Chapter 23: Medical Mycology

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Welcome to the deep dive.

Fungi?

They're basically everywhere, right?

From the yeast in to mushrooms in the woods.

Absolutely, all around us.

But what about the fungi living on us, or even inside us?

It's this whole microscopic world that frankly most people just don't consider.

But it has a huge impact on our health, sometimes in really surprising ways.

These organisms, they're constantly interacting with our bodies.

And that's exactly what we're digging into today, the world of medical mycology.

We're using Bryce Kendrick's fantastic book, Fifth Kingdom, as our guide.

It's a cornerstone text in the field.

Our mission here is to really walk you through how these fungi interact with us, from common annoyances to serious diseases.

We want you to grasp the key ideas, the terminology,

and sort of visualize this hidden world, even without a microscope handy.

Yeah, whether you're maybe studying this in college or just curious, we want to make it clear and engaging.

Okay, so to start, let's frame how fungi generally cause problems for humans.

There are like three main strategies they use.

That's a good way to put it.

First, you've got the obligately parasitic fungi, think dermatophytes.

These are the specialists.

They've specifically evolved to target our outer bits, skin, hair, nails.

Got it.

The keratin crew, focusing on that tough protein.

Exactly.

Then second, there are the thermodimorphic sap robes.

Now, these usually live in the soil, just decomposing stuff, but they have this incredible ability to adapt.

Adapt how?

Well, when they get into the much warmer, hostile environment of the human body, they actually change the physical form.

Their morphology shifts usually from a mold -like form to a yeast -like form.

Oh, sheep shifters, okay.

And the third type?

Those are the opportunistic sap robes.

These guys are generally harmless decomposers too, but they seize the chance, the opportunity, when our body's defenses are lowered.

Ah, so if someone's immune system is weak, maybe from illness or medication.

Precisely.

That's when these opportunists can move in and cause trouble.

And we can also think about the types of infections, right?

Like where they happen.

Yes.

Three broad categories there.

First, cutaneous infections.

These affect the outer layers, skin, hair, nails.

They cause allergic reactions or inflammation.

You see these on the surface.

Things like athlete's foot.

Exactly.

Then, number two, subcutaneous infections.

These usually get in through a wound, like a cut or a puncture.

They tend to stay localized under the skin or maybe spread quite slowly.

Okay.

And the last one?

The most serious systemic infections.

These can be caused either by those true pathogens, the dimorphic ones we mentioned, or by the opportunists.

The key thing is they get into the bloodstream and can spread throughout the entire body, affecting internal organs.

Right.

This deep dive isn't just academic then.

Understanding this stuff helps make sense of common things, like maybe dandruff or that stubborn toenail fungus.

Or it gives insight into really serious global health issues.

It connects our everyday lives to this vast fungal kingdom.

Okay.

I'm ready.

Let's unpack this.

Let's start right on the surface, literally getting under our skin with cutaneous infections.

Sounds good.

And the main players here are the dermatophytes, as you said, the keratin crew.

They are keratinolytic.

They possess enzymes that break down keratin.

That tough protein in our skin's outer layer, our hair, our nails.

Exactly.

There are about 40 species, mostly in three main groups, or genera.

Epidermophyton, microsporum, and trichophyton.

They're incredibly specialized.

And some are really specialized, right?

Like, only living on humans.

Yes.

About half of them are human specific.

They cause diseases we often call keratinia or, you know, ringworm, even though there's no worm involved at all.

There's a fungus growing in a ring pattern sometimes.

Right.

And these human specific ones, they don't live in soil, they don't live on animals, they only grow on people.

But, and this is amazing, their spores, these little infectious bits called arthrit canidia, can survive for ages.

How long?

Potentially up to two years in places like carpets or fallen hair, just waiting for bare skin to come along.

Wow.

Persistent little things.

What about the other half?

Those usually come from animals.

A classic example is microsporum canis.

Its main home is on cats.

It can infect humans or dogs, but it doesn't really thrive or persist there long term.

It needs to get back to a cat eventually for its cycle to continue properly.

Fascinating specificity.

Are there examples linked to specific conditions?

Oh, definitely.

Trichophyton rubrum is notorious for causing chronic infections, especially on the feet and toenails.

Someone infected can shed infectious material for a very long time.

Makes treatment tricky, I bet.

It can be.

And then there's trichophyton concentricum.

It causes a very distinct type of chronic ringworm, Tinea imbricata, almost exclusively in people of Polynesian descent.

Even if other ethnic groups live side by side, they typically don't get it.

That really highlights how tightly adapted these fungi can be to specific hosts, maybe genetic factors or something.

It seems likely.

And for common stuff you'd recognize, Epidermophyton flacosum is often the culprit behind athlete's foot.

The medical term is Tinea pedis and also jock itch, Tinea caris.

So a really key point you mentioned earlier, these dermatophytes, they're not actually eating our living skin, are they?

No, that's a common misconception.

They're breaking down the dead keratin layer, the itching, the redness, the inflammation you feel, that's caused by irritating chemicals.

The fungus releases enzymes like proteases and peptidizes.

So it's the fungal waste products,

essentially, causing a reaction, a sort of toxic dermatitis.

Exactly.

It's not munching on live tissue.

It's the chemical byproducts doing the damage.

Okay.

Moving slightly up, I guess.

What about dandruff?

Another super common issue.

Right.

The most frequent cause there is a yeast called Malassezia globosa.

It's actually a Basidiomycete yeast, related more closely to mushrooms than many other yeasts.

It has a weird quirk, doesn't it?

Something about fats.

It does.

It has a tiny genome and it cannot produce its own fatty acids.

It's completely dependent on us for them.

So how does it get them?

It lives on our skin, particularly the scalp, and feeds on sebum.

That's the oily stuff our skin glands produce to waterproof and protect skin and hair.

Malassezia produces enzymes, lipases, that break down the sebum.

Okay.

And that causes dandruff how?

The breakdown process releases oleic acid.

This acid can penetrate the top layer of the skin.

And in about half the population, this triggers inflammation and increases skin cell turnover, leading to the flakes and irritation we call dandruff.

So it's our own oils processed by the yeast, causing the problem for many of us.

Wow.

Exactly.

It's a fascinating little ecosystem on our heads.

Scientists even sequenced its genome back in 2007, revealing these metabolic dependencies.

Let's talk about another common yeast, Candida.

Specifically, Candidiasis.

Right.

Candida albicans.

This yeast is actually a mucous membrane.

Usually it lives there harmlessly.

But sometimes it overgrows.

Yes.

Things like excessive moisture, maybe from wet clothes or tight non -breathable clothing, can create conditions where Candida rapidly multiplies on the skin.

Things like diaper rash in babies, infections in skin folds, think armpits, groin area, under the breasts, and sometimes around fingernails, especially if hands are frequently wet.

And it affects mucous membranes too, right?

Like in the mouth.

Absolutely.

Oral Candidiasis, commonly known as thrush, is quite common in newborns.

And vaginal Candidiasis is frequent, especially during pregnancy, when hormonal changes affect vaginal secretions, making the environment more favorable for Candida.

Men can also get infections called Candida Balanitis.

Is widespread skin Candida ever a sign of something deeper?

It can be.

Chronic, persistent, cutaneous Candidiasis, especially if it's severe or current, can sometimes indicate an underlying issue with the immune system.

Maybe problems with the thymus gland, thyroid, or certain white blood cell functions.

It's a potential red flag.

Okay.

Let's move deeper now, beneath the surface,

to subcutaneous infections.

Right.

These are typically caused by fungi that aren't inherently very aggressive.

They're often suborbic, meaning they normally live on dead plants or soil debris.

So how do they infect us?

They usually get introduced through a break in the skin, a splinter, a thorn prick, a cut.

And once inside, they have to adapt.

Sometimes they change their structure, their morphology, or their physiology to survive in our tissues.

You mentioned Scorchicosis earlier, caused by Sporithrich's Secchi.

That's one of these.

Yes, a classic example.

It's found worldwide in soil and on plants.

You get it from, say, a contaminated rose thorn.

And this is one of those shapeshifters, the dimorphic ones.

Exactly.

That's what's really interesting here.

In the soil or on the plant, Sporithrich's grows as a filamentous mold.

But once it gets into the warmer human body, it converts into a yeast -like form.

Clever survival tactic.

How does the infection progress?

It usually starts as a small localized lesion at the site of inoculation.

This might ulcerate, drain a bit, and might even seem to heal over.

But the fungus can then travel along the lymphatic channels draining that area.

Ah, so it spreads internally.

Yes, causing a chain of secondary lesions along the lymphatic vessel.

In some cases, especially if the person's immunity is weak, it can become systemic, spreading via the bloodstream to joints, bones, and even internal organs.

That sounds pretty serious.

Are there other types of subcutaneous infections?

There are.

Chromoblastomycosis is one, often seen in tropical areas among people who go barefoot.

Fumgii, like Phelophora or Fonsaceae, get in via minor trauma and cause these chronic, warty, cauliflower -like growths, usually on the feet or legs.

Oof, sounds unpleasant.

And another one is mycotic myositoma, again, often in barefoot populations in the tropics.

Fungi get into a wound, and they stimulate the body to form a kind of tumor -like mass.

Inside this mass, the fungus grows as compact colonies called grains.

Sometimes these grains can even be pushed out through openings in the skin.

Okay, so that covers infections just below the skin.

Now for the big ones.

Systemic mycosis, infections throughout the body.

Right.

And we can divide these into two main groups based on the type of fungus.

First,

infections caused by true specialized pathogens.

Second, infections caused by those opportunistic sap robes we talked about earlier.

Let's tackle the true pathogens first.

These are the dimorphic ones again.

Yes.

The four major ones are all dimorphic pathogens.

They exist in one form, usually mycelial or mold -like, in the environment, typically soil, and switch to a different form, usually yeast -like, inside the host's body to cause disease.

Three are quite common in North America, one mainly in South America.

Okay, walk us through them.

Let's start with histoplasmosis, or histo for short, caused by histoplasma capsulatum.

This one loves soil enriched with nitrogen, especially from bird droppings in starlings, chickens, or bat guano.

So caves, old chicken coops, places like that.

Exactly.

If you disturb that soil or guano, you can inhale the fungal spores, the canidia.

That leads to a primary lung infection.

Is it always serious?

Actually, no.

About 95 % of the time, people who get infected have no symptoms, or maybe just mild flu -like ones.

Their immune system handles it, often leaving just a tiny calcified spot in the lungs and providing some immunity.

But the other 5 %?

That's where it gets problematic.

The inhaled spores turn into yeast cells inside the body, parasitizing immune cells.

It can cause a more severe lung disease that can mimic tuberculosis, or, in the worst cases, it disseminates spreads throughout the body via the bloodstream attacking internal organs like the liver and spleen.

This systemic form can be fatal if not treated.

Where is this most common?

It's highly endemic in the Mississippi and Ohio River valleys in the U .S.

It's estimated maybe 40 million people there have been infected, most without ever knowing it.

Wow.

Good next one.

Coccidioidomycosis, often called cocci, or, more commonly, valley fever.

The fungus is Coccidioides imitis.

This one thrives in dry alkaline soils, particularly in the southwestern U .S.

places like Arizona, California's Central Valley, and parts of Mexico.

And the disease is similar to histo.

The pattern is very similar.

Most infections are mild or asymptomatic, but it can cause significant lung disease or disseminate.

One difference is the form it takes in the body instead of yeast.

Coccidioides forms these unique spherical structures called spirals, which fill up with spores called endospores.

Again, millions have likely been infected, but severe disseminated disease, while possible and potentially fatal, is less common, though certain groups seem more susceptible.

Okay, two down.

What's the South America one?

That's pericoccidioidomycosis, caused by pericoccidioids brasiliensis.

It's found mainly in Central and South America, especially in humid tropical forest areas.

Lung infection is probably common, but serious disease is relatively rare.

What happens when it does get serious?

The really characteristic feature when secondary infections occur is severe, painful ulceration of the mucous membranes, particularly in the mouth and nose.

It can be quite destructive, sometimes even leading to loss of teeth and damage to the face.

Grim.

And the last of the four true pathogens.

Blastomycosis, caused by blastomyces dermatitis.

This one is found primarily in the Eastern and Central US and parts of Canada.

It's often associated with the decaying wood and moist soil, maybe near waterways.

How does it typically present?

It starts as a primary lung infection, which might be mild or severe, sometimes forming granulomas or abscesses.

But it has a tendency to spread, often to the skin, especially exposed areas like the face and neck.

It causes these characteristic raised, warty looking lesions that can scar badly and destroy tissue.

It can also spread to bones, the prostate in men, and occasionally the brain.

So these four dimorphic fungi are the ones that can infect even healthy people, just by inhaling spores from the environment.

Exactly.

They are true pathogens.

But now we need to talk about the other category of systemic infections.

The opportunistic pathogens.

Right.

These are fungi like various species of Aspergillus, Candida, Cryptococcus, and fungi belonging to the order Muceralis.

These organisms are all around us, and they can generally grow at human body temperature.

But they don't usually cause disease in healthy folks.

Correct.

They usually only cause serious systemic disease when our body's defenses are significantly weakened.

Think of conditions like diabetes, especially uncontrolled diabetes, AIDS, advanced cancers like leukemia or lymphoma, patients undergoing chemotherapy or long -term steroid therapy, or people who have received organ transplants and are on immunosuppressive drugs.

So they take advantage of a compromised host.

Let's revisit Candida.

We talk about skin and membrane infections, but it can cause systemic disease too.

Oh, yes.

Systemic Candidiasis is a major concern, especially in hospitalized or severely ill patients.

In adults, it's strongly associated with things like diabetes, AIDS, cancer, steroid use, broad spectrum antibiotic therapy, which wipes out competing bacteria, intravenous lines, and IV feeding.

And how serious is it?

It can become truly systemic.

Getting into the bloodstream that's called septicemia or fungi, and spreading to multiple organs.

It carries a very high mortality rate.

Okay.

What about zygomycosis?

That sounds ominous.

It is.

This is caused by fungi from the order mucoralis, like rhizopus or mucore species.

They cause several devastating types of infection.

One is rhinocerebral zygomycosis.

Brinocerebral.

Nose and brain.

Exactly.

This form has a terrifying association with patients who have diabetic ketoacidosis, high blood sugar, and high levels of ketones, making the blood acidic.

The fungus typically starts in the nasal sinuses, but then it grows incredibly rapidly, invading through tissues into the eye sockets and directly into the brain.

That sounds incredibly aggressive.

It is.

Patients can develop bulging eyes, facial paralysis.

It's often fatal within about a week, if not diagnosed and treated extremely aggressively, which usually involves surgery and antifungal drugs.

Are there other forms of zygomycosis?

Yes.

There's a thoracic or lung form, often seen in leukemia or transplantations, mimicking pneumonia but often invading blood vessels.

There's a gastrointestinal form, sometimes seen in severely malnourished children.

And a cutaneous form that can colonize severe burns and spread rapidly.

All are very serious.

Let's move to cryptococcosis.

Caused by cryptococcus neiformens, you said.

Often linked to pigeon droppings.

That's the one.

It's an encapsulated yeast, meaning it has this protective capsule around it.

It's widespread in the environment, especially where pigeons roost.

We probably all inhale the spores or dried yeast cells quite frequently.

And usually it's fine.

For most healthy people, yes.

You might get a mild subclinical lung infection that your body clears without you even noticing.

But in immunocompromised individuals,

again, think leukemia, lymphoma, AIDS, transplant recipients, it's a different story.

What happens then?

It can cause significant But the real danger is its tendency to spread, particularly to the central nervous system,

causing cryptococcal meningitis.

Meningitis.

Inflammation of the membranes around the brain and spinal cord.

Exactly.

It presents with symptoms like increasingly severe headaches, fever, confusion.

Untreated cryptococcal meningitis is invariably fatal.

You mentioned another cryptococcus species earlier, seagaddiei.

That's a bit different.

Yes.

That's a really interesting and somewhat concerning story.

Cryptococcus seagaddiei was historically associated with eucalyptus trees, mainly in places like Australia.

But starting in the late 1990s, it unexpectedly emerged as a significant pathogen in the Pacific Northwest of North America.

Wait, exactly.

Primarily Vancouver Island in British Columbia initially, but then it spread to mainland BC and down into Washington State, Oregon, and even California.

It's been isolated from native trees there, from the air, from soil.

Why the sudden emergence and spread?

Any ideas?

The reasons aren't fully understood, but climate change is strongly suspected as a contributing factor.

Perhaps changing weather patterns help disperse the spores, or warmer temperatures allowed it to establish in new areas.

It's an active area of research.

Does seagaddiei cause the same disease as c.

neoformans?

It can cause similar diseases, including lung infections and meningitis.

One difference is that seagaddiei seems more causing disease even in people with apparently normal immune systems, although immunocompromised individuals are still at higher risk.

Symptoms often include a prolonged cough, sharp chest pain, fever, night sweats, weight loss, and severe headache if meningitis develops.

Is it treatable?

Yes, fortunately.

Like c.

neoformans, it's treatable with antifungal medications, especially if caught early.

And importantly, it's not spread from person to person.

You get it from inhaling the spores from the environment.

Okay, one more opportunistic group.

Aspergillosis.

Caused by aspergillus species.

Yes, particularly aspergillus fumigatus, which is incredibly common in the environment, soil, decaying vegetation, air.

We inhale its spores constantly.

And like the others, usually harmless, unless?

Unless your immune system is compromised, or sometimes if you have pre -existing lung damage.

There are different forms.

One is allergic bronchopulmonary aspergillosis and allergic reaction in the airways.

Another is an aspergilloma or fungal ball.

A fungal ball?

Yeah, where the fungus grows in a pre -existing cavity in the lung, maybe left over from tuberculosis, it forms this tangled mass.

It might not invade tissue, but it can cause coughing, sometimes bleeding.

And the most serious form.

That's invasive aspergillosis.

This occurs in severely immunocompromised patients, advanced aids, leukemia patients undergoing intense chemo transplant recipients.

The fungus starts in lungs but then invades tissues, gets into blood vessels, and spreads throughout the body.

That sounds incredibly difficult to treat.

It is.

It's an insidious disease, often diagnosed very late, sometimes only at autopsy.

The mortality rate is extremely high.

And as medicine advances and more people live longer with compromised immune systems, we're seeing infections caused by other, previously rare opportunistic fungi, too.

It really underscores the link between immunity and these fungal infections.

AIDS, in particular, seems to have highlighted this connection.

Absolutely.

The AIDS epidemic brought opportunistic fungal infections to the forefront in a major way.

Patients with severely depleted CD4 T -cell counts became highly susceptible.

To the point where some fungal infections became markers for AIDS.

Exactly.

Certain opportunistic mycosis, if they occurred in someone without other known risk factors for immunosuppression, like cancer therapy or transplantation, became part of the diagnostic criteria for AIDS itself.

Which one specifically?

Hisopagel candidiasis, that's thrush extending down the esophagus, was a big one.

And cryptococcosis, especially cryptococcal meningitis, affecting the central nervous system.

Seeing those in an otherwise unexplained context strongly suggested underlying HIV infection leading to AIDS.

The prevalence varied geographically, but the link was undeniable.

So,

faced with all these potentially deadly fungi, how do we actually fight them?

What about treatment?

Well, for a long time it was incredibly challenging.

Effective and safe antifungal drugs were really scarce.

Many of the systemic mycosis we've discussed were almost universally fatal before modern antifungals.

But regular antibiotics don't work.

Worse than useless.

Antibacterial antibiotics target bacteria, not fungi.

In fact, by killing off competing bacteria in the body, they can sometimes create an environment where fungi can overgrow even more easily, potentially worsening a fungal infection.

Right, so what were the breakthroughs?

There were some early successes.

Simple potassium iodide solution, taken orally, was found to be effective for certain forms of spore trichosis way back in 1903, and it's still used sometimes.

Okay, what else?

A big step forward came in 1950 with nystatin.

This was one of the first polyene antibiotics specifically targeting fungi.

It's particularly effective against candida, used mostly for superficial infections like thrush or skin candidiasis and sometimes for esophageal candidiasis.

And there's a nice story behind its discovery.

There is.

It was discovered by two remarkable women scientists working for the New York State Department of Health, Dr.

Rachel Brown and Dr.

Elizabeth Hazen.

They decided to donate all the royalties from nystatin, millions of dollars over the years, to establish a foundation supporting research, particularly in medical mycology.

Really inspiring.

That's amazing.

But nystatin wasn't the answer for the deep systemic infections.

Not really.

The major breakthrough for those potentially fatal deep mycosis came in 1957 with amphotericin B, often called fungizone.

This had to be given intravenously.

The heavy hitter.

Exactly.

It was, and in many ways still is, a crucial drug for life -threatening systemic fungal infections like disseminated histoplasmosis, cryptococcal meningitis, or invasive aspergillosis.

It saved countless lives.

There is.

It's always a but with powerful drugs, isn't there?

There is.

Amphotericin B is notoriously toxic.

Patients often experience significant side effects, fever, chills, nausea, vomiting during infusion.

It can cause inflammation of the veins, phlebitis, and most seriously, it can cause kidney damage, sometimes permanent.

Ouch.

So it's reserved for really dire situations.

Absolutely.

It's a risk -benefit calculation.

You use it when the fungal infection itself is life -threatening.

Plus, unfortunately, some fungi can be resistant.

There have been tragic cases where infections caused by resistant strains, like some aspergillus flavus, didn't respond even to amphotericin B.

Were there other options developed?

Yes.

Myconazole monostat was another one used intravenously for systemic infections, but it had similar toxicity issues.

For the dramatified infection's ringworm, athletes foot an oral drug called griso fulvin became available, which was a big help.

We have lots of creams and powders now for those, right?

We do.

Newer topical treatments like tolniftate and clotrimazole are very effective for common superficial infections.

Then, in 1981, ketoconazole nizoral came along.

It was one of the first azole antifungals available orally that could treat severe systemic mycosis.

Another breakthrough.

It was, but again, with significant drawbacks.

Ketoconazole can have serious side effects, including liver toxicity and effects on hormone production.

It can suppress adrenal function and cause impotence or reduce sperm count in men.

So, like amphotericin B, its use for severe systemic disease is limited to cases where benefits outweigh the risks.

So where are we now?

What's the modern approach?

We have a much broader arsenal now, thankfully.

Many newer drugs belong to the azole class, like fuconazole, intraconazole, voriconazole, or the echinocandon class.

They work by targeting specific things fungi have that human cells don't.

Like what?

A key target is ergosterol.

That's the main sterol in fungal cell membranes, analogous to cholesterol in our membranes.

Many azole drugs inhibit its synthesis, disrupting the fungal membrane.

Others, like amphotericin B, bind directly to ergosterol, creating pores in the membrane.

Attacking a unique fungal component.

Smart.

Exactly.

Other drugs target the synthesis of the fungal cell wall components, like chitin or glucans, which human cells lack entirely.

The echinocandins, for example, inhibit glucanin synthesis.

By hitting these specific fungal vulnerabilities, newer drugs can often be more effective and, crucially, less toxic to the human host.

Okay, so wrapping this up, what are the main takeaways from this deep dive into our fungal neighbors?

I think the first thing is just how incredibly adaptable and diverse fungi are as potential pathogens.

They range from causing fairly minor, though annoying, skin issues to truly devastating, life -threatening systemic diseases.

And their ability to survive in different environments, change form, exploit weaknesses in our immune systems.

It makes them pretty formidable.

Absolutely.

Understanding those main categories, cutaneous, subcutaneous, systemic, and knowing about the key players, both the true pathogens like histoplasma and the opportunists like candida and aspergillus, is really crucial.

We've also seen that medical science has made huge strides.

We've gone from having almost no effective treatments for systemic mycosis to having a range of antifungal drugs.

True.

But those drugs, especially the older ones, often come with significant toxicity challenges.

And resistance is an ongoing concern.

Plus, new threats can emerge, like we saw with Cryptococcus gaudii, possibly linked to environmental changes like climate change.

It reminds us this is a dynamic relationship.

It really does feel like a complex dance.

So while learning about all these diseases might seem a bit alarming.

It's important to remember the conclusion from Tendrick's chapter.

Most healthy people will never contract a serious systemic mycosis.

Common skin stuff like athlete's foot, probably.

But the really dangerous ones are less common in the general population.

It puts it in perspective.

This dive really highlights how intimately connected we are the microbial world, inside and out, and how our health depends on maintaining a delicate balance with that environment.

Definitely.

And it underscores why continued research into these often overlooked organisms is so important.

Understanding fungi helps us understand our own health, our environment, and the intricate biology playing out all around us and within us every single day.

Well, we hope this deep dive into medical mycology has given you, our listener, a clearer picture and a more engaging understanding of this complex but fascinating topic.

Thanks so much for joining us for the deep dive.

Keep that curiosity alive.