CDI

Clostridioides difficile Infection (CDI) Treatment Protocol

1.0 Purpose and Scope

This protocol establishes a standardized, evidence-based framework for the diagnosis and management of Clostridioides difficile infection (CDI). Its strategic importance lies in unifying our clinical approach to improve patient outcomes, reduce the incidence of recurrence, and ensure the appropriate stewardship of antimicrobial and biologic therapies. By adhering to this protocol, we aim to optimize care from the initial diagnosis through the management of complex, recurrent disease.

The scope of this document applies to the diagnosis, severity assessment, and staged treatment of initial and recurrent CDI in adult patients within our clinical and hospital settings. It provides clear therapeutic pathways based on disease severity and treatment history. Successful management begins with a precise and timely diagnosis, the criteria for which are detailed in the following section.

2.0 Diagnostic Criteria and Definitions

Accurate diagnosis is the cornerstone of effective CDI management. This principle prevents the inappropriate treatment of asymptomatic colonization, which can further disrupt the gut microbiome, while ensuring that timely and decisive intervention is initiated for true infection. This section defines the precise criteria required to diagnose an active infection and to classify a subsequent recurrence.

2.1 Defining Active CDI

A diagnosis of active CDI is a clinical diagnosis supported by laboratory evidence. It requires the presence of BOTH of the following criteria:

Clinical Symptoms: The patient must present with clinically significant diarrhea, defined as the passage of three or more unformed stools in a 24-hour period for which there is no other obvious cause (e.g., laxative use, new enteral feeding formula).

Laboratory Evidence: A stool sample must test positive for the presence of a toxin-producing strain of C. difficile.

Crucially, patients with formed stool or who are asymptomatic should not be tested for CDI. A positive laboratory test in an asymptomatic individual signifies colonization, not active infection, and does not warrant antimicrobial therapy.

2.2 Interpreting Laboratory Tests

This protocol is based on a standard two-step testing algorithm involving a nucleic acid amplification test (PCR) and a toxin enzyme immunoassay (EIA). The combination of these results dictates the clinical interpretation and subsequent action. When both PCR and toxin EIA are positive, this indicates active CDI requiring treatment. When PCR is positive but toxin EIA is negative, this suggests colonization rather than active infection, and treatment should be withheld unless clinical suspicion remains high. When both tests are negative, CDI is ruled out.

2.3 Defining Recurrence

A CDI recurrence is formally defined as the reappearance of clinical symptoms (≥3 unformed stools/24 hours) accompanied by a positive stool test within 8 weeks of completing therapy for a prior episode. This timeline suggests a relapse from persistent spores. An episode that occurs more than 8 weeks after the completion of therapy is typically considered a reinfection or a new episode.

Once an active infection is confirmed, the next critical step is to assess its severity, which directly guides the initial therapeutic choice.

3.0 Initial Patient Assessment and Severity Staging

The strategic staging of disease severity is a critical decision point in CDI management. This assessment determines not only the choice and dose of antimicrobial therapy but also dictates the need for a higher level of care, intensive monitoring, and immediate surgical consultation.

3.1 Non-Fulminant CDI

A case of CDI is classified as non-fulminant if it does not meet any of the criteria for fulminant disease listed below. This category encompasses the majority of initial CDI episodes.

3.2 Fulminant CDI

Fulminant CDI is a severe, life-threatening presentation characterized by systemic toxicity and colonic collapse. A diagnosis of fulminant CDI is made if any of the following are present:

• Hypotension or shock
• Ileus (paralysis of the bowel)
• Megacolon (significant dilation of the colon on imaging)

The following sections will outline the specific treatment pathways based on this crucial severity assessment.

4.0 Management of an Initial CDI Episode

The primary goals for treating an initial episode of CDI are to achieve clinical resolution of symptoms and, critically, to minimize the risk of subsequent recurrence. The choice of therapy is guided by disease severity and patient-specific risk factors for relapse.

4.1 Treatment of Non-Fulminant Initial CDI

Preferred Therapy: Fidaxomicin

• Regimen: 200 mg orally twice daily for 10 days.
• Rationale: Fidaxomicin is the preferred agent due to its targeted, narrow-spectrum activity that functions like a sniper, eliminating C. difficile with minimal collateral damage to the protective gut flora. This microbiome-sparing property preserves and promotes the restoration of colonization resistance, resulting in a significantly lower rate of recurrence compared to the "scorched-earth" effect of broader agents like vancomycin.

Alternative Therapy: Vancomycin

• Regimen: 125 mg orally four times daily for 10 days.
• Rationale: Oral vancomycin is a highly effective agent for achieving initial clinical cure. It is an acceptable alternative when fidaxomicin is unavailable or access is limited by cost.

Not Recommended: Metronidazole is no longer recommended as a first-line agent for the treatment of an initial episode of CDI in adults due to inferior cure rates.

4.2 Treatment of Fulminant CDI

The management of fulminant CDI requires an aggressive, multi-modal antibiotic regimen to maximize drug delivery to all compartments of the compromised colon.

• Vancomycin: 500 mg orally or via nasogastric (NG) tube every 6 hours.
• Metronidazole: 500 mg intravenously (IV) every 8 hours. This provides systemic delivery to the inflamed bowel wall, which is critical in the setting of ileus and poor perfusion.
• Rectal Vancomycin: If ileus is present, add 500 mg of vancomycin in 100 mL of normal saline administered per rectum as a retention enema every 6 hours.

Fidaxomicin has no role in the management of fulminant CDI, as its efficacy depends on a functioning gastrointestinal tract for drug delivery, which is compromised in the setting of ileus.

4.3 Surgical Consultation for Fulminant CDI

A surgical consultation must be obtained immediately upon diagnosis of fulminant CDI. This is a co-management strategy initiated at diagnosis, not a rescue consult for when medical therapy fails. The following clinical triggers indicate an immediate need for surgical evaluation for colectomy:

• Presence of toxic megacolon or perforation
• A rapidly rising serum lactate level (>5 mmol/L)
• Worsening leukocytosis (>50,000 cells/µL)
• Clinical shock that is unresponsive to 24-48 hours of maximal medical therapy

4.4 Adjunctive Therapy to Reduce Recurrence Risk

For patients with an initial episode who are at high risk of recurrence, the addition of bezlotoxumab is recommended.

• Agent: Bezlotoxumab (Zinplava), a monoclonal antibody that neutralizes C. difficile toxin B.
• Dosage: A single infusion of 10 mg/kg administered intravenously.
• Timing: The infusion is given during the course of standard-of-care antibiotic therapy (fidaxomicin or vancomycin).
• Target Population: Patients at high risk for recurrence. Key risk factors include: age ≥65 years, immunocompromised status, or a history of CDI recurrence within the last six months.

After resolving the first episode, clinicians must be prepared to manage the complexities of recurrent infections.

5.0 Management of Recurrent CDI

Managing recurrent CDI requires a strategic shift from simply treating the acute infection to actively preventing the next relapse. The therapeutic approach must address the underlying microbiome disruption and the persistence of bacterial spores that lead to the cycle of recurrence.

5.1 Management of a First Recurrence

The choice of therapy for a first recurrence is dictated by the agent used to treat the initial episode.

If Initial Therapy was Vancomycin: The recommended treatment is Fidaxomicin 200 mg orally twice daily for 10 days. The rationale is to change the drug class to a microbiome-sparing agent, as the recurrence signals a failure of ecological recovery that a broad-spectrum agent like vancomycin is unlikely to correct.

If Initial Therapy was Fidaxomicin: The recommended treatment is a Vancomycin taper-and-pulse regimen. The rationale is to change the therapeutic strategy. Since the initial microbiome-sparing approach was insufficient, this prolonged, intermittent suppression is designed to hunt and kill successive waves of persistent, germinating spores while allowing the native flora to recover in between doses. An example regimen is:

• 125 mg orally four times daily for 10–14 days, followed by
• 125 mg orally twice daily for 7 days, followed by
• 125 mg orally once daily for 7 days, followed by
• 125 mg orally every 2–3 days for 2–8 weeks.

Alternative Strategy: For high-risk patients, an extended-pulsed fidaxomicin regimen (200 mg orally twice daily for 5 days, then 200 mg orally every 48 hours on days 7-25) is another supported option that combines a microbiome-sparing agent with a pulse strategy.

5.2 Management of a Second or Subsequent Recurrence

After two or more recurrences, antibiotic therapy alone is often insufficient to prevent relapse. The primary goal becomes the definitive restoration of the gut microbiome.

The core strategy is to first treat the active infection with an appropriate antibiotic course (e.g., fidaxomicin or a vancomycin taper-and-pulse regimen). Immediately upon completion of antibiotics, this should be followed by an intestinal microbiota transplant (IMT) product to restore colonization resistance and prevent another relapse.

The following section details the available IMT options.

6.0 Intestinal Microbiota Transplant (IMT) for Recurrence Prevention

Intestinal Microbiota Transplant (IMT), which includes FDA-approved live biotherapeutics and conventional Fecal Microbiota Transplant (FMT), is a cornerstone of late-stage recurrence prevention. The purpose of IMT is not to treat the active infection but to restore the gut's natural colonization resistance after antibiotics have cleared the acute episode. This re-establishes a healthy microbial community capable of suppressing C. difficile spore germination.

6.1 FDA-Approved Microbiota-Based Therapies

VOWST (fecal microbiota spores, live-brpk)

• Indication: Prevention of CDI recurrence after at least one prior recurrence.
• Dosing: Four capsules taken orally once daily for 3 consecutive days.
• Timing: Therapy must begin 2–4 days after the final dose of anti-CDI antibiotics.
• Prerequisites: Requires a standard magnesium citrate bowel preparation on the day before the first dose is administered.

REBYOTA (fecal microbiota, live-jslm)

• Indication: Prevention of CDI recurrence after at least one prior recurrence.
• Dosing: A single 150 mL dose administered rectally by a healthcare provider.
• Timing: The dose is administered 24–72 hours after the final dose of anti-CDI antibiotics.

6.2 Conventional Fecal Microbiota Transplant (FMT)

Conventional, donor-derived FMT retains two primary roles in modern CDI management:

• For patients with multiple recurrences when FDA-approved IMT products are unavailable or have failed.
• As a potential rescue therapy for select patients with severe or fulminant CDI who have failed maximal antibiotic therapy and for whom surgery is not a feasible option.

Successful CDI management relies not only on adhering to these evidence-based therapeutic sequences but also on understanding the key principles that underpin them.

7.0 Critical Clinical Principles

This final section codifies essential principles that underpin the entire protocol. Internalizing these concepts is critical to prevent common management errors and optimize patient care.

Do Not Test for Cure: Stool tests, particularly PCR, can remain positive for weeks or even months after clinical cure due to the shedding of non-viable bacterial DNA and spores. A positive test in an asymptomatic patient signifies colonization, not treatment failure, and must not be used as a reason to re-treat.

Timing of Microbiota Therapies is Critical: Intestinal microbiota transplant products (VOWST, REBYOTA) are designed to restore the microbiome after the infection has been cleared. They must only be administered after the patient has completed the full course of anti-CDI antibiotics. Administering them concurrently will result in the transplanted microbes being killed by the antibiotic.

Colonization Resistance is the Goal: The long-term goal of CDI therapy, particularly in recurrent disease, is to restore the gut microbiome's natural ability to suppress C. difficile. This active ecological barrier, known as colonization resistance, is maintained by a healthy microbiome that chemically suppresses spore germination, largely through the production of secondary bile acids. This is why microbiome-sparing agents and restorative therapies are central to preventing relapse.

Understand Treatment Failure in Fulminant CDI: The failure of antibiotics in fulminant CDI is not a result of microbial resistance. It is a failure of drug delivery and physiology caused by anatomic and circulatory collapse (ileus, ischemia, toxic megacolon). Therefore, early surgical consultation for source control is paramount; antibiotics alone cannot resolve necrotic tissue, and as the source notes, "late surgery just documents futility."

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Welcome to the Deep Dive.

Today, we're tackling something more than just a bad bug.

Claustroids difficile infection, CDI.

It's really an ecological crisis in the gut..

That's exactly right.

And the fight isn't just about knocking it out the first time.

It's about stopping this cycle, preventing the whole system from collapsing again and again.

Yeah, the recurrence rate is, well, it's frustrating.ly high .

So the real game is protecting the gut's natural defenses, that colonization resistance.

Precisely.

And that's the paradox, isn't it?

The antibiotics we use to treat it can actually pave a way for it to come back.

So that's our mission for you today.

We're going to walk through the clinical playbook, step by step, first infection recurrences , what drugs, why, and when we pivot to newer microphone.biome fixes.

We'll break down the logic behind each step in that escalation ladder.

Okay, let's untack this.

First stop, the initial nonfulminate episode.

What's job number one?

Well, before you even think about CDIF drugs, you absolutely have to stop any other antibiotics the patient might be on, if possible .

The ones that likely triggered the CDI in the first place.

Right.

Clear the decks.

Then what's the preferred opening move these days?

The guy guidelines now lean towards FIDE Oison.

That's 200 milligrams, twice a day for 10 days.

And the Y behind that shift?

It used to be all Van Comycin.

It's all about being selective.

Fedax Oin is kind of like a sniper.

It's narrow spectrum.

It hits C diffI hard, but leaves most of the other beneficial gut bacteria alone.

The good guys.

Exactly.

Especially those c crucial anerobes that help prevent spores from germinating later. Preserving the microbiome, you get better colonization resistance.

And that means fewer recurrences down the line.

That's the data.

Recurren rates with Fedax Elmin are significantly lower, maybe around 15% compared to Vomecin.

So if Fedax Omin is the sniper , Venomomycin is more.

Scorched earth.

It's a good analogy.

Oal Veno, 125 milligrams, four times a day.

For 10 days, it definitely kills C diff.

No question.

But it also wipes out a huge portion of the protective flora.

So, yes, you treat the infection, but you leave behind this , this empty landscape.

An ecological vacuum.

Perfect term.

And those dormant sea diff spores.

They wake up, find no competition, and boom recurrence.

Historically, rates were closer to 25% Sometimes higher.

Okay, so FyX sum icin sounds clearly better for preventing real lives.

Why isn't it just used all the time then?

Is it costs?

That's usually the main hurdle.

Yeah.

Fedx icing can be a lot more expensive than generic Venomeomycin.

So, you know, you have to weigh that lower recurrence risk against the immediate cost.

Real world medicine.

Absolutely.

So Venomeomycin is still a very valid, solid, first line choice. Especially if cost, or maybe insurance formula, it's a major issue.

Makes sense.

Now, what about those really high risk patients, older folks,munocompromised, maybe someone who had C diff six months ago..

Can we add something extra up?

Yes, there's bezletox amount.

It's interesting because it's not an antibiotic..

A monoclonal antib against toxin B. Ah, so it neutralizes the toxin, not the badacteria itself.

Exactly.

You give a single IV dose while they're getting their antibiotic treatment, like fedaxomyomycin or fuyin.

It doesn't kill C diff, but it mops up the toxin that causes the damage the symptom.

So it's like an extra layer of protection against relapse while the antibiotic does its work.

Precisely.

It significantly cuts down the risk of that rebound infection, especially in those vulnerable groups.

Okay, so that's the standard first approach.

But sometimes things go sideways, fast , Fulminant CDI, that sounds like the emergency alarm bell.

How do we define that?

Fulminant is severe complicated disease.

We're talking systemic toxicity.

Key signs are things like hypotension, shock,ias, where the bowel just stops working, or toxic megacolon, which is a massively dilated colon, usually or six centimeters, plus signs of sepsis.

So the patient is critically ill.

Treatment has to escalate immediately.

Immediately.

No question.

You move straight to what we call the fulminate bundle, maximum force.

And that bundle involves.

Hidosphomecin plus IV Metronid dol.

The V is 500 milligrams orally or down an NGube every six hours .

And crucially, IV Metronid dole, 500 millig.

Hold on.

IV Metronid, why intravenous if the infection's in the colon?

Okay, this is key.

In fulate disease, the colon is often isic, meaning poor blood supply, and it's not moving well.

It's a tonic.

Right.

Right.

So the strugetrate into thatamed , it gets into the inside.

The IVid through the blood into the sick bowel wall from the outside.

You need that two pronged attack.

Hitting it from both sides makes sense.

What if the alias is complete?

Like, nothing's moving through the gut at all.

Good point.

If Oal Van Pico is't going to reach the distal colon because of the alias, you add a third route, rectal Vomeomycin.

Okay.

How' that?

You give 500 milligrams ofomecin mixed in about 100 millil of tine as a retention enema every six hours. Ensures you get drug concentration right where it's needed .

And note, FeedX is not used here.

Its delivery is too unreable if the is paralyz.

This all sounds incredibly urgent.

What about surgery?

Call them immediately.

The moment you diagnose fulminate CDI, you get the surgical team involved.

And when do they actually operate?

The trigger point, the absolute threshold, is failure to improve clinically after, say , 24 to 48 hours of these maximal antibiotics, especially if they have confirmed toxic megacolon or their lactate level is climbing, particularly above 5 millimal.

Why the urgency for surgery, then?

Because at that point, the colon itself is often necrotic, dead tissue.

It's just acting as a reservoir, pumping out toxins.

Medical therapy won't fix that.

You need to remove the source, usually a subtotal collectomy for the patient to survive.

Wow.

Okay.

Grim scenario .

Let's shift back to the more common but still tricky problem, recurrence.

Patient finishes treatment, feels better, weeks later, diarrs back.

How do we confirm it's really CDI again?

Typically it's defined as return of symptoms, the diarrhea plus another positive CDI test. Usually within about eight weeks of stopping the last treatment.

And the strategy for this first recurrence, do we just try the same drug again?

No, that's generally not the best approach .

The key is to switch strategies based on why the first treatment likely failed.

It's about correcting the mechanism of failure.

Okay, walk us through the two main scenarios.

What if they got Van Kissen the first time?

If Vo failed, remember our scorched Earth problem, the likely issue was the collateral damage to the gut flora .

So the logical switch is to feed axomycin, standard 10 day course.

Use the sniper this time to spare the microbiome.

Exactly.

Give the remaining good flora a fighting chance to recover.

Usually no fancy dosing needed.

But what if they already had the sniper fit axomomycin and still recurred?

Ah, now, that's suggesting. A different problem.

If Faxxyin failed, it's less likely damage and more likely persistent .

T spores just keeperminating in waves. 10 day wasn't long enough to outlast them.

So we need a different tactic.

Right.

We need to change the timing strategy.

This is where you switch to Echomycin, taper and pulse regimen.

Taper and pulse sounds methodical.

How does that work?

It is.

You start with a standard Vanco course, maybe 10, 14 days, 125 milligram, four times daily .

Then you taper the frequency, maybe twice a day for a week, then once a day for a week.

And then comes the pulse.

It's the pulse being.

Giving that 125 milligram dose only every two or three days, and you continue that for several weeks, maybe two to eight weeks, depending on the situation.

So, short bursts of antibiotic separated by drug free periods.

What's the goal of those off days?

It's clever, actually.

The off period allows the native gut flora, whatever is left, some breathing room to try and recover and start making those protective secondary bids again.

Okay.

And the pulse is just new bact that managed to germinate during that brief antibiotic break .

It's prolonged suppression to break that cycle of germin while letting the ecosystem slowly heal.

Is there a similar prolonged strategy using Fedexomin?

Yes, for patients considered high risk where you still want that microbiome steering effect, there's an extended pulseed Fedaxon regimen.

It's 200 milligrams twice daily for five days, then it drops to 200 milligrams, just every other day out to day 25.

Same principle, prolonged pressure, but kinder to the flora.

Okay, but what happens when even these strategies fail?

Second, third recurrence?

Are we just stuck in this antibiotic loop?

This is where the paradigm really shifts.

After two or more recurrences, the odds of another antibiotic course working long term are just not good.

It's time to stop chasing the spores and focus on rebuilding the entire gut ecosystem.

And that means microbiota-ased therapies, FMT.

Exactly.

IMT.

Intestinal microbito transplant, is the broader term we use now.MT fecal microbito transplant usually refers to the older , less standardized donor stool method, but the goal is the same.

Restore that missing colonization resistance.

And we now have FDA approved options for this.

Yes, which is a huge step forward.

These are specifically approved to prevent further recurrence after you've treated the current active infection with antibiotics .

Timing is everything here.

Critical point.

So you finish the antibiotic course first, then you use these.

Absolutely critical.

Do not use them during antibiotic treatment.

The antibiotics will just kill the beneficial microbes you're trying to transplant.

Makes sense.

What are the approved products?

We have two main ones right now.

VAG and Ra.

Tell us about VOWS.

VIA is an oral capsule therapy.

It contains purified bacteriaal spores from healthy donors.

The patient takes four capsules, once a day, for three days straight, and they start this about two to four days after finishing their antibiotics.

There is a bowel prep needed beforehand, usually magnesium citrate.

Oal capsules sound convenient?

What about rebiota?

Rebiota is different.

It's a liquid suspension, given rectally.

It's a single, prep packaged 150 millilt dose administered by a healthcare provider, typically 24 to 72 hours after the last antibiotic dose.

So different delivery routes, but the same biological aim.

Precisely.

Both are designed to flood the g with a diverse community of beneficial microbes to basically outcompete any remaining CD spores and restore that natural balance.

And just to hammer at home, start these after antibiotics stop.

Cannot stress that enough.

Otherwise, you're just wasting the therapy.

Traditional FMT, using screen donor tool is still sometimes used maybe for patients who failed the approved products, or occasionally as a rescue therapy in very sphere cases where surgery isn't option.

Okay, that covers the treatment ladder.

But let's talk diagnosis for a second, because I know this causes a lot of confusion , especially with testing, the PCR test.

Ah, the PCR trap.

Yes.

Yeah.

This is probably the single biggest area for potential missteps.

So how should we be diagnosing active CDI?

Diagnosis really requires three things.

Compatible symptoms usually unexplained diarrhea, plus detection of a toxin producing strain.

And the problem with PCR or Nate's?

The PCR test is incredibly sensitive.

It detects the gene for the toxin, TCDB. Usually.

The issue is that gene material, or even dormant spores carrying the gene, can hang around for weeks or months after the patient is cured.

So a positive TCR doesn't automatically mean active infection.

Absolutely not.

If the patient is feeling well or even has diarrhea from another cause , a positive PCR alone often just means colonization.

They have the bug, but it's not actively causing disease.

How do we prove it as active disease right now, then?

You need to test for the actual toxin protein using an EIA, an enzyme ammino acay.

Detecting the toxin confirms the bacteria are alive , multiplying and actively producing the poisons that make the patient sick.

So the rule is, PCR positive, toxin negative, usually means.

Colonization.

Unless the patient is clearly crashing with fulminate disease, you do not treat colonization .

Adding more antibiotics just damages the recovering microbiome and sets them up for a real recurrence later.

Crucial distinction.

And what about diarrhea after successful treatment?

Test comes back negative, but they still have loose stools.

That's super common.

It's almost always post infectious IBS, or maybe some bile acid malabsorption.

The gut lining is still healing, the microbiome is still rebalancing it's full functional, not infectious.

So don't retest, don't retreat with antibiotics.

Please don't.

Yeah.

Supportive care, maybe a bacid binder trial, if it persists, but give the gut time to heal.

This all circles back to beautifully to that core concept we started with, colonization resistance.

It really does.

It's the unifying principle.

The healthy gut microbiome doesn't just passively take up space.

It actively fights back against C diffF.

And the key mechanism involves bacids, right?

Exactly.

This is fascinating.

Your liver makes primary bile acids to digest fat.

In a healthy gut, certain bacteria, like claustridium sindons, chemically modify these primary bacids into secondary bacid.

Okay.

And what do these different bacids do to C diff?

Primary bial acids actually act as a germination signal for C dis spores.

They tell the spores to wake up and start growing .

But secondary bol acids do the opposite.

They strongly inhibit spore germination.

Wow.

So the good bacteria literally create the chemical defense system that keeps C diffIF spores dormant.

That's it in a nutshell.

Antibiotics, especially broad spectrum ones like Van Gen, wipe out those crucial converter bacterials like Ccendons .

Primary b acids build up, secondary b acids disappear, and suddenly it's germination City for any sea diff spores lying around.

So the whole treatment ladder, fedaximescent to spare the converters, tapers to outlast germination waves, IMT to bring back the converters , it's all fundamentally about restoring that bassid balance.

That's the deep biological logic.

It's about either preserving or directly reinstalling the gut's natural chemical defense system.

That is a powerful way to look at it.

So, quick recap.

Fedaxximusspares the flora, taper pulse targets persistent spores , IT reboots the whole ecosystem, and surgery is for removing a necric tissue in fulminant cases.

You've nailed the core strategies, and it leads to a really interesting final thought.

Go on?

Well, think about it.

The most effective therapy we have for the toughest cases, recurrent CDI, is IMT.

And it works not by killing the bug better , but by restoring the gut's own chemical defenses those secondary bids.

Right.

So maybe the future of tackling infections like this isn't solely focused on finding the next stronger antibiotic.

Maybe it's more about finding clever, standardized ways to, you know, ecologically engineer or chemically manipulate the gut environment back to a state where it can defend itself.

Restoring health rather than just fighting disease ?

That's definitely something to mull over.

A different perspective on antiinfective strategy.

Indeed.

Well, that's all the time we have for this deep dive.