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Communicable takes on hot topics in infectious diseases and clinical microbiology. Hosted by the editors of CMI Communications, the open-access journal of ESCMID, the European Society of Clinical Microbiology & Infectious Diseases.
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Annie: Hello, and welcome back to Communicable for our first episode of 2026. Communicable is brought to you by the Journal CMI Communications, ESCMID's Open Access Journal, covering infectious diseases and clinical microbiology. My name is Annie Joseph, clinical microbiologist at Nottingham University Hospitals in the UK and associate editor at CMI Comms co-hosting.
With me today is Josh Nosanchuk, fellow editor at CMI Comms, infectious Diseases clinician and Professor of Infectious Diseases and microbiology and immunology at Albert Einstein College of Medicine in New York City. Hi Josh.
Josh: Hi, Annie. Thanks for doing this with me today. We're really excited to welcome two outstanding guests to discuss meaningful papers in clinical microbiology published in 2025.
The first guest is a rockstar in infectious diseases [00:01:00] and medical microbiology, my friend Robin Patel, the Elizabeth p and Robert E. Allen, professor of Individualized Medicine, professor of microbiology and professor of Medicine at Mayo Clinic in Rochester, Minnesota. Robin is the director of the Infectious Diseases Research Laboratory at Mayo Clinic and co-director of its clinical Bacteriology laboratory.
Robin, welcome to Communicable.
Robin: Thank you Josh and Annie. It's my pleasure to be here.
Our second guest is a super awesome member of ESCMID's executive committee, responsible for education and the affiliated societies, and a terrific resource for music suggestions. Fidelma Fitzpatrick is the head of the Department of Clinical Microbiology and the Royal College of Surgeons in Ireland, university of Medicine and Health Sciences, and a consultant clinical microbiologist in Beaumont Hospital Dublin. Thank you for joining us on Communicable
Fidelma: thanks very much Josh, and thank you Annie
so as our listeners know, we like to start with a get to know you question [00:02:00] So the question this week is, what is the most memorable or strangest thing that has happened to you in 2025? Robin.
Robin: Well, I'm gonna tell you about a couple of papers and something that I don't, often talk about. So we get some special funding from the Centers for Disease Control and Prevention, in the pathogens, genomic Centers of Excellence, program, and our, Work is naming the unnamed. And so we are naming previously unnamed bacteria that we encounter in the clinical microbiology lab, that really stump us and put us in a difficult position because we can't issue a report for an unnamed bacteria and naming bacteria for anyone who's done that is quite a task.
So we were very thankful to get funding, from the CDC to do this. And this past year we described four new species. And I also wanna tell you about the naming process because that was something that I learned something about. not just, sort of what name is allowed [00:03:00] and so forth, but the names we chose.
So, we described Rinni Bacterium, maus and Dry co maus, but then we described two other cola species and I couldn't use that same Mayo Clinic associated species name. So we decided to name, two prominent microbiologists. So there's a Dry Cola Sharpie. And a Dry Cola Baroni, and they're named after Susie Sharp and Ellen Joe Baron respectively.
And that was very exciting to be able to name, microorganisms after, famous microbiologists.
Annie: That's so cool.
Fidelma.
on a personal level, I was sick last year and I came back to work and I started working with ESCMID and it reminded me how fantastic my colleagues are and how fantastic my friends and family are.
Fidelma: And I suppose as a doctor that works all sorts of hours. It's important to remember what really supports you and enables you to do your job. The research that I was most proud of this year is one of our hospital staff, Marade s sc [00:04:00] sat down with patients and asked them about their experience of hospital infection in AMR.
Annie: Fantastic. For the first episode of this new year, we've asked our esteem guests to select top three papers published in 2025 in the field of clinical microbiology papers that they found interesting or impactful. And the papers are extremely varied, as is the field of clinical microbiology itself.
And we'll be going from the lab to the ward, some epidemiology, science, communication, and even back in history.
Josh: Okay, so, Robin, you're up first. Shall we start in the clinical microbiology laboratory with your first paper? the microbe that you'll be discussing is named in honor of the amazing microbiologist Elizabeth O.
King, who worked at the CDC and she named the pathogen in 1960s. Though it was first called Moraxella kingii. Robin,
Robin: thanks Josh. So I picked this paper that was published in the Journal of Clinical Microbiology called an in-house Kingella kingae PCR, in a Large Pediatric [00:05:00] Cohort, impact on Diagnosis, antimicrobial stewardship, and Clinical Outcomes.
And I will say it was really hard to choose just three papers. but I'll tell you why I chose this one. And actually all of them have a personal connection. Kingella kingae is associated with bone and joint infections in children and, I was part of a team that designed the Kingella kingae PCR assay that we run here at Mayo Clinic, and we've been testing since 2017, and I think we've learned a lot.
And this study is very well done and emphasizes a lot of what we've learned in our own clinical practice that I think is important to share with a broader community. So the objective of this study was to characterize the performance of a Kingella kingae PCR and determine its impact on antimicrobial utilization and clinical management in children.
It was carried out from 2014 to 2024 in children who had Kingella kingae PCR performed, and it was done at Nationwide Children's Hospital testing. There was offered once daily. During the study period, 500 children had the [00:06:00] test performed, among whom 45 had a positive result by PCR or by culture. So compared to clinical diagnosis, the Kingella kingae PCR had a sensitivity and specificity of 96 and a hundred percent respectively, super high.
There were 44 patients with positive PCR results, who were simultaneously, tested by culture, and among them, 36 were culture negative. there was only one patient who was culture positive and PCR negative, so PCR improved case identification by fourfold. Compared to culture. So I think that's really important.
Most of the kids in this study were previously healthy. afebrile, and the clinical presentations included mostly septic arthritis and acute hematogenous osteomyelitis. Now all the children were classified into a group called Lessen or equal to five years old. I have a little issue with the authors on that.
I think, lumping all children [00:07:00] into, zero to five years is kind of a broad age group. but I'll come back to that in a minute. that's just how they design their study in this group of less than or equal to five years old, though Kingella kingae was the most common organism detected. More commonly than staphylococcus aureus causing bone and joint infections.
And that's a very important message and consistent with what we see in our clinical practice. But the piece about the age I think is important. So the median age was 18 months and all the children were one to three years old. So it's, not really zero to five years. It's a much narrower and special window.
although not all the organisms grew in culture, they did do some susceptibility testing on Kingella kingae isolates, and they were all susceptible to Trimethoprim/sulfamethoxazole, meropenem, ciprofloxacin, levofloxacin, ampicillin, amoxicillin, clavulanate, penicillin, and azithromycin. And they were all beta-lactamase negative.
And that's important in terms of selecting antimicrobial therapy. The median time to result for the PCR was 27 [00:08:00] hours, and 84% of subjects had antimicrobial modifications made within a day of that PCR report resulting in deescalation. In most cases, the children were treated for this infection for a median of 21 days, and all had complete resolution of symptoms.
Also very important. So my takeaways are that Kingella kingae is the most common cause of acute septic arthritis and acute hematogenous osteomyelitis in children one to three years of age. In my mind, PCR is the incontrovertible test of choice for these children. If you're trying to make a diagnosis in the United States, there are no FDA approved standalone tests available to these children, and for that reason, testing for these children is not widely available, and that's a problem.
Clinical outcomes, fortunately, are excellent in fact. That leads me to ask some questions. Do these children need any surgical intervention? [00:09:00] Do they even need to be hospitalized? And how long do they need antimicrobial therapy? They got a median of 21 days. That seems long. is that really needed? All questions for future studies.
So, I loved this paper . I think, , this is really important to those one to 3-year-old children who are affected, by this particular organism, and obviously to their parents as well.
Annie: Yeah, it's such a cool paper, Robin. And I think the access to molecular diagnostics is really helping us to understand epidemiology in a different way, particularly, it's not zero to five, it's really, less than three or maybe median ages about 18 months.
It does make me wonder though, what is going on around that time immunologically? Is it a first exposure to Kingella kingae? Why? Is it this age range that seems to suffer with this pathogen?
Robin: Yeah, that's a really good question. there are several infectious diseases in children. That manifest at a specific age. for some of them, I think we can say we maybe know that answer. And for [00:10:00] others at least, I don't know that answer. when I thought about that, idea, the closest organism that I could come up with was Haemophilus influenzae.
So I trained in an era before the Haemophilus influenzae vaccine, and at our children's hospital in Montreal , it was just full of kids infected by Haemophilus influenzae. By the way, it was a disaster. Like the outcomes were very bad and, the vaccine just like turned that whole thing around.
But, Haemophilus influenza affects a slightly younger population than Kingella kingae. So I don't think we can directly translate what's going on, but. It must be, some combination of immunity. So there must be some protective immunity that's coming from mom. I'm guessing there must be an exposure factor that they're being exposed to this organism.
Certainly respiratory transmission in daycares has been, reported. So that may be playing a role here. But then the other thing that's I think really interesting and that I don't have an explanation for [00:11:00] is these are bone and joint infections and just bone and joint infections for the most part.
I have a hard time thinking of another organism that does exactly that. So there must be something about the bone and joint space in this age group of children that is making them at risk for these infections. But I don't know. Josh, do you know the answer to this question?
I don't. I think it's really interesting, the physiology of bone and, how fast it's remodeling.
Josh: the ILS don't fuse until you're much, much older. So it's not that, that's keeping the 11 and 12 year olds from having this, it's really fascinating. I do also think that the fact that this was done in North America is. Important to highlight, like you said, Robin, because certain places, like in Africa where they see salmonella in small kids, is important.
And so when you're coming up with your design, you have to take into consideration where you are. Things are getting closer globally in some things, but [00:12:00] not in some of these other areas like, salmonella. So another twist.
Annie: Yeah, that's a really good point, Josh. And I think you, touched on it, Robin, about the, prevalence of fever in the Kingella kingae group I mean, that surprised me less than a third had a fever and the median CRP was only 2.9, which, was a take home message for me really thinking about, these aren't necessarily sick, unwell kids, they're presenting with probably quite generally well, but with an acute bone and joint infection at the right age range.
So yeah. Can maybe target testing. Towards the right kids.
Josh: Yeah. So they, didn't really tell you whether they just had a limp or they weren't crawling as well, like what brought them in, , versus a, staph aureus septic joint. so interesting to get more information about the individual presentations.
That was really an interesting conversation . We're gonna stick with you, Robin, on our second paper, which is more of an epidemiological slant, what have you [00:13:00] chosen?
Robin: This next paper that I chose comes from Lancet Microbe and it's called Invasive Streptococcus dysgalactiae Subspecies equisimilis compared with streptococcus pyogenes in Australia.
2011 to 2023 and the emergence of a multi continent STG 6 2 6 4 7 Lineage, a retrospective clinical and genomic epidemiologic study. So Streptococcus dysgalactiae, subspecies equisimilis. Closely related to streptococcus pyogenes with overlapping disease manifestations. I picked this one because , this is something that I've observed in our clinical practice.
We run a 16 s ribosomal, R-N-A-P-C-R sequencing assay on normally sterile body fluids and tissues. And, I see this organism frequently. In fact, I just pulled data from 2024 and 2025 to date, the numbers of strep pyogenes detections were 123 and strep [00:14:00] dysgalactiae were 92. So they're pretty similar. that I think is.
Maybe something that's under recognized in clinical practice. I also lump streptococcus a glacier into this, and we detected 155. That's not the topic of this paper, but it might be something for clinicians to think about when they think about beta hemolytic streptococci. So back to streptococcus dysgalactiae, subspecies equisimilis and streptococcus pyogenes.
The two share niches in the human throat and skin, and they're thought to transmit via a respiratory route or maybe direct contact. But like I said, I think clinicians know a lot about streptococcus pyogenes group a strep, but maybe not so much about streptococcus dysgalactiae. This Australian study compared the clinical and genomic epidemiology of invasive streptococcus dysgalactiae with invasive streptococcus pyogenes and phylo genomically contextualized streptococcus dysgalactiae sequences against the [00:15:00] global cohort of genomes.
So invasive streptococcus dysgalactiae isolates from normally sterile sites were identified and sequenced across hospital networks in Melbourne and Sydney, Australia, and the northern territory of Australia. Genomic transmission clusters were inferred between isolates from different people by single linkage clustering using a single nucleotide polymorphism threshold of less than or equal to seven for strep dysgalactiae, and less or equal to five for strep pyogenes.
The study was carried out on isolates between 2011 and 2023, and there were 693 invasive streptococcus dysgalactiae and 995 invasive streptococcus pyogenes cases. So not too dissimilar. Invasive streptococcus dysgalactiae occurred almost exclusively in adults, so now we have an adult infection here. 30 day mortality, in hospital mortality, and ICU admission were similar across the [00:16:00] two species.
The overall incidence of invasive streptococcus dysgalactiae in Melbourne and Sydney was very much like that of invasive streptococcus pyogenes. Interestingly in Melbourne and Sydney where COVID-19 mitigation strategies were enforced in 2020 and 2021, they witnessed a plateau of the number of cases of streptococcus dysgalactiae, but a decline of the number of cases of streptococcus pyogenes suggesting differential effects of those strategies on the two species.
In the Northern Territory, streptococcus dysgalactiae incidents was lower than streptococcus pyogenes incidents, but higher than in Melbourne and Sydney and disproportionately affected first nations Australians. Also in the Northern Territory where COVID-19 mitigation strategies were not implemented like in Melbourne and Sydney.
Robin: Rates of infections with the two species did not change during the pandemic. Now looking at the whole genome sequence data. [00:17:00] Only 6% of streptococcus dysgalactiae cases were assigned to genomic transmission clusters compared to 52% of streptococcus pyogenes cases. One quarter of the streptococcus dysgalactiae genomes belong to an STG 6 2 6 4 7 lineage.
Analysis then of sequences, not just from Australia, but from Europe and North America showed international expansion of this lineage in all three regions between 1990 and 2005. This lineage is estimated to have emerged in the first place in 1956 or so. of this study is that in high income regions, invasive streptococcus dysgalactiae is just as prominent and common as invasive streptococcus pyogenes infections and is dominated today by a global lineage.
I think this might be an under-recognized pathogen globally, at least amongst [00:18:00] clinicians. I think a lot of us weren't trained to think about these two strep species in this way. The few cases were assigned to transmission clusters and that cases did not decline with COVID. 19 mitigation strategies different than streptococcus pyogenes suggest that the two species behave differently.
Invasive streptococcus dysgalactiae may arise from long-term carriage rather than acute transmission like streptococcus pyogenes. But more work is really needed to understand carriage and immunity and molecular drivers of emergent lineages to inform potential disease management and control measures.
Annie: I don't think microbiologists help ourselves, particularly with the naming of these species, Robin, when you were saying about, everyone kind of knows strep pyogenes. I mean, pyogenes tells you what it is, like the name's on the tin, isn't it?
Whereas, we've got dysgalactiae, agalactiae. Like, I just don't think clinicians generally have a feel for what strep dysgalactiae subspecies equisimilis is. And [00:19:00] does, I'm still kind of a little bit old school and have that thought about, it's a group G, it's a group G strep and G for geriatric. And I just kind of remember that.
And actually these patients were older on average than the strep pyogenes, cases, weren't they? So I think that's possibly true, but, it kind of surprised me that the incidents overall was very similar to strep pyogenes. want to know what it is in the uk. I did try and look it up after reading this paper, but it surprised me.
Robin: That's why I chose it because like I mentioned in our own experience, I was a bit surprised because based on our sequencing work, it's kind of on par with strep pyogenes for these invasive infections. this is Australia, we're in the United States. I think other people should maybe look at this.
I, bet that's what's going on. in other areas, you're absolutely right. We in the lab, we're probably a bit to blame for this the reason is that we've changed the way we identify organisms and we report organisms That has maybe led to a lot of confusion over time because, there are [00:20:00] strep that are closely related to dysgalactiae that are not necessarily human pathogens, right?
And so I think now that we can better identify these organisms and MALDI-TOF mass spectrometry works just fine. we should be able to better identify these organisms and then that should better inform clinical interpretation and pathogenicity. but there's a lot of confusion on the naming side of things, as well as on the interpretive side of things that goes on here.
So, that's why I think this is important, you know, recognize this, species streptococcus dysgalactiae as a very important human pathogen.
Josh: I was struck by how many individuals had recurrent infections in both of the species. And, the finding that with the dysgalactiae, they had more likely to have the same, recurrent one, whereas Pyogenes was often different.
But the fact that these individuals are having multiple ones, but most people never have a significant strep infection at [00:21:00] all, makes me wonder about is there an immune process in these individuals that makes them more susceptible to this particular disease? And also, they didn't give us much information about toxin production of this, Lineage and whether it's a high toxin producer or a low toxin producer, or if those that had recurrent, even though it's the same lineage, if they had variants that were higher or lower, producers of various strepto, lisen and super antigens. So I think there's a lot more that we need to learn, that may help explain some of the disease processes that they're recording here.
Robin: I completely agree. and the fact that they have all that genomic data, might mean they could dig a little bit more around those pieces. But, I really chose this just because I think it, starts with the lab, identifying and recognizing that this is an important pathogen and reporting as such, and then clinicians, interpreting in that way.
then we need to get to the why, like why these people are getting infected, how they're getting infected. [00:22:00] Can we do something to, prevent these infections? can we, better manage them so that they don't have recurrences? and what will that involve? what do we need to be doing?
Is it, more aggressive surgery? When surgery is performed? Is it, different? Antibiotics, prolonged treatment, adjunctive therapies, lots of questions that, we can now ask. But until we begin to identify these properly in the laboratory and then understand, that they are significant pathogens, we can't even get to that point
Josh: again, argues for why clinical microbiology is vital.
Robin: Definitely.
Annie: In many places in the world, the next two papers might be seen as more strictly in the sphere of Id rather than clin micro. However, in a lot of countries like Ireland where Fidelma practices and the UK where I do, clinical microbiologists are quite patient facing rather than purely in the laboratory.
And the lines between the two specialties are much more fluid. and CMI, comms and ESCMID is for all of us wherever we sit along this clinical spectrum. So, [00:23:00] Fidelma, you've chosen first, the DOTS Trial, which is dalbavancin for the treatment of Staph Aureus bacteremia, published in JAMA in August, 2025.
And interestingly, these trial results were presented at ESCMID Global back in 2024 in Barcelona in the late Breakers session, and were discussed on our very first episode of Communicable, which was the Late Breakers trial roundup . So listeners can go back and check that episode out if they haven't already listened to all our back catalog.
So obviously it's taken quite a long time from conference presentation to publication, and I know many people who insist on waiting for the full publication before changing their clinical practice. So Fidelma over to you..
Fidelma: So I, chose this, for a few reasons.
First of all, this is common. We see a lot of patients with staph aureus, bloodstream infection, certainly in the Irish healthcare. system. we are at capacity in our hospitals. So anything that aids safe and earlier discharge is a good, and having recently been a patient and had several IVs in anything [00:24:00] that stops me, having lots of invasive devices is a good thing.
So that's the preamble. So this was a randomized trial, and there was two arms. Then patients either got dalbavancin or they got standard therapy for complicated staph aureus, bloodstream infection, or right-sided endocarditis. So there was 22 hospitals in the us, one in Canada, and it ran from April 21 to December 23.
And importantly, patients were enrolled. After their blood cultures had cleared. So we're now comparing consolidation treatments. So these are very stable patients. So what attracted me to this is when you think of standard therapy, standard therapy means having to get a PICC line in, which is not much fun.
Keeping a PICC line in for four to eight weeks, it may limit your mobility and it certainly carries clot risks like clots and secondary infections. even just simplistically, it's kind of a no-brainer from a patient end of things to have two [00:25:00] short IV infusions on day one and day eight. when you can go home and carry about your normal life.
So the investigators, not surprisingly expected alpha balance and to reduce side effects and improve treatment completion and enhance quality of life. And surprisingly, it wasn't superior to the other arm. And I'll go through how they measured this in a minute. but it was non-inferior for efficacy, so it was equally as good and it was equally as safety. the bottom line for this is it got me thinking and got my colleagues thinking that actually this may offer a way to finish therapy without the hassles and the hazards of prolonged IV access. while it's not better than standard care and what they talk about standard care is if you hadda methicillin susceptible staph, you got an antis, staphylococcal penicillin or cefazolin.
And if you had an MRSA van Doto. So that's the comparison, but it was equally as good. Going through the trial, who are they? Well, they were adults over 18 and what's important here is who is included. The definition of [00:26:00] complicated staph aureus bloodstream infection was essentially people that were not uncomplicated.
If that makes sense. So I have to reread that sentence a little bit myself. So uncomplicated bloodstream infection means you don't have endocarditis, you don't have an implanted prosthesis. Your follow-up blood cultures are sterile and your fever has settled and you don't have a secondary site. So you're not that.
But then when you looked at the exclusion criteria, there was lots of patients that I would see that I would've called complicated staph aureus bloodstream infection that weren't included. So more double negatives. So CNS infection, not surprisingly, and patients with left-sided endocarditis weren't included, or peri valvular abscesses, if you'd, any sort of prosthesis in you that couldn't be pulled out, you weren't included, be it heart valves or prosthetic joints or prosthetic grafts.
So I think that's important when we carry on to talk about the results that while these are complicated Staph Aureus bloodstream infection, [00:27:00] it's a limited subset of complicated patients. Now from a laboratory bit, it was interesting. They did what we all did up until recently. They inferred dalbavancin susceptibility from the vanc susceptibility and the recent EUCAST update has told us we shouldn't be doing that.
We need to check our dalbavancin susceptibilities, and that's what we're currently doing ourselves. the primary outcome was another acronym. It was a thing called the DOOR Criteria. So I obviously like my dots and my doors. So what door was, is I think it's quite interesting. It was a composite endpoint and it was much more patient centered than being cured alive or dead.
And there was five elements. It was clinical success, whether they had infectious complications. Safety, complications, mortality, and then health related quality of life, which when we're talking about dalbavancin, I would've thought is kind of important. and the health related quality of life was, measured by patient reported health status.
So the highest door ranking [00:28:00] was if you treatment success, ta-da, and you'd no complications. And the lowest door ranking was If you died at the study endpoint at day 70, and there was bits in between. So I thought this was an interesting primary outcome when we look at this, because you kind of would inherently think because you don't have a PICC line inside you that health related quality of life, it might skew it to favor dalbavancin.
The bottom line, as I said, It was non-inferior and there was 200 patients, a hundred in each group. Only 10 though had right-sided endocarditis. And again, I had to reread the way they reported the outcome because it's kind of a probability thing with the DOOR criteria.
Fidelma: So the probability of Dalbavancin and being superior was 47.7%, which meant it didn't meet superiority criteria. So then I thought if you randomly picked somebody outta the dalbavancin group, they were 47.7% likely to have a better overall treatment outcome than somebody selected from the other group.
now to the investigator's surprise, [00:29:00] when they broke down all the five door criteria, the health related quality of life was very similar. Which was interesting considering what I said at my first preamble, that you have a choice between a PICC line or a peripheral line.
So maybe actually from a patient end of things, the way an antibiotic is delivered isn't as important as we all thought. Personally. I would've thought so. But that's the results. Or else maybe just the criteria and the questions we asked, weren't the right questions to ask. And they go through that a bit in the editorial.
So being very dutiful, I pulled all the supplementary material and went hunting for the door criteria because I couldn't figure it out. And in one of the supplementary, some of the questions they asked is, could you go up and down stairs as normal? Can you walk at least 15 minutes?
Can you do some chores? Can you run errands? And you probably can do that with a pick line. As well as not, so I, it just got me thinking maybe sometimes when we're asking questions, we need to be more specific. So, while it [00:30:00] didn't show superiority, it did confirm similar outcomes.
So it means that, from a patient perspective, there's practical benefits. You're not having a pick. You don't need oat. And if you were on Vancomycin, which we wouldn't ever prescribe on, oat, but some people do, you don't need vanc levels, you don't have people coming into your home.
You don't have a risk of thrombosis, et cetera, et cetera. But it's important again. To look exactly at the types of complicated infection that we're talking about. So while it's complicated infection, there's lots of exclusion criteria, but I, like this trial because it's got us talking in my own hospital about this expensive drug, we probably need to start getting better at, the full health economics argument. but I do think it's a reasonable option for completing therapy. and that's the trial dots, doors, and give, dalbavancin a go.
Josh: thank you. a population that you, sort of referred to when you said going home.
We have, unfortunately, too many unhoused individuals, [00:31:00] and unfortunately some of those are at high risk for. These staph aureus infections, and it's always complicated how to address their long-term care. And switching to orals early is certainly something that we've been pushing a lot. But, you know, especially in this population, this type of approach is something that is life-changing for those individuals.
So I do wanna recognize that.
Fidelma: 15% of their, patients were intravenous drug users. And you're absolutely right. And like anything without a device is obviously best, but oral medication are not without their issues either.
Like you actually have to take them and if anybody's ever tried to take TDS or QDS or three or four times a day, you kind of need to be a ninja on your timing, you know? So, I agree with you. we too have a, group of patients that don't have a home to go to and, for other reasons then this is also a good option because [00:32:00] they'll at least get one dose and the dose they're using is 1.5 grams, so 1500 milligrams.
So it's a high dose.
Josh: Yeah. We also have individuals who. Can't stay in the hospital longer because they have no childcare and other issues like that. Yeah. And so in the US it's very hard in some of these populations to set up home infusion. And so this is really a life changing Yeah, I agree.
Opportunity to administer this. I will circle back to ask about the economics, because that is in many countries what really drives some of the decision making and they did not really analyze that in this paper. Yeah. And I'm wondering what your thoughts on that are.
Fidelma: Yeah. Like I think the drug cost, but also the opat comes with a cost too.
I kind of had a look, in Ireland. So if the dose they're using it would probably be about one and a half thousand euro for one dose. So about 3000 euro for the course. But oat also costs money. And you have to pay staff and you have to pay staff to go there and pay their [00:33:00] expenses. You have to pay for the drugs, nevermind the poor patient and people coming into their home.
So everything has a cost. but that does not take away from the fact that these are costly drugs. but I do think that if we're going to try and move this forward, we need to be a bit more holistic about how we talk about cost. we also need to bring in our health economists and our patients into this research because the health economists can talk about the Euros or the dollars or the pounds, but actually maybe our patients also need to start telling us about their quality of life and what they can't do, and can they go back to work and do they have to stay at home and what have they lost?
I don't have the answers to that, but yes, it's an expensive drug, but the other options don't come without cost either.
Annie: that's a really good point. And I think, the setting in which the health economics are done and is gonna be crucial really, isn't it? 'cause the NHS in the UK and the Irish system compared to the states, you know, it's just a [00:34:00] completely different kettle of fish, isn't it? In terms of, whether this will be cost effective and how that's spread across the healthcare system.
It's much easier when you're in a, public healthcare system where costs are, spread across everybody. Cost savings are spread as well. but I
Fidelma: suppose like in Ireland we have a mixed public and private system. at the moment, the way OAT is funded, it's funded separately from the hospital.
, And it's slightly different from the uk. for example, unlike the UK a lot of our, our gps are private, but they're contracted by the public healthcare service to look after patients. if I had to think about this in our hospital, to do this, you would have to have a daycare facility or a day ward.
So to bring your patient in so that they can safely get an IV stuck into them and sit there for their hours. So, and get the infusion. So that's not rocket science, but you still need to have that facility, or else get your opat team trained up to be able to put in a peripheral iv. and administer it at home.
So there's certain ways to crack [00:35:00] this, nut, but I agree with you, we do need to be much more holistic in the way we talk about cost. and maybe that's an idea for 2026.
Fidelma, thank you for, picking this, article. It was executed by the Antibacterial Resistance Leadership Group.
Robin: And just to declare my conflict of interest, I am the laboratory center director for that group. I think that's important, because we need to be looking at this kind of studies and I think sometimes we, as, physicians, we, think we already know the answer to the question. And so the, patient perspective, a highlight that you brought out, we thought we already knew the answer to that question because we applied our physician's, perspective to that.
And we said, well. Patients will prefer this because that's what I would prefer. but in fact, you're right. maybe we didn't ask the right questions, but maybe we're also not the right people to answer those questions that we need our patients to answer those questions. So it's very nice that you picked this paper and I, think it showed a lot, but we also learned a lot about study design and the importance of the patient perspective.
All right, we're gonna change the game [00:36:00] here. The next one up is another clinical trial that has only been published this year in October in Lancet Infectious Diseases, after also being a late breaker in Barcelona in 2024. And. It's the Game Changer trial Fidelma. Yeah. Can you give us some more information about this?
I like my tabloid acronyms, but I also, heard David Paterson speak in the GAMRIC Conference in London, and I must say he's one of the most fantastic engaging speakers I've ever come across. So then that piqued my interest along with the Game Changer trial.
Fidelma: So what is it? So it's cefiderocol versus standard therapy for patients with either hospital acquired or healthcare associated gram negative. Bloodstream infection. and this was an open label parallel group randomized trial, and it was an adults, so it was all gram negatives, but it did include carbapenem resistant organisms and importantly, patients were randomized within 48 [00:37:00] hours of blood culture collection, which I don't know about any of you lot, but I thought that was pretty fast.
So, wow. what they were trying to find out is whether or not cefiderocol was either non-inferior or superior to standard therapy in terms of survival and infection clearance. The gram negative bloodstream infection has a very high mortality, especially when you get to being carbapenem resistance. One in three patients will die at 30 days. Even third generation cephalosporin resistant enterobacterales, just under 10% of people die. So this is an issue. So cefiderocol is one of those Trojan horse antibiotics that since it's first come out, certainly in my hospital, we've been scratching our heads trying to figure out when we should use it.
the bottom line here is. I'm still not sure, but I'll tell you about the trial. and definitely there was, from previous trials, there was a little bit of concern about, ooh, should we really be using this in carbapenem resistant organisms? But this trial looked at all gram negatives. So it was a big trial.
[00:38:00] Started at the end of 2019, finished towards the end of 2023. And it was in 17 hospitals between Australia, Malaysia, Singapore, Taiwan, Thailand, and Turkey. and they were adults. Interestingly, adults were over 21 in Singapore, the rest were over 18. And to get in, you had to have a gram negative bacillus on your gram stain.
And in terms of exclusion criteria, just I suppose for me importantly to remember patients that had vascular catheter related bloodstream infections where the catheter stayed in were not included, as were palliative type patients. And patients, as I said to you, were randomized within 48 hours of blood culture collection, which means in practice you're probably not going to have known the susceptibility.
And that's probably why the investigators allowed a second antibiotic to be combined with cefiderocol until it was confirmed as susceptible. So the primary outcome this time was a bit more straightforward in terms of getting your head around. It was all cause mortality at 14 days from the date of [00:39:00] randomization, and there was a number of secondary outcomes as well.
So in terms of, the results section, they screened a lot of patients over 9,000 patients. So, despite this being a, common infection, certainly in my practice, they had to screen a lot to get 504 patients. 250 in the cefiderocol arm. Now when you look at, I think it's one of the tables, or maybe it's one of the supplementary tables, their standard of care antibiotics is a bit of a mishmash.
So there's carbapenem, there's pip-tazo, which we certainly commonly use in my hospital for healthcare associated gram-negative bloodstream infection, cefepime and a bit of aminoglycoside use. But for me, I, maybe it's to do with the timing of the trial. There was very few patients got the newer beta-lactam, beta-lactamase inhibitors.
So in our practice, you know, if you think somebody possibly has a multi-drug resistant gram-negative and you see a gram-negative on gram, you probably would. Go in with ceftaz-avi that's kind of ours. So in terms of the population, the sources of, gram [00:40:00] negatives, I was surprised that only 19% had a UTI, I think they talked about that in your first podcast as well, and the rest was pretty kind of what we'd expect in our practice.
the gram negatives were e coli and Klebsiella. So for me personally, they were quite representative of the patients I'd see. And what I don't see is one in four patients had a carbapenem resistant organism. So that to me was, whoa, that's, definitely not what I'd see in, our population.
when I started trying to extrapolate these patients, About 27% had a third generation cephalosporin resistant enterobacterales. So in Ireland, just to put that in context, about 12% of our e coli and 15% of our Klebs have a third generation ceph resistant. So it's slightly different to my context. And when we looked at the carbapenem resistant organisms, there was only four KPCs, 26 OXAs, and 58 Metallo, beta-lactamases.
So if that's [00:41:00] your, population, that's fine, but that's. Definitely not our population. and the primary outcome of the all cause mortality after all of that is drum roll. there wasn't much difference. So at 14 days, 8% versus 7% for cefiderocol and standard therapy. So they were similar, but, when we looked at the carbapenem resistant organism subset, there was a slight difference, but the numbers are very small, 14% versus 10%.
But what that actually is, is nine patients versus six patients. And with the MBL, the difference was again. Larger but small numbers. So it was 31% for cediderocol mortality versus 0%, but we're to five outta 16 versus 11 patients. So that's what I mean, like I'm not really sure what to do with this drug.
the other thing that I thought was interesting, and maybe it's just because of my recent patient history, when I looked at the table three, it just reminded me how sick and [00:42:00] debilitated these patients are because when you looked at their functional status, at, the end of the study on day 30, only 36% and 39% were described as out of hospital and basically healthy.
So this study showed that cefiderocol was non-inferior, but not superior to standard of care. Bearing in mind that was a mishmash of lots of stuff, based on a primary outcome of 14 day all cause mortality. And we're still really not sure what to do in carbapenem-resistant organisms. And to be honest with you, I wouldn't be using cedfiderocol straight off in a gram negative.
on bloodstream. I probably use either Piptazo if it's healthcare, if I was worried about resistance, I may add an aminoglycoside. If I was worried about carbapenem resistance, I'd probably use ceftaz-avi And while this study is, fantastic and really well designed, it hasn't changed my practice.
Josh: That's fabulous. And the first thing is, we pronounce the drug differently. I
Speaker 6: was gonna say that. I was gonna say, we should have talked beforehand. How are we [00:43:00] all gonna say it? 'cause I'm gonna say it totally different.
Josh: I'm gonna do it now as Fidelma does.
But I think your, comments on, selection of drug is really important and the authors do. State that they recognized it as well. They said very few patients in the standard of care group received the newer beta, lactam, beta-lactamase inhibitors such as the ceftaz-avi. So I think they are, in the same camp as you on that another area was on source control that they didn't have data on that, that was super important too for me.
Yeah,
Fidelma: yeah, yeah. They go through the discussion. Actually, it's interesting one of the points David Patterson made, on his talk in GAMRIC was not only should we be talking about it as being an antimicrobial resistance problem, it's an antimicrobial resistance and access problem. So many of the countries that are included in this study may not have had ready access to ceftaz-avi and the newer antimicrobials.
Josh: The timing of this and evolution of drug resistance to this particular, compound [00:44:00] is also different today.
Robin: the comments that came up about, standard of care, standard of care is not necessarily the same everywhere. And it can be for a number of reasons, including lack of availability in certain countries of actually compounds that might be needed to manage the infections that they're seeing.
But it's still on a technicality standard of care. The problem is that then the results don't generalize to other environments where the standard of care is different. that makes these things complicated, but also emphasizes a problem with standard of care in, certain countries.
Fidelma: and your point, Josh, about the source control, you right?
Actually in the discussion, they have quite some relevant points about that. including the IVs, and, intraabdominal sources. So that's all very pertinent. But I suppose not withstanding, it's a huge trial, like even to get people. Enrolled within 48 hours. That's pretty fast. I listened back to your first [00:45:00] podcast and one of those speakers made the point that maybe we need to start using the adaptive platforms because We need bigger numbers to answer the question because I don't probably need cephiderocol for. Most of my gram-negative bloodstream infections, but I might need it for some. at the moment, we don't in our own hospital have in-house testing, but we send it off to our colleagues in the UK in Colindale.
And with thanks to my wonderful colleague, Benu Dinesh, who rapidly got some data from me, we all had the impression that every time we sent it off, it was resistant. And actually we were right. So in about two years, we sent 69, isolates off, for cefiderocol susceptibilities and Bart two, isolates most of the Enterobacterales were resistant.
Now that's obviously we don't send everything off. and a lot of these were MDMs. Interestingly, we sent 35 pseudomonas and nine were only resistant. But again, we're not going to use that in pseudomonas. But, in this trial. you wouldn't have [00:46:00] continued cefiderocol if it was resistant, whereas we don't have that luxury.
So I think until we get it in-house for our own center, this is probably going to be a conversation. We'll be all going, Hmm, should we use this or not?
Josh: Annie, I think you have some experience in your institution.
Annie: Yeah. So I mean this paper really for me boils down to what is your local epidemiology in terms of what flavor of beta-lactamase you seeing locally?
And we've had sort of grumbling issues with NDM, in our institution over the past sort of five to 10 years. And I think we were all, waiting for cefiderocol I'm gonna go with OL to come. We were waiting, you know, you here at conferences and we were like, it's nearly here. We've got such an NDM issue.
We can't wait. We're sick of trying to do these combinations of ceftaz-avi and Aztreonam and Amino Glycosides. And pretty much everything we see in our is resistant. Our N dms are all resistant. That really rings true what you were saying. and also testing is not easy either. I dunno.
Robin, if you want to make a comment about the practicalities [00:47:00] difficult testing in terms of, whether you can reliably use this or not, and, testing guidance has changed a fair bit over the past few years as well, hasn't it?
Robin: the points are interesting. I'm guessing, Annie, that you hadn't used a lot of this compound.
And yet you're describing high rates of resistance and exactly the organisms you wanted to target and Exactly, yeah. So that's one of the challenges with antimicrobial resistance is you would think that having not used it in your clinical practice, you would be good to go.
But in fact that's not the case. And we're seeing that from some of the work that we're doing. In Europe as well. so that's a challenge. And then, the susceptibility testing to this agent is, also challenging, because of its mechanism of action. It, needs special media for testing and that's not, universally available.
and so you don't, even have that information. So, now we have resistance that's already arrived ahead of using an antibiotic in clinical practice and challenges with availability of [00:48:00] susceptibility testing. the other thought is that we do need, still.
More implementation of diagnostics to tell us what drugs to use to treat gram-negative bacteremia, because we have now rapid diagnostics that can really inform that there's been a huge explosion, on the phenotypic susceptibility testing side to make those results available rapidly. I think for idealized patient care, that would be the way to go.
Obviously there are logistics and expense involved in that, and they're probably not available from a regulatory standpoint everywhere, just like we talked about with the, therapeutics. But I think, globally, we have some solutions in our toolbox that we're not necessarily deploying, and we're also learning that in many cases, the horse already got outta the barn before, we even, got to thinking about, what we're gonna do in our own clinical practices.
So it's a great conversation. Complicated.
Annie: Yeah, I should say most of our, NDM infections are imported. we're kind of seeing resistance coming into our institution, but then spinning off [00:49:00] and having our own little outbreaks to deal with as a result. So, yeah, a tricky one with, cedfideroc ol.
Okay, now onto Robin's last chosen paper. I have to say this paper really is the coolest. I actually came across it listening, to an anthropology podcast a little while ago. So when I saw that you'd selected it, Robin, and you sent it through, I was like, oh, yes, I knew I'd heard something about this.
So it just combines everything that's got microbiology, archeology. Paleo anthropology, whole genome sequencing, and, randomly the squirrels of the British Isles as well, all in one. so it's got a lot going on. Robin, can you unpack this one for us?
Robin: absolutely. so first of all, let me explain a little bit about why I personally chose this, because I mentioned, I chose all my papers because of a personal connection.
So in 2017, we launched our 16 s ribosomal, RNA, PCR sequencing assay. And one of the first tests that I reported out, was a patient with leprosy one of my colleagues had diagnosed. And they said, [00:50:00] oh, hey, can you run your, fancy new test on this patient's? Skin biopsy. And I kind of said, well, why you, you know what's going on?
They have leprosy and it's caused by Mycobacterium leprae. So what question am I answering that's going to help you, in this, diagnostic odyssey? they kind of said, well, just because you have this cool new assay and, we hadn't specifically validated the diagnostic for diagnosis of leprosy, although Bioinformatically, we knew it would work.
So my arm got twisted and we ran it, and then I got the results back and I looked at the sequence data and I was like, wait a second. It's not Mycobacterium leprae, it's Mycobacterium lepromatosis. Which caused me to say, and I'll just be honest, what is Mycobacterium lepromatosis? Because I had never heard of it.
the sequence data was, clear by the way. It was not Mycobacterium leprae. It was very nicely separated by the assay we had designed, despite the fact that we hadn't designed the assay to make this distinctions, which is [00:51:00] also really cool. And highlights genomics. So this in a way, answers some of the questions of what is Mycobacterium lepromatosis, and also tell some interesting stories as you point out.
So leprosy we know a lot about as physicians, it was discovered by Hansen in Norway in 1871. It's caused by Mycobacterium leprae, and it was the sole cause of leprosy actually until 2008 when Mycobacterium lepromatosis was identified in two patients with diffuse lap promi leprosy in the US who were from Mexico.
also interesting here is that the consensus is that the introduction of Mycobacterium leprae into the Americas was a consequence of European colonization. And that's a story that we tell over and over again. But interestingly, most cases of Mycobacterium lepromatosis have been identified in the Americas.
And so this, you know, right off the bat, suggested a different possible origin and epidemiological path. what is this disease? A 2023 [00:52:00] review identified 27 cases of Mycobacterium lepromatosis, infection, 19 from North America, 10 found in the us. But seven of those 10 patients were originally from Mexico, six in Mexico, three in the Dominican Republic, and one each in Paraguay, Cuba and Canada.
In addition, there have been two reported cases in Singapore, two in Myanmar, and one in Indonesia. clinically of the 27 patients, 15 had diffused Lepromatous leprosy 10 had Lepromatous, leprosy, and two had borderline Lepromatous leprosy. So this study was published in science and it's called pre-European Contact Leprosy in the Americas, and its current persistence.
It's a nice title. It really kind of tells you the whole story. so Lopopolo and colleagues investigated the evidence indicating that Mycobacterium lepromatosis initially emerged in the Americas rather than having been introduced via European colonization like Mycobacterium leprae, they found Mycobacterium lepromatosis, [00:53:00] DNA in 34 samples.
They, looked at leprosy samples. Across five countries in the Americas, the us, Mexico, French Guiana, Brazil, and Paraguay. And then they combined high throughput, short read sequencing and targeted enrichment, and were able to recover genomic data from 23 of 34 positive samples. interestingly, technologically, they overcame limitations of short read sequencing by generating high quality long read mycobacterial lepromatosis, DNA, from mouse footbed samples inoculated with a strain from human sample that came from Costa Rica.
They then also went on to examine a collection of 389 ancient DNA datasets from pre-European contact. Ancestors in the Americas, and they recalculated the time of divergence between mycobacterium leprae and lepromatosis. This had been previously calculated, so, these are modeling and in one model, the most recent common ancestor was 720,000 years [00:54:00] ago in the Pleistocene age.
And in a second model, it was 2 million years ago in the late Triassic. In either case, divergence happened a long time ago. this apparently was sooner than prior estimate. S they also looked at the remains of three human American ancestors who tested positive for Mycobacterium lepromatosis. One was from Canada, and two were from Argentina, and they were dated by radiocarbon to a time approximately a thousand years ago.
So that is before European contact. And they indicate a genetic ancestry that's indigenous to the Americas. They also went on to combine that ancient and present day DNA data to look at Clades, and they found five clades of Mycobacterium lepromatosis four, which were first detected the Americas. And now we are getting to the squirrels.
Annie the fifth CLA was identified in red squirrels in Britain and Ireland in 2016. But even though that's where it was found, it was subsequently shown to belong to an American [00:55:00] lineage that had been likely introduced into the British Isles toward the end of the 19th century. So we're actually taking this organism from the Americas.
Over to the British Isles, which is interesting of the 26 present day strains analyzed using maximum likelihood phylogenetic reconstruction. All but two belong to a single present day dominant phylogenetic clade that was near clonal. So analysis of ancient genomic DNA and Phylo genomic evaluation clearly demonstrates that Mycobacterium leprae was brought to the Americas from Europe and Asia.
But this work now provides definitive evidence that Mycobacterium lepromatosis was endemic in the Americas before the arrival of Europeans. It also shows that it was geographically widespread across the Americas. So this study shows the value of ancient genomics to understand the history of infectious diseases.
But also I think, highlights yet another bacterium beyond Kingella kingae, streptococcus [00:56:00] dysgalactiae that is likely underappreciated by clinicians. So hopefully everybody now has heard of Mycobacterium lepromatosis.
Josh: Wow. Yeah, I really enjoyed this. I really enjoyed going back and reading more about leprosy. And again, in the US we don't see it very often, if at all. some people in their practice. And the fact of the matter is, is that in some countries, like India and Brazil, for example, they have 10,000 cases a year of this.
And that's really remarkable. it shows that we need to take better note of where our patients are coming from and because of global travel, where people are going, and also just to continue to read and learn lifelong when we are in these areas of work.
Robin: And I think also it speaks to diagnostics, right?
Because I began with, someone asked to run an advanced diagnostic, and I was like, why? You already know the answer. And then it turned out that it wasn't the answer that I thought it would be. So I'm not suggesting [00:57:00] we need to go crazy and using molecular diagnostics, but we learn a lot by using molecular diagnostics.
this is just a great example of that.
Annie: I love that it kind of overturn that assumption that everybody thought they knew.
we've kind of touched on that a bit. Everybody thought, oh, well, you know, the Europeans took it to the Americas. And I just love that, we can use science to try and find the truth to things. and how amazing is it that, sequencing has come so far, even in the past decade, it is just beyond what people would've imagined possible, isn't it?
I'm so excited to know what else we're gonna pick, what diseases are we gonna find the origins of, I think
Robin: if you look at the list of contributors, they are from all over the world. It's, truly an international collaboration, amazing, body of work to pull everybody together, and execute, the sequencing analysis that was done.
And, I mentioned, mouse foot pads were also involved in this work, so, there was a lot going on on the technical side and on the collaborative side.
Josh: I think that, [00:58:00] foreshadowing the future, looking at epigenomics is another step even. What would you do that for? Well, to define why one strain might be more virulent than another, or what changed to allow the hop to the red squirrels.
so I think this is really the tip of the iceberg for where we're going to be going in the next several years.
Fidelma: And I think that's a great example, Robin of storytelling and illustrating how diagnostics. So it's a bit like CSI, if I may use an example, I could almost see that you were telling a story there. So when we start talking about communication, that would be an amazing way of demonstrating the use of diagnostics.
In my head, I could see just a, TV program or a cartoon, and it could be used really good educationally because it's such a good story.
Josh: The issue of communication is a beautiful segue into our final paper of the 2025 clinical microbiology top picks, Fidelma has chosen an opinion piece from.
A [00:59:00] SHE rather than original research to round things up and it gets to the point of communication. Fidelma, can you take us into the echo chamber?
Fidelma: It's called Beyond the Echo Chamber, reframing AMR awareness efforts to reach the other 99.9%.
So , I like the idea of clear communication and in a way I'd summarize that title of, it's not what you say, it's how you say It. and the paper quite rightly makes a point that we are all specialists in infection and we're very passionate about addressing AMR.
And we talk about a lot and we write about it a lot and we talk to each other about it a lot. but this kind of enthusiasm is essentially self-contained most of the time to all of us. So we're talking within an echo chamber and we're really scratching the surface of, the public, our other clinicians, and policy makers.
And actually these are the people that are going to get us a bit of traction. so the 99.9% refers to the fact that infection specialists are less than 0.1% of the [01:00:00] population. So we're targeting the others. what the paper talks about, is various public opinion surveys.
About a quarter of people have never heard of AMR. And then when they've heard of it. They really don't think they can do much about it in over half of them, which is kind of shocking and to me, has parallels with climate change. This is such a big problem that when it starts involving everybody, when you're a little old me, you don't really know.
What you personally can do, but they also make the point, which is kind of a reality check for me, and I know it because I see it every day, is most healthcare professionals, while they might understand it, they're kind of at best ambivalent about AMR because they've other priorities like obesity or diabetes or cigarette smoking or whatever.
and like certainly since I started in clinical microbiology in the mid nineties, there's been. A sea change in terms of awareness. Politically, we might say not enough, but at least there is. It's been discussed at the un but I think [01:01:00] generally most of us would agree that, all these commitments and documents probably haven't been matched with consistent funding and consistent policy instruments, to see them through.
I think if we look at AMR in the whole One Health perspective, there's lots of competing interests. We have surveillance systems, but there are lots of them are incomplete.
We don't have consistent coordination across sectors. There's lots of regulatory gaps. there still places in the world you can go and buy your sweets and your antibiotics at the same time. The role of science is under threat internationally, and it's becoming very much eroded, using science to make decisions.
And we kind of don't help ourselves either because AMR is not an easy thing to get across. It's complicated and it's very nuanced, so it's not a, very straightforward message. And the other thing is, if we're trying to engage policy makers, the political cycle is very short. It's certainly very short.
In Ireland, we have general elections of very frequent, cycles. [01:02:00] And to get some kind of traction on AMR, you need long-term planning and long-term investment. So if you're a politician, well why should you focus on that where you can get a lot more kudos in something like improving your trolley weights.
so what this paper does is takes all of this and goes, what can we actually do? They picked four areas and the first is, knowledge translation, and it's what we've been talking about. It's what I said to Robin about that story.
We need to be able to translate our message in different ways, I suppose, using different languages to different audiences and appreciating that. some people can read, some people may not. Some people find visuals more helpful, some people want the snappy answer. So we have to kind of get better at translating our message into very clear, simple, and I suppose actionable things.
investing in public engagement. That's the second one, there has been public information campaigns, but there tends to be a tendency, oh, we've done that and it's [01:03:00] over, but that's not true. we've to constantly keep kind of highlighting that we need these public information campaigns, we need clear messaging, but it needs to be actionable.
Otherwise the individual gets lost in the complexity and it's very easy to go, what can I do myself? then the other two parts are leveraging One Health. we talk about that a lot. And actually in many countries, including my own, there's been huge advances in the One Health Dialogue. And in Ireland we are now on our third national action plan for antimicrobial resistance.
So that's fantastic. but we need to continue doing that. And then the last thing, which I think is important specifically as we start the new year in 2026, is we have to get science and policy partnerships. We just simply have to do that. we have to co-develop things. we have to get AMR understood by our policy makers.
use some kind of language that we can all get. And certainly at last year's [01:04:00] ESCMID of 2025 the AMR Science Policy Forum, which I attended, I thought was really exciting. So you'd all the appropriate people around the table, and that's where the discussion starts. I liked this paper because it got me thinking and it reminded me we're doing what we're doing on this podcast. We're talking to ourselves and presumably the people that listen will infection experts. But probably what we need to do is do a different podcast sometime for the general public and go through all these papers and try and explain them in, plain English.
Fidelma: And I think Robin's story is probably going to be the one that the general public will like the best, but I might be able to give her a run for her money on the dots and the door criteria.
Josh: the line that was most powerful to me is that AMR is a shared problem and I, really like that.
at the same time, I will say that many people, even in infectious diseases and Clin Micro that I talk to, you bring up AMR, they talk about antibacterial issues and AMR is bigger than that. [01:05:00] We have antivirals that don't work for complicated. herpes. We have, malaria drugs that don't work and we have antifungals that don't work.
And I think it's on us as a community to make sure that we bring that as a shared problem together because we're much stronger when we include everybody in these discussions.
Regardless of whether it's a eukaryote or a prokaryote or a virus, they are all causing devastating problems globally and we need to have a very clear voice on this topic.
Fidelma: Mm-hmm. And I think we need to get better telling stories. So locally, when I'm teaching about AMR I pick a patient with a problem and demonstrate the problem through the patient, because otherwise it's not tangible. I think we have to get better at, being more inclusive ourselves, as you rightly point out, and then broadening it out first to our own colleagues and then broader still, because we tend to talk about the policy [01:06:00] makers, but actually between us and the policy makers or the electorate, and they tend to kind of influence the policy makers as well.
By engaging the, public, we are the public, but the non-specialist public and listening to our patients and trying to bring them into our discussions and our research, I think the conversation and the action can be all the more richer.
Robin: I think that we as scientists, we're also very poor at communicating our science with the public.
Maybe we just aren't doing it that much, but we're also very bad at it. And so we need to reflect on how we can do better there. maybe it's our younger folks who can really help us, and think about how they would do it and, try different approaches to doing that. Also, wanted to thank you again for picking dots.
I think thinking about trials that really take a patient perspective is important because all of this is that echo chamber of talking to ourselves, which we're doing here today. and we're really nerding out and we all love it. Right? That's great. [01:07:00] But. for the people that we're really trying to help with what we're doing, they're not involved and they need to be involved because that's the whole reason we're doing this in the first place.
So thank you for picking the articles that you did, and especially this last one.
Annie: Great. that's it for the papers. Josh, out of the papers we've discussed, which one had the biggest impact on you?
Josh: easily would say the leprosy one.
And I really agree with Fidelma when she said it could be made into. Something that we could watch. And I really was looking at it more like a Raiders of the Lost Arc type of thing. And I don't know, Robin, you know, if you would play the lead there, but I think it would be an incredible way of, showing how history matters.
I was a history major in university and so I always go back to what did we know about this and how come we didn't do better? And so this is an area where we've learned a lot and can continue to do better. So it's very exciting to me and I really appreciated [01:08:00] all six of the papers, but that one was a standout for me.
What about you, Annie?
Annie: I do have soft spot for the paleo microbiology paper. So I think probably at my heart I'd say that one, but I do think the strep dysgalactiae subspecies equisimilis paper is gonna make me think a little bit more in my own practice. 'cause we see so many of these, it's so common. It's usually elderly, frail patients.
it is our bread and butter as microbiologists and ID physicians and it's just gonna make me think a little bit harder about whether I've been underestimating that as an invasive infection.
Josh: well, we certainly covered a tremendous breadth of clinical microbiology and I do wanna give our amazing, amazing guests the opportunity for some final thoughts.
I think that my point about AMR and communication is what I'd like. To take home for myself. And it's not just what you say, it's how you say it. And we need to engage different audiences and be consistent on our message.
Fidelma: And remember that the AMR is antimicrobial resistance. thank you all. [01:09:00] Thank you, Robin. And thank you to Josh and Annie for Inviting me.
Oh, thank you Fidelma for the kind words. it's a pleasure to do this. And, these articles are all great and there are many more. I picked mine from personal experience and also because they really reflect things that we thought to be otherwise.
new knowledge that maybe is going to change some of our practice or the way that we care for our patients. And I think they also emphasize that we need more science. Right there are things that we don't know.
Robin: We need to continue to, investigate in these areas what's the right diagnostic for the right patient, what's the right therapeutic for particular patients? And then importantly, Fidelma your perspective on what does the patient actually want. Because a lot of times we take our own perspective. I know best because I'm the expert, but actually this is about our patients.
So what do they want?
that's our top clinical ology papers of 2025 and we'll of course link to all of the papers in our show notes so that listeners [01:10:00] can check these manuscripts out for themselves. Thank you again to our guests, Robin Patel from the Mayo Clinic in Rochester. Minnesota, and Fidelma Fitzpatrick at the Royal College of Surgeons in Beaumont Hospital in Dublin Ireland.
Annie: And thank you for listening to communicable the CMI Comms podcast. This episode was hosted by Josh Nosanchuk in New York, USA and me Annie Joseph in Nottingham, uk. Associate editors at CMI, comms ESCMID's Open Access Journal. It was edited and produced by Dr. Katie Hostetler, oy and peer reviewed by Dr. Sinéad Kilgarriff of the National Virus Reference Laboratory University College, Dublin in Ireland.
Theme music was composed and conducted by Joseph McDade. This episode will be citable with a written summary referenced by A DOI in the next eight weeks. And of course, all our papers and any other literature we've discussed today will be linked in our show notes. You can subscribe to Communicable wherever you get your podcasts, or you can find it on ESCMID's website for the CMI Comms Journal.
Thank you for listening and helping CMI, [01:11:00] comms and ESCMID move the conversation in infectious diseases and clinical microbiology. Further along.