier, often linked to mutations in the filaggrin gene. This allows irritants, allergens, and microbes to penetrate the skin more easily, triggering inflammation.Differential DiagnosisAtopic dermatitis can sometimes mimic other skin conditions, so it's important to keep a differential in mind: -Contact dermatitis – triggered by allergens or irritants; often limited to the area of exposure but also tends to be very itchy. -Seborrheic dermatitis – greasy scales, typically on the scalp, eyebrows, and nasolabial folds -Psoriasis – well-demarcated plaques with silvery scales; sometimes found in similar areas of the body as eczema. -Tinea (fungal infections) – ring-shaped lesions with active, scaly borders -Important to note that treatment of tinea with topical steroids can make the rash much worse. -Scabies – intense itching, especially at night, with burrows between fingers. Ruling out these conditions helps guide the right treatment and prevent chronic mismanagement. As a recap our main differential diagnosis: contact dermatitis, seborrheic dermatitis, psoriasis, tinea, and scabies.The treatment cornerstone: Moisturizers The most important daily treatment for atopic dermatitis is regular moisturizing. Moisturizers repair the skin barrier, reduce water loss, and protect against irritants. They should be applied at least twice daily, ideally right after bathing while the skin is still damp (within 3 minutes is most ideal). Use greasy ointments or thick creams rather than lotions — think products with ceramides or glycerin (hydrates and protects skin). It is best to choose ointments or creams without additives, perfumes or fragrances. Greasier ointments are the preferred vessel; however, patient compliance may be less as they may be unpleasant to some.Bleach Baths For patients with frequent skin infections or severe eczema, dilute bleach baths can be a game-changer. How to do it? Use ¼ to ½ cup of household bleach in a full standard bathtub of water (about 40 gallons) and soak for 10 minutes, twice a week. This helps reduce bacterial colonization — particularly Staphylococcus aureus — which commonly worsens eczema. After the bath, pat the skin dry and immediately apply a moisturizer (within 3 minutes). Bleach baths are endorsed by the American Academy of Pediatrics and the American Academy of Dermatology as an adjunctive treatment for atopic dermatitis, especially in patients with moderate to severe disease and frequent bacterial infections, but the evidence for their efficacy is mixed, and further well-designed studies are needed.Medical Treatments-Topical corticosteroids: When moisturizers alone aren't enough, we move to anti-inflammatory therapy. Topical corticosteroids are the first-line treatment for flares. Some studies suggest that a short burst of a high-potency topical corticosteroid to rapidly control active disease, followed by a quick taper in potency, is most effective, whereas others use the lowest-potency agent thought to be needed and adjust upward only if this fails. Common steroids used are hydrocortisone (low potency), triamcinolone (medium potency), or betamethasone (high potency). -High-potency steroids should never be applied to sensitive skin like the face. With short-term use of lower-potency steroids, there is a low likelihood of skin atrophy but use for more than 6 months is linked with greater levels of skin thinning -Wet wrap therapy: Wet wrap therapy improves absorption of topic steroid. Apply a topical steroid, then layer a wet dressing and then a dry dressing over the top of that. This can be beneficial in providing  both relief of symptoms and prevention of itching. In pediatric patients it is called “daddy's socks therapy” because large socks may be used to cover the arms of kids.-Topical calcineurin inhibitors — like tacrolimus — are great alternatives for sensitive areas or for maintenance once inflammation is under control. They may burn upon application which can scare patients away from their use.-PO antihistamines can help with itching, especially at night, but they don't treat inflammation itself.-Systemic therapies, like dupilumab (Dupixent®), an IL-4 receptor antagonist, are reserved for moderate to severe cases unresponsive to topical therapy. This is a great time to refer to your local dermatologist for management! Many of the newer treatments are highly effective but can require more frequent monitoring.Recent Research One recent study is the 2024 Cochrane network meta-analysis comparing effectiveness of topical anti-inflammatory treatments for eczema that was recently published in the AFP Journal in July of 2025.Here are the highlights:-Over 291 RCTs with ~45,846 participants were included. -The analysis ranked potent topical corticosteroids, JAK inhibitors (for example ruxolitinib (Opzelura® 1.5 %), and tacrolimus 0.1 % among the most effective for reducing signs and symptoms of eczema. -In contrast, PDE-4 inhibitors [like crisaborole (Eucrisa®) 2 %] were among the least effective in this comparison. -Regarding side effects: tacrolimus and crisaborole were more likely to cause burning or stinging at the application site; corticosteroids were less likely in the short term to cause local irritation.-Long-term outcomes regarding effectiveness or safety of treatments for eczema were not addressed by the review because they are rarely reported.”-Another insight from this study is considering cost when initiating treatment. Most topical steroids are significantly more cost effective than JAK inhibitors or calcineurin inhibitors so it may be best to start with a cheaper solution in an uninsured patient considering their relative effectiveness. Additional Tips & Lifestyle -Keep baths and showers short and in lukewarm water.-Avoid harsh soaps and detergents — use gentle, fragrance-free cleansers.-Wear soft cotton clothing instead of wool or synthetics.-Identify and avoid triggers — common ones include stress, sweating, allergens, and certain foods (especially in kids).-Ice packs can help reduce itching and relieve any burning sensation.-Keep fingernails short, especially in children, help cause less trauma to the skin from repeated itching. Living with eczema Many celebrities like Kerry Washington, Jessica Simpson, Kelly Rowland, Brad Pitt and Kristen Bell have spoken out about their lives with eczema. They have shared personal stories about how they were diagnosed, what treatment works for them, and the general impact it has had on their lives and mental health. I feel like it can be so important for celebrities to speak out about their lives with certain conditions because it helps to normalize the condition, raise awareness of the struggles, and encourages more open dialogue.It is important to remember that for patients living with eczema, the persistent itch-scratch cycle can be very distressing, causing patients to struggle with their sleep and day-to-day activities. Anxiety and depression are common in patients with eczema so as physicians it is vital to monitor for signs of distress. Support groups can be incredibly helpful for patients [National Eczema Association]If you are interested in providing additional information to your patients or getting this for yourself, you can find more resources on altogethereczema.org or nationaleczema.org. Key Takeaways Atopic dermatitis is chronic but manageable. Moisturizers are the foundation of treatment. Topical steroids and calcineurin inhibitors control inflammation. Bleach baths help reduce bacterial load and flare severity. Always rule out other skin conditions to ensure appropriate management. Atopic dermatitis can be managed by the primary care physician but in certain cases (cases refractory to standard topical treatment, recurrent infections, etc.), a referral to dermatology can be especially helpful.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! References:Coping with eczema. Allergy & Asthma Network. (2025, May 20). https://allergyasthmanetwork.org/what-is-eczema/coping-with-eczema/.Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014 Feb;70(2):338-51. doi: 10.1016/j.jaad.2013.10.010. Epub 2013 Nov 27. PMID: 24290431; PMCID: PMC4410183. https://pubmed.ncbi.nlm.nih.gov/24290431/.Yancey, J. R., & Green, S. (2025, July 15). Effectiveness of topical anti-inflammatory drugs for eczema. American Family Physician. https://www.aafp.org/pubs/afp/issues/2025/0700/cochrane-eczema.html.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Amprologix chief scientific officer Mathew Upton talked with Proactive's Stephen Gunnion about how the company aims to use £740,000 in fresh funding to push forward work on a treatment for drug-resistant infections, including MRSA. Amprologix, a Frontier IP Group, PLC (LSE:FIPP) portfolio company, is developing Epidermicin NI01, a novel antibiotic aimed at treating methicillin-resistant Staphylococcus aureus, or MRSA. Upton explained that the recent funding will be used to complete preclinical studies for Epidermicin NI01, ensuring the compound's safety ahead of human clinical trials. “This money is going to be used to advance our lead technology,” said Upton. “We need to run some final assays to prove that the lead molecule Epidermicin is not toxic before we go into human trials.” The urgency to develop new classes of antibiotics remains high, with the World Health Organisation (WHO) repeatedly identifying a shortage of effective antimicrobials in the pipeline. Epidermicin represents a first-in-class solution that works differently from existing treatments, including those to which many bacteria have developed resistance. Upton also highlighted the company's broader strategy, including the use of an AI-driven accelerated evolution engine to expand its pipeline. The goal is to generate additional novel drug candidates targeting WHO-prioritised pathogens such as Clostridioides difficile. Looking ahead, Amprologix is initiating Series A funding to support first-in-human trials and portfolio expansion. Visit Proactive's YouTube channel for more interviews and updates like this one. Don't forget to like the video, subscribe to the channel, and turn on notifications so you never miss new content. #Antibiotics #DrugDevelopment #BiotechNews #FrontierIP #Amprologix #Epidermicin #AntimicrobialResistance #WHO #BiotechInvesting #ClinicalTrials

rWotD Episode 3084: RsaOG Welcome to random Wiki of the Day, your journey through Wikipedia's vast and varied content, one random article at a time.The random article for Monday, 13 October 2025, is RsaOG.RsaOG (an acronym for RNA S. aureus Orsay G) is a non-coding RNA that was discovered in the pathogenic bacteria Staphylococcus aureus N315 using a large scale computational screening based on phylogenetic profiling. It was first identified, but not named, in 2005. RsaOG has since been identified in other strains of Staphylococcus aureus under the name of RsaI, it has also been discovered in other members of the Staphylococcus genus (such as Staphylococcus carnosus) but in no other bacteria.The RsaOG gene is conserved in all Staphylococcaceae sequenced genomes, its secondary structure contains two highly conserved unpaired sequences which have the ability to form a pseudoknot. Northern blot experiments show that RsaOG is expressed in several S. aureus strains. Mapping of RsaOG ends indicates a size of 146 nucleotides in S. aureus. RsaOG ncRNA is thought to have trans-acting regulatory functions, possibly on fine tuning toxin production or aiding with invasion.This recording reflects the Wikipedia text as of 01:11 UTC on Monday, 13 October 2025.For the full current version of the article, see RsaOG on Wikipedia.This podcast uses content from Wikipedia under the Creative Commons Attribution-ShareAlike License.Visit our archives at wikioftheday.com and subscribe to stay updated on new episodes.Follow us on Bluesky at @wikioftheday.com.Also check out Curmudgeon's Corner, a current events podcast.Until next time, I'm long-form Patrick.

Long-term care facilities face unique challenges in preventing healthcare-associated infections (HAIs) and managing multidrug-resistant organisms (MDROs). In this episode of The ICHE Podcast, Dr. Loren G. Miller (UCLA), Dr. Lyndsay M. O'Hara (University of Maryland School of Medicine), and Dr. Mary-Claire Roghmann (University of Maryland School of Medicine) share insights from their recent studies on decolonization and enhanced barrier precautions—two promising approaches for reducing infection risk among residents. They explore what the latest research tells us, where evidence gaps remain, and how facilities can apply practical, evidence-based interventions today to improve safety and quality of care. UCI SHIELD Nursing Home Decolonization Toolkit: https://www.ucihealth.org/healthcare-professionals/shield/nursing-home-decolonization-toolkit Enhanced barrier precautions to prevent transmission of *Staphylococcus aureus* and Carbapenem-resistant organisms in nursing home chronic ventilator units: https://www.cambridge.org/core/journals/infection-control-and-hospital-epidemiology/article/abs/enhanced-barrier-precautions-to-prevent-transmission-of-staphylococcus-aureus-and-carbapenemresistant-organisms-in-nursing-home-chronic-ventilator-units/43FBB459BB569B052DEDF87EA57193FB Impact of routine chlorhexidine bathing and nasal iodophor on MDRO colonization and environmental contamination in nursing homes: https://www.cambridge.org/core/journals/infection-control-and-hospital-epidemiology/article/abs/impact-of-routine-chlorhexidine-bathing-and-nasal-iodophor-on-mdro-colonization-and-environmental-contamination-in-nursing-homes/EE2288CCE486EB4822A545BFE6210BA5

Karl Matthews, Ph.D., Professor of Microbial Food Safety at Rutgers University, discusses ways to eliminate pathogens like Salmonella, E. coli O157:H7 and Listeria from fresh fruits and vegetables. He highlights the importance of preventative measures from farm to table, including the use of water antimicrobials, like chlorine, and photosensitizers, like curcumin. Watch this episode: https://youtu.be/6Wkef9RyUVE Ashley's Biggest Takeaways We consume billions of microorganisms in the food that we eat each day. Fresh fruits and vegetables that are not thermally processed are likely to carry a higher microbial load than cooked foods. Many of those microbes are not concerning to human health. However, when pathogens of human health concern are present, the food can become unsafe to eat. Scientists use many methods from pre-harvest through post-harvest to keep food free of human pathogens. Water antimicrobials, such as chlorine, and photodynamic inactivation using photosensitizers, such as curcumin, are 2 preventative measures that Matthews and colleagues are investigating. Curcumin is a natural chemical compound found in the turmeric plant. It is responsible for giving tumeric its yellow color. Curcumin is also a photosensitizer, meaning that it can absorb light energy and transfer it to another molecule to initiate chemical reactions that produce cytotoxic singlet oxygen. Featured Quotes When I look at [what makes fruits and vegetables safe to eat] as far as from a microbiological perspective, it's are they free of pathogens of human health concern? And so, we might think about organisms, such as Salmonella or the Shiga toxin producing E coli or Listeria. There are a number of processes and initiatives that are put into place, from the pre-harvest through post-harvest levels to try to ensure that the product is not contaminated with microorganisms of human health concern. Each day, we're consuming literally billions of microorganisms in the foods that we eat, and particularly the raw fruits and vegetables that we're eating that are not being thermally processed in any fashion by which you might reduce the microbial load. Oftentimes we think about the bacteria that might well be there. But we do know that there's viruses that could be present. There's certain type of protozoa that might be present. Many of us know of norovirus and the concerns associated with that particular pathogen. So, there's a multitude of microorganisms that might well be associated with fresh fruits and vegetables, but there's really a very limited number or types that are actually of concern from a human health standpoint. In my program, we're working on E. coli O157:H7, in particular. It's a certain serotype of E. coli, a diarrheagenic E. coli, what's also known as a Shiga toxin-producing E. coli. We work with Salmonella, and we work with Listeria monocytogenes, but there's other microorganisms, such as Campylobacter, Yersinia, Staphylococcus aureus. All of those types of pathogens can also be associated with foods—and different types of foods, at that—and be of concern to the general public—the consumer. If we look at a lot of the processing of foods that are taking place, not only here in the United States, but globally, many times, what will happen is they're utilizing some type of a water antimicrobial, and I stress that because, oftentimes, these antimicrobials are added to the water to control the microbial load in the water. So, ultimately, you're not basically putting on water and putting on a whole load of microorganisms along with it. And also, you can prevent cross contamination through that. Here in the U.S. and elsewhere, we'll often put additional chlorine into the water. So, let's say we're increasing the chlorine concentration to 20 parts per million, or 50 parts per million, or maybe in poultry processing, they're utilizing peracetic acid. These are 2 common antimicrobials that are being used. What we wanted to do is find out could we utilize some other types of methods that might well control microorganisms on the commodity itself? And that's where we started looking at photodynamic inactivation and coupling that with the use of a photosensitizer. And in this particular case, the photosensitizer we were using was curcumin. The reason for working with curcumin is that it's naturally used in foods as a food dye. It's also used as a flavoring agent, and so forth. So, it's there, and it's being used—not just in the U.S., but [also] globally. And we thought we would try to see if we utilize this compound, could we have an additive effect to it? If you apply certain wavelengths of light, you can inactivate microorganisms, but if you apply that wavelength to something like a photosensitizer type molecule (curcumin), you could generate singlet oxygen molecules. And those singlet oxygen molecules would act like little explosions on the cell membrane and basically blow it apart and, therefore, inactivate the organism. We looked at the ability of this to inactivate Listeria monocytogenes, Salmonella, as well as E. coli O157:H7, so these Shiga toxin-producing E. coli, and what we did indeed find is that it was very effective. We looked at it in comparison to peracetic acid use in the poultry industry, and we found it to be equivalent, at least to treatments that we were utilizing on poultry skin, with inactivation of the microorganisms, such as Listeria, on the poultry skin. So, it is really exciting. Links for This Episode ​​​​​​Preventing Foodborne Outbreaks Starts in the Field. Influences of photosensitizer curcumin on microbial survival and physicochemical properties of chicken during storage.

Le “triangle de la mort” désigne une zone du visage comprise entre l'arête du nez et les commissures des lèvres, formant un triangle. Cette appellation spectaculaire vient d'une particularité anatomique : dans cette région, les veines superficielles (veine faciale, veine angulaire) communiquent directement avec des veines profondes de l'orbite (veines ophtalmiques) et, au-delà, avec le sinus caverneux, une grande veine située à la base du crâne. Or ces veines sont dépourvues de valvules efficaces, ce qui autorise un reflux du sang vers le crâne en cas d'inflammation, de pression ou d'infection locales.Concrètement, une lésion cutanée banale du triangle — bouton manipulé, poil incarné, gerçure, furoncle dans le vestibule nasal — peut, très rarement, permettre à des bactéries (souvent Staphylococcus aureus, parfois streptocoques ou anaérobies) de gagner la circulation veineuse puis le sinus caverneux. Cela expose à une thrombose du sinus caverneux (formation d'un caillot infecté), à une méningite ou à un abcès intracrânien. Ces complications restent exceptionnelles à l'ère des antibiotiques, mais leur gravité explique la réputation de cette zone.Les signes d'alarme qui doivent faire consulter en urgence après une infection du nez ou de la lèvre supérieure sont : fièvre, céphalée intense, douleur autour d'un œil, œdème palpébral, rougeur conjonctivale, diplopie (vision double), douleur aux mouvements oculaires, proptose (œil “qui ressort”), diminution de la vision, engourdissement du front ou de la joue (atteinte des nerfs V1/V2), voire paralysie oculomotrice (nerfs III, IV, VI). Le diagnostic repose sur l'examen clinique et l'imagerie (IRM avec angio-IRM ou TDM), et le traitement associe antibiothérapie intraveineuse rapide, prise en charge en milieu spécialisé, parfois anticoagulation selon les cas.Pourquoi le risque augmente-t-il quand on “triture” un bouton ? En pressant, on provoque microtraumatismes et diffusion bactérienne dans des tissus très vascularisés, avec un gradient de pression qui peut favoriser la remontée du sang vers les veines profondes. Le risque est majoré par le diabète, l'immunodépression, une sinusite non traitée ou une infection dentaire maxillaire.Les gestes de prévention sont simples : éviter de percer ou manipuler les lésions dans cette zone ; nettoyer la peau avec une solution douce ; traiter les croûtes/sécheresses nasales (salines isotoniques, baumes adaptés) ; consulter en cas de douleur, fièvre, extension de la rougeur, écoulement purulent nasal, ou atteinte de l'œil. En résumé, le “triangle de la mort” n'est pas une fatalité : c'est le rappel qu'ici, la connexion veineuse directe avec l'intérieur du crâne impose de respecter les règles d'hygiène et de ne pas jouer les dermatologues amateurs. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

Antimicrobial resistance (AMR) continues to grow as a global health threat, making infections harder to treat and leaving fewer options for patients. The need for new antibiotics is an urgent matter — but traditional discovery methods are slow and limited. In this episode of Let's Talk Micro, Luis is joined by Dr. James Collins, professor at MIT and researcher at the Broad Institute, who is leading efforts to apply AI to antibiotic discovery. We discuss how his team used deep learning to uncover promising new compounds, including NG1 and DN1, which showed activity against drug-resistant Neisseria gonorrhoeae and Staphylococcus aureus. We also talk about the challenges of bringing discoveries from computer models to the clinic, and what this approach could mean for the future of the fight against superbugs.   Link to study: https://www.cell.com/cell/abstract/S0092-8674%2825%2900855-4   Check out the website: https://www.letstalkmicro.com/ Questions? Feedback? Send those to letstalkmicro@outlook.com Want to support the podcast? Here's how: Venmo: https://venmo.com/u/letstalkmicro Buy me a Ko-fi: https://ko-fi.com/letstalkmicro  

À l'ère du smartphone et du télétravail, les écouteurs font désormais partie de notre quotidien. Que ce soit pour écouter de la musique, téléphoner ou suivre une visioconférence, ils restent des heures durant dans nos oreilles. Mais ce geste anodin est-il sans risque pour notre santé ? Plus précisément, peut-il favoriser l'apparition d'otites ?La réponse est oui, dans certains cas. Les spécialistes ORL s'accordent sur un point : l'usage prolongé et répété d'écouteurs intra-auriculaires peut créer un environnement propice aux infections, en particulier les otites externes, c'est-à-dire les inflammations du conduit auditif.Une étude publiée en 2008 dans le Journal of Laryngology and Otology (par Leong et al.) a comparé le conduit auditif de deux groupes : un groupe portant régulièrement des écouteurs, et un groupe n'en utilisant jamais. Résultat : les utilisateurs fréquents d'écouteurs présentaient un taux significativement plus élevé de bactéries pathogènes, notamment Staphylococcus aureus et Pseudomonas aeruginosa, des germes souvent impliqués dans les otites externes.Pourquoi ce lien entre écouteurs et otites ? Plusieurs mécanismes sont en cause :1. Obstruction du conduit auditif : les écouteurs, surtout intra-auriculaires, empêchent la bonne ventilation du canal. L'humidité naturelle ne s'évacue pas correctement, créant un terrain chaud et humide, idéal pour la prolifération des bactéries.2. Microtraumatismes : le frottement régulier des embouts ou leur insertion brutale peut irriter la peau du conduit, facilitant l'entrée des agents infectieux.3. Manque d'hygiène : peu d'utilisateurs nettoient leurs écouteurs régulièrement. Or, ces dispositifs sont souvent posés sur des surfaces non stériles ou partagés entre plusieurs personnes. Les germes présents sur les écouteurs peuvent ainsi être introduits dans l'oreille à chaque usage.Les symptômes d'une otite externe liée aux écouteurs sont classiques : douleurs, démangeaisons, rougeur du conduit auditif, voire écoulement. Dans certains cas, l'audition peut temporairement diminuer. Si ces signes apparaissent, il est recommandé d'arrêter immédiatement l'usage des écouteurs et de consulter un médecin.Pour limiter les risques, quelques gestes simples suffisent :Ne pas porter d'écouteurs plus de deux heures d'affilée.Les désinfecter régulièrement avec un chiffon doux imbibé d'alcool à 70 %.Éviter de les partager.Aérer ses oreilles entre deux utilisations.En conclusion, si les écouteurs ne sont pas à l'origine directe de toutes les otites, leur usage excessif et négligent peut en augmenter la probabilité, notamment en cas de mauvaise hygiène. Pour écouter en toute sécurité, mieux vaut penser aussi à… laisser respirer ses oreilles. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

On episode #87 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 7/31/25 – 8/18/25. Host: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Adjuvanted recombinant zoster vaccine is effective against herpes zoster ophthalmicus, and is associated with lower risk of acute myocardial infarction and stroke in adults aged ≥50 years (CID) Bacterial Dalbavancin for Treatment of Staphylococcus aureus Bacteremia (JAMA) Propensity-Matched Comparison of Timely vs. Delayed Antibiotic Therapy in Stenotrophomonas maltophilia Pneumoni (OFID) The proportion of Treponema pallidum PCR-positive primary syphilis infections which are seronegative for syphilis (OFID) Cefixime versus benzathine penicillin G for the treatment of early syphilis (Journal of Antimicrobial Chemotherapy) Dalbavancin for Treatment of Staphylococcus aureus Bacteremia (JAMA) Fungal The Last of US Season 2 (YouTube) Parasitic Increasing Length of the Babesia Season in New England in the Climate Change Era (OFID) Ivermectin to Control Malaria (NEJM) Miscellaneous ACIP Recommendations Summary (CDC: Influenza) Relative effectiveness of high-dose versus standard-dose influenza vaccine against hospitalizations and mortality according to frailty score (JID) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

Agradece a este podcast tantas horas de entretenimiento y disfruta de episodios exclusivos como éste. ¡Apóyale en iVoox! En 1928, Alexander Fleming, un bacteriólogo escocés, realizó uno de los descubrimientos médicos más importantes de la historia: la penicilina. Mientras trabajaba en el Hospital St. Mary’s de Londres, Fleming notó que una placa de cultivo de bacterias Staphylococcus aureus había sido contaminada por un moho de color verde. Observó detenidamente lo que había sucedido y advirtió que, alrededor del moho, las bacterias no crecían, lo que indicaba que el moho producía una sustancia que las inhibía. Este moho fue bautizado como Penicillium notatum, y la sustancia, como penicilina. Esto marcó el inicio de la era de los antibióticos. Aunque Fleming publicó sus hallazgos en 1929, no pudo purificar la penicilina ni producirla a gran escala. Fue en la década de 1940 cuando científicos como Ernst Chain y Howard Florey lograron aislar y estabilizar el compuesto, permitiendo su uso médico. La industria farmacéutica estadounidense hizo el resto. Durante la Segunda Guerra Mundial, la penicilina salvó innumerables vidas al tratar infecciones bacterianas en soldados lo que supuso toda una revolución para la medicina. El descubrimiento de Fleming fue accidental, pero su observación meticulosa y su curiosidad científica las bases para un avance que transformó el tratamiento de enfermedades infecciosas. La penicilina no solo redujo la mortalidad por infecciones, sino que también abrió la puerta al desarrollo de otros antibióticos. Escucha el episodio completo en la app de iVoox, o descubre todo el catálogo de iVoox Originals

Agradece a este podcast tantas horas de entretenimiento y disfruta de episodios exclusivos como éste. ¡Apóyale en iVoox! En 1928, Alexander Fleming, un bacteriólogo escocés, realizó uno de los descubrimientos médicos más importantes de la historia: la penicilina. Mientras trabajaba en el Hospital St. Mary’s de Londres, Fleming notó que una placa de cultivo de bacterias Staphylococcus aureus había sido contaminada por un moho de color verde. Observó detenidamente lo que había sucedido y advirtió que, alrededor del moho, las bacterias no crecían, lo que indicaba que el moho producía una sustancia que las inhibía. Este moho fue bautizado como Penicillium notatum, y la sustancia, como penicilina. Esto marcó el inicio de la era de los antibióticos. Aunque Fleming publicó sus hallazgos en 1929, no pudo purificar la penicilina ni producirla a gran escala. Fue en la década de 1940 cuando científicos como Ernst Chain y Howard Florey lograron aislar y estabilizar el compuesto, permitiendo su uso médico. La industria farmacéutica estadounidense hizo el resto. Durante la Segunda Guerra Mundial, la penicilina salvó innumerables vidas al tratar infecciones bacterianas en soldados lo que supuso toda una revolución para la medicina. El descubrimiento de Fleming fue accidental, pero su observación meticulosa y su curiosidad científica las bases para un avance que transformó el tratamiento de enfermedades infecciosas. La penicilina no solo redujo la mortalidad por infecciones, sino que también abrió la puerta al desarrollo de otros antibióticos. · Canal de Telegram: https://t.me/lacontracronica · “Contra la Revolución Francesa”… https://amzn.to/4aF0LpZ · “Hispanos. Breve historia de los pueblos de habla hispana”… https://amzn.to/428js1G · “La ContraHistoria de España. Auge, caída y vuelta a empezar de un país en 28 episodios”… https://amzn.to/3kXcZ6i · “Lutero, Calvino y Trento, la Reforma que no fue”… https://amzn.to/3shKOlK · “La ContraHistoria del comunismo”… https://amzn.to/39QP2KE Apoya La Contra en: · Patreon... https://www.patreon.com/diazvillanueva · iVoox... https://www.ivoox.com/podcast-contracronica_sq_f1267769_1.html · Paypal... https://www.paypal.me/diazvillanueva Sígueme en: · Web... https://diazvillanueva.com · Twitter... https://twitter.com/diazvillanueva · Facebook... https://www.facebook.com/fernandodiazvillanueva1/ · Instagram... https://www.instagram.com/diazvillanueva · Linkedin… https://www.linkedin.com/in/fernando-d%C3%ADaz-villanueva-7303865/ · Flickr... https://www.flickr.com/photos/147276463@N05/?/ · Pinterest... https://www.pinterest.com/fernandodiazvillanueva Encuentra mis libros en: · Amazon... https://www.amazon.es/Fernando-Diaz-Villanueva/e/B00J2ASBXM #FernandoDiazVillanueva #penicilina #fleming Escucha el episodio completo en la app de iVoox, o descubre todo el catálogo de iVoox Originals

Dalbavancin, a long-acting IV lipoglycopeptide, may be an option for the treatment of complicated Staphylococcus aureus bacteremia without requiring long-term IV access. Author Thomas L. Holland, MD, MSc, from Duke University School of Medicine discusses key points of the DOTS randomized clinical trial and more with JAMA Deputy Editor Preeti Malani, MD, MSJ.Related Content: Dalbavancin for Treatment of Staphylococcus aureus BacteremiaManagement of Staphylococcus aureus Bacteremia

Dalbavancin, a long-acting IV lipoglycopeptide, may be an option for the treatment of complicated Staphylococcus aureus bacteremia without requiring long-term IV access. Author Thomas L. Holland, MD, MSc, from Duke University School of Medicine discusses key points of the DOTS randomized clinical trial and more with JAMA Deputy Editor Preeti Malani, MD, MSJ. Related Content: Dalbavancin for Treatment of Staphylococcus aureus Bacteremia Management of Staphylococcus aureus Bacteremia

No episódio de hoje do Check-up Semanal, nosso editor-chefe médico, Ronaldo Gismondi, traz as principais atualizações do último mês sobre Clínica Médica publicadas no Portal Afya.Confira os temas do episódio:- Diretrizes para ajuste de antibioticoterapia em pacientes obesos;- Câncer de sítio primário oculto: ainda vale buscar o local de origem?;- Roteiro estratégico para investigação de diarreia aguda e crônica;- Quando indicar antibióticos na pancreatite aguda;- Ecocardiograma transesofágico na bacteremia por Staphylococcus aureus: sempre necessário?Aperte o play e ouça agora os destaques que impactam a prática clínica na atenção ao paciente adulto!

Cauda Equina Syndrome • Neurosurgical emergency due to compression of cauda equina nerve roots, usually from disc herniation, tumor, or trauma Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Key Differentiators Epidural Abscess • • Spinal epidural infection commonly caused by Staphylococcus aureus Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Key Differentiators […] The post 131 Neuro: Spinal Cord issues appeared first on Physician Assistant Exam Review.

On episode #85 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 7/3 – 7/21/25. Hosts: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Elimination of HIV Reservoirs Harboring Intact Proviruses (JID) Bacterial Expansion of tetM-Carrying Neisseria gonorrhoeae in the United States, 2018–2024 (NEJM) Study hints doxyPEP use coincides with rise in tetracycline-resistant gonorrhea in US (CIDRAP) Potential Impact of Doxycycline Post-Exposure Prophylaxis on Tetracycline Resistance in Neisseria gonorrhoeae and Colonization With Tetracycline-Resistant Staphylococcus aureus and Group A Streptococcus (CID) Methenamine hippurate asprophylaxis for recurrent urinary tract infections in older women – a triple-blind, randomised, placebo-controlled, phase IV trial (ImpresU). (CMI: Clinical Microbiology and Infection) Diagnosis and Management ofCommunity-acquired Pneumonia(American Journal of Respiratory and Critical Care Medicine) Complicated Urinary Tract Infections (cUTI): Clinical Guidelines for Treatment and Management (IDSA) The impact of an intervention to increase follow-up blood cultures for patients with Staphylococcus aureus bacteriuria (Antimicrobial Stewardship & Healthcare Epidemiology) Fungal The Last of US Season 2 (YouTube) Candida auris Containment Responses in Health Care Facilities that Provide Hemodialysis Services (CDC: MMWR) Candidozyma auris: an emerging threat (Reflections on Infectious Prevention and Control) Effects of postoperative antifungal therapy on the recurrence of Aspergillus infection after pulmonary aspergilloma resection (BMC Infectious Diseases) Triazole-resistant Aspergillus fumigatus in the Netherlands between 1994 and 2022: a genomic and phenotypic study (LANCET: Microbe) Large language models and their performance for the diagnosis of histoplasmosis (PLoS Neglected Tropical Diseases) Parasitic Field evidence of Trypanosoma cruzi infection, diverse host use and invasion of human dwellings by the Chagas disease vector in Florida, USA (PLoS Neglected Tropical Diseases) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

Dr. Don and Professor Ben talk about the risks of making pancakes from old sourdough leftovers. Fedica text: Dr. Don - not risky

Is it time to rethink how we treat atopic dermatitis?Atopic dermatitis is more than skin deep—and naturopath and award-winning clinician Rebecca Hughes is here to prove it. In this practical and insightful episode, Rebecca shares her integrative, root-cause approach to eczema that goes far beyond suppressing symptoms with topical steroids.Drawing from extensive clinical experience, Rebecca highlights the importance of accurate diagnosis, noting that conditions such as psoriasis, seborrheic dermatitis, and lupus are often misidentified as eczema—leading to ineffective treatment. She walks practitioners through key investigations, from food intolerance and intestinal permeability testing to genetic susceptibilities, that help identify true inflammatory drivers.Rebecca also outlines her foundational nutrient protocol, including zinc, vitamin D, vitamin A, quercetin, and glutamine, and discusses how these work synergistically to modulate immune response, stabilise mast cells, and repair gut integrity. She also addresses overlooked environmental triggers like mould and water-damaged buildings, as well as the clinical importance of emotional support, sleep hygiene, and managing the psychological toll of visible skin conditions.Clinicians will find practical strategies for supporting patients through topical steroid withdrawal, tips on using bleach baths safely for Staphylococcus aureus overgrowth, and why children with eczema require particularly vigilant care.With a soon-to-be-released practitioner course on atopic dermatitis, Rebecca equips healthcare professionals with the tools they need to treat this complex condition confidently and holistically.Connect with Rebecca: Home - Rebecca Hughes Naturopath Explore Rebecca's Managing Atopic Dermatitis Course: Use code SAVE30 for a 30% discount. More information on the course can be found here: Managing Atopic Dermatitis | Natural Skin Medicine CoursesGet in touch! Shownotes and references are available on the Designs for Health websiteRegister as a Designs for Health Practitioner and discover quality practitioner- only supplements at www.designsforhealth.com.au Follow us on Socials Instagram: Designsforhealthaus Facebook: Designsforhealthaus DISCLAIMER: The Information provided in the Wellness by Designs podcast is for educational purposes only; the information presented is not intended to be used as medical advice; please seek the advice of a qualified healthcare professional if what you have heard here today raises questions or concerns relating to your health

Story at-a-glance Your scalp hosts a dense microbial ecosystem that protects against inflammation and disease. When disrupted, it can lead to flaking, itching, thinning hair, and inflammatory scalp conditions like seborrheic dermatitis The scalp microbiome is dominated by key bacteria like Cutibacterium acnes and Staphylococcus epidermidis. These microbes help protect your skin barrier, manage inflammation, and regulate other harmful organisms Scalp dysbiosis can be triggered by overwashing, harsh shampoos, excessive oil production, and even genetic factors like hair density or dandruff-prone skin. These disrupt the balance of good and bad microbes Dandruff is linked to reduced microbial diversity and fungal overgrowth. Studies show healthy scalps have more protective bacteria, while dandruff-prone scalps are overrun with inflammatory microbes like Malassezia restricta and Malassezia globosa Long-term relief comes from restoring beneficial microbes, not just killing fungi. Using microbiome-safe natural products, avoiding daily shampooing, and consuming foods that promote the growth of probiotics, prebiotics, and postbiotics are effective ways to rebalance your scalp naturally

This episode of Communicable takes on a special format where editors of CMI Comms, Marc Bonten, Josh Davis, Erin McCreary, Emily McDonald, all clinical trialists in their own right, take turns to summarise and discuss late-breaker trials presented at ESCMID Global 2025 in Vienna. These include the CloCeBa trial on Staphylococcus aureus bacteraemia treatment options, the Taper V trial on vancomycin as prophylaxis for Clostridioides difficile infection, the ASTARTÉ trial on temocillin versus meropenem for bacteraemia due to third-generation cephalosporin-resistant Enterobacterales, the HARVEST trial investigating high doses of rifampicin for tuberculosis meningitis, and the CAP5 trial on shortening antibiotic treatment for community-acquired pneumonia.   This episode was peer reviewed by Dr. Barbora Píšová (Czech Republic) and is the first of a two-part series covering selected clinical trials presented at ESCMID Global 2025. References: Lescure X, et al. Cloxacillin versus cefazolin for methicillin-susceptible Staphylococcus aureus bacteraemia (CloCeBa): a randomised, controlled, non-inferiority trialMcDonald EG, et al. Initial vancomycin taper for the prevention of recurrent Clostridioides difficile infection: the TAPER-V randomised controlled trialCogliati Dezza F, et al. Temocillin versus meropenem for the targeted treatment of bacteraemia due to third-generation cephalosporin-resistant Enterobacterales (ASTARTÉ): a randomised, pragmatic trialVan Crevel R, et al. High-dose rifampicin in the treatment of tuberculous meningitis: results of the HARVEST phase III multi-country randomised clinical trialBastrup Israelsen S, et al. Shortened antibiotic treatment for 5 days in patients hospitalised with community-acquired pneumonia (CAP5): a multicentre randomised controlled noninferiority trial

Send us a textEpisódio 54 – Hipotermia, Crescimento, Infecção Metabólica e Nariz Eletrônico na NeonatologiaNeste episódio especial, apresentamos os destaques do Encontro Internacional de Neonatologia, realizado nos dias 4 e 5 de abril em Gramado, sob a mais uma vez brilhante organização dos professores Rita e Renato Procianoy. Um evento que reuniu especialistas do Brasil e do mundo para discutir os avanços mais recentes no cuidado neonatal — e nós não poderíamos deixar de compartilhar com vocês, ouvintes que acompanham quinzenalmente o nosso Journal Club em língua portuguesa.Selecionamos quatro estudos que marcaram as discussões científicas durante o encontro:1. Whole-Body Hypothermia vs Targeted Normothermia for Neonates With Mild Encephalopathy – Este ensaio clínico multicêntrico coloca em pauta uma pergunta que muitos de nós enfrentamos à beira do leito: recém-nascidos com encefalopatia leve devem ser resfriados?2. Glucose supply and glycolysis inhibition shape the clinical fate of Staphylococcus epidermidis-infected preterm newborns – Uma fascinante investigação experimental que conecta metabolismo energético e resposta inflamatória em prematuros infectados, com possíveis implicações clínicas na prevenção da disfunção orgânica.3.Monitoring the Postnatal Growth of Preterm Infants: A Paradigm Change – Este artigo propõe uma verdadeira mudança de paradigma na forma como monitoramos o crescimento de prematuros, destacando a importância de uma abordagem individualizada e centrada no bebê. 4. Longitudinal fecal microbiota and volatile metabolomics preceding necrotizing enterocolitis in preterm infants– Um estudo que combina análise do microbioma e metabolômica para identificar marcadores precoces de enterocolite necrosante, uma das doenças mais temidas da neonatologia.Esperamos que este episódio especial amplie seu repertório científico e inspire práticas ainda mais seguras e baseadas em evidências. Se você gosta do nosso conteúdo, avalie o programa na sua plataforma de streaming e compartilhe com colegas e interessados. Seu apoio é essencial para continuarmos promovendo a neonatologia em língua portuguesa!Até o próximo episódio! Não esqueça: você pode ter acesso aos artigos do nosso Journal Club no nosso site: https://www.the-incubator.org/podcast-1 Lembrando que o Podcast está no Instagram, @incubadora.podcast, onde a gente posta as figuras e tabelas de alguns artigos. Se estiver gostando do nosso Podcast, por favor dedique um pouquinho do seu tempo para deixar sua avaliação no seu aplicativo favorito e compartilhe com seus colegas. Isso é importante para a gente poder continuar produzindo os episódios. O nosso objetivo é democratizar a informação. Se quiser entrar em contato, nos mandar sugestões, comentários, críticas e elogios, manda um e-mail pra gente: incubadora@the-incubator.org

Breakpoints joins forces with CMI Communications' Communicable podcast to discuss the highly anticipated SNAP trial updates presented at ESCMID Global 2025. Hosts Drs. Erin McCreary and Angela Huttner interview SNAP trial investigators, Drs. Joshua Davis and Steven Tong, on results from penicillin-susceptible and methicillin-susceptible Staphylococcus aureus domains. Conflict of Interest for DSMC Members: Conflicts of interest were evaluated when choosing individuals to serve on the SNAP DSMC. Aside from being compensated for their duties on the committee, DSMC members have no ongoing financial relationship that relate to the trial and are not involved in the conduct of the trial in any role other than that of a DSMC member. DSMC members have no intellectual conflict of interest or bias and reviewed SNAP data in a fully objective manner. Each DSMC candidate was well vetted.

In this first-ever collaboration between Communicable and Breakpoints, the podcast of the US Society of Infectious Diseases Pharmacists, hosts Angela Huttner (Geneva, Switzerland) and Erin McCreary (Pittsburgh, USA) join trial investigators Josh Davis (Newcastle, Australia) and Steve Tong (Melbourne, Australia) to unpack the first results coming from the SNAP adaptive platform trial, which were recently presented at ESCMID Global in Vienna. Learn whether penicillin and cefazolin are non-inferior to—and maybe even safer than—flucloxacillin for penicillin-susceptible and methicillin-susceptible Staphylococcus aureus, respectively.This episode was edited by Julie Anne Justo, transcribed by Katie Lambert and Sarah Groom, and peer-reviewed by Megan Klatt and Lacy Worden. Note on conflict of interest for SNAP Data Safety Monitoring Committee (DSMC) members:Conflicts of interest were evaluated when choosing individuals to serve on the SNAP DSMC. Aside from being compensated for their duties on the committee, DSMC members have no ongoing financial relationships that relate to the trial and are not involved in the conduct of the trial in any role other than that of a DSMC member. DSMC members have no intellectual conflict of interest or bias and reviewed SNAP data in a fully objective manner. Literature:Steven Y. C. Tong, Joshua S. Davis, Emily Eichenberger et al. Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management. Clin Microbiol Rev. 2015 Jul;28(3):603-61.SNAP Adaptive trial platform/results of the PSSA & MSSA domains: https://www.snaptrial.com.au/ESCMID Global April 2025 presentation:www.online.escmid.org *https://www.escmid.org/congress-events/escmid-global/programme/scientific-programme/CloCeBa trial results (ESCMID Global April 2025 presentation): www.online.escmid.org *https://www.escmid.org/congress-events/escmid-global/programme/scientific-programme/Note on access to online video of ESCMID Global presentations:In the six months following the congress:Non-ESCMID members have access if they registered for ESCMID GlobalMembers have access only if they registered for ESCMID GlobalSix months after the congress:Non-members do not have access, whatever their ESCMID Global registration statusAll members have access, whatever their ESCMID Global registration statusCAMERA 2 trial: Steven Y. C. Tong, David C. Lye, Dafna Yahav, et al. Without an Antistaphylococcal β-Lactam on Mortality, Bacteremia, Relapse, or Treatment Failure in Patients With MRSA BacteremiaA Randomized Clinical Trial. JAMA. 2020;323(6):527-537. doi:10.1001/jama.2020.0103 POET trial: Kasper Iversen, Nikolaj Ihlemann, Sabine U. Gill et al. Partial Oral versus Intravenous Antibiotic Treatment of Endocarditis. N Engl J Med 2019;380:415-424POET trial follow-up: Mia M. Pries-Heje, Christoffer Wiingaard, Nikolaj Ihlemann. Five-Year Outcomes of the Partial Oral Treatment of Endocarditis (POET) Trial. N Engl J Med 2022;386:601-602

What exciting times! Clinical trials into the management of SAB! SNAP publication on the horizon! But how do we interpret and apply the results of these trials to our patients? This week Jame and Callum are joined by Dr Clark Russell, Clinical Lecturer in Infectious Diseases to discuss:The difficulty in interpreting current clinical trials in SAB.The emerging concept of "low risk" SAB and how to define this.The heterogeneity of SAB and how this might be exploited.Notes for this episode here: https://idiots.notion.site/107-SAB-update-1316a1ea09d8800ba701ca7ebc8d4093 Previous episodes for the basics of Staphylococcus aureus and SABATO & SNAP trials:1. It starts with Staph65. SNAP trial protocol72. SABATO trial & 73. SABATaddendumSend us a text Support the showQuestions, comments, suggestions to idiotspodcasting@gmail.com or on Bluesky @idiots-pod.bsky.socialPrep notes for completed episodes can be found here (Not all episodes have prep notes).If you are enjoying the podcast please leave a review on your preferred podcast app!Feel like giving back? Donations of caffeine gratefully received!https://www.buymeacoffee.com/idiotspod

Do you keep relapsing after treating candida, SIBO or other conditions? The culprit behind these never-ending cycles may be biofilms. In this episode, I'll explain how biofilms form, help you identify signs that you have them, and recommend the best antibiofilm agents. Tune in!   Learn more about biofilms and improve your gut now! Reach out to our virtual clinic: https://drruscio.com/virtual-clinic/  

Dr. Jackie Sherbuk, Assistant Professor of Medicine at the USF Morsani College of Medicine, Division of Infectious Diseases, presents a case-based discussion of gram positive organisms producing disease in humans. Infections discussed include Staphylococcus aureus, Coagulase negative Staphylococcus, Pneumococcus, Streptococcus spp., Enterococcus, Corynebacterium, Bacillus, and Erysipelothrix. Associated clinical syndromes are also discussed.

Dr. Don - not risky

We are pleased to announce the first of a new series of upcoming episodes, titled ‘Pulse Check – Key Papers at a Glance'. Our host Can discuss two recent and impactful EJCTS articles on infective endocarditis. Joined by the renowned, Michael Borger and Torsten Doenst, we explore firstly the implications of preoperative septic cerebral embolism for patients undergoing valve surgery. Then followed by an exploration into the use of haemoadsorption therapy, addressing the key issue of controlling inflammation during cardiac surgery for endocarditis. Listen to gain rapid insight into the associated articles: Effect of haemoadsorption during cardiac surgery for Staphylococcus aureus endocarditis: a REMOVE trial post hoc analysis Outcomes following heart valve surgery in patients with infective endocarditis and preoperative septic cerebral embolism: insights from the CAMPAIGN study group'

Man Says He Visited Heaven, Met Jesus During Near-Death Experience Watch this video at- https://youtu.be/3FQmcCFZ8Ng?si=x4U0Eezqh21CuDDg CBN News 2.28M subscribers 123,685 views May 16, 2024 Randy Kay's "afterlife" experience still leaves him visibly emotional as he recounts details of visiting heaven, meeting Jesus, and returning to share his harrowing journey. Kay, author of the book, "Heaven Stormed: A Heavenly Encounter Reveals Your Assignment in the End Time Outpouring and Tribulation," told CBN News he was once a denier of near-death experience claims — until he faced his own purported heaven journey. He recalled his own afterlife experience, which began with a sore calf. At first, he thought he had strained a muscle, but while working out and going on a bike ride, his calf began to swell. "I was able to make it back home and then went to the doctor to get an anti-inflammatory prescription, and lo and behold, when I pressed my heel into the floor as the doctor had suggested, I collapsed," Kay said. "And I was rushed to the emergency room." It turns out, the pain and swelling were due to seven blood clots that had formed. He then contracted Methicillin-resistant Staphylococcus aureus (MRSA), a drug-resistant bacteria. "The doctor said I was a walking dead man," Kay said. "And then the septic shock which entered into my body caused a traffic jam in my vessels, my vascular system." The chaos landed Kay in a dire situation — one that he believes sent him to heaven. "Everything went dark initially and the next moment of recall, I was looking down on my body," he said. "I was being pulled by this light. I know that sounds cliche, almost, but it's absolutely true." Kay continued, "I was in a kind of very vague, ethereal space initially where I saw these figures in front of me, and they were warring against each other. There's no other way of putting it." After his return from his after-death experience, Kay discerned he was watching spiritual warfare play out. Regardless of what people choose to believe, Kay's physical body was dead at this point, making these memories and claims quite fascinating. "My heart had stopped," he said, noting that hospital records indicate he was clinically dead for 30 minutes and 49 seconds. During that time, Kay believes he was experiencing heaven, noting he was aware that her was himself but suddenly was seeing and visualizing the world quite differently. "I was seeing things, hearing things beyond which I would be able to do otherwise in my body," he said.

In this episode of Skin Anarchy, host Dr. Ekta welcomes Dr. Barbara Paldus, founder of Codex Labs, to explore breakthrough insights into eczema treatment. Dr. Paldus delves into the science behind the skin-gut-brain microbiome axis and explains how addressing both internal and external factors can revolutionize eczema care. Drawing on her recent TED Talk, she reveals that supporting gut health, reducing systemic inflammation, and restoring a balanced skin barrier can yield up to three times the benefits of traditional topical treatments.Dr. Paldus outlines the two main theories behind eczema—whether it starts with a leaky gut or a weakened skin barrier—and emphasizes that true relief comes from a holistic approach. She shares compelling data and real-world results from Codex Labs' innovative products, including the Bia Unscented Soap, Bia Eczema Relief Lotion, and Antü Skin Barrier Support Supplement. These products are designed to soothe, hydrate, and strengthen the skin from within, proving effective even in rigorous clinical trials.The conversation highlights the importance of understanding the genetic and environmental factors that contribute to eczema, from mutations in the filaggrin gene to the role of Staphylococcus aureus. Dr. Paldus also offers practical advice on integrating dietary changes, stress management, and gentle skincare into a comprehensive routine that supports long-term skin health.Tune in to discover how combining cutting-edge science with holistic wellness is paving the way for a new era in eczema treatment and learn why taking care of your skin from the inside out is the future of dermatology.Shop Codex's NEW Bia Eczema Relief Lotion.To learn more about Codex Labs, visit their website and social media. Don't forget to subscribe to Skin Anarchy on Apple Podcasts, Spotify, or your preferred platform. Reach out to us through email with any questions.Shop all our episodes and products mentioned through our ShopMy Shelf! Hosted on Acast. See acast.com/privacy for more information.

Arctic air is on the move southward and eastward into the United States in the coming days and will create harsh conditions for millions prior to the end of February. Also, the "superbug bacteria" is the methicillin-resistant Staphylococcus aureus, which resists most antibiotics, causes lung scarring and could cause death. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Drs. Henry “Chip” Chambers and Warren Rose join Dr. Megan Klatt to tackle rifampin dosing for gram-positive infections. In this episode, they break down rifampin synergy studies and discuss what is the optimal dosing of rifampin for challenging gram-positive bacterial cases, in particular Staphylococcus aureus infections with or without retained hardware/devices.   Listen to Breakpoints on iTunes, Overcast, Spotify, Listen Notes, Player FM, Pocket Casts, TuneIn, Blubrry, RadioPublic, or by using our RSS feed: https://sidp.pinecast.co/ References: Deconstructing the Dogma: Systematic Literature Review and Meta-analysis of Adjunctive Gentamicin and Rifampin in Staphylococcal Prosthetic Valve Endocarditis. Open Forum Infect Dis. 2022 Oct 31;9(11):ofac583. doi: 10.1093/ofid/ofac583. PMID: 36408468. Effectiveness of adjunctive rifampicin for treatment of Staphylococcus aureus bacteraemia: a systematic review and meta-analysis of randomized controlled trials. J Antimicrob Chemother. 2023 Oct 3;78(10):2419-2427. doi: 10.1093/jac/dkad214. PMID: 37583062. Adjunctive Rifampin Following Debridement and Implant Retention for Staphylococcal Prosthetic Joint Infection: Is it Effective if not Combined With a Fluoroquinolone? Open Forum Infect Dis. 2022 Oct 31;9(12):ofac582. doi: 10.1093/ofid/ofac582. PMID: 36504699.

Drs. Nico Cortes-Penfield (@Cortes-Penfield), Kerry LaPlante (@Kerry_LaPlante), Jessica Seidelman (@JessieLSeidel) join Dr. Julie Ann Justo (@julie_justo) to discuss the pesky slime that is biofilm in periprosthetic joint infections. They review biofilm composition & development, have an honest discussion about whether antibiotics can ever really eradicate it, and provide updates on the promising non-pharmacologic strategies on the horizon (bacteriophages, electromagnetism, & more). Learn more about the Society of Infectious Diseases Pharmacists: https://sidp.org/About X: @SIDPharm (https://twitter.com/SIDPharm) Instagram: @SIDPharm (https://www.instagram.com/sidpharm/) Facebook: https://www.facebook.com/sidprx LinkedIn: https://www.linkedin.com/company/sidp References Nixing the Nidus: Managing Retained Sources in Prosthetic Joint Infections. Breakpoints Podcast Episode #67. Society of Infectious Diseases Pharmacists. Dosing Consult: Rifampin Part 1. Breakpoints Podcast Episode #104. Society of Infectious Diseases Pharmacists. Review on Staphylococcal biofilm development: Schilcher K, Horswill AR. 2020 Aug 12;84(3):e00026-19. doi: 10.1128/MMBR.00026-19. PMID: 32792334. Antibiotics can fail to kill biofilm cells even if they penetrate the biofilm: Singh R, et al. Pathog Dis. 2016 Aug;74(6):ftw056. doi: 10.1093/femspd/ftw056. Epub 2016 Jul 7. PMID: 27402781. Subinhibitory antibiotic concentrations can promote biofilm formation: Schilcher K, et al. Antimicrob Agents Chemother. 2016 Sep 23;60(10):5957-67. doi: 10.1128/AAC.00463-16. PMID: 27458233. Clinical and genetic risk factors for biofilm-forming Staphylococcus aureus: Luther MK, et al. Antimicrob Agents Chemother. 2018 Apr 26;62(5):e02252-17. doi: 10.1128/AAC.02252-17. PMID: 29530854. Meta-analysis showing poor clinical outcomes with debridement, antibiotics, and implant retention (DAIR): Kunutsor SK, et al. J Infect. 2018 Dec;77(6):479-488. doi: 10.1016/j.jinf.2018.08.017. PMID: 30205122. Thieme L, et al. MBEC versus MBIC: the lack of differentiation between biofilm reducing and inhibitory effects as a current problem in biofilm methodology. Biol Proced Online 21, 18 (2019). https://doi.org/10.1186/s12575-019-0106-0. Ongoing trial investigating use of MBEC in the treatment of PJIs: Tillander JAN, et al. BMJ Open. 2022 Sep 15;12(9):e058168. doi: 10.1136/bmjopen-2021-058168. PMID: 36109038. Maale, G. Complete eradication of biofilm using low frequency electromagnetic force (EMF) and antibiotics at MIC. 34th Annual Meeting Musculoskeletal Infection Society. 2024 Aug. Abstract 1232 (see full program). Meta-analysis on bacteriophages for biofilm: Kovacs CJ, et al. Mil Med. 2024 May 18;189(5-6):e1294-e1302. doi: 10.1093/milmed/usad385. PMID: 37847552. Berking BB, et al. Biofilm disruption from within: light-activated molecular drill-functionalized polymersomes bridge the gap between membrane damage and quorum sensing-mediated cell death. ACS Biomater Sci Eng. 2024 Sep 9;10(9):5881-5891. doi: 10.1021/acsbiomaterials.4c01177. PMID: 39176452. Aboelnaga N, et al. Deciphering the dynamics of methicillin-resistant Staphylococcus aureus biofilm formation: from molecular signaling to nanotherapeutic advances. Cell Commun Signal. 2024 Mar 22;22(1):188. doi: 10.1186/s12964-024-01511-2. PMID: 38519959. Conway J, et al. Phase 1 study of the pharmacokinetics and clinical proof-of-concept activity of a biofilm-disrupting human monoclonal antibody in patients with chronic prosthetic joint infection of the knee or hip. Antimicrob Agents Chemother. 2024 Aug 7;68(8):e0065524. doi: 10.1128/aac.00655-24. PMID: 39012102. Mulpur P, et al. Efficacy of intrawound vancomycin in prevention of periprosthetic joint infection after primary total knee arthroplasty: a prospective double-blinded randomized control trial. J Arthroplasty. 2024 Jun;39(6):1569-1576. doi: 10.1016/j.arth.2024.01.003. PMID: 38749600. Dong Y, et al. Synergy of ultrasound microbubbles and vancomycin against Staphylococcus epidermidis biofilm. J Antimicrob Chemother. 2013 Apr;68(4):816-26. doi: 10.1093/jac/dks490. PMID: 23248238. Miltenberg B, et al. Intraosseous Regional Administration of Antibiotic Prophylaxis for Total Knee Arthroplasty: A Systematic Review. J Arthroplasty. 2023 Apr;38(4):769-774. doi: 10.1016/j.arth.2022.10.023. PMID: 36280158. Viswanathan VK, et al. Intraosseous regional antibiotic prophylaxis in total joint arthroplasty (TJA): Systematic review and meta-analysis. J Clin Orthop Trauma. 2024 Oct 3;57:102553. doi: 10.1016/j.jcot.2024.102553. PMID: 39435324. SOLARIO trial: Dudareva M, et al. The European Bone and Joint Infection Society Meeting, 2024 Sept. SOLARIO trial press release from BoneSupportTM. 2024 Oct 3. Fehring TK, et al. Does treatment at a specialized prosthetic joint infection center improve the rate of reimplantation. J Arthroplasty. 2023 Jun;38(6S):S314-7. PMID 37004968. ROADMAP trial website. 2024.

In this episode of the Micro Binfie Podcast, host Andrew Page takes listeners to the heart of the microbial genomics hackathon in Bethesda, Maryland, for an engaging conversation with special guest Megan Phillips, a PhD student from Emory University. Megan delves into her research on Staphylococcus aureus (MRSA), highlighting its fascinating dual nature as both a harmless and potentially serious pathogen. Megan discusses the complexities of tetracycline resistance, particularly focusing on plasmid-mediated mechanisms involving the pt181 plasmid. She explains how this plasmid's efflux pump, encoded by the gene tetK, contributes to variable resistance levels and the factors influencing MIC (Minimum Inhibitory Concentration) variability. Listeners will learn about the intricacies of plasmid copy numbers, their global spread across clonal complexes, and the occurrence of horizontal and vertical gene transfer. Throughout the episode, Megan shares insights on working with short-read sequencing data and the strategies she employs to detect plasmid presence using tools like BLAST. She also touches on the challenges and fascinating discoveries of tracking historical sample data and integrating findings from older research papers, showcasing her appreciation for the poetic style of scientific writing from the 1940s. For those interested in antimicrobial resistance, evolutionary microbiology, and the subtleties of bacterial genome analysis, this episode offers a compelling blend of technical details and engaging storytelling. Tune in to hear more about Megan's upcoming publications, her experiences navigating complex genomic data, and her thoughts on antimicrobial stewardship and historical perspectives on drug resistance.

Guest: Dr. Christian de Virgilio is the Chair of the Department of Surgery at Harbor-UCLA Medical Center. He is also Co-Chair of the College of Applied Anatomy and a Professor of Surgery at UCLA's David Geffen School of Medicine. He completed his undergraduate degree in Biology at Loyola Marymount University and earned his medical degree from UCLA. He then completed his residency in General Surgery at UCLA-Harbor Medical Center followed by a fellowship in Vascular Surgery at the Mayo Clinic.   Resources:  Rutherford Chapters (10th ed.): 174, 175, 177, 178 Prior Holding Pressure episode on AV access creation: https://www.audiblebleeding.com/vsite-hd-access/ The Society for Vascular Surgery: Clinical practice guidelines for the surgical placement and maintenance of arteriovenous hemodialysis access: https://www.jvascsurg.org/article/S0741-5214%2808%2901399-2/fulltext  KDOQI Clinical Practice Guideline for Vascular Access: 2019 Update: https://pubmed.ncbi.nlm.nih.gov/32778223/    Outline: Steal Syndrome Definition & Etiology Steal syndrome is an important complication of AV access creation, since access creation diverts arterial blood flow from the hand. Steal can be caused by multiple factors—arterial occlusive disease proximal or distal to the AV anastomosis, high flow through the fistula at the expense of distal arterial perfusion, and failure of the distal arterial networks to adapt to this decreased blood flow.  Incidence and Risk Factors The frequency of steal syndrome is 1.6-9%1,2, depending on the vessels and conduit choice Steal syndrome is more common with brachial and axillary artery-based accesses and nonautogenous conduits. Other risk factors for steal syndrome are peripheral vascular disease, coronary artery disease, diabetes, advanced age, female sex, larger outflow conduit, multiple prior permanent access procedures, and prior episodes of steal.3,4  Long-standing insulin-dependent diabetes causes both medial calcinosis and peripheral neuropathy, which limits arteries' ability to vasodilate and adjust to decreased blood flow. Patient Presentation, Symptoms, Grading Steal syndrome is diagnosed clinically.  Symptoms after AVG creation occurs within the first few days, since flow in prosthetic grafts tend to reach a maximum value very early after creation. Native AVFs take time to mature and flow will slowly increase overtime, leading to more insidious onset of symptoms that can take months or years. The patient should have a unilateral complaint in the extremity with the AV access. Symptoms of steal syndrome, in order of increasing severity, include nail changes, occasional tingling, extremity coolness, numbness in fingertips and hands, muscle weakness, rest pain, sensory and motor deficits, fingertip ulcerations, and tissue loss.  There could be a weakened radial pulse or weak Doppler signal on the affected side, and these will become stronger after compression of the AV outflow. Symptoms are graded on a scale specified by Society of Vascular Surgery (SVS) reporting standards:5  Workup Duplex ultrasound can be used to analyze flow volumes. A high flow volume (in autogenous accesses greater than 800 mL/min, in nonautogenous accesses greater than 1200 mL/min) signifies an outflow issue. The vein or graft is acting as a pressure sink and stealing blood from the distal artery. A low flow volume signifies an inflow issue, meaning that there is a proximal arterial lesion preventing blood from reaching the distal artery. Upper extremity angiogram can identify proximal arterial lesions. Prevention Create the AV access as distal as possible, in order to preserve arterial inflow to the hand and reduce the anastomosis size and outflow diameter.  SVS guidelines recommend a 4-6mm arteriotomy diameter to balance the need for sufficient access flow with the risk of steal. If a graft is necessary, tapered prosthetic grafts are sometimes used in patients with steal risk factors, using the smaller end of the graft placed at the arterial anastomosis, although this has not yet been proven to reduce the incidence of steal.  Indications for Treatment Intervention is recommended in lifestyle-limiting cases of Grade II and all Grade III steal cases. If left untreated, the natural history of steal syndrome can result in chronic limb ischemia, causing gangrene with loss of digits or limbs. Treatment Options Conservative management relies on observation and monitoring, as mild cases of steal syndrome may resolve spontaneously. Inflow stenosis can be treated with endovascular intervention (angioplasty with or without stent) Ligation is the simplest surgical treatment, and it results in loss of the AV access. This is preferred in patients with repetitive failed salvage attempts, venous hypertension, and poor prognoses. Flow limiting procedures can address high volumes through the AV access. Banding can be performed with surgical cutdown and placement of polypropylene sutures or a Dacron patch around the vein or graft. The Minimally Invasive Limited Ligation Endoluminal-Assisted Revision (MILLER) technique employs a percutaneous endoluminal balloon inflated at the AVF to ensure consistency in diameter while banding Plication is when a side-biting running stitch is used to narrow lumen of the vein near the anastomosis. A downside of flow-limiting procedures is that it is often difficult to determine how much to narrow the AV access, as these procedures carry a risk of outflow thrombosis. There are also surgical treatments focused on reroute arterial inflow. The distal revascularization and interval ligation (DRIL) procedure involves creation of a new bypass connecting arterial segments proximal and distal to the AV anastomosis, with ligation of the native artery between the AV anastomosis and the distal anastomosis of the bypass. Reversed saphenous vein with a diameter greater than 3mm is the preferred conduit. Arm vein or prosthetic grafts can be used if needed, but prosthetic material carries higher risk of thrombosis. The new arterial bypass creates a low resistance pathway that increases flow to distal arterial beds, and interval arterial ligation eliminates retrograde flow through the distal artery.  The major risk of this procedure is bypass thrombosis, which results in loss of native arterial flow and hand ischemia. Other drawbacks of DRIL include procedural difficulty with smaller arterial anastomoses, sacrifice of saphenous or arm veins, and decreased fistula flow. Another possible revision surgery is revision using distal inflow (RUDI). This procedure involves ligation of the fistula at the anastomosis and use of a conduit to connect the outflow vein to a distal artery. The selected distal artery can be the proximal radial or ulnar artery, depending on the preoperative duplex. The more dominant vessel should be spared, allowing for distal arterial beds to have uninterrupted antegrade perfusion. The nondominant vessel is used as distal inflow for the AV access. RUDI increases access length and decreases access diameter, resulting in increased resistance and lower flow volume through the fistula. Unlike DRIL, RUDI preserves native arterial flow.  Thrombosis of the conduit would put the fistula at risk, rather than the native artery.  The last surgical revision procedure for steal is proximalization of arterial inflow (PAI). In this procedure, the vein is ligated distal to the original anastomosis site and flow is re-established through the fistula with a PTFE interposition graft anastomosed end-to-side with the more proximal axillary artery and end-to-end with the distal vein. Similar to RUDI, PAI increases the length and decreases the diameter of the outflow conduit. Since the axillary artery has a larger diameter than the brachial artery, there is a less significant pressure drop across the arterial anastomosis site and less steal. PAI allows for preservation of native artery's continuity and does not require vein harvest.  Difficulties with PAI arise when deciding the length of the interposition graft to balance AV flow with distal arterial flow. 2. Ischemic Monomelic Neuropathy Definition Ischemic monomelic neuropathy (IMN) is a rare but serious form of steal that involves nerve ischemia. Severe sensorimotor dysfunction is experienced immediately after AV access creation. Etiology IMN affects blood flow to the nerves, but not the skin or muscles because peripheral nerve fibers are more vulnerable to ischemia. Incidence and Risk Factors IMN is very rare; it has an estimated incidence of 0.1-0.5% of AV access creations.6 IMN has only been reported in brachial artery-based accesses, since the brachial artery is the sole arterial inflow for distal arteries feeding all forearm nerves. IMN is associated with diabetes, peripheral vascular disease, and preexisting peripheral neuropathy that is associated with either of the conditions. Patient Presentation Symptoms usually present rapidly, within minutes to hours after AV access creation. The most common presenting symptom is severe, constant, and deep burning pain of the distal forearm and hand. Patients also report impairment of all sensation, weakness, and hand paralysis. Diagnosis of IMN can be delayed due to misattribution of symptoms to anesthetic blockade, postoperative pain, preexisting neuropathy, a heavily bandaged arm precluding neurologic examination. Treatment Treatment is immediate ligation of the AV access. Delay in treatment will quickly result in permanent sensorimotor loss.   3. Perigraft Seroma Definition A perigraft seroma is a sterile fluid collection surrounding a vascular prosthesis and is enclosed within a pseudomembrane. Etiology and Incidence Possible etiologies include: transudative movement of fluid through the graft material, serous fluid collection from traumatized connective tissues (especially the from higher adipose tissue content in the upper arm), inhibition of fibroblast growth with associated failure of the tissue to incorporate the graft, graft “wetting” or kinking during initial operation, increased flow rates, decreased hematocrit causing oncotic pressure difference, or allergy to graft material. Seromas most commonly form at anastomosis sites in the early postoperative period. Overall seroma incidence rates after AV graft placement range from 1.7–4% and are more common in grafts placed in the upper arm (compared to the forearm) and Dacron grafts (compared to PTFE grafts).7-9 Patient Presentation and Workup Physical exam can show a subcutaneous raised palpable fluid mass Seromas can be seen with ultrasound, but it is difficult to differentiate between the types of fluid around the graft (seroma vs. hematoma vs. abscess) Indications for Treatment Seromas can lead to wound dehiscence, pressure necrosis and erosion through skin, and loss of available puncture area for hemodialysis Persistent seromas can also serve as a nidus for infection. The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines10 recommend a tailored approach to seroma management, with more aggressive surgical interventions being necessary for persistent, infected-appearing, or late-developing seromas.   Treatment The majority of early postoperative seromas are self-limited and tend to resolve on their own Persistent seromas have been treated using a variety of  methods-- incision and evacuation of seroma, complete excision and replacement of the entire graft, and primary bypass of the involved graft segment only. Graft replacement with new material and rerouting through a different tissue plane has a higher reported cure rate and lower rate of infection than aspiration alone.9     4. Infection Incidence and Etiology The reported incidence of infection ranges 4-20% in AVG, which is significantly higher than the rate of infection of 0.56-5% in AVF.11  Infection can occur at the time of access creation (earliest presentation), after cannulation for dialysis (later infection), or secondary to another infectious source. Infection can also further complicate a pre-existing access site issue such as infection of a hematoma, thrombosed pseudoaneurysm, or seroma. Skin flora from frequent dialysis cannulations result in common pathogens being Staphylococcus, Pseudomonas, or polymicrobial species. Staphylococcus and Pseudomonas are highly virulent and likely to cause anastomotic disruption. Patient Presentation and Workup Physical exam will reveal warmth, pain, swelling, erythema, induration, drainage, or pus. Occasionally, patients have nonspecific manifestations of fever or leukocytosis. Ultrasound can be used to screen for and determine the extent of graft involvement by the infection.   Treatments In AV fistulas: Localized infection can usually be managed with broad spectrum antibiotics.  If there are bleeding concerns or infection is seen near the anastomosis site, the fistula should be ligated and re-created in a clean field. In AV grafts: If infection is localized, partial graft excision is acceptable. Total graft excision is recommended if the infection is present throughout the entire graft, involves the anastomoses, occludes the access, or contains particularly virulent organisms Total graft excision may also be indicated if a patient develops recurrent bacteremia with no other infectious source identified. For graft excision, the venous end of the graft is removed and the vein is oversewn or ligated. If the arterial anastomosis is intact, a small cuff of the graft can be left behind and oversewn. If the arterial anastomosis is involved, the arterial wall must be debrided and ligation, reconstruction with autogenous patch angioplasty, or arterial bypass can be pursued. References   1. Morsy AH, Kulbaski M, Chen C, Isiklar H, Lumsden AB. Incidence and Characteristics of Patients with Hand Ischemia after a Hemodialysis Access Procedure. J Surg Res. 1998;74(1):8-10. doi:10.1006/jsre.1997.5206 2. Ballard JL, Bunt TJ, Malone JM. Major complications of angioaccess surgery. Am J Surg. 1992;164(3):229-232. doi:10.1016/S0002-9610(05)81076-1 3. Valentine RJ, Bouch CW, Scott DJ, et al. Do preoperative finger pressures predict early arterial steal in hemodialysis access patients? A prospective analysis. J Vasc Surg. 2002;36(2):351-356. doi:10.1067/mva.2002.125848 4. Malik J, Tuka V, Kasalova Z, et al. Understanding the Dialysis access Steal Syndrome. A Review of the Etiologies, Diagnosis, Prevention and Treatment Strategies. J Vasc Access. 2008;9(3):155-166. doi:10.1177/112972980800900301 5. Sidawy AN, Gray R, Besarab A, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg. 2002;35(3):603-610. doi:10.1067/mva.2002.122025 6. Thermann F, Kornhuber M. Ischemic Monomelic Neuropathy: A Rare but Important Complication after Hemodialysis Access Placement - a Review. J Vasc Access. 2011;12(2):113-119. doi:10.5301/JVA.2011.6365 7. Dauria DM, Dyk P, Garvin P. Incidence and Management of Seroma after Arteriovenous Graft Placement. J Am Coll Surg. 2006;203(4):506-511. doi:10.1016/j.jamcollsurg.2006.06.002 8. Gargiulo NJ, Veith FJ, Scher LA, Lipsitz EC, Suggs WD, Benros RM. Experience with covered stents for the management of hemodialysis polytetrafluoroethylene graft seromas. J Vasc Surg. 2008;48(1):216-217. doi:10.1016/j.jvs.2008.01.046 9. Blumenberg RM, Gelfand ML, Dale WA. Perigraft seromas complicating arterial grafts. Surgery. 1985;97(2):194-204. 10. Lok CE, Huber TS, Lee T, et al. KDOQI Clinical Practice Guideline for Vascular Access: 2019 Update. Am J Kidney Dis. 2020;75(4):S1-S164. doi:10.1053/j.ajkd.2019.12.001 11. Padberg FT, Calligaro KD, Sidawy AN. Complications of arteriovenous hemodialysis access: Recognition and management. J Vasc Surg. 2008;48(5):S55-S80. doi:10.1016/j.jvs.2008.08.067

I've touched on the topic of endotoxemia in past episodes of the Defiant Health podcast. In this episode, let's dive deeper into this topic that is absolutely crucial to understanding and managing SO many aspects of health, from subduing anxiety and panic, to depressive, to joint pain and skin rashes, to gastrointestinal conditions, even weight management. What is endotoxemia? Fecal microbes, so-called Gram-negative species because of the way these microbes take up stain for examination under a microscope, species such as E. coli and Salmonella, have something called lipopolysaccharide endotoxin in their cells walls. Other species, so-called Gram positive species such as Enterococcus, Staphylococcus, and Streptococcus, that stain in a different manner, have something called lipoteichoic acid in their cell walls. When these microbes die, both Gram-negative and Gram-positive, these toxic factors are released into the intestines. If these fecal microbes are confined to the colon, where they belong, a section of GI tract adapted to their presence, the entry of these toxic components are limited and current evidence is unclear in how importat this process is. The real trouble occurs, however, when fecal microbes have invaded the 24-feet of small intestine, a process we label small intetinal bacterial overgrowth, or SIBO, because the small intestine—the stomach, duodenum, jejunum, and ileum are not well-adapted to the invasion of fecal species. Here, they die, release their toxic components, which then enter the bloodstream, the process labeled endotoxemia. People with SIBO therefore have high blood levels, typically 200-400% higher, levels of endotoxin. This is how microbes in the GI Tract export their effects to all other parts of the body. So let's discuss this process and how you can take control over it to be be better able to take control over your emotions, mood, sleep, energy, weight, and numerous other aspects of health. _______________________________________________________________________________For BiotiQuest probiotics including Sugar Shift, go here.A 15% discount is available for Defiant Health podcast listeners by entering discount code UNDOC15 (case-sensitive) at checkout.*_________________________________________________________________________________Get your 15% Paleovalley discount on fermented grass-fed beef sticks, Bone Broth Collagen, low-carb snack bars and other high-quality organic foods here.* For 12% off every order of grass-fed and pasture-raised meats from Wild Pastures, go here._____________________________________________________________________________MyReuSupport the showBooks: Super Gut: The 4-Week Plan to Reprogram Your Microbiome, Restore Health, and Lose Weight Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health; revised & expanded ed

We are back with more exciting IDWeek 2024 content. In this episode, Breakpoints hostesses Drs. Erin McCreary, Julie Ann Justo, Jeannette Bouchard, and Megan Klatt highlight more of our favorite sessions and posters at IDWeek, this episode is a must listen if you are an IDWeek nerd like us! References: Perret et al. Application of OpenAI GPT-4 for the retrospective detection of catheter-associated urinary tract infections in a fictitious and curated patient data set. 10.1017/ice.2023.189 Wiemken et al. Assisting the infection preventionist: Use of artificial intelligence for health care–associated infection surveillance. 10.1016/j.ajic.2024.02.007 Leekha et al. Evaluation of hospital-onset bacteraemia and fungaemia in the USA as a potential healthcare quality measure: a cross-sectional study. 10.1136/bmjqs-2023-016831 Diekema et al. Are Contact Precautions "Essential" for the Prevention of Healthcare-associated Methicillin-Resistant Staphylococcus aureus? 10.1093/cid/ciad571 Martin et al. Contact precautions for MRSA and VRE: where are we now? A survey of the Society for Healthcare Epidemiology of America Research Network. 10.1017/ash.2024.350 Browne et al. Investigating the effect of enhanced cleaning and disinfection of shared medical equipment on health-care-associated infections in Australia (CLEEN): a stepped-wedge, cluster randomised, controlled trial. 10.1016/S1473-3099(24)00399-2 Protect trial: Decolonization in Nursing Homes to Prevent Infection and Hospitalization. 10.1056/NEJMoa2215254 Aldardeer et al. Early Versus Late Antipseudomonal β-Lactam Antibiotic Dose Adjustment in Critically Ill Sepsis Patients With Acute Kidney Injury: A Prospective Observational Cohort Study. 10.1093/ofid/ofae059 Schmiemann et al. Effects of a multimodal intervention in primary care to reduce second line antibiotic prescriptions for urinary tract infections in women: parallel, cluster randomised, controlled trial. 10.1136/bmj-2023-076305 Vernacchio et al. Improving Short Course Treatment of Pediatric Infections: A Randomized Quality Improvement Trial. 10.1542/peds.2023-063691 Advani et al. Bacteremia From a Presumed Urinary Source in Hospitalized Adults With Asymptomatic Bacteriuria. 10.1001/jamanetworkopen.2024.2283 Saif et al. Clinical decision support for gastrointestinal panel testing. 10.1017/ash.2024.15 Bekker et al. Twice-Yearly Lenacapavir or Daily F/TAF for HIV Prevention in Cisgender Women. 10.1056/NEJMoa2407001 Montini et al. Short Oral Antibiotic Therapy for Pediatric Febrile Urinary Tract Infections: A Randomized Trial. 10.1542/peds.2023-062598 Nielsen et al. Oral versus intravenous empirical antibiotics in children and adolescents with uncomplicated bone and joint infections: a nationwide, randomised, controlled, non-inferiority trial in Denmark. 10.1016/S2352-4642(24)00133-0 Kaasch et al. Efficacy and safety of an early oral switch in low-risk Staphylococcus aureus bloodstream infection (SABATO): an international, open-label, parallel-group, randomised, controlled, non-inferiority trial. 10.1016/S1473-3099(23)00756-9 AMIKINHAL: Inhaled Amikacin to Prevent Ventilator-Associated Pneumonia. 10.1056/NEJMoa2310307 PROPHY-VAP: Ceftriaxone to prevent early ventilator-associated pneumonia in patients with acute brain injury: a multicentre, randomised, double-blind, placebo-controlled, assessor-masked superiority trial. 10.1016/S2213-2600(23)00471-X AVENIR: Azithromycin to Reduce Mortality — An Adaptive Cluster-Randomized Trial. 10.1056/NEJMoa2312093 Thomas et al. Comparison of Two High-Dose Versus Two Standard-Dose Influenza Vaccines in Adult Allogeneic Hematopoietic Cell Transplant Recipients. 10.1093/cid/ciad458 Schuster et al. The Durability of Antibody Responses of Two Doses of High-Dose Relative to Two Doses of Standard-Dose Inactivated Influenza Vaccine in Pediatric Hematopoietic Cell Transplant Recipients: A Multi-Center Randomized Controlled Trial. 10.1093/cid/ciad534 Mahadeo et al. Tabelecleucel for allogeneic haematopoietic stem-cell or solid organ transplant recipients with Epstein-Barr virus-positive post-transplant lymphoproliferative disease after failure of rituximab or rituximab and chemotherapy (ALLELE): a phase 3, multicentre, open-label trial. 10.1016/S1470-2045(23)00649-6 Khoury et al. Third-party virus-specific T cells for the treatment of double-stranded DNA viral reactivation and posttransplant lymphoproliferative disease after solid organ transplant. 10.1016/j.ajt.2024.04.009 Spec et al. MSG-15: Super-Bioavailability Itraconazole Versus Conventional Itraconazole in the Treatment of Endemic Mycoses—A Multicenter, Open-Label, Randomized Comparative Trial. 10.1093/ofid/ofae010

On episode #67 of the Infectious Disease Puscast, Daniel reviews the infectious disease literature for the weeks of 10/24 – 11/6/24. Host: Daniel Griffin Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Microbial dynamics and pulmonary immune responses in COVID-19 secondary bacterial pneumonia(Nature) Bacterial Implementation of a Pharmacist-Driven Vancomycin Area Under the Concentration-Time Curve Monitoring Program Using Bayesian Modeling in Outpatient Parenteral Antimicrobial Therapy (OFID) Rifaximin prophylaxis causes resistance to the last-resort antibiotic daptomycin (Nature) Oral Versus Intravenous Antibiotic Therapy for Staphylococcus aureus Bacteremia or Endocarditis(CID) Fungal The Last of US Season 2 (YouTube) Notes from the Field: Trichophyton mentagrophytes Genotype VII — New York City, April–July 2024 (CDC MMWR) Evaluation of Crushed Posaconazole Delayed Release Tablets in Lung Transplant Recipients(Transplant Infectious Disease) Parasitic Outcomes of kidney transplant recipients exposed to Chagas disease under Benznidazole prophylaxis(Transplant Infectious Disease) Fake Aristotle Fakely Rails Against Fighting Inequality (Sententiae Antiquae) Need for a paradigm shift in soil-transmitted helminthiasis control (PLoS Neglected Tropical Diseases) Miscellaneous IDSA Advocacy Results in Big Win for ID in 2025 Final Medicare Rule (IDSA) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice

Drs. Cesar Arias (@SuperBugDoc) and Katie Barber join Dr. Julie Ann Justo (@julie_justo) to discuss what is hot-off-the-presses for gram-positive bacterial infections and it's a total party vibe! They review the latest news for recent and ongoing clinical trials (DOTS, DISRUPT, and SNAP trials), discuss hope for novel clinical tests of the cefazolin inoculum effect in staphylococci, and explore the fascinating changes in virulence and potential therapeutic options for the most challenging enterococci. Learn more about the Society of Infectious Diseases Pharmacists: https://sidp.org/About X: @SIDPharm (https://twitter.com/SIDPharm) Instagram: @SIDPharm (https://www.instagram.com/sidpharm/) Facebook: https://www.facebook.com/sidprx LinkedIn: https://www.linkedin.com/company/sidp References Climate Change and Antimicrobial Resistance. Editors in Conversation Podcast. American Society for Microbiology. Oct 2023. Is More Better? The Role of Combination Therapy for MRSA. Breakpoints Podcast Episode #30. Society of Infectious Diseases Pharmacists. Turner NA, et al. DOTS: Dalbavancin as an Option for Treatment of Staphylococcus aureus Bacteremia. ESCMID Global 2024. April 2024. NCT04775953. Real-world dalbavancin observational cohort: Rebold N, et al. Infect Dis Ther. 2024 Mar;13(3):565-579. doi: 10.1007/s40121-024-00933-2. PMID: 38427289. Exebacase DISRUPT trial : Fowler VG Jr, et al. Clin Infect Dis. 2024 Jun 14;78(6):1473-1481. doi: 10.1093/cid/ciae043. PMID: 38297916. @snap_trial tweet of Breaking News. Aug 2024. Investigator Resources for the SNAP trial. Sept 2024: https://www.snaptrial.com.au/for-investigators#interim Cefazolin inoculum effect on mortality in MSSA bacteremia : Miller WR, et al. Open Forum Infect Dis. 2018 May 23;5(6):ofy123. doi: 10.1093/ofid/ofy123. PMID: 29977970. Prevalence of cefazolin inoculum effect in MSSA and modified rapid nitrocefin test for detection: Carvajal LP, et al. Antimicrob Agents Chemother. 2024 Sep 30:e0089824. doi: 10.1128/aac.00898-24. PMID: 39345182. LiaX as surrogate for cell envelope stress in Enterococus faecium: Axell-House DB, et al. Antimicrob Agents Chemother. 2024 Mar 6;68(3):e0106923. doi: 10.1128/aac.01069-23. PMID: 38289081. Shorter is better for uncomplicated streptococcal bacteremia: Clutter DS, et al. Antimicrob Agents Chemother. 2024 Aug 7;68(8):e0022024. doi: 10.1128/aac.00220-24. PMID: 38975753. Short vs. long antibiotic duration in Streptococcus pneumoniae bacteremia: Crotty M, et al. Open Forum Infect Dis. 2024 Aug 30;11(9):ofae478. doi: 10.1093/ofid/ofae478. PMID: 39257675. This podcast is powered by Pinecast.