29% of Explant Samples Had Bacterial DNA — Here's What That Means

The talk tonight is about biofilm and capsular contracture. So biofilm does not explain every single problem. So the more useful question is, what are the microbial signals we detected in the samples of the patients we took care of, and how do we interpret those results, and how do we understand them, and what can we learn from them and help our patients? So we will separate obviously samples from patients, and we want to separate detection from an infection and association from causation. There's a lot made about direct implications that I find on implants, and I think obviously I like to follow the evidence and see where it leads us. So the distinctions are where we really need to, you know, make strides and try to close out gaps. So I'm Dr. Whitfield. I'm in Austin, Texas. I want to thank you all for joining me tonight. You know, our paper looked at 694 samples. So we looked at what biofilm, how it showed up in our practice, because I had this frustrating experience in 2018 where I took care of somebody and did a conventional culture and it showed nothing. But I was a little bit taken aback because I know better than that. I've been in practice a long period of time. I knew there was something else wrong. So although biofilm doesn't directly implicate a cause and effect relationship with capsular contracture, it certainly can be a contributor. So obviously I'm the first author of that paper and I was the The physician who collected all the samples in that study. So we did those all sterilely, implants on the back table, case was done. And we're gonna try to go through the data and try to make sense of it for you and try to help you better understand, you know, capsular contracture. And this is educational only. It's not, you know, me giving you specific medical advice on your situation. Always try to help everybody, but you got to have in-person consultations or calls and visits to get your specific case analyzed. The testing discussed tonight is obviously, like I said, a prevention. By itself, it doesn't diagnose anybody. If you have more symptoms or questions— so, uh, oh, somebody's already asking about my paper. Yeah, my paper is listed in my bibliography on my website, drrobertwhitfield.com. It is, if you just type in my Google Scholar ID, which is also listed on my website, but I have a whole list of my publications on my website. The paper's there. You can click on it. It's in PubMed. It's open access. Okay. But once again, take specific symptoms, questions about those implants, laboratory results, or treatment options to your provider. And if you Want to work with us, obviously we'll help get you connected. We have a team that helps vet and takes calls, does discovery calls for me. So, if you go to drrobertwhitfield.com, they'll help you get a complimentary call set up. And so, when I do these tests, I get asked a lot, what do we do afterwards? Well, we don't use oral antibiotics. And I don't In particular, have a specific regimen for supplementation or anything afterwards. We have a curated set of tests and supplements and guidance on nutrition that we use pre-op and post-op, and that's how we just help patients move through the process more simply and clearly. So let's let's talk about a capsule, right? So the body normally forms a capsule or layer of scar tissue around any implant. Now we're talking about just and focusing on breast implants, and that's the expected response. Capsular contracture is different. The capsule can become unusually firm, and in some instances almost you know what I find in the operating room is tight. And it may become painful to the patient. It may change shape or position of the breast. It can be a real problem for patients, both in how it feels, how their clothing fits. Capsular contracture is, as we talk about today, considered to be a multifactorial problem. The patient's individual biology, of course, Inflammation, of course. At the time of surgery, was there bleeding or problems in the pocket? Other surgical factors or implant-based factors? And of course, any microbial processes are relevant depending on the circumstances of the patient. So biofilm is one plausible contributor, and it's not a universal explanation. So that distinction matters for patients who are trying to make sense of their symptoms. 2 people can have similar implants, very different clinical experiences. One person may develop a firm capsule, another may have pain without a severe contracture, another may have local symptoms, um, or simply have nothing at all. So any of the findings may be relevant in one clinical picture or another. The study that we designed, it wasn't designed in a way to sort through symptoms or categorize them. It was designed to describe the findings of any microbes on the devices. So That was my intent in trying to set the true incidence of bacterial contamination on implants. So, a biofilm is simply an organized community of those microbes associated with— basically, think of a layer of goo, and it just helps protect them. It makes it harder for your body to deal with them. In medicine, biofilms are not new. They can behave differently from feet, free-floating bacteria, though. They may be unevenly distributed and difficult to characterize in a single type of sampling method. But here is a critical distinction: detecting bacteria through genetic material by itself, it doesn't really demonstrate a mature biofilm. It does not prove that there is an active infection. So in my paper, it certainly does not do that, and that's, you know, why the language I use refers back to that all the time. So there have been a number of papers published about biofilm. I reviewed one of them recently by Dr. Mathun Sina and colleagues about biofilm and oxylipin tenhorm. I also reviewed a paper about the transcriptome. So I think it's important, you know, my paper was published in Microorganisms in 2024. The title of which is Clinical Evaluation of Microbial Communities and Associated Biofilms with Breast Augmentation Failures. So the IRB-approved study was my surgical experience, and excuse me, it covered really a sample from February of 19 to September of 22. Total of 694 explant samples were examined through next-gen sequencing for microbial profiling. So, you know, that's a large number of samples. Also, this was a specific set of samples. Obviously, people are coming to me for explant surgery. The specimens came from that particular population who were Removing their implants. And so that's the selection of the patient population that I'm taking care of. So the study can describe findings that are submitted obviously by those specimens I took. It cannot establish the prevalence of these findings among all people with implants. It cannot tell us what we'd find in a general screening population. And because the review is retrospective, it cannot identify any patterns and associations. Um, outside the limitations of the study, those, those are the limits, right? I was looking specifically like, all right, how many of these explants have bacterial contamination that are existing within this? Like, what's the true incidence? How do we figure that out? And so the literature was really confusing to me. It ranged all over the place, and the sample sizes were relatively small. So we used next-gen sequencing. So the testing used this NGS, next-gen sequencing, including bacterial 16S ribosomal RNA profiling. In plain language, this approach looks for bacterial genetic material and compares the detected sequences with the reference information that already exists in the database to estimate Which organisms may be present. This can identify bacterial DNA that routine growth-based methods may not be able to identify. That includes genetic material from organisms that are difficult to grow, organisms that are no longer viable, or very small amounts of material. That is key. All right, so in culture medium, the thing has to be alive, it has to grow, so there has to be enough of it. That's an important distinction. The strength of this other method is about Finding it, is it there? And it can be in small amounts, and that makes it still relevant. A 16S result tells us that a bacterial genetic signal was detected under the assay's condition. It does not tell us by itself that the organism was alive at the time of testing. If everybody remembers from my livestream previously, I talked about the transcriptome, which is basically the RNA signatures. of live organisms or cell types. And that's, that's like the next step in this, if I were to be like perfectly blunt about it. So once again, it doesn't prove that there was structural material, biofilm present or anything like that. So obviously results can be affected by how I, you know, collected the sample, how it was handled, how it was transported, all those things. So I think it's important that, you know, in a culture-based setting, as we get back to traditional cultures, if something didn't grow in the culture-based setting, you know, they send us this, you know, no growth at 24 hours, no growth 72 hours final, or they'll show you a culture result of bacteria placed on a petri dish and it'll say Normal flora, so that's like skin flora: Staph epi, Cutibacterium, Propionibacterium, all these like normal Campylobacter, all these skin bacteria. But they don't end up showing up in high enough amounts, so they don't actually consider those to be pathogens. They're not a problem. So I'm. Very cognizant that those are problems. And so although no single microbiology result should be interpreted outside, you know, the clinical picture— so I have all these, um, examples of patients with chronic inflammatory symptoms of which I explant, and then 29% in my study had bacterial contamination. So that's a contributor to inflammation. You know, think of the methods As just different windows in the same room. A culture asks whether an organism can grow under laboratory conditions provided. Next-gen sequencing asks whether the targeted genetic material can be detected and classified. So, using the microscope, you can see the structure of organisms and tissue, while pathology evaluates the tissue changes. One window may reveal something, another does not, but no single window shows the entire room. So interpretation asks, you know, whether or not these findings agree with one another and whether they fit the history, exam, operative findings, symptoms. It also asks whether contamination during collection or processing is reasonable alternative explanation. I've done so many of these thoroughly, so you all know, um, and if, if there's a contamination, then typically both samples have the same contaminants, which is not the case. We would always identify that as a pattern and concern. So sensitivity can reveal information that older methods miss, and that's why I switched to PCR, but clinical meaning still has to be established. The correct response to a molecular result like the ones we get is it's another piece of the puzzle. I don't, uh, overrespond to it, and I don't just be dismissive if there's nothing there. And I think probably I, I, I had, uh, To hedge a little bit, I would like to see something there that would reassure me that that's another signal the patient was dealing with. So of the 694 samples submitted, 203 returned positive findings, so that's 29%. And again, this is a sample-level result. It is not correct to say that 29% of patients had infection. It is not correct to say that 29% of all the people with Preston plants have biofilm. The accuracy, I mean, just, you know, of the specimens that I took care of, 29% were positive. And across these positive samples, the analysis detected 103 unique types of bacterial species. The median was 3 per positive sample. 72% of the positive samples had fewer than 5. These results suggest that the detected signals were often not limited to a single species. They also show variation across specimens. What they do not establish is equally important. More detected species does not automatically mean more severe disease. Fewer species does not automatically mean less severe disease. Descriptive counts do not provide a validated diagnostic threshold, severity score, or treatment guide, or anything like that. They are measurements from my dataset. They are not, you know, the end-all be-all of every analysis. So, it always needs further work. The 3 names that showed up the most were Cutibacterium acnes, Staph epidermidis, and Corynebacterium. So, the dominant organisms included those. And, there was also Pseudomonas that was relatively prominent. Some of these names, they kind of sound wild, but many of them are just skin bacteria. Organisms commonly associated, you know, in our skin are and have been relevant to surgery for a long period of time and device placement. But finding their genetic material in a tissue sample still does not tell us on its own whether they were viable, whether they formed a mature biofilm, or whether they caused that person's symptoms. So the microbial findings, you know, so what we found, you have to take it in larger context. I did this very purposefully to help create a better idea and incidence in patients with Symptoms and bacterial contamination on devices. So the study gives us a more detailed picture of what microbial signals appeared in those specimens I took. It does not convert any one species into the the culprit specifically. That is important when results list several organisms. A long list can look a little bit more daunting. Scientifically. It is still just a molecular profile that requires interpretation. So I think it adds another piece to an already interesting puzzle. The paper also examines species richness. Richness means the number of different species detected in a sample. It does not mean the amount of live bacteria, the strength of biofilm, or establishing the biofilm. It's an initial comparison. Implant filling appeared related to richness, but age and implant filling were also related to— I'm sorry, were also related in the dataset. So after the analysis controlled for age, implant filling was no longer significantly associated with the species richness, but age remains significant. So that's why, you know, I didn't do this analysis. The company that we work with for the examination of the samples Did the scientific analysis, and it is you know it's important not to like overinterpret results. I think these findings like they don't prove that aging causes a greater microbial richness. I know that's not true. It does not tell us the specific pathways. It does not show that changing implant fill types would change a result. It should not be obviously used to predict. an individual's symptoms or outcomes or anything like that. So the responsible, like, thing that I concluded from it is a bit narrower. In, you know, in my set, in my study, we had this 29%, implant fill really didn't matter. And that's kind of where I stopped, you know, trying to make stronger and stronger conclusions about the data. So really, what does the data support? The data supports when you target and profile these bacteria, obviously you can get in a large sample size a pretty good example of what's going on at the microbial signal level. It describes the diversity of species detected in these positive samples. It identifies several commonly detected organisms. And it does offer us, you know, options for further research into these microbial communities, acute and chronic inflammation, implant failures, capsular contractures. You know, what does it establish? Well, for a long time, you know, I always kind of thought anybody who had fluid around an implant, anybody who had a capsular contracture, basically I'm always worried about an infection. And I was worried that we didn't have as sensitive a technique to examine it. I think this is a much more sensitive and specific technique. So if we had a lot of studies that looked at biofilm relative to capsular contracture, we may have a lot more answers. It does not establish the prevalence among all implant patients, of course. It does not prove that a positive sequencing result represents an active infection. It doesn't obviously show that this is correlated with capsular contracture. I didn't look at that. It does not prove that a detected organism caused capsular contracture, local symptoms, systemic symptoms, or implant failure. It does not establish that a negative result rules out microbial contribution. And it does not show that antibiotic supplement surgery or another treatment improves outcomes based on these findings. This is not— and once again, it's not a weakness of the study. It's basically— this study is a retrospective sample analysis. of my series to help, like, clarify to me personally, like, this is the incidence I see in my practice. And for those who, you know, for instance, have a very similar practice, this— if they reported similarly, this would be great. Scientific restraint, you know, is not the same as saying the finding does not matter. It means matching, you know, the strength of our statements to the strength of the evidence. And I think this is a great start in terms of evidence. It's the largest published series in the world. And we can say we detected the signal. We can report how often it appeared in these samples. We can describe which organisms. So we've added quite a bit to the literature in terms of evidence. But, you know, I don't jump to any conclusions or make any broader claims about it. I think biofilm does matter. I think we're going to learn more and more about it. One of the reasons I was really excited about the transcriptome paper is because if you took my technical paper about incidents and then added RNA analysis to it, then you would really have something combined and powerful, uh, from the same, uh, patients. And if you paired that with an age-matched cohort, that would be a powerful tool. So can we— and I just basically gave the end of the talk— so we, we want to create research protocols, obviously, that compare groups and have control groups. And what I just said is that's my favorite thing would be to, you know, have a group of patients probably just undergoing another breast procedure and you're checking their PCR and you're checking their RNA analysis. And then you're comparing that to a sample like I have of a, you know, implant-based situation. Or you can do it on exchanges if patients are getting exchanges and compare those age-matched cohorts. I'm getting a little long in the tooth to run that kind of study, but maybe some young folks want to do that. Other things to look at are, do these specific patterns dictate specific outcomes? Meaning, do the bacteria of certain patterns we find have different outcomes? I haven't seen that yet, but that would be good to study. And then obviously, can independent teams produce— reproduce, you know, the data? We also need studies designed specifically to evaluate these, like, diagnostic testing and treatment outcomes because there's not good tools right now, you know, that we can utilize for that. We have a very specific curated prep and recovery protocol, so it's not a fair fight to run my patients against others typically. Um, but I, I think trying to get more ideas about outcomes, um, helps patients. Um, I know that's an optimistic message, but I think that helps patients the most. I would like to see that. And patients really deserve, uh, more and better research that respects obviously their experiences and also protects them from conclusions that the data Doesn't get support, and I think we can do both. We can obviously. I always take symptoms very seriously. These symptoms are sometimes very hard for for providers and to understand, and for patients to like you know convey. I want to give you some takeaways tonight. One, the sample size right six hundred ninety four samples. It's a good sample size. So um. I'm glad our clinic could produce that with our co-authors for MicrogenDX. And 2, 29%, I believe that number. I believe that's a real number in my patient population. I don't think it's a vague general number at all. I think the sequencing method is great for detecting bacterial genetic material, but it, once again, it doesn't establish that they're alive. Or dead, right? That's an RNA function, not a DNA function. It doesn't dictate active infection. 4, you know, we still think, uh, in my study, even though I wasn't looking specifically at capture contracture, the biofilm plays a role. We just don't know the, the level of the role in each patient. Testing is informational, obviously. It's not diagnostic by itself. We don't prescribe antimicrobial therapy or supplementation based on findings. That would be something you have to pursue with Uh, your provider. I will say I recently got a call and took care of a patient who had a rapidly evolving breast process, a breast process pre-surgery, and I, you know, had to take care of it, but it increased in size. It was drained, ruled out for ALCL. We'll get the final analysis on that, but if you have signs of Increase your redness, warmth, swelling, drainage, fever, any kind of severe pain. You don't feel well. Obviously, with a device in place, you need to seek attention. Reach out, go get examined. If you don't feel like you're being heard, obviously we've we've put out a lot of data. We have a book out about breast implants, explant surgery, and breast implant illness, and then my short method. There's a book out about that. We have all sorts of free podcasts and educational material things. That we put out are for education only. Doesn't replace working with a provider. And for Q&A, I'm going to take some off of Instagram and TikTok and then shut those down and go to the private community, Dr. Rob's Circle. So that is it for my talk. All right, let me get some— let me see if there's a question. There's a question. It says, how many bacteria do you actually test for? Also funguses? Yes, it tests for over 150 bacteria, mycobacterium, and fungus. So, it's asking me, do I still do implants? No, I haven't placed implants in the last 6 years. All right. Aphrodite2985, yes, we do. My team will do them complimentary. All right, who do we have now? We have Diana. Well, Diana, you have textured implants. Textured implants are always ones I worry about having more symptoms. They have the most preponderance from our research in the literature or just reviewing the literature of obviously breast implant-associated anaplastic large cell lymphoma, of which I've taken care of a case with a B-cell lymphoma from a textured implant. Not a T-cell. Okay. Um, yeah, Elena, that's a great question. Um, I like to do simultaneous fat transfers. I've done several live streams about it, and, um, you can find the live streams that I've done if you join the circle. There are also some inside of my YouTube channel. I prefer to do simultaneous fat transfer if I can get you in the right state of health. I feel like that's best. I think it's best because I can offset volume changes. I should clarify that. I want to always offset the volume changes if I can. I think it's very, very hard on patients if you can't do that, and especially the smaller, low BMI, low body weight patients, it's much harder for them. So I don't want to ever like not provide that if I can do it. So All right. Yeah, I got a question here. Is it common for implants to be linked to other cancers in the body? Can implants do weird things to genes, or is that far-fetched? Um, I mean, nobody has any data on whether that's really, uh, the case or not. So implants have been used extensively They certainly don't increase the incidence of breast cancer because they're used for that as a reconstructive tool. They don't increase the incidence of sarcomas because they're used to reconstruct those defects. So from that standpoint, in my experience, no. But once you've had a cancer, you're more susceptible to have other cancers if you want to think of it that way. Now y'all are supposed to get off Instagram and go to my community. Do you know how to do that? Do you want me to explain it? Okay, you can go to drrobertwhitfield.com and click the circle, and then you can sign up there. All you gotta do is put in your email. There's no fee. You get a magic link. Boom, you join. Now, um, I guess I could, uh, how could I do that? I could do— Oh, you can't put a join link in there. You can't put that in Facebook, or I'm sorry, Instagram. Gosh, it's been a long day, y'all. I got up at 4 this morning. I'm officially an empty nester now. Both my kids are out and about. Last one had an early flight this morning, so. All right, did I get all the questions answered on Instagram here? Mm. Oh, there's Lisa. All right, I'm gonna shut down Instagram. You guys can go into the Circle. Okay. Yeah, Lisa, that's a good question. So, you know, if you look at the literature, the literature predates PCR testing on capsular contracture. So I would say in my experience, I would always be concerned about a capsular— I'm sorry, an infection with capsular contracture. The things that I, I wish I had a little bit better handle on. And if you understand, capsular contracture is a really subjective, examiner-dependent diagnosis. It's not a scientific diagnosis at all. So if you have a capsular contracture, can you have BII symptoms? Sure. You can have BII symptoms without a capsular contracture. Um, I think bacterial contamination plays a role in capture contracture. I just don't know how much. Everybody's going to obviously be very different and different side to side even. So those are— I think those are things that we have to learn more about, to be honest. And, um, studies like Jason Posner did one about capture contracture and biofilm. It's really small sample size. Um, I think there just should be, um, okay, you're seeing your surgeon next week in Dallas. Have a list of things to go over. I have implants from double mastectomy. Oh, okay. So if I had someone in your position and I could convert it to a flap when I did reconstruction, that's what I would do. Choices would be deep flap reconstruction, and then the second choice depending on tissue would be like TMG or TUG. I did SGAPs. SGAPs are just harder to do, um, and, and almost you would, uh, stage them typically. So I mean, that would be my thought process. That's what I did starting in 2005, basically. One of the first patients that ever came to me was somebody with a, uh, capsular contracture. All right, who's next? We got another question? Okay. So, Deanna, what we do is we treat the pocket. So the secret to pollution is dilution. So you can rinse a pocket out. We use a low pH solution because bacteria, fungus, viruses— none of them survive at a low pH. Think of like during the pandemic, you could clean things with an Acid type solution or basic solution. We prefer to do a dilute acid. Yeah, Lisa, then the second choice is a TUG flap or TMG depending on that. Um, a really older operation I did was a bilateral latissimus dorsi flap. If someone's small enough and can support that as a standalone reconstruction, I did that as well in bilateral cases for bilateral capsular contractures and patients who had previous tummy tucks or couldn't have Deep flap. I want to hear from everybody in this chat, how many of my YouTube videos, podcasts, or live streams have y'all gone through? And have you read, or do you know that I have a book out on BII? I bet you most of you don't. Thank you, Lisa. Yeah, um, getting books done is a challenge. I knew I needed to write a BI book because one hadn't been specifically written about or given the patients a lot of airtime. So we did a lot of airtime in the book for patients. Oh, wow. Thank you, Diana. That's awesome. Yeah, we've been trying to advertise these on Facebook. It's— yeah, I feel like we get suppressed a lot. Certainly YouTube was my main forum for a long time. That's why you see my YouTube channel connected on the homepage now. And basically we got in trouble. They said I didn't have family-safe content because I talk about the breast, I guess. I don't know. Anyway, we'll be all right. We just keep trying to do the good work. That's all. Take care of patients best we can. There was somebody letting a person basically slander and defame me in their group. So, I mean, it's like a never-ending battle, social media. I wish I didn't have to be on it or deal with it. Oh, there's Miss Lori. She's now a member of the club for lots of reasons, but you're probably hearing and seeing more of Miss Lori. Just got to get her healed up a little bit more. Well, I'll ask a favor. So for everybody on the live, if you have a friend or loved one or family member, um, who needs the information, just share the information or share the The livestream or share the book or what have you. Just try to help them out. I think it's a very bad place to be if you're not getting, um, heard or if you're not getting enough of your questions answered. And I, I just hear that all the time. It's really frustrating. So glad to hear it, Miss Lori. Had to tone down your work. Lori's a nurse and she works hard like almost every nurse I've ever met. They're hard workers. They are hard workers. Only person worse to take care of than a nurse is a doctor, in my opinion. Nicole hates me. Nicole's under suspicion for having doctors pay her to be listed on her Facebook. So Diana, you're in West Virginia. Okay. Diana, I think in West Virginia, the— um, trying to think of who I know there. The only folks I see are in actually Virginia, not West Virginia, and these are in Virginia Beach. There was a good group there for a long time. Um, if you go— Diane, uh, is that right? Diana, go to, um, So there's a society, uh, this society is the only one I still belong to from a, a plastic surgery perspective. So that lists all the folks in and around the United States who do reconstructive microsurgery. And I apologize, I don't remember everybody like in the Virginia area. Plus now I'm 57. The people that I would've known and been in practice or colleagues with, many of them have retired. Or, um, stop doing microsurgery like I have. I stopped, um, several years ago because it was, uh, more of an issue with my neck. Yeah, I think that's— you try to use their physician finder and see if that helps you. Um, if you get some names, you know, you can direct message me in the circle and I can look at them and, and let you know what I think. If, if I don't know them, I can't comment on them. If they're my age group So you don't look— look for somebody born between, you know, '65 and '75 or '65 and '80. So they're not too old and they're not like super young. And if you can travel, then I can definitely recommend some other people. All right, you all, I think we're gonna shut it down for tonight. Thank you so much for, for hopping on. I really enjoyed it. Make sure— we'll be here next Thursday. I think next Thursday I'll stir some shit up and talk about breast implant-associated anaplastic large cell lymphoma. How about that? It's always something causing trouble. Yeah, I mean, the thing with, uh, the thing with ALCL is it's super, super rare. And if you have textured devices in, obviously you're the— you're in the, in the riskier group. But the thing with it is It's a really, really rare condition, and I think there has to be something else going on. And I say that from somebody who's who's done you know like several thousand of these, and and I've sent one of the only B cell. I think it was the eighth case of B cell lymphoma from a breast implant in the world when I found it. And we can talk about that on my next live. And I'll, I'll tell you, uh, what I think, and then we can go from there. All right, so, all right, that's what we're going to talk about next week. We'll do a BIA, ALCL, and breast implant-associated cancers. How about that? All right, it's a wrap.