Paul Feuerstadt, MD

Advances in Managing Recurrent C Diff Infection, with Paul Feuerstadt, MD

 has long posed a major clinical challenge, with few effective, durable treatment options and until recently no FDA-approved microbiota-based therapies.

For decades, management revolved around antibiotic courses that often failed to prevent recurrence—leaving patients caught in a debilitating cycle and providers with limited tools. The FDA approval of fecal microbiota, live-jslm (Rebyota) signalled a major shift in the trajectory of C. diff treatment.

 is recurrence,” Paul Feuerstadt, MD, a clinical gastroenterologist and an associate clinical professor of medicine at Yale University School of Medicine/PACT-Gastroenterology Center, explained to 

, noting that an estimated 35% of individuals treated with guideline-based treatments will recur.

He goes on to describe how antibiotics only treat part of the infection and do not fully resolve the underlying microbial imbalance. When it comes to addressing recurrence, Feuerstadt references historical approaches with microbiota restoration therapy or fecal microbiota transplant and, more recently, the FDA approval of fecal microbiota, live-jslm.

New data presented at Digestive Disease Week (DDW) 2025 highlight findings from 5 pooled trials of live-jslm, showing a consistent favorable safety profile with similar rates of treatment-emergent adverse events (TEAEs) reported in all live-jslm recipients (70.9%), 1-dose recipients (67.6%), and placebo recipients (60.2%). Most TEAEs were mild or moderate in severity, gastrointestinal in nature, and related to C. diff recurrence and/or preexisting conditions, with few events (<1%) being considered possibly related to live-jslm.

In a second abstract at DDW, Feuerstadt and colleagues explored the safety and clinical effectiveness of live-jslm when administered by colonoscopy. Physician experiences with the 41 procedures included in the study were largely positive, with 90% of investigators reporting at least a ‘positive’ or ‘very positive’ experience across all aspects of administration. Additionally, material preparation time and ease of passage through the colonoscope were mentioned as reasons for ‘positive’ or ‘very positive’ experiences.

Of note, among the 39 participants who completed 8-week visits, all (100%) were assessed as either having ‘much improved’ or ‘very much improved’ CGI-I.

“As we're starting to evolve these FDA approved treatments, RBL is diversifying its data, showing that across 5 trials, including 3 phase 2 trials and 2 phase 3 trials, it's incredibly safe,” said Feuerstadt. “When we apply this knowledge to putting the material through a colonoscope, [we see] that is also safe and effective and a potential modality that can be broadly used.”

Editors’ note: Relevant disclosures for Feuerstadt include Rebiotix Inc, Takeda Pharmaceuticals, Ferring Pharmaceuticals, Seres Therapeutics, and Probiotech.

Khanna S, Awad T, Guthmueller B, et al. PHYSICIAN EXPERIENCES AND USABILITY OF FECAL MICROBIOTA, LIVE-JSLM (RBL) ADMINISTERED VIA COLONOSCOPY TO ADULTS WITH RECURRENT CLOSTRIDIOIDES DIFFICILE INFECTION: ANALYSIS OF A PHASE 3B STUDY. Abstract presented at Digestive Disease Week (DDW) 2025 in San Diego, CA from May 3 - May 6, 2025.

Lee C, Feuerstadt P, Louie T, et al. SAFETY OF FECAL MICROBIOTA, LIVE-JSLM, IN ADULTS WITH RECURRENT CLOSTRIDIOIDES DIFFICILE INFECTION: AN INTEGRATED SAFETY ANALYSIS FROM 5 PROSPECTIVE CLINICAL TRIALS. Abstract presented at Digestive Disease Week (DDW) 2025 in San Diego, CA from May 3 - May 6, 2025.

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Feuerstadt explains recent advances in treating recurrent C diff and reviews new data on the safety and administration of fecal microbiota, live-jslm (Rebyota).

: Hello, and thank you for joining this MEDcast series titled “Restoring Balance with Advanced Fecal Microbiota Transplantation in 

 Infections.” I am David Hudesman, MD, codirector at the Inflammatory Bowel Disease Center at NYU Langone Health in New York, New York.

I am Jordan Axelrad, MD, MPH, director of clinical and translational research at the Inflammatory Bowel Disease Center at NYU Langone Health in New York, New York.

In this program, we’ll explore the latest advances in treating recurrent 

 infections with fecal microbiota transplantation [FMT] and examine the clinical evidence supporting its use. To discuss more of this, we are joined by Paul Feuerstadt, MD, FACG, AGAF, assistant clinical professor of medicine at Yale University School of Medicine in New Haven, Connecticut. Paul, tell us a little about what type of patients or people are at increased risk of 

 There is a wide array of patients that are at risk for 

 infection, which is why so many patients get it. About a half a million people will get diagnosed with 

 in the United States every year. The risk factors for 

 fall under 3 categories: demographics, medication exposure, and environment.

Demographically, seniors and women are at increased risk for 

 infection, as well as those living with chronic kidney disease, HIV, diabetes, or inflammatory bowel disease [IBD]. Patients that have had 

 in the past are also at significantly increased risk.

As for medication exposures, the classic association is with antimicrobials. The most common antimicrobials associated with 

 are amoxicillin, ampicillin, erythromycin, fluoroquinolones, cephalosporins, and piperacillin and tazobactam. These antimicrobials have an impact on our colonic microbiota, which creates an environment that’s much more welcoming for 

 to proliferate. In my practice, patients often come in on a PPI [proton pump inhibitor] or histamine blocker to treat diseases such as GERD [gastroesophageal reflux disease]. H2 [histamine type-2] blockers and PPIs are also risk factors for 

The third group is environment. Any individual that lives in a skilled nursing facility or spends significant amounts of time in the hospital are at greatest risk. They probably fulfill the other risk factors I listed in terms of demographics and medication exposures, and they are also surrounded by other patients that might have 

You illustrated nicely how prevalent this disease really is. What is the recurrence rate of a patient who has previously recovered from 

? Does 1 recurrence increase the risk of further recurrences?

 That is a really important question. Recurrences are a major Achilles heel with 

An estimated 35% of properly treated patients will recur within 8-12 weeks. Of those recurring infections, 45% will recur a third time, and up to 60% will recur after that. Patients get caught in this vicious cycle of recurrence after recurrence after recurrence. That causes a huge burden on our health care system. Recurrences predict an increased risk of sepsis and colectomy, as well as increased risk of 

-related mortality. It is a significant financial burden. There is a burden on the patients beyond abdominal pain and diarrhea associated with 

. They may experience a health care-related quality of life impact, anxiety, or PTSD [post-traumatic stress disorder]. These patients live in fear that they are going to get 

again because the rates are so high for recurrence.

Could you tell us about how the gut microbiota is linked to 

 The microbiota is a complicated space. It is estimated there are a hundred trillion different microorganisms in a healthy colon. It is made up of bacteria, archea, fungi, yeast, and viruses. In the medical field, we gravitate towards the things that we have defined the best and understand the most. We understand the bacterial phyla within the colon the most. The most common bacterial phyla in a healthy colon are the Bacteroidetes, Firmicutes, Actinobacteria, Proteobacteria, Verrucomicrobia, and Fusobacteria. I believe that’s what makes our society great is our diversity. Different people from different backgrounds approach things in a different way to solve problems efficiently. It is the same thing in the microbiota. The more diverse the microbiota is, the healthier the microbiota is because it can approach problems in a more sophisticated, efficient way.

The composition of the microbiota is what is most eloquently defined, but what this bacteria is doing is more important. 

 is a really interesting bacteria because 

 has 2 phases: the spore phase and the vegetative phase. The spore phase is really resistant. It’s possible that 

 is sitting on a surface right in front of you in its spore phase, because the spore phase can last on that surface up to 8 months and remain viable. It’s the spore phase that gets transferred from person to person. Healthy microbiota eradicates the spore phase. Antimicrobials have minimal to no impact on 

spores, instead impacting the vegetative phase. The vegetative phase of infection releases toxins and causes symptoms, such as abdominal pain, diarrhea, nausea, fevers, and sweats. Antimicrobials control the vegetative phase, which is why when patients are on antimicrobials, they respond, their symptoms go down. The spore phase [of] 

 then stays in a patient’s system, and it’s up to a healthy, diverse microbiota to give that spore phase the knockout punch.

 has changed. Walk us through your approach and tell us how the IDSA [Infectious Diseases Society of America] and ACG [American College of Gastroenterology] guidelines have changed. What should providers be doing when they evaluate a patient with diarrhea?

 The incidence of health care-associated infections is decreasing because of better infection control and antimicrobial stewardship. Essential to understanding a patient with 

 is understanding the diagnostic tools. There are 3 commercially available tests: the enzyme-linked immunosorbent assay [EIA], the GDH [glutamate dehydrogenase] assay, or the PCR [polymerase chain reaction]/NAAT nucleic acid amplification testing.

Let’s start with the EIA, or enzyme-linked immunoassay. In the distant past, doctors would have to send off 3 consecutive bowel movements to diagnose

, because the sensitivity of the EIA at that time with 1 test was completely insufficient. In about 2008-2009, the sensitivity improved, but it wasn’t great. The enzyme-linked immunoassay is the only test that we have commercially available that detects a true diagnosis of the 

 toxin itself. We don’t necessarily care if 

 is in a patient system, we care whether it’s in the patient system and producing toxin. But the EIA still has an unacceptably low sensitivity. If it’s positive, you can confidently say that the patient has 

. But if it’s negative, you can’t say that they don’t have 

We do secondary tests to boost the overall accuracy. One of those secondary tests is the GDH assay. This assesses for an enzyme that is broadly released by 

. A positive test means you possibly have

, and a negative test means it is incredibly unlikely that you have 

. It has a high negative predictive value. If you put the EIA and GDH together, you get a pretty good test. If they’re both positive, you’re positive. If they’re both negative, you’re negative.

However, we frequently will get discordant results. We adjudicate those discordant results with a test called the PCR assay. The PCR assay is an assay that detects the genes that code for the toxin, not the toxin itself. So it detects the organism, but not whether the organism is actively releasing toxin. Well, when you’re adjudicating discordant results, perfectly acceptable test. If you’re positive, you say the patient’s positive. If they’re negative, you can say that the patient is negative.

But there’s been a significant shift in our society. A study published in the 

 in 2020 looked at the frequency of testing in the United States in 2011 versus 2017. In 2011, the predominant assay that was used was the enzyme-linked immunoassay. The estimate for the number of cases in the United States was 476,400. That was based on the frequency of EIAs being true positives.

However, in 2017, the frequency of positive tests was essentially the same, but the PCR assays were being used as a single test about 80% of the time. They adjusted the frequency of diagnosis of 

 down to 365,200 to account for colonizers. Fifteen percent of all health care providers, of all individuals that spend significant amounts of time in the hospital have 

 within their system without an active infection. PCR assays on their own will over-diagnose. Following IDSA/AHA guidelines and clinically contextualizing those patients will fix that. The patient should be having at least 3 liquid bowel movements in a 24-hour period. The stool should take the shape of the specimen collection container.

We see a lot of inflammatory bowel disease patients in the hospital system. Be very careful on who you’re testing.

Know what tests your institution has available and know how to use them.

Exactly. If a patient tests positive, is your first-line agent metronidazole, vancomycin [Vancocin], or fidaxomicin [Dificid]? How do you make that decision?

 The guidelines say that fidaxomicin is superior to vancomycin. Fidaxomicin has a narrow spectrum. What that means is that when you treat 

, having a minimal effect on the surrounding microbiota. Vancomycin treats 

, but also alters that surrounding microbiota, creating an environment that results in higher recurrence rates. If they are positive, the tendency is to want to treat. If you treat with vancomycin, you can alter the microbiota in a way that causes 

 to reactivate because you’re weakening the colonization resistance. True diagnosis is key. Fidaxomicin is preferred.

In my clinical practice, I wait if patients have 2 or more risk factors for recurrence. In that group, considering the financial elements, I use fidaxomicin. An acceptable alternative is vancomycin 125 mg 4 times daily. Metronidazole has largely been phased out. There’s data from 2005-2007 showing that metronidazole was inferior to vancomycin. That gap has widened even more significantly over the last 15-17 years. In the guidelines, they recommend metronidazole if neither fidaxomicin nor vancomycin are available, if the white cell count is less than 15,000 and the creatinine is less than 1.5 mg per deciliter.

A lot of these patients do in fact recur. The first recurrence, according to the guidelines, should be treated again preferentially with fidaxomicin 200 mg, twice daily, for 10 days, or fidaxomicin 200 mg twice daily for 5 days, bought by 1 tablet every other day, day 7-25. An acceptable alternative is vancomycin in a taper and pulse fashion more than 6 weeks. And then finally, if somebody failed metronidazole, initially, we could consider giving a 10-day course of vancomycin. In clinical practice, I use fidaxomicin for first regards. If they fail fidaxomicin, I use vancomycin taper pulse for that first recurrence. This is also where a product called bezlotoxumab was added. Bezlotoxumab [Zinplava] is a fully humanized monoclonal antibody designed to bind toxin B in a specific way. It is an infusion given during the standard of care antimicrobial that helps prevent recurrence.

Let’s talk about the duration of standard care antibiotics. How much benefit does the bezlotoxumab give patients as far as reduction and recurrence?

 For an IBD population, I would tend to use a more prolonged cause of vancomycin. I don’t necessarily go full 20 days. I usually go about 14 days as opposed to the 10 as recommended in the IDSA/SHEA [Society for Healthcare Epidemiology of America] guidelines and the ACG guidelines. I am more aggressive in patients that have higher risks for future recurrence, such as IBD.

Bezlotoxumab has fascinating data associated with it. From the MODIFY I [NCT01241552], MODIFY II [NCT01513239] trials, the number needed to treat to reduce 1 recurrence overall was 10. When they looked at … risk factors for recurrence, such as being over 65 years old, having any form of immune compromise, having history of 

 within the previous 6 months, the presence of the NAP1/B1/O27. or hypervirulent strain. or severe infection defined by a white cell count greater than 15,000 and or creatinine greater than 1.5 milligrams for deciliter; these patients benefited specifically the age over 65, the number needed to treat was 6. It almost cut the number to treat in half. The bulk of the patients that we see with 

in general are those over 65, so that is a sweet spot for bezlotoxumab.

A subgroup analysis looked at those 5 risk factors and it found that if a patient had just 1 risk factor for recurrence, the recurrence rates were about 31.3% with placebo versus 17.1% bezlotoxumab. In clinical practice we usually use at least 2 risk factors for recurrence. IBD, a great population to certainly consider with regards to this. There is very heterogeneous data that show a significant benefit, but in my clinical practice I will use this more aggressively in an IBD population. The 1 population we have to be careful with bezlotoxumab with is in patients with CHF [congestive heart failure]. Within the MODIFY I and MODIFY II trials, there was a slight increased risk of CHF exacerbation.

Could you give us an overview of what we have now? When are you implementing next-stage microbial therapeutics for recurrent 

 We’ve gone from the rudimentary fecal transplant world to a more sophisticated approach. Fecal transplant works because we know that there’s deficiencies of bacteroidetes and firmicutes in patients that have 

 infection. We know that those bacteroidetes and firmicutes create an environment in the colon that helps eradicate that spore phase. Unfortunately, our body’s ability to naturally regrow the bacteroidetes and firmicutes does not work well, which is why recurrences are so high. The theory with fecal transplant to replace what is deficient, thus reducing rates of recurrence. This has worked wonderfully over the last 10 years in widespread practice.

We were really learning along the way what we were doing. It seemed to work, and [when] we reinforced that it seemed to work. We had a bunch of open label studies. We had a couple of randomized controlled trials. There are a couple safety signals, but fecal transplant was overall safe. But there was a lot of heterogeneity of the trials. What the next phase looks like are pharmaceutically-produced products. In November of 2022, we had a major step forward with the FDA approval of a product called FMBL [fecal microbiota, live-jslm]. That is a treatment previously referred to as RBX2660 and this is under the class in the FDA of live biotherapeutic products, or LBPs.

This is the first product in this class. Our hope both in the 

 world, and maybe eventually in the ulcerative colitis world, that we see microbiota altering treatments that can help patients prevent 

 or minimize symptoms of ulcerative colitis, etc. This product is indicated in adults 18 and over for the prevention of recurrence of 

. You also asked where it fits in clinical practice. A product like this probably fits according to the guidelines, which is second recurrence and beyond. Within the guidelines for second recurrence and beyond it was felt both in the IDSA/SHEA guidelines and the ACG guidelines that there was significant benefit with fecal transplant so therefore we would stay with these live biotherapeutic products. In clinical practice, some of the LBP trials included patients with first recurrence. In patients with inflammatory bowel disease, it might be considered appropriate to use an LBP earlier in the treatment because we know the safety profile, we have open label study data in an IBD population. Therefore, it’s worth consideration for those patients that we’re fearful are going to get caught in that cycle of recurrence.

When we are seeing these patients in their first and second recurrences, do you take into account the time between the recurrences?

treatment is not as organized as the IBD world. For the last 15 years, recurrences have been defined by 1 month, 2 months, or 3 months. The bezlotoxumab trials were 3 months, the fidaxomicin trial was 1 month, and the live biotherapeutic trials were 2 months. How do you sort this through?

Three months is relatively conservative. The majority of recurrence is happening within 1 month, but in clinical practice, the good rule of thumb is about 6 months. The microbiota turns over about every 90 days so if you’ve lasted 90 days, which I like to call the window of vulnerability, you’re much less likely to get a recurrence of 

. In 6 months, the microbiota has turned over twice. The likelihood that it’s the same 

that is causing the symptoms goes down remarkably after 6 months. If somebody had 

 3 years ago and then they’re presenting again with 

, you start right back at the top. If somebody has 

e and then 6 months and 1 day later gets a recurrence, I would treat that as first recurrence. If it’s 8 months to a year, then I would start back at the initial treatment algorithm.

We saw efficacy results around 70%. How long was there follow up? Was there good long term follow up looking at the microbiota in those patients? Was it just 2 months, or do we have longer follow up than that?

 LBP trials follow up for a minimum of 6 months. With the FMBL, that product in their phase 2 data had 2 years of safety follow up and sustained response follow up. In the pivotal phase 3 trial, the PUNCH CD3 [NCT03244644] trial, it was 6 months of follow up. Overall efficacy was 70.6% for FMBL versus placebo which was 57.5%.

We commonly will encounter in practice patients who are put on a standard of care antibiotic while still persistently symptomatic. Sometimes, these patients may be referred to us for fecal transplant. Is there a way that you evaluate these patients that have sort of persistent symptoms through their therapies whether that’s truly recurrence of their PCR testing may not be reliable and so forth?

 About 25% of patients that come to see me with 

. Sometimes it’s a lack of understanding of diagnostic testing, but frequently it’s a situation that you actually just presented; the patient has resistant symptoms. What does that actually mean? The potency and efficacy of vancomycin and fidaxomicin for active infection is excellent. Any patient that is having resistant symptoms to either of those antimicrobials should be considered not to have 

. If they are on those antimicrobials and their bowel habits have not at least improved a little bit, we will use the confounder of inflammatory bowel disease. They should at least improve and come down maybe half as frequent in terms of frequency of bowels. It’s probably their underlying inflammatory bowel disease. In the real world, when patients come in and say, “I’m on vancomycin and I’m not responding,” it’s up to us as gastroenterologists to think through the differential diagnosis. Is this a post-infection irritable bowel syndrome [IBS] seen in about 25% of these patients? Is it inflammatory bowel disease? Is it a microscopic colitis? Is it some other medication-induced effect? Did they start on new medications? Have they traveled recently? It’s the usual suspects and then as gastroenterologists we have the power to do a colonoscopy and take a look and take some biopsies and see what’s going on. The majority of these patients are not resistant to the antimicrobials. It’s up to us to create that differential diagnosis and figure out what’s going on.

That’s a really important conversation that I have with so many patients. These microbial therapeutics are for 

 recurrence prevention. They are not a therapeutic necessarily for active 

 infection, especially for recurrent episodes.

Do you ever recommend probiotics or prebiotics? We know what the guidelines say, but what are your thoughts?

 They are very controversial. I am a big probiotic proponent with the caveat that probiotics are supplements. Supplements have virtually no data associated with them. When you look at probiotics, the probiotic of choice is Saccharomyces boulardii for 

 infection. Saccharomyces boulardii alters the metabolic environment within the colon to prevent inversion from spore phase to vegetative phase by altering the bile salt. There is basic science data that came out of Boston a number of years ago that showed that, and there is some clinical data that looked into it.

The ACG guidelines say the certainty of evidence is insufficient to recommend probiotics. The AGA position paper by Crytus et al from August 2021 also said the certainty of evidence is insufficient. My belief is that you’re not doing harm by giving probiotics. I do not use Saccharomyces boulardii after a fecal transplant. Fecal transplants give you the ultimate probiotic. I consider Saccharomyces boulardii in patients with a recurrence or multiple recurrences that we’ve cured with an antimicrobial alone to prevent recurrence in the future. If it is one recurrence I usually use about a month’s worth. If it is multiple recurrences I will use up to 3 months. There’s one population that we absolutely should never use a probiotic in and those are our patients who are severely immune compromised, ICU [intensive care unit], septic. There have been reports of fungemia from those probiotics, so we do need to be careful. I am a proponent of it, but I absolutely see the other side and the argument, and the certainty of evidence is insufficient right now to make a definitive statement.

Is there anybody that you will not or should not use an FMT in?

 There is a school of thought from Monika Fischer’s [MD, Indiana University Health] lab in Indiana that we can use FMT in patients that have fulminant disease. These patients are too sick to go to the [ED] and they have excellent results. There is not a safety signal that is overly concerning. I think the safety signals that have come up with regards to FMT over time are results of us learning appropriate screening and us learning the diagnostic tools that we discussed with 

. We also need to apply those diagnostic tools to screening of individuals who are donating for transplant and those individuals need to have both EIA and PCR assays. EIA is looking for whether they actually have an active infection, but PCR is looking for presence or absence of the bug. If we just transcribe the bug to somebody else, then it can reactivate in somebody else’s system and have failed the patient.

How are you using this recent FDA approved product in your office? How practically are you getting a patient this? Are you doing it in your office? Are you doing it at a center? Can they do it at home? Is that even an option?

 Doing it at home is not an option. It is incredibly easy to do in the office. It is a rectally instilled product, like an enema. It comes with a bag, a tube, a clip on the tube and a black circle at the end of the tube. If the patient has a recurrence, they take the full antimicrobial course. Then, there is what we call a washout period, where we want the antibiotics to wash out of the patient’s system. Vancomycin treats 

 but can also cause it, so we want the patient to have 1 to 2 bowel movements before we administer the material. The patient comes to the office, they get gowned up, in any exam room they get into left lateral decubitis position. We lubricate the tube, insert the tube about 5 inches, open the clip, the material flows in. It’s about 150 cc that take about 2 minutes to flow in. We monitor the patient for another 5 minutes, and the patient can go on their way. This treatment is given after the standard of care antimicrobial.

Dr Paul Feuerstadt joins Dr David Hudesmand and Dr Jordan Axelrad in a discussion about treatment approaches for C difficile infections, and the latest advances in treating recurrent infections with fecal microbiota transplantation.

Restoring Balance with Advanced Fecal Microbiota Transplantation in C. difficile Infections

To watch the video series component of this episode, click here.

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Restoring Balance with Advanced Fecal Microbiota Transplantation in C difficile Infections

: If you could give one piece of advice to physicians caring for patients with C. difficile infection or recurrent C. difficile infection, Teena, what would that be?

For me, the big one is the follow-up of these patients with recurrent C. diff. We need to keep a close eye on these patients, because they can be really high risk for high morbidity and mortality given that some of them can be no compromised all the patients and recurrence can really take them downhill. We should be following up with them, giving them a good contact number, so they can reach out. While on therapy, are they taking their medications, or do they have access to their medications? It’s so important. A lot of times we prescribe them fidaxomicin, they are not able to fill it, and they are suffering from recurrence. For me, that is the most important thing.

: Bincy, what are your thoughts about the most important thing for management of either initial or recurrent C. difficile?

I will keep it simple to summarize everything. My main advice is to act early. Early for the diagnosis, and you have the suspicion. Once you know that, you start them on treatment, and assess them early after treatment to make sure they’re responding, so you don’t need to make adjustments immediately after that.

Paul, I know you’re asking about recurrent C. diff, but I must start with the good antibiotic stewardship. Only use antibiotics particularly in your high-risk patients. Having said that, we treat patients, and we talk to all about the emotional, physical, and all the different sequelae that’s associated with this disease. Unlike other domains and infectious diseases, we have drugs with superiority data. We need to be more aggressive. I think you did a good job highlighting the changes in the microbiota over time, particularly those with recurrent disease. For prompt treatment, I’m a very big advocate of fidaxomicin. I think we should be thinking about bezlotoxumab a bit earlier in the course. Then when we have these live biotherapeutics, and we have to prioritize their use. Again, there’s always issues, which is the right one to use. As more data become available, there will probably be certain circumstances where one may be preferred than the other. But the wait and see approach with this disease; you got a patient in front of you, number seated a 3 to 5 to 10, I’m unaware of this in any other domain. The data are compelling. We’re beginning to appreciate the underlying pathophysiology. Everything we’re doing makes sense. I think this is something that patients suffer with, and we actually have more options to reduce and extinguish that suffering. When I think about CDI [C. difficile infection], people need to think about that patient and all the sequelae otherwise, and really take a very proactive approach in terms of prioritizing somebody’s new treatments.

: We’ve had really important points here. We have treating earlier from Bincy. We have access from Teena. We have Tom, aggressive, which is appropriate. Not in the negative way, but aggressive treatment upfront to try to shut this down. What I’ll say is accurate or indicated treatments, phasing out metronidazole, considering fidaxomicin, considering bezlotoxumab, considering live biotherapeutic products, if and when they get approved, fecal transplant as it is now, so that these patients don’t go through all that suffering that they have gone through, going through recurrence after recurrence after occurrence. Now during this presentation, we’ve covered a lot of information. We spoke about the mechanics of C. difficile, when to refer patients with C. difficile, differential diagnoses, important educational initiatives. We spoke about a subset of patients with inflammatory bowel disease in C. diff that are kind of a special unique element and a unique group that we need to consider differently. We shifted gears. We spoke about the mechanisms of treatment of C. difficile, antimicrobials treating the vegetative phase, the microbiota eradicating the spore phase. We updated ourselves on the IDSA/SHEA [Infectious Diseases Society of America/Society for Healthcare Epidemiology of America guidelines from 2021. We then shifted gears, spoke about bezlotoxumab, fecal transplant, microbiota based live biotherapeutic products, the trials, the differences. And here we are, at the end of this presentation. I want to thank you for watching this 

. If you enjoy the content, please subscribe to the e-newsletters to receive upcoming peer exchanges and other great content right in your inbox. Thank you so much for all the panelists for being here tonight. It was such a pleasure working with you.

Experts share advice for physicians taking care of patients with C. difficile infection (CDI).

Paul Feuerstadt, MD

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