Infectious Colitis

[00:00] Host:

Unmasking GI Chameleons: The Campylobacter Appendicitis Mimic

You know, you’re scrubbed in.

It’s it’s 2:00 in the morning.

[00:03] Guest:

Oh yeah, the classic nightmare scenario.

[00:05] Host:

Right, a 45 year old patient rolled into the trauma Bay a few hours ago with, I mean, just exquisite, right?

Lower quadrant pain.

[00:15] Guest:

Let me guess, fever of one O 1 elevated white count?

[00:19] Host:

Exactly.

White count of 16,000.

Yeah, get the CT scan and there is prominent fat stranding right around the cecum.

[00:26] Guest:

So it looks like a a total slam dunk case of acute complicated appendicitis.

[00:32] Host:

100% You make your incision, you get into the abdomen and you look down.

[00:35] Guest:

And the appendix is completely pristine.

[00:37] Host:

Not a single hint of inflammation.

[00:39] Guest:

That’s perfect.

[00:40] Host:

But the terminal ilium and the cecum, they are angry, hyperemic and edematous.

[00:44] Guest:

Yeah, you just stepped on a massive diagnostic landmine.

[00:47] Host:

Called Campylobacter.

Yep, welcome to colorectal surgery Review.

Today we are taking a deep dive into the absolute chameleons of the gastrointestinal tract.

[00:56] Guest:

The infectious calidities.

[00:58] Host:

Exactly.

Now if you are listening to this, you are likely a practicing board certified colon and rectal surgeon.

[01:03] Guest:

You already know your way around the after, but.

[01:06] Host:

You know the gross anatomy, you know the standard operations, but our mission today for this deep dive is to extract the the highly clinical, incredibly relevant material that keeps us up to date as practicing clinicians.

[01:19] Guest:

The stuff that actually changes how you practice on a Tuesday afternoon.

[01:22] Host:

Precisely, we are pulling this from the latest comprehensive science on infectious colitis.

Specifically, we’re looking at the data compiled by Craig A Reichert and Maher A Abbas.

[01:32] Guest:

A fantastic detailed text.

[01:35] Host:

It really is.

We are hunting for those evolving practice change, the high stakes, medical legal pitfalls, and you know, the testable minutiae for your recertification exams.

[01:45] Guest:

Because The thing is, infectious colitis rarely introduces itself politely.

[01:50] Host:

It really doesn’t.

[01:51] Guest:

It masquerades.

It totally mimics our most common surgical emergencies a patient will present looking exactly like that acute appendicitis we just talked about.

[01:59] Host:

Or like a new onset severe Crohn’s disease flare.

[02:02] Guest:

Right.

Or even a right sided clonic malignancy.

So we are going to systematically breakdown the bacterial, parasitic, fungal and viral pathogens that lay these traps.

[02:13] Host:

And we will conclude with the ultimate diagnostic minefield, which is the immunocompromised patient.

[02:17] Guest:

The stakes there are incredibly high.

[02:20] Host:

For you, the surgeon, standing at the bedside or or staring at an endoscopic monitor, recognizing subtle histologic clues matters.

[02:29] Guest:

Or taking a careful geographic history.

[02:31] Host:

Exactly.

Knowing the absolute contraindications in medical management, I mean that can literally mean the difference between a patient having a routine recovery and a catastrophic surgical complication.

[02:42] Guest:

We’re talking toxic megacolon, profound sepsis, or a full thickness perforation.

[02:48] Host:

Because if you operate when you shouldn’t, or if you escalate immunosuppression when you should be giving an antimicrobial, the morbidity absolutely skyrockets.

[02:56] Guest:

Mortality too.

We really have to recalibrate our index of suspicion, and I think we should start with the most common encounters in clinical practice.

[03:03] Host:

The bacterial infection.

3:05Campylobacter: Complications, Resistance, and Azithromycin Shift

Let’s jump right back into that 2:00 AM operation.

We started with the campylobacter trap.

Statistically, this is the heavy hitter.

[03:12] Guest:

Right.

Oh, absolutely.

It is the most common cause of bacterial colitis worldwide.

Wow.

Yeah, we are looking at an incidence of roughly 25 to 30 paces per 100,000 people globally.

[03:25] Host:

And what about in the US?

[03:26] Guest:

Just shy of 20 per 100 those in here.

It’s usually contracted from contaminated food or water.

[03:34] Host:

Undercooked poultry is the classic culprit there.

[03:36] Guest:

Right, though unpasteurized milk and contaminated water sources are also massive vectors.

[03:43] Host:

Now the incubation period sits right around 2 to 4 days, but let’s look at the cellular mechanics of what actually happens when a patient swallows that contaminated chicken, because I always found this fascinating.

[03:53] Guest:

It’s pretty wild.

[03:54] Host:

The bacteria don’t just passively wash through the gut, they actually travel down, survive the gastric acid, and multiply in the bile.

[04:01] Guest:

Yeah, they are resilient.

[04:03] Host:

And then they actively invade the gastrointestinal mucosa all the way to the depth of the lamina propria.

[04:09] Guest:

That depth of invasion is critical.

You know it’s not a superficial toxin mediated wash, right?

The bacteria cause a really intense edematous enteritis and the specific tropism, like the areas they target most aggressively are the terminal ileum and the cecum.

[04:25] Host:

And there’s the exact setup for our 2:00 AM surgical nightmare.

[04:28] Guest:

Yep, intense localized mucosal and submucosal inflammation right at the ileocecal valve.

[04:34] Host:

Clinically, the patient is having right lower quadrant pain, fever, maybe some nausea and vomiting.

[04:39] Guest:

And usually there’s bloody diarrhea, but you know, if the patient hasn’t had a bowel movement yet, the clinical picture is totally identical to appendicitis.

[04:47] Host:

So if you aren’t actively putting infectious idolitis on your differential, you are taking that patient to the OR for an appendectomy they absolutely do not need.

[04:56] Guest:

Exactly.

And while taking a normal appendix out isn’t the end of the world.

[05:01] Host:

I mean, we’ve all done it.

[05:02] Guest:

Right, but subjecting a patient with an active systemic mucosal infection to the physiologic stress of surgery, general anaesthesia, and an enderotomy is just inviting complications.

[05:12] Host:

Totally.

But let’s talk about the complications of the disease itself, which are highly testable points for board exams.

[05:20] Guest:

Crucial for inpatient management too.

[05:22] Host:

Because while the illness is usually self limiting, over a week or so things can escalate.

[05:27] Guest:

Right.

The mucosal damage can be so severe that you see massive lower GI bleeding.

We can also see toxic colitis requiring intensive care.

[05:36] Host:

And then you have the systemic immunologic sequel A The molecular mimicry of Campylobacter is notorious.

[05:42] Guest:

Oh, it’s heavily tested.

The antibodies your immune system forms against the campylobacter cell wall antigens can cross react with human tissues.

[05:51] Host:

This is the mechanism behind post infectious reactive arthritis, right?

[05:54] Guest:

Formerly known as Ryder’s Syndrome, Yes.

[05:56] Host:

And most dangerously, killing Bar’s syndrome.

[05:59] Guest:

Exactly where the antibodies attack the myelin sheath of the peripheral nerves, leading to that scary ascending paralysis.

[06:05] Host:

So the stakes are really high.

Now let’s talk about a major practice change regarding management.

[06:10] Guest:

This is a big one.

[06:11] Host:

Let’s say this patient is hospitalized, they’re toxic, they have severe bloody diarrhea, and you decide you need to initiate antimicrobial therapy.

Historically, for a gram negative enteric rod like this, surgeons instinctively reached for a fluoroquinolone.

[06:28] Guest:

Oh yeah, Ciprofloxacin was handed out like candy.

[06:32] Host:

Right.

And that is exactly where the practice has drastically evolved.

[06:35] Guest:

Because that historical reliance on fluoroquinolones has created a massive resistance problem.

[06:40] Host:

How bad is it?

[06:41] Guest:

We are currently seeing over 25% resistance to fluoroquinolones in the United States and in some parts at the globe, particularly areas with heavy agricultural use of the drug, resistance approaches an astounding 80%.

[06:54] Host:

80% So if you empirically start a sick patient on Cipro today, there is a very good chance you are doing absolutely nothing to the bacteria.

[07:03] Guest:

Basically nothing, which is why the current standard and a highly testable practice update is to use azathromycin.

[07:09] Host:

A Macrolite.

[07:10] Guest:

Yes, azithromycin is now considered almost as effective as fluoroquinolones were historically, but it boasts significantly lower rates of dry resistance.

[07:20] Host:

And a typical course is just three days.

[07:22] Guest:

Nice and short.

[07:23] Host:

But what about the shedding phase?

You treat the patient, their symptoms resolve.

They want to go back to work.

Maybe they work in food service or healthcare.

[07:31] Guest:

You have to counsel them heavily on hand hygiene.

[07:34] Host:

Because they’re still contagious.

[07:35] Guest:

Highly up to 16% of patients can have persistent colonic colonization and fecal shedding for up to 10 weeks after the acute symptoms resolve.

[07:45] Host:

10 weeks, I mean, that’s a massive window for community transmission.

[07:49] Guest:

It really is.

[07:49] Host:

So we’ve solved the appendicitis mimic.

We avoid the unnecessary operation.

We give azithromycin instead of fluoroquinolone and we watch for a Guillain bar.

[07:57] Guest:

Perfect.

7:58Yersinia & GI TB: Avoiding the Crohn’s Disease Trap

But what happens when the clinical picture isn’t acute right lower quadrant pain?

[08:03] Guest:

The slow burners, right?

[08:05] Host:

What happens when a patient presents with chronic grumbling, right sided pain, weight loss and diarrhea and the inflammatory markers point toward a long term disease process like inflammatory bowel disease?

[08:17] Guest:

This is where surgeons get lured into the Crohn’s disease trap.

[08:19] Host:

The Crohn’s disease mimics are incredibly insidious, and the two primary culprits you must know inside and out are Eusinia and gastrointestinal tuberculosis.

[08:28] Guest:

Let’s start with Eusinia and Teracolitico.

[08:31] Host:

The classic transmission route here is handling contaminated animals.

[08:34] Guest:

Farming communities.

Abattoir workers.

[08:37] Host:

Or ingesting undercooked pork, particularly chitterlings or contaminated unpasteurized milk products.

[08:43] Guest:

And the symptom timeline is what starts to push you away from an acute bacterial infection and toward an IBD diagnosis.

[08:51] Host:

Because it lingers.

[08:52] Guest:

Exactly.

The diarrhea, the low grade fevers, the smoldering abdominal pain.

These can easily last up to 21 days or more.

[08:59] Host:

But the real trap is what you see when you scope them.

You take this patient to the endoscopy suite to work up suspected Crohn’s.

[09:06] Guest:

You intubate the terminal ileum.

[09:08] Host:

And you see massive mesenteric adenitis and a severe ileitis.

You look at the right colon and you see distinct mucosal erosions.

[09:17] Guest:

Visually, grossly, it looks perfectly like Crohn’s disease.

[09:20] Host:

And the deception extends beyond the gut, too.

[09:23] Guest:

Just like Campylobacter, Ursinia triggers extra intestinal manifestations.

Patients can develop migratory polyarthritis and erythema nodosum.

[09:32] Host:

Those painful red subcutaneous nodules on the shins.

[09:35] Guest:

Yeah, usually on the anterior shins.

[09:38] Host:

I mean if I have a 25 year old patient with right sided colonic erosions, terminal iolitis, and areadimenodosum, my brain immediately screams inflammatory bowel disease.

[09:48] Guest:

Of course it does.

I’m.

[09:49] Host:

Getting ready to consult gastroenterology to start steroids and biologics.

[09:52] Guest:

And if you do that, if you initiate heavy aminosuppression on a patient with an active Ursinia infection, you will induce A fluorid bacteremia and potentially fatal sepsis.

[10:02] Host:

It is a massive diagnostic dilemma.

[10:04] Guest:

It really is.

[10:05] Host:

So how do we avoid it?

If the endoscopy looks like Crohn’s and the extra intestinal symptoms look like Crohn’s, how do we catch the Ursinia?

[10:12] Guest:

That’s the challenge.

[10:13] Host:

Because from what I understand, standard stool isolation methods like the routine cultures we order everyday frequently fail to identify.

[10:21] Guest:

It they absolutely do.

Standard stool cultures are often grown at body temperature right around 37°C.

Sure, but Yersinia is unique.

It prefers cooler temperatures for optimal in vitro growth around 25°.

[10:34] Host:

So it literally just gets missed on routine plating.

[10:37] Guest:

Yes, to catch it you have to specifically suspect it based on their history, maybe that farming exposure, and then order specialized testing the.

[10:46] Host:

Literature specifically highlights hemagglutinin testing, looking for titers in a 1 to 128 ratio.

[10:53] Guest:

Yes, the hemoglutinin titers are a classic board review marker.

Though practically speaking, in a modern well equipped hospital you are going to rely on Multiplex PCR based stool assays that specifically target the Ursinia virulence genes.

[11:09] Host:

OK, so that’s Ursinia, but there’s another pathogen that mimics Crohn’s disease so perfectly that it’s a global crisis, particularly in developing nations or for immigrant populations.

[11:18] Guest:

Mycobacterium tuberculosis.

[11:20] Host:

Right.

We are so conditioned to think of TB strictly as a pulmonary disease.

[11:25] Guest:

Which is a dangerous oversight for a general or colorectal surgeon.

Gastrointestinal TB is a highly destructive entity.

[11:33] Host:

I want to break down the path of Physiology here because the mechanism of how it gets to the bowel is just fascinating.

[11:39] Guest:

It’s a journey a.

[11:40] Host:

Patient has primary pulmonary TB.

They are coughing up heavily infected sputum, but instead of spitting it all out, they swallow a portion of it.

[11:48] Guest:

Millions of mycobacteria traveled down the esophagus, survived the stomach acid thanks to their waxy mycolic acid cell wall, and they land in the GI tract.

[11:57] Host:

And the lymphoid tissue in the terminal ilium and cecum.

The pyre’s patches are incredibly rich.

[12:02] Guest:

The mycobacteria recognize this immune dense area, invade, and set up a granuloma disinfection.

[12:07] Host:

So again, you have massive inflammation centered squarely on the iliacolic region.

[12:11] Guest:

In mimics complicated appendicitis or new onset Crohn’s.

[12:14] Host:

But what?

Really really strikes me as imaging.

You get a C key scan of the abdomen and you see massive dissemination.

There is thick complexes sites, there is extensive omental infiltration and caking.

[12:25] Guest:

To the untrained eye, or even to a seasoned surgeon, that CT scan looks exactly like advanced peritoneal carcinomatosis.

[12:33] Host:

It looks like a disseminated ovarian or GI malignancy or a severe perforating granulomatous disease.

[12:39] Guest:

You see a scan like that and the surgical instinct is to get a tissue diagnosis.

[12:44] Host:

You want to schedule a diagnostic laparoscopy?

Maybe take out that inflamed ileocecal segment to cure the problem.

[12:50] Guest:

But here is the critical take away for the practicing surgeon.

What are the absolute surgical indications for GITB?

[12:57] Host:

They are incredibly narrow.

[12:59] Guest:

Very surgical intervention for gastrointestinal tuberculosis is strictly reserved for two very specific scenarios.

[13:06] Host:

Scenario one being.

[13:07] Guest:

It is completely undiagnosed case, the patient is deteriorating and you absolutely need a tissue biopsy to establish the diagnosis because all non invasive workups have failed.

[13:17] Host:

And scenario 2.

[13:17] Guest:

You already know the patient has TB, but the disease has progressed to a mechanical catastrophe.

[13:22] Host:

Meaning the granulominous influence inflammation has healed with severe fibrosis creating a stricturing hard bowel obstruction.

[13:28] Guest:

Exactly.

Or the ulcers have eroded full thickness and caused a free perforation.

[13:34] Host:

Right.

You operate to fix the mechanical plumbing problem, you fix the hole or you bypass the stricture.

You do not operate simply to resect the inflammation.

[13:42] Guest:

Never if you perform a massive ileocolectomy on a patient with active medically untreated GI TB.

Just to quote remove the disease you are cutting through actively infected inflamed friable tissue just.

[13:55] Host:

Going to fall apart.

[13:56] Guest:

The anastomosis is almost guaranteed to leak, the patient will develop devastating interocutaneous fistulas, and the mortality rate is horrendous.

[14:04] Host:

So the primary treatment for GI TB is always always 6 to 9 months of systemic anti tubercular chemotherapy.

[14:11] Guest:

Surgery is just for the structural failures.

14:14STEC: The Deadly Contraindications of Antibiotics & Antidiarrheals

Let’s pivot now.

We’ve talked about the appendicitis mimic, and we’ve talked about the Crohn’s mimics.

I want to transition to a pathogen that lays perhaps the most dangerous medical management trap of all, a situation where our standard reflexive doctoring instinct actually kills the patient.

[14:30] Guest:

Oh, this is a huge topic.

[14:32] Host:

I’m talking about Escherciacoli, specifically the S tec pathotype.

[14:36] Guest:

The E coli landscape is incredibly broad.

For the most part, you know E coli is a normal, highly beneficial part of our colonic flora.

[14:44] Host:

It synthesizes vitamin K.

It competes with pathogens.

[14:47] Guest:

Right, but there are 5 distinct pathotypes conclusively associated with virulent diarrhea for the colorectal surgeon.

The one we must focus on heavily is SEC.

[14:56] Host:

She got toxin producing E coli.

[14:58] Guest:

Yes.

You may also see it referred to in older literature as EHEC or enter a hemorrhagic E coli.

[15:06] Host:

Now when we say SEC, almost everyone’s mind immediately jumps to the O 157 dot H7 strain the.

[15:12] Guest:

Famous one by.

[15:13] Host:

The strain that gained global notoriety in the 1980s and 90s heavily associated with massive outbreaks from undercooked ground beef at fast food chain.

[15:21] Guest:

Cows are the primary reservoir, so beef and unpasteurized milk are the usual vectors.

[15:25] Host:

Well, O 157 is incredibly dangerous.

Focusing solely on it is a massive epidemiologic trap.

A.

[15:30] Guest:

Huge trap.

A crucial piece of data from the current literature is that non O 157 strains actually account for 75% of SEC infections today.

[15:38] Host:

Let me repeat that because it is vital. 75% of these infections are not O 157.

Yep.

Why does that matter practically?

Because if you send a stool sample to the lab and just order a specific culture for O 157 and it comes back negative, you might falsely conclude the patient doesn’t have a Shiga toxin infection.

[15:56] Guest:

And that false sense of security leads to deadly mismanagement.

[16:00] Host:

You cannot rule out STEC with just an O 157 plate.

[16:03] Guest:

No, you need a stool analysis that specifically assays for the presence of the Shiga toxin itself, regardless of the bacterial strain producing it.

Or you must use a rapid Multiplex PCR panel.

[16:16] Host:

And here’s why diagnosing it correctly is so paramount.

This is the absolute board review.

Medical legal.

Do not do not miss contraindication.

Let’s take the clinical picture.

[16:26] Guest:

OK, let’s do it.

[16:26] Host:

You are on call.

The ER docs consult you.

For a 30 year old patient with severe crampy abdominal pain and a massive, frankly, bloody diarrhea, they’re going to the bathroom 20 times a day just passing blood and mucus.

Sounds awful.

Intuitively, as a physician, your instinct is to stop the suffering.

16:45

You want to stop the diarrhea with an anti motility agent like loperamide, or you want to kill the bacteria causing the bleeding by hanging a bag of broad spectrum IV antibiotics.

But current guidelines state that using anti motility agents or antibiotics in this specific scenario is like throwing gasoline on a fire.

17:04

I use that analogy deliberately.

Why?

Why does our standard therapeutic instinct make things exponentially worse here?

[17:12] Guest:

This is perhaps the most vital clinical principle we will discuss today.

Let’s breakdown the mechanics.

The danger of STACK isn’t really the bacteria itself, it’s the Shiga toxin it produces.

If you give an anti motility agent like lopramide, you are paralyzing the gut.

17:27

You are stopping the peristalsis that the body is desperately using to flush the pathogen out.

[17:32] Host:

So intuitively, using loperamide isn’t just masking the symptom, it’s basically boarding up the wind rig while the house is filling with carbon monoxide.

[17:40] Guest:

That’s a great way to put it.

By increasing the intestinal transit time, you are causing the bacteria and the toxin to stagnate in the colon.

[17:47] Host:

Which means more time for the body to absorb it.

[17:49] Guest:

Exactly.

This dramatically increases the time the colonic mucosa is exposed to the Shiga toxin, leading to massive systemic absorption.

[17:57] Host:

Now what about antibiotics?

Why not just kill the bug, Kill the factory, stop the the toxin?

That’s the logic.

[18:04] Guest:

It’s logical, but fatally flawed here.

When you introduce an antibiotic, you put extreme stress on the bacterial cell wall.

Right as the bacteria undergo stress, or as they physically undergo cell lysis and burst open, they release all of their preformed intracellular Shiga toxin at once into the gut lumen.

[18:22] Host:

A massive, sudden surge of poison.

[18:25] Guest:

Exactly.

And that sudden exponential surge in toxin absorption directly damages the endothelial cells of the microvascular.

[18:31] Host:

It triggers a cascade.

[18:32] Guest:

A terrible one.

It leads to hemolytic uremic syndrome or HUS.

[18:37] Host:

HUS is a life threatening, often fatal triad.

[18:40] Guest:

It causes a microangiopathic hemolytic anemia, where red blood cells are literally sheared apart as they pass through damaged capillaries.

[18:48] Host:

It consumes platelets, leading to profound thrombocytopenia and bleeding risks.

[18:52] Guest:

And it brutally damages the micro vessels of the kidneys, leading to anuric acute kidney injury requiring dialysis.

[19:01] Host:

Throwing gasoline on the fire, you give lopromide and ciprofloxacin to a patient with bloody diarrhea, and three days later they are in the ICU on a ventilator requiring continuous renal replacement therapy.

[19:13] Guest:

So the treatment for SEPTEC is strictly supportive aggressive early IV hydration to maintain renal perfusion.

[19:20] Host:

Careful correction of electrolyte derangements.

[19:22] Guest:

No antibiotics, no anti motility agents.

You support the patient’s Physiology and let their immune system clear the infection naturally.

[19:30] Host:

That is an incredible reminder of why we can’t just practice algorithm medicine without understanding the underlying biology.

[19:37] Guest:

We really can’t.

19:38Salmonella, Shigella, Vibrio: Key Clinical Pearls & Management

Let’s round out the bacterial roster with some rapid fire clinical pearls from the text.

Pathogens that might not have a massive surgical decision tree, but are heavily tested and frequently encountered.

Let’s start with Salmonella.

[19:50] Guest:

Salmonella is broadly divided into non typhoidal strains and typhoidal strains.

[19:54] Host:

Typhoid fever specifically describes a severe systemic presentation.

[19:59] Guest:

Right, it’s not just diarrhea, it’s high prolonged fevers, profound lethargy or delirium, and often a faint salmon colored maculopapular rash on the trunk known as rose spots.

[20:10] Host:

And this entire cascade relates to the fact that the bacteria don’t stay in the gut, they cross the mucosa and cause a true bacteremia.

[20:18] Guest:

Exactly.

[20:19] Host:

And the classic transmission route for the non typhoidal Salmonella is taught in medical school as the five FS food, feces, fingers, fomites and flies.

[20:28] Guest:

Highly contagious through poor sanitation for the average healthy adult.

Non typhoidal salmonella is self limited.

You don’t treat it.

[20:36] Host:

But there are exceptions.

[20:37] Guest:

Yes, you must recognize the frail populations if the patient is an infant, elderly, profoundly immunocompromised, or if they have a known vascular graft or prosthetic joint.

[20:47] Host:

Where a transient bacteremia could see the devastating hardware infection.

[20:50] Guest:

Exactly.

Then you reach for antibiotics and again fluoricomolones or third generation cephalosporins are typical, though you must verify local sensitivities.

[20:59] Host:

Next on the rapid fire list is Shigella.

[21:01] Guest:

Shigella typically involves contaminated drinking water or recreational water exposure.

It is highly virulent.

It takes a very small inoculum to cause disease.

[21:11] Host:

It starts as a watery non bloody diarrhea but rapidly progresses to its severe bloody colitis with profound tenesmus.

[21:19] Guest:

That constant painful urge to pass stool even when the vault is empty due to the intense rectal inflammation.

[21:26] Host:

And the crucial detail here involves the shedding and the treatment paradigm.

[21:29] Guest:

Right.

Patients can continue to shed the Shigella Organism in their feces for up to six weeks, completely asymptomatic.

[21:36] Host:

But despite this prolonged shedding, empiric antibiotic treatment is generally not advisable.

It’s not why?

I mean, if they are shedding A virulent pathogen for a month and a half, why aren’t we treating everyone to eradicate it?

[21:48] Guest:

Because of explosive, globally rising antibiotic resistance, if we blanket treat every case of Shigella, we will run out of effective drugs.

[21:57] Host:

So you only treat high risk populations where public health transmission is a massive concern.

[22:02] Guest:

We are talking about food handlers, childcare providers or institutionalized patients.

[22:06] Host:

And even in those select groups, you strictly limit the antibiotic course to a short three to five day burst, guided purely by the specific culture sensitivities, not empiric guessing.

[22:18] Guest:

Exactly right.

[22:19] Host:

What about Vibrio?

[22:20] Guest:

Vibrio infections are universally linked to marine environments, specifically the consumption of raw or undercooked shellfish like oysters.

[22:28] Host:

We have to clearly differentiate the species here, right?

Yes.

[22:31] Guest:

Vibrio parahemolyticus causes a miserable but generally self limited watery diarrhea, but Vibrio cholerae, specifically the toxigenic strains O1 and O 139 is a completely different beast.

[22:44] Host:

Cholera is terrifying from a physiological standpoint.

The cholera toxin doesn’t destroy the bowel wall like an amoeba, it fundamentally hijacks the cellular machinery.

[22:53] Guest:

It irreversibly binds to the adenylate cyclist complex, causing massive cyclic AMP production.

[22:59] Host:

This forces the CFTR chloride channel to lock in the open position.

[23:03] Guest:

Which means the crypt cells are just pumping chloride ions into the bowel lumen and water follows osmotically at an incredible rate.

[23:09] Host:

The current literature notes that a patient with severe cholera can lose up to one liter of fluid per hour.

[23:14] Guest:

One liter per hour.

[23:16] Host:

A standard human has roughly 5 liters of blood.

At that rate, you are staring down profound dehydration, acute renal failure and lethal hypovolemic shock within hours.

[23:29] Guest:

The medical management here isn’t a casual liter of saline, it is massive, aggressive, high volume crystalloid resuscitation, often requiring multiple large bore Ivs.

[23:40] Host:

Once you are replacing the fluid, you give a single large dose of ciprofloxacin or doxycycline to shorten the duration of the diarrhea.

[23:48] Guest:

To quickly finish the bacterial landscape, we should briefly note Arimonas.

[23:52] Host:

Right, which causes a watery diarrhea you should suspect in travelers to developing nations often treated with fluoroquinolones.

[23:59] Guest:

Is bacteroids fragilis normally a friendly commensal but it has a specific subclass that secrets an entero toxin causing disease?

[24:06] Host:

And finally, Listeria monocytogens.

[24:09] Guest:

Listeria is famous for surviving in cold temperatures, which is why it’s linked to deli meats and soft cheeses.

[24:14] Host:

In healthy adults it might just cause a mild gastroenteritis, but it is highly lethal to pregnant women and the immunocompromised, frequently causing meningitis.

[24:23] Guest:

If you identify a GI Listeria infection in an immunocompromised individual, you must treated aggressively, specifically using trimethoprim sulfamethoxazole.

24:34Amoebiasis: Flask Ulcers, Amoebomas, and Surgical Pitfalls

Which perfectly sets the stage for how much a patient’s immune status, their diet, and their geographic history truly matters.

[24:42] Guest:

It’s everything.

[24:43] Host:

And that takes us from the bacterial mimics to the second major category of our deep dive.

[24:48] Guest:

The parasitic calidities.

[24:49] Host:

When modern urban surgeons hear the word parasites, we often default to thinking of Tropical Medicine.

We think of medical mission trips or textbooks from the 1950s, right?

But with massive global travel, shifting immigration populations and culinary trends, these pathogens are a very real presence in everyday clinical practice, whether you operate in London, New York or rural Ohio.

[25:13] Guest:

They absolutely are, and while bacteria primarily cause disease through toxins or superficial mucosal inflammation, parasites operate differently.

[25:21] Host:

Many of them physically destroy tissue where their sheer physical mass causes mechanical problems in the gut.

[25:27] Guest:

Let’s start with a parasite that literally consumes human flesh and amoeba hystolytica.

[25:32] Host:

The causative agent of amoeba colitis.

The pathophysiology here is elegant and brutal.

[25:38] Guest:

A human ingests the mature amoebic cysts via fecal oral contamination, usually tainted water.

[25:44] Host:

These cysts are incredibly Hardy.

They survive the stomach acid easily, but once they hit the lower GI tract, they undergo exestation.

[25:52] Guest:

They break open and release active motile trophozoites.

[25:56] Host:

And these trophozoites are highly invasive.

They secrete proteases that literally melt away the mucosal lining, allowing them to Burrow deep into the colonic wall.

[26:05] Guest:

And as they Burrow, they leave a very specific, highly testable architectural signature.

[26:10] Host:

If you were taking a board exam, or if you were reading a pathology report from a colonic biopsy, the pythognomonic phrase you are looking for is deep flask shaped ulcers.

[26:20] Guest:

Let’s visualize that why Flask shaped?

[26:22] Host:

Well, because the initial point of entry through the mucosa is relatively narrow, but once the trochozoids reach the submucos, which is looser and heavily vascularized, they spread out laterally, consuming tissue in all directions.

[26:34] Guest:

So you have a narrow neck at the surface and a wide necrotic base underneath a flask.

Exactly.

And the surgical relevance of these deep burrowing ulcers is immense.

[26:44] Host:

It’s terrifying because they don’t always stop at the subbucosa.

They can keep eating right through the muscularis propria and the serosa, leading to a full thickness blowout of the colon.

[26:54] Guest:

The literature sites an incredible landmark 30 year study from a surgical group in Mexico City that highlights just how lethal this is.

[27:02] Host:

Yes, that study is a cornerstone in understanding surgical amoebiasis.

They looked retrospectively at patients who suffered acute colonic perforations from amoebic colitis.

[27:13] Guest:

They identified 112 cases of perforation over 3 decades.

[27:18] Host:

Here are the staggering statistics you need to know.

Over 90% of those perforations occurred in the right colon.

[27:23] Guest:

74% of those patients didn’t just have one hole, they had multiple perforations scattered across the right colon.

[27:29] Host:

And the mortality rate was a massive 40%.

[27:32] Guest:

40% mortality.

[27:33] Host:

Almost half the patients who perforated died even with surgery.

Why is it so unique, lethal compared to say, a perforated diverticulitis?

[27:41] Guest:

Because you aren’t just dealing with a mechanical hole spilling stool, you are dealing with a bowel wall that is actively being digested by millions of parasites.

[27:50] Host:

The tissue is profoundly friable.

[27:52] Guest:

It’s like trying to suit your wet tissue paper.

If you try to do a primary anastomosis in that environment, it will fail 100% of the time.

The tissue simply will not hold a staple or a stitch.

[28:03] Host:

So if you are dealing with a right colon perforation and a patient with a travel history to an endemic area like Central or South America, Africa, Southeast Asia, you must consider amoebiases and you must plan for wide resection and fecal diversion.

[28:18] Guest:

But amoebiases doesn’t just present as an acute, sudden perforation.

It can also be a slow burn that creates a massive diagnostic illusion.

Right.

If the body tries to wall off this parasitic invasion, it mounts an intense, chronic inflammatory response.

[28:34] Host:

Over months, this creates a large fibrous granulomatous mass in the wall of the colon known as an amoebama.

[28:40] Guest:

Clinically, the patient presents with weight loss, anemia and obstructive symptoms.

You get ACT scan and there’s an apple core lesion in the ascending colon.

You do a colonoscopy and you see a bulky fungating mass.

[28:54] Host:

Visually, radiographically and endoscopically it looks exactly like a locally advanced right sided colon cancer.

[29:01] Guest:

You would be fully prepared to do a formal right hemiclectomy with an oncologic lymph node harvest.

[29:06] Host:

And if you just took a superficial biopsy of the overlying inflamed mucosa, you might miss the trophozoites deep in the mass.

[29:13] Guest:

You really have to have a high index of suspicion checking serum amoebic antibodies or stool PCR to avoid doing a major cancer operation for a curable parasitic infection.

[29:24] Host:

We also have to mention the X-ray intestinal complications of E histolytica.

The trophozoites don’t always stay in the bowel wall.

They can invade the mesenteric venules and get swept up into the portal circulation.

[29:34] Guest:

Which takes them directly to the liver.

[29:36] Host:

There they carve out massive spaces filled with a necrotic a cellular debris, the classic anchovy paste exudate of an amoebic liver Abscess.

[29:45] Guest:

And the text notes these abscesses, particularly in the right lobe of the liver, can actually erode right through the diaphragm and rupture into the pleural space of the chest cavity, leading to an amoebic empyema or a lung Abscess.

[29:59] Host:

It’s a systemic destroyer.

Yeah.

Let’s talk about the medical treatment.

Let’s say you’ve confirmed active amoebic colitis with APCR test.

What is the pharmacological strategy?

[30:08] Guest:

If the patient has invasive tissue disease, active colitis, or a liver Abscess, the first line therapy is a 10 day course of systemic metronidazole.

[30:18] Host:

This kills the tissue invading trophozoids.

[30:20] Guest:

Correct.

[30:21] Host:

But wait, if I give 10 days of Flagyl and the patient’s symptoms resolve, the ulcers start healing.

Why can’t I just stop there?

Aren’t we done?

[30:28] Guest:

No, and this is a frequent, dangerous oversight.

Metronidazole is excellent at penetrating tissues, but it is very poorly active against the dormant cysts sitting freely in the gut lumen.

[30:38] Host:

So if you stop at metronidazole, the active diseases cure, but the patient remains an asymptomatic cyst passer.

[30:44] Guest:

They will continue to shed the parasite into the water supply and more importantly, those cysts can exist months later causing a massive relapse.

[30:51] Host:

You must follow the metronidazole with a luminal agent, typically paramomycin or iodoquinol, to completely eradicate the cystic reservoir in the gut.

[31:00] Guest:

10 days of systemic therapy followed by luminal eradication.

That’s the complete package.

31:05Sushi Worms & Megacolon: Anisakidosis and Chagas Disease

OK, from flask shaped ulcers we move to a parasite heavily tied to modern culinary habits and it’s psychedosis.

[31:13] Guest:

This infection is directly related to the consumption of raw or inadequately cooked marine fish and squid.

[31:19] Host:

We’re talking about sushi, sashimi, ceviche.

[31:22] Guest:

The life cycle involves marine mammals and crustaceans, but humans become accidental hosts.

When we eat the infected raw fish, the larvae entered the GI tract.

[31:31] Host:

Most reported cases, particularly out of Japan where the raw fish diet is ubiquitous, involve the stomach, but roughly 4% of cases involve the colon.

[31:40] Guest:

And the pathophysiology here isn’t a toxic cascade, it’s a profound localized allergic reaction.

[31:46] Host:

The larva physically Burrows into the muscular wall of the bowel.

[31:49] Guest:

They can’t complete their life cycle in a human, so they die there, but their presence and their antigens trigger a massive hypersensitivity reaction characterized by dense infiltrates of eatslanophils and the formation of granulomas.

[32:02] Host:

So clinically, what does a focal 3 centimeter area of intensely inflamed, thickened bowel wall packed with granulomas look like on ACT scan?

[32:12] Guest:

It looks exactly like acute appendicitis, severe terminal ileitis, or acute diverticulitis.

[32:17] Host:

The bowel wall is thick, there is localized fat stranding, maybe even a small micro perforation.

[32:23] Guest:

The diagnostic trap is that the imaging and the physical exam scream acute surgical abdomen.

[32:29] Host:

The clinical literature notes that anasagidosis is very often diagnosed purely via surgery.

You take the patient to the OR at midnight for suspected acute appendicitis.

You find a severely inflamed segment of ileum.

[32:41] Guest:

You do an ILEA cystectomy to remove the problem, send the specimen to pathology, and three days later the pathologist calls and says there’s no appendicitis, but the bowel wall is full of dead worm larvae and eosinophils.

[32:52] Host:

It’s an incidental retrospective diagnosis.

[32:55] Guest:

Now, if you are lucky enough to suspect it preoperatively, say the patient had massive sushi consumption a few days prior and their CBC shows an unexplained peripheral EOC enophilia, you might diagnose it medically.

[33:07] Host:

In that rare case, A7 to 21 day course of albendazole can be effective.

[33:13] Guest:

But most colonic cases meet the scalpel first.

[33:16] Host:

Another crucial geographically distinct parasite for the colorectal surgeon to understand is Trypanosome mcruzi, the agent of Chigus disease.

[33:25] Guest:

Endemic to Central and South America, transmitted by the reduvid bug or the kissing bug, the acute phase of the infection is often mild and resolved spontaneously, but the parasite then enters A latent phase that can last for decades.

[33:39] Host:

And the board testable pathology here is what the parasite is doing during that latency.

It isn’t just sleeping, it is slowly causing chronic progressive destruction of the autonomic ganglion cells within the gastrointestinal tract and the heart.

[33:53] Guest:

Specifically, it destroys the enteric nervous system the My Enteric Plexus of Auerbach.

[33:58] Host:

And when you destroy the nerves that coordinate peristalsis, you get profound dysmotility.

Over years, the bowel dilates massively because it lacks the tone and the coordinated contractions to move content forward.

[34:11] Guest:

The patient develops a massive megacolon and often a Meg esophagus.

[34:15] Host:

They present to your colorectal clinic in their 50s or 60s with intractable, life altering Constipation.

They haven’t had a bowel movement in three weeks.

[34:24] Guest:

Or they present to the ER in absolute extremists with a massive colonic volvulus where the dilated, redundant sigmoid colon has twisted on its mesenteric axis, cutting off its own blood supply.

[34:37] Host:

And here is the sobering fundamental surgical principle regarding Chagas.

Surgery is palliative, not curative.

[34:44] Guest:

When you take a patient with a chagassic sigmoid volumes to the OR and you resect that massive dilated floppy segment of colon, you are purely fixing the mechanical plumbing problem.

You are preventing gangrene and restoring transit.

[34:56] Host:

But you have done absolutely nothing to cure the underlying Trypanosoma cruzi infection.

[35:00] Guest:

The parasite is still in their system, still damaging their hearts, still damaging the rest of their gut.

[35:05] Host:

They absolutely require referral to infectious disease for medical treatment with specialized agents like denzinidazole.

35:13Ascaris, Strongyloides, Schistosomiasis: The World of GI Parasites

We’ve covered the amoebas and the protozoans.

Now we need to discuss the helmets and the nematodes, the worms.

[35:20] Host:

It’s not the most pleasant topic for the squeamish, but the global scale is undeniable.

Let’s start with Ascarius lumbaricoids.

[35:28] Guest:

This single parasite infects up to 1.2 billion people globally.

It is an enormous public health burden.

[35:35] Host:

And the life cycle is something out of a science fiction movie.

The human host consumes the eggs via contaminated soil or food.

The eggs hatch into larvae in the small intestine.

[35:45] Guest:

But they don’t just stay there and grow, they penetrate the intestinal wall and to the venous, return and travel through the heart into the lungs.

[35:52] Host:

They break out of the pulmonary capillaries into the alveoli, causing a transient pneumonitis.

They crawl up the bronchial tree to the trachea, get coughed up into the pharynx, and are swallowed back down into the GI tract.

[36:03] Guest:

Only then, after that massive migration, do they settle in the small bowel and mature into adult worms.

[36:08] Host:

And these adult worms are not microscopic.

They look like large earthworms.

He can live for up to two years in the human gut, with the females producing hundreds of thousands of eggs a day.

[36:18] Guest:

From a surgical perspective, a heavy worm burden creates A purely physical mechanical problem.

[36:24] Host:

A tangled ball of dozens or hundreds of adult worms can completely obstruct the lumen of the small bowel.

[36:30] Guest:

The patient presents with a classic mechanical small bowel obstruction, cramping distension, bilious vomiting.

On imaging, you might actually see the outline of the worm mass.

[36:42] Host:

The surgical management is unique.

If you operate for an Ascaris obstruction, you try to avoid cutting the bowel open if possible, because the worms can migrate through the suture line and cause a leak.

[36:51] Guest:

The preferred technique is to manually milk the mass of worms distally crushing them gently or pushing them through the ileo sickle valve into the colon where they can be passed in the stool.

[37:02] Host:

If the bowel is ischemic, of course a formal resection is unavoidable.

[37:07] Guest:

Physical reality of milking a bolus of worms through the ileum is something every surgeon remembers.

Let’s move to stranguloids.

Stychoralis.

[37:14] Host:

This is highly relevant because while it’s prevalent in the tropics, there is a notable established endemic incidents right here in the United States, particularly in the rural Appalachian areas.

[37:25] Guest:

Stranguloids is insidious because of its auto infection cycle.

Most parasites require the eggs to leave the host and mature in the soil, but with stranguloids, the larvae can actually hatch and mature within the human gut and then immediately penetrate the colonic mucosa or the perianal skin to restart the cycle.

[37:42] Host:

This means a patient who acquired the infection 50 years ago in military service can still be actively infected today with 0 new external exposures.

[37:51] Guest:

And when it manifests in the colon, it causes a severe pancolitis.

The mucosa is edematous, friable and ulcerated.

To the endoscopist.

It perfectly mimics a severe pan ulcerative colitis.

[38:02] Host:

First line treatment here is distinct.

Ivermectin for two days is highly effective.

[38:06] Guest:

Next on the list of nematodes is Tricurus tracheura, commonly known as the whipworm.

[38:11] Host:

For board exams, Tricurus is heavily tied to visual microscopy clues.

If they show you a picture of stool microscopy featuring distinct barrel shaped eggs with bipolar plugs, they look almost like little lemons.

You immediately think Trecurus.

[38:25] Guest:

And the clinical manifestation that a colorectal surgeon might get called to the ER for.

[38:30] Host:

While light infections are asymptomatic, a massive worm burden in a child or malnourished adult causes severe mucosal inflammation and tinesmus.

The constant straining can actually lead to a symptomatic full thickness rectal prolapse.

[38:43] Guest:

You evaluate the prolapsed rectal tissue in the ER and you can literally observe the adult worms embedded into the edematous mucosa.

[38:51] Host:

And finally, for the nematodes, we have Enterobius vermicularis, the pinworm.

[38:55] Guest:

Incredibly common globally, particularly in pediatric populations and daycares, the adult worms live peacefully in the cecum, but the pregnant females migrate down the colon and emerge onto the periodontal skin at night to lay thousands of eggs.

[39:07] Host:

This causes intense, madding periodontal puritis.

[39:11] Guest:

Diagnosis here is low tech but highly effective.

The classic tape test.

You press a strip of clear adhesive tape against the periodontal skin first thing in the morning, pull it off and place it on a slide for microscopy.

You will easily see the asymmetrical eggs.

[39:26] Host:

To complete the parasitic picture, the literature touches on several key protozoans and trematodes that round out the differential.

Cryptosporidium is notable from a public health standpoint because the Udian cysts are highly resistant to standard water chlorination.

[39:40] Guest:

It causes massive, explosive outbreaks of watery diarrhea from municipal pools or water parks.

[39:47] Host:

In a healthy, immunocompetent patient, Cryptosporidium is miserable but self limited.

But in an HIV patient with a low CD4 count, the disease is protracted, devastating and unresponsive to standard antibiotics.

[39:59] Guest:

The most effective treatment is actually optimizing their immune status with heart highly active antiretroviral therapy.

[40:05] Host:

We also frequently see Giardia lamblia contracted from drinking unfiltered stream water.

It causes a classic greasy, foul smelling malabsorptive stool.

Treated first line with metronidazole.

[40:15] Guest:

Balantidium colae is a great trivia fact.

It is the only ciliated protozoan known to infect humans, and it’s almost exclusively associated with exposure to pigs or pig feces.

[40:26] Host:

And we absolutely must mention schistosomiasis.

This is caused by blood flukes trematodes that use freshwater snails as intermediate hosts.

Specifically, Kistosoma mansoni and Schistosoma japonicum affect the gastrointestinal tract.

[40:42] Guest:

The adults live in the mesenteric venules, they lay eggs, and those eggs are deposited into the tissues of the small bowel and the colonic mesentery.

[40:49] Host:

The body reacts to these foreign bodies by triggering a massive granulomatous immune response.

This leads to intense local tissue destruction, strictures and profound portal hypertension as the liver also becomes fibrotic.

[41:02] Guest:

So if we synthesize all this parasitic data, we have seen parasites that mimic advanced colon cancer like the Emma boma.

We have seen parasites that mimic acute surgical abdomens like Anesacus mimicking appendicitis or amoebic ulcers causing right colon blowouts.

[41:16] Host:

The practicing surgeon has to be wondering, how do we avoid unnecessary bowel resections?

How do we not operate on a parasite?

[41:23] Guest:

It comes down to deliberately expanding your diagnostic toolkit before you reach for the scalpel first.

Specific, granular geographic history taking is paramount.

Don’t just ask if they’ve traveled.

Where exactly did they live?

What bodies of water did they swim in?

41:38

What wild game or raw seafood have they eaten?

[41:41] Host:

Second, lean heavily on advanced diagnostics.

Routine stool cultures will completely miss these.

You need Multiplex PCR antigen testing, which is incredibly sensitive.

[41:51] Guest:

And third, look at the systemic peripheral clues.

A standard CVC showing an unexplained eosinophilia strongly hints at a parasitic hypersensitivity reaction, which should instantly broaden your differential beyond simple bacterial appendicitis.

42:06CMV Colitis: Biopsy Edges, Microvascular Thrombosis, and Fungal Mimics

We have spent the first half of this review covering bacteria that trigger acute inflammatory cascades and parasites that physically consume or obstruct tissue.

Now we need to shift our focus to a completely different class of invaders.

[42:18] Guest:

The viral and fungal threats.

[42:20] Host:

These pathogens operate differently.

They don’t typically cause massive, explosive, bloody diarrhea right out of the gate.

They are insidious.

They often present with subtle microscopic changes.

[42:30] Guest:

They are the endoscopic illusions requiring the surgeon or gastroenterologist to know exactly where and how to biopsy to prove their existence.

Let’s start with the surgeon’s primary viral foe, said a megalovirus, or CMV.

[42:45] Host:

CMV is a large double stranded DNA virus belonging to the herpes virus family and the most important epidemiological factor GRASP is that it is ubiquitous.

Global seroprevalence is estimated to be up to 83%.

[42:59] Guest:

Meaning the vast majority of your adult patients have already been exposed to it.

[43:02] Host:

In a healthy, immunocompetent person, a primary CMV infection is usually completely asymptomatic, or at worst, it feels like a mild case of mononucleosis.

The virus then goes dormant, hiding out in the monocytes and endothelial cells.

[43:16] Guest:

The clinical catastrophe arises when there is a reactivation of that latent infection.

[43:20] Host:

And that reactivation occurs due to a specific alteration or depression in the patient’s T lymphocytes.

Cell mediated immunity.

This usually it’s an organ transplant patient, an HIV patient, or an IBD patient on a heavy steroids.

[43:32] Guest:

Clinically, CMV colitis is a master of disguise.

[43:35] Host:

Let’s talk about what it looks like when you put a scope in endoscopically.

CMV can present as a patchy area of mucosal friability and punched out ulcerations that look exactly like an acute ischemic colitis.

[43:46] Guest:

Or, paradoxically, it can present as a large fungating polypoid mass that is highly suspicious for a malignancy.

[43:53] Host:

So you are in the endoscopy suite.

You are looking at a deep ulcer crater.

You suspect CMV.

The technical testable question is does it matter where you place your biopsy forceps?

[44:04] Guest:

My instinct, if I’m trying to diagnose an ulcer, is to grab tissue right from the deepest, grossest part of the crater.

That’s where the damage is.

But for CMV, is that the wrong move?

[44:14] Host:

It is entirely the wrong move.

If you biopsy the center of the ulcer, you were just going to get dead.

Necrotic Slough viruses are obligate intracellular parasites.

They need living cells to replicate.

[44:25] Guest:

Therefore, you must biopsy the edges of the colonic ulcers.

The viral cytopathic effect, the act of replication, and the characteristic cellular damage is concentrated exclusively in the viable inflamed tissue margins.

[44:37] Host:

OK.

So you biopsy the margin, you send it to pathology.

When the pathologist looks at that viable tissue on a standard H&E stain, the classic boar testable finding they’re hunting for is the owl’s eye inclusion body.

[44:49] Guest:

Yes, it is a massive eosinophilic intranuclear viral inclusion surrounded by a clear Halo, making it look like an owl’s eye staring back through the microscope.

It is highly specific for CMV.

[45:01] Host:

But here is the major diagnostic trap.

Relying solely on H&E staining is dangerous.

H&E has a relatively low sensitivity for early or mild CMV infection.

[45:12] Guest:

If the H&E stain comes back negative but your clinical suspicion is high, say the patient is a transplant recipient with severe bloody diarrhea.

You cannot stop there.

You must push the lab for PCR testing of the tissue itself or CME specific immunohyster chemistry stains.

[45:26] Host:

Because missing a CMV diagnosis can be fatal.

[45:29] Guest:

And let’s discuss why it’s fatal, specifically regarding the surgical intervention.

Let’s say the CMV colitis goes unrecognized or progresses despite medical therapy and the patient suffers A colonic perforation.

[45:40] Host:

The text notes this typically occurs somewhere between the terminal ilium and the splenic flexure.

[45:44] Guest:

You take them to the OR you find the whole, and the practice standard here is completely unambiguous.

If you are operating on a procrated CMV colitis, you must perform a resection and you must bring up an endostomy.

Primary anastomosis is absolutely contraindicated.

[46:00] Host:

And we need to explain the Physiology of why you can’t join the bowel back together.

Even if the bowel proximal and distal to the perforation looks pink and healthy from the outside, the margins are a lie.

[46:11] Guest:

CMV causes an intense diffuse microvascular thrombosis.

It infects the endothelial cells lining the tiny blood vessels in the subbucosa, causing them to swell and occlude.

[46:22] Host:

So even though the serosa looks pink, the tissue level is profoundly ischemic.

If you staple 2 pieces of ischemic bowel together, that anastomosis will fail, leak, and cause overwhelming sepsis.

[46:33] Guest:

Diversion is mandatory, and even with aggressive perfect surgery and potent antiviral therapy like IV Gansa, Clovier or foscarnet, the mortality remains incredibly high.

[46:44] Host:

The literature sites a 31% mortality rate even in relatively immunocompetent patients who perforate.

In the severely immunosuppressed, that number is much higher.

[46:52] Guest:

Let’s quickly review the fungal calidities.

Fungal infections of the colon are exceedingly rare in healthy individuals.

They almost universally signify profound advanced immune compromise.

[47:03] Host:

Histoplasma capsulottum is a key player here.

Heavily endemic to the Ohio and Mississippi River valleys in the United States.

Well, usually a pulmonary infection from bird or bad guano.

Progressive disseminated histoplasmosis can severely affect the GI tract.

[47:18] Guest:

Endoscopically, it causes deep colonic ulcers and raised pseudo polyps, again mimicking inflammatory bowel disease or a primary colonic malignancy.

[47:27] Host:

You confirm it not just with biopsy, but with specific fungal tissue cultures, and the treatment shifts entirely away from antivirals or antibiotics, requiring potent systemic antifungals like IV Amphotericism B.

[47:39] Guest:

We also occasionally see Candida in severely neutropenic or ICU bound patients presenting endoscopically as thick white plaque like lesions coating the mucosa and advanced disseminated Aspergillus or Cryptococcus can cause spontaneous colonic perforations or large submucosal GI nodules that mimic Crohn’s disease.

47:58IBD, HIV, Transplant: Navigating Infectious Colitis in Vulnerable Patients

Which brings us to the final and undoubtedly the most complex section of to our deep dive.

We now have to take all of these pathogens, the bacteria, the parasites, the viruses and the fungi and apply them to a patient population where the rules of engagement completely change.

[48:13] Guest:

I’m talking about the immunocompromised patient.

[48:16] Host:

The margin for error in this population is effectively 0.

Let’s start with a group you see constantly in your practice.

Patients with inflammatory bowel disease, specifically ulcerative colitis and Crohn’s disease.

[48:28] Guest:

The ultimate trap here is that the clinical presentation, the vital signs, and the endoscopic findings of a severe IBD flare are virtually indistinguishable from an acute infectious colitis.

[48:39] Host:

And this overlap leads to a highly dangerous, potentially lethal clinical cascade.

Let’s walk through it.

A patient with known biopsy proven ulcerative colitis comes into the ER.

They have worsening bloody diarrhea, tachycardia and a high white count.

[48:55] Guest:

The ER does a standard stool culture for common bacteria, and it’s negative.

You assume logically that this is just a severe exacerbation of their underlying autoimmune disease.

[49:04] Host:

So what is the standard algorithmic response for an IVD flare?

You escalate their immunosuppression, you admit them and start IV Methylprednisolone or you initiate A biologic like an anti TNF agent.

[49:17] Guest:

But what if they actually have a superimposed hidden infectious colitis?

What if they acquired Campylobacter, or their latent CMV reactivated, or they picked up a ME biases on a recent trip?

[49:27] Host:

If you give massive systemic doses of steroids to a patient with an active invasive colonic infection, you are turning off their immune systems only defense.

You are inviting disastrous, overwhelming sepsis, deep tissue necrosis, and a massive colonic blowout.

[49:43] Guest:

It’s like misdiagnosing a raging structural fire inside the walls of a house as just a heating system glitch and deciding the best solution is to turn up the thermostat.

You aren’t fixing the problem, you are actively fueling the destruction.

[49:55] Host:

That analogy perfectly captures the danger, and the textbook provides a truly harrowing case example to illustrate this reality.

It’s referred to as the Abbas case.

[50:04] Guest:

A patient presented to the hospital with a clinical picture that was completely completely presumed to be a severe exacerbation of ulcerative colitis.

Because of this presumption, they were treated aggressively with prolonged high dose steroid therapy.

[50:18] Host:

But the patient didn’t approve.

In fact, they rapidly deteriorated, developed peritonitis, perforated and were rushed to the operating room for an emergency colectomy.

[50:26] Guest:

And when the surgical resection was analyzed by pathology, it revealed severe full thickness amoebic colitis.

The colonic wall was destroyed by Antimoeba hystolytica.

[50:36] Host:

But here is the absolute kicker.

Upon final review, there was no underlying inflammatory bowel disease at all.

The entire initial presentation was purely an amoebic infection, totally masked and lethally exacerbated by the assumption of IBD and the blind administration of steroids.

[50:52] Guest:

So how do we, as careful surgeons and clinicians, avoid repeating that tragedy?

A multidisciplinary approach with rigorous repeated testing is absolutely mandatory.

We all know show the mantra to routinely test for Clostridium difficile in every single IBD flare, but that isn’t enough.

[51:08] Host:

It isn’t.

The data shows that cytomegalovirus is prevalent in 10 to 33% of IBD patients experiencing a severe flare, and it is notably more common in ulcerative colitis than in Crohn’s disease.

[51:21] Guest:

Because the standard stool cultures and even the H&E biopsies miss so much, as we discussed with the cooler growth times for your Cinia or the margin biopsies for CMV, the current literature emphasizes that a Multiplex PCR assay of the stool is critical.

[51:36] Host:

Is rapidly becoming the gold standard.

It’s one of the best methods to rapidly concurrently screen for a massive array of viral, bacterial and parasitic pathogens in a matter of hours.

[51:47] Guest:

Interestingly, there is emerging data noted in the text suggesting that identifying and treating a superimposed CMV infection with antiviral therapy might actually yield long term benefits for the overall management of the patient’s underlying IBD, potentially altering the long term trajectory of their autoimmune disease.

[52:03] Host:

Let’s shift from IBD to HIV.

The critical physiologic threshold here is ACD 4 + T cell count of less than 200 cells per cubic millimeter.

That is, the line with the immune system loses its structural integrity and the risk for bizarre, opportunistic infections drastically increases.

[52:22] Guest:

The gastrointestinal tract is actually a major primary site for HIV viral replication and profound early CD4 cell depletion.

While an HIV patient is perfectly susceptible to every common pathogen we’ve discussed today, like Salmonella or Campylobacter, the most common opportunistic colitis you will encounter in this specific depleted population is CMV.

[52:42] Host:

And while you obviously treat the specific pathogen Ganza Clover for the CMV heart optimized therapy for Cryptosporidium, the absolute cornerstone of long term gastrointestinal management in these patients is optimizing their underlying immune architecture.

[52:55] Guest:

Highly active antiretroviral therapy, or heart, restores gut immunity by increasing that CD 4 or count, giving the body the soldiers it needs to help clear the infection.

[53:03] Host:

Finally, we must briefly consider the solid organ transplant patients kidney, liver and heart recipients.

Diarrhea is an incredibly common frustrating complaint in this population.

Incidence rates during admissions range anywhere from 22 to 52%.

[53:18] Guest:

The major diagnostic and therapeutic challenge here is differentiating between a true infectious diarrhea and diarrhea that is simply a toxic side effect of their crucial life saving immunosuppression medications, particularly agents like mycophenolatemophotol.

[53:33] Host:

The Reichert and Abbison text highlights a massive retrospective review of over 400 transplant patient admissions specifically for diarrhea.

The results are enlightening.

[53:44] Guest:

The vast majority of those cases actually had no identifiable infectious etiology.

They were medication induced or self limited.

[53:51] Host:

But when an actual infectious agent was identified, the top three culprits were Clostridium difficile, norovirus and cytomegalovirus.

[54:00] Guest:

Again, relying on a rapid PCR Multiplex GI panel is paramount here.

You need to rapidly sort out if it’s a bug or a drug.

[54:07] Host:

Because if it’s a bug, you treat it, but if you falsely assume it’s a bug and it’s actually drug toxicity, you might needlessly lower their anti rejection medications and throw them into acute organ rejection.

[54:20] Guest:

So to synthesize all of this complex data for the practicing surgeon.

Infectious colitis is the ultimate shape shifting chameleon in colorectal surgery.

[54:29] Host:

We have seen how Campylobacter mimics the acute right lower quadrupain of appendicitis.

We’ve seen how Yersinia mimics the chronic ileitis of Crohn’s disease.

We’ve seen how Amabo is mimic the bulky mass of a right sided colon cancer.

We’ve seen how anasacidosis mimic diverticulitis.

[54:45] Guest:

Navigating this minefield is all about recognizing the mimics and knowing the microscopic detail.

[54:50] Host:

It’s knowing that if a pathologist describes a flask shaped ulcer, you are dealing with amoebiasis.

[54:55] Guest:

It’s knowing that if you are endoscopically biopsying a suspected CMV ulcer, you strictly target the viable tissue edges, not the necrotic center.

[55:03] Host:

It’s deeply understanding the absolute physiologic contraindication of giving lopromide or ciprofloxacin to a patient with Cestac E coli because you will precipitate a massive toxin driven hemolytic uremic syndrome.

[55:16] Guest:

Your best tools in the hospital are not just your scalpel or your lapar.

They are a high, unwavering index of suspicion, A granularly detailed geographic and dietary history, and the aggressive use of precise modern diagnostic testing like Multiplex PCR.

[55:33] Host:

And he was always questioned the obvious diagnosis, especially in the immunocompromised before you commit to irreversible surgical or pharmacologic pathways.

[55:42] Guest:

I want to leave you with one final, deeply provocative thought from the text to Mull over as we close out this review.

[55:48] Host:

We talked earlier about serologic antibody testing for parasitic infections, specifically amoebiasis.

The literature notes that these antibodies usually become positive after about two weeks of active tissue infection.

[55:59] Guest:

But here is the critical, potentially dangerous detail.

Those specific antibodies can remain positive in the bloodstream for years, long after the patient has been successfully treated and cured.

[56:10] Host:

That pharmacokinetic reality creates A fascinating and highly dangerous clinical scenario in the emergency department.

[56:16] Guest:

Exactly.

Imagine a 60 year old patient presenting to your ER tonight.

They have free air on the abdominal X-ray, a rigid abdomen and a perforated right colon.

[56:26] Host:

You take a quick history while prepping them for the OR.

They mentioned casually that they traveled to Central America five years ago on a church mission trip and had a terrible bout of dysentery, but they took some pills and fully recovered.

[56:38] Guest:

If your ER team runs a rapid serology test right now, it might flag positive for amoebiasis based entirely on that old cured exposure.

[56:46] Host:

And that single positive test could lead your entire surgical team and the infectious disease consultants down a completely false bias diagnostic pathway.

[56:55] Guest:

You might alter your entire surgical approach assuming you were dealing with a friable amoebic perforation, while the true underlying pathology may be a perforated right sided adenocarcinoma or a massive acute ischemic event addresses unchecked and unrecognized in your operative planning.

[57:11] Host:

As a surgeon, you are not just treating the data on the screen or the current test results.

You have to treat the entire timeline.

[57:18] Guest:

You have to interpret the lab data strictly within the context of the patient’s entire lived history.

That synthesis of data, history and biology is the true essence of surgical clinical judgment.

[57:29] Host:

Thank you for joining us on this Colorectal surgery review deep dive.

We hope this exploration of the chameleons the GI tract has equipped you with the tools to navigate these muddy diagnostic waters.

Keep your differentials wide, keep questioning the obvious diagnosis, and as always, keep your scalpels sharp.