0:44

Hi, I'm Aaron Welsh and this

0:46

is this Podcast Will Kill You. I

0:49

am so excited to welcome

0:51

you all to another episode

0:53

in our tp w K Y book

0:55

Club series this season, where

0:57

we interview authors about their wonderful

1:00

books in science and medicine. The

1:02

effects these books have on us or

1:04

the inspiration we draw from them, can be

1:06

as varied as the topics of the books

1:09

themselves. With the books just

1:11

this season, I've been on the edge

1:13

of my seat, reading as fast as I can

1:15

to find out what happens next in a book

1:18

about an element essential to all

1:20

of life. I've been absolutely

1:23

raging over a story of misogyny

1:25

in academia. My jaw fully dropped.

1:28

I've been delighted to learn about the regenerative

1:31

power of the endometrium. And I've

1:33

been moved in so many other ways

1:35

by the incredible things I've learned from

1:38

these authors. If you'd like to check

1:40

out the books that we've covered so far in this

1:42

book Club, head to our website This

1:44

Podcast Will Kill You dot Com, where

1:46

you can find pages for each of our released

1:48

book club episodes. And

1:51

if you, like me, were one of those

1:53

nerds always going past your assigned

1:55

reading in middle school and you want to sneak

1:57

peek at the rest of the books for this season.

2:00

You can also find that through our website

2:02

under the Extras tab by clicking on a

2:04

link to our bookshop dot org affiliate account,

2:07

which will take you to a list of lists,

2:09

including a book club list which features

2:11

all of the books from this season and the one

2:13

before. But now let's

2:16

turn back to the present and the book will

2:18

be chatting about today Blight Fungi

2:21

and the Coming Pandemic by author

2:23

and environmental toxicologist doctor

2:25

Emily Monison. Here

2:27

at TPWKY, we love

2:30

talking about fungi, even if we

2:32

don't do it maybe as often as we

2:35

should. We've covered kittrid

2:37

fungus, which affects amphibians,

2:39

white nose syndrome, which has devastated

2:42

some bat populations, as well

2:44

as a couple of fungal diseases of public

2:46

health relevance, cocidioidomycosis

2:49

and blastomycosis, which

2:51

was one of my favorite topics to research

2:54

last season because I got to talk about

2:56

dinosaurs. Go check it out if

2:58

you haven't already. This handful

3:00

of fungal pathogens represents

3:02

only a teeny tiny

3:05

proportion of fungi that can be pathogenic

3:07

to humans or animals, and that

3:09

group itself is minuscule

3:11

compared to the mind boggling

3:14

beautiful diversity of fungal species

3:16

that play so many crucial roles

3:18

in ecosystems and make life

3:21

possible. Fungi truly

3:24

are amazing, and all

3:26

fungal species are certainly worthy

3:28

of appreciation and attention. But

3:30

today we're setting our sites on the

3:33

select few that have the power

3:35

to do us and plants

3:37

and other animals harm, especially

3:40

harm on what is an almost incomprehensible

3:43

scale. Allow me to

3:46

take a quick trip down memory lane

3:48

to explain in part why I

3:50

love this book Blight so very

3:52

much. When I was an undergrad

3:55

at the University of Kentucky, I spent

3:57

many weekends escaping the end

4:00

traffic on Nicholasville Road on football

4:02

game days, my teeny apartment

4:05

with the bright orange walls, and of

4:07

course the homework and studying that

4:09

I probably should have been doing, and

4:12

I would head down to Red River Gorge.

4:14

For some hiking and camping.

4:15

It's an amazing place, and you

4:18

should absolutely go if you get the chance.

4:20

But sometimes while I was driving through the

4:22

park to get to a trailhead, I would stop

4:25

at the visitor center, initially for the

4:27

opportunity to use a nice, clean bathroom

4:29

rather than the pit toilet at camp. Once

4:32

I had luxuriated and washing my hands

4:35

with soap and warm water, I would

4:37

wander around the displays at the center, peeping

4:39

at the photos showcasing its history,

4:42

the respectably done taxidermy of

4:44

local fauna, and what quickly

4:46

became my favorite attraction and

4:49

my reason for future pit stops. At

4:51

the center a massive

4:53

cross section of a tree whose

4:55

label read something to the effect of

4:58

This cross section is of an American

5:00

chestnut tree. The tree was one hundred

5:02

and eighty something years old when it was killed,

5:05

along with millions of other chestnut trees,

5:07

by the chestnut blight fungus in the early

5:10

twentieth century. Next

5:12

to this cross section was a grainy black

5:14

and white photo showing a forest of

5:16

living chestnut trees, whose colossal

5:19

size was made very clear

5:22

by the tiny humans standing

5:24

in their shade. My mind

5:26

was blown. I could

5:29

not fathom, even with the help

5:31

of more old photographs, the sheer

5:33

size of these forests. How the

5:35

forests that I walked in today were

5:37

so dramatically different than those of

5:40

one hundred years before. How it all

5:42

changed so quickly and all

5:44

due to a fungus.

5:47

That chestnut tree cross section has

5:49

never left my mind, and I

5:51

admit to every month or two googling

5:53

historical chestnut forests out

5:55

of this morbid fascination. The

5:58

story of the chestnut blight is only

6:00

one of many told in Emily Monisson's

6:03

captivating book Blight, which

6:05

delves into the history of fungal epidemics

6:08

and pandemics and asks what these

6:10

fungal pathogens may have in store

6:12

for us in the future, as our climate

6:15

changes, as global movement and travel

6:17

increases, and as these

6:19

notoriously hard to eliminate species

6:22

see the chestnut blight fungus establish

6:24

strongholds in our hospitals and

6:27

across the world. So let's

6:30

take a quick break and then get into

6:32

it. Doctor

6:57

Monison, thank you so very

6:59

much for joining me today. Your

7:01

book, Blight Fungui in the Coming

7:04

Pandemic was such a fascinating

7:06

read, and I loved learning more

7:08

about this world of infectious disease that

7:10

we you know we on the podcast, but also

7:13

we as a general public, don't

7:15

really give enough attention to. And

7:17

I'm super excited to dig into some of these

7:20

fungal pathogens and the patterns

7:22

that we've been seeing lately. But

7:24

first, can you tell me where the

7:26

idea for this book first came about?

7:29

Sure, And first I just want to say thank

7:32

you for having me, and I love your show, so

7:34

I'm excited to be So this

7:37

is something that kind

7:40

of was running in the back of my mind for a

7:42

long time. So many years ago.

7:45

My first kind of experience with a

7:48

fungus like pathogen was

7:51

a thing called late light in

7:53

tomatoes. So people grow tomatoes,

7:55

I think they probably know about late light, especially if they're

7:57

on the East Coast, and that is an

8:00

organism that I think there was

8:02

sort of an outbreak of it in around two

8:05

thousand and six or seven or something like that, and

8:08

it was a disease where you're growing tomatoes. They

8:10

look beautiful end of the summer,

8:13

and all of a sudden something just came and hit them

8:15

and within a day, the tomatoes

8:18

and their leaves just were dead, hanging

8:20

on the stock, looking really pretty ugly. And

8:23

what it turned out was that that was a

8:26

disease called pause

8:28

by an organism called phytophra infestins,

8:32

and it was new to the

8:34

East Coast for tomatoes. And

8:36

it turns out that that disease was

8:38

probably distributed by a big box distributor

8:41

who was growing tomatoes starts down in I

8:43

think Florida and then shipping them up

8:46

the East Coast and infected

8:49

the Holy East Coast. And we are we

8:51

have had phytopha infestins infections

8:54

pretty much every year or maybe every

8:56

other year ever since then, because once it you

8:58

know, So what I learned from that, that was just that I

9:01

was writing and I was trying to understand the disease,

9:03

and what I learned was that it's caused

9:05

by phytopher infestins, same organism

9:08

that caused or contributed to

9:10

the Great famine in Ireland,

9:13

the potato blight, same organism,

9:16

that it could be spread so easily

9:18

through buying plants and being

9:21

distributed up the coast, and

9:23

that once it got established, it's

9:25

very hard to get rid of, if not impossible.

9:27

So that was sort of an introduction to a

9:30

sort of new disease that just kind

9:32

of came and you know, caused

9:34

havoc. And like

9:36

I said, it's not a fungus, but it behaves

9:40

like a fungus. I think when it was first discovered.

9:42

They probably thought it was a fungus. It's really something

9:44

called a water mold. Then

9:47

around that time, there was a paper that came out

9:49

in a scientific publication a

9:52

group of scientists who were across

9:54

different disciplines about

9:56

the emerging fungal threats across species.

9:59

And so what they were saying was, hey, hey, people,

10:02

you need to take you know, be aware. And they actually

10:04

included phytopher infestins because it's

10:06

fungus like in this paper.

10:08

But they were talking about frogs and bats and

10:10

humans and crops and that you know, there

10:12

are fungal pathogens across all of these

10:16

species, and they weren't getting a

10:18

whole lot of attention. So

10:20

together that seemed like a really good

10:22

topic for a book. I

10:25

had just finished a book about how all sorts

10:27

of things were getting resistant to all the chemicals we used

10:29

to kill them, which was a

10:31

pretty depressing book, and then this

10:33

would have been a pretty depressing book. And I

10:36

was talking with the editor and I was like, this is kind

10:38

of depressing, and she agreed, and so I

10:40

wrote a different book that was kind of hopefully more

10:42

hopeful. So I put this off and

10:44

I didn't really think about it, and then in

10:47

what was it whenever a fairly

10:50

recently Canada orius. So

10:52

the yeast fungus that's

10:54

been infecting people started infecting

10:57

people and it became a problem, and the

11:00

CDC started putting out alerts.

11:02

I think that was twenty sixteen maybe,

11:05

So when that came about, that was sort

11:07

of seemed like, Okay, maybe it's time to revisit

11:09

and write a book about emergent fungal

11:12

pathogens.

11:13

Of which there are many, and

11:16

not just in sort of these

11:18

big devastating epidemics that we

11:21

have come across the news, like in amphibians

11:24

or in frogs, or in

11:26

bats, but also, as you mentioned, in

11:28

humans. And so, what are

11:31

some of the unusual patterns that we've

11:33

been seeing lately in this rise

11:35

in these human fungal infections

11:37

that have been observed over the past few decades.

11:41

So I think the biggest

11:43

one. I remember speaking to an

11:46

infectious disease doctor who specialized

11:48

in fungal pathogens,

11:51

and he said he got his degree

11:53

in the eighties, and he said, and if somebody

11:56

were to come to Rounds with a

11:59

heart to treat fungal problem, that would have been

12:02

news like that would have been a big deal, and

12:05

then came HIV human immune

12:07

deficiency virus, and people

12:09

started becoming immunocompromised because

12:11

of it, and fungal diseases started

12:14

to rise. So that was one of the

12:16

things because a lot of fungal pathogens.

12:18

So I should say first of all that there

12:21

are a lot of fungi in the world. Most

12:24

of them are beneficial, some of them don't do anything,

12:26

and only a very small proportion

12:28

of them cause problems. So

12:30

that's you know, important to keep in

12:32

mind that we really most

12:35

we rarely rely on fungus for a lot of things.

12:37

So in most fungi, you

12:39

know, we're not really the target for a lot of

12:41

fungal pathogens, so there are very few compared

12:44

to viruses and bacteria. They're

12:46

a small proportion of those kind of pathogenic

12:48

problems. But

12:51

so it would would have been unusual. And

12:53

one of the reasons is we have a pretty robust immune

12:55

system, and when we do have a robust immune

12:57

system, we can you know, we're

13:00

breathing in fungal spores all the time, and

13:02

most of us it's not you know, for most of us, it's

13:04

not a problem. So when

13:06

people are compromised, then fungi

13:09

are ouptimistic and they

13:11

take advantage and they can start

13:13

to infect you. So back

13:15

in the eighties they were rise. There was a rise.

13:19

There's also been there was some

13:21

commentary that I came across that in the fifties

13:24

when we started using antibiotics on

13:26

a large scale, so

13:29

that there was had a quote somewhere

13:31

where, you know, they fungal

13:34

pathogens were kind of a disease of the antibiotic

13:37

age. And the

13:39

thinking there is in part because of

13:42

our microbiome, although back then they didn't really

13:44

talk about that in those terms because I don't think we

13:46

you know, nobody really realized

13:49

how much of a part of us our microbiome

13:51

is. But so we have, you know, fungi

13:54

and bacteria that keep other fungi in

13:56

bacteria in check. So once we start

13:58

using antibiotics, you wipe out the bacteria

14:01

they're not keeping the fungi in check.

14:04

And we've been seeing some unusual

14:06

cases in terms of like person to person

14:08

spread or outside of hospitals

14:11

or outside of people who are have immunal

14:13

compromise of some kind. Is

14:15

it sort of a mix of all of these things where we

14:17

have overuse or potential overuse

14:19

of antibiotics, we have higher rates

14:22

or higher detection of immunal compromise.

14:25

And is it just that we're better at finding

14:27

and isolating and treating, well maybe

14:30

not treating, but finding an isolating or

14:32

detecting fungal infections period.

14:36

You know, And it's not just you know, the other thing

14:38

is there's antibiotics, is immune compromise, and

14:40

there's a lot more tissue transplants, so just a lot

14:42

of good you know, medical

14:45

advances have also contributed to this because

14:47

if you get you know, tissue t plant

14:49

or an organ transplant, I mean, you

14:52

know, then you can be on you

14:55

know, suppressence to prevent rejection,

14:57

that sort of thing. So we have a large population people that

14:59

are also you know, transplant recipients

15:02

and things like that. So there's a lot of reasons why people

15:04

can be imm compromised. The

15:06

part about are we detecting you know,

15:08

what changed and are we detecting it? So one

15:12

difference in almost all

15:14

most fungal pathogens is that when

15:16

we think about bacteria viruses, we think about spreading

15:18

it from one to another, you know, where you sneeze on

15:20

somebody and you spread the virus. We all know that so

15:24

fun I don't spread like that. Usually it's

15:26

there isn't that sort of person to person contact.

15:29

So that's one thing that was raised

15:33

sort of red flags with Canada Orus.

15:35

So when this was the yeast that

15:38

you know, emerged somewhere around twenty sixteen,

15:40

at least came to recognition

15:42

in twenty sixteen as a problem. I think it was twenty

15:45

sixteen. I can't remember the year that the CDC issued

15:47

their warning. And part

15:49

of it was because here we had a yeast, and

15:52

yeast is you know, it's the fungus

15:54

we have Canada albacans.

15:57

That's very common use that a lot of us, you know,

16:00

we all have it on us and some of us problems, some

16:02

of it's not. Canada Orus is another

16:04

kind of yeast, and this one was

16:07

one that had a high mortality

16:09

rate when it infected people in the hospitals, and

16:12

it seemed to spread person to person, so it

16:14

could spread around the hospital room and

16:16

it could spread, you know, they thought

16:18

maybe health workers were spreading Canada ors.

16:22

It was very hard to clear from the room. So there were

16:24

a lot of problems with Canada ors. And

16:27

the other odd thing about Canada ors was

16:29

that it emerged here in the US

16:31

and in many other places around the world

16:33

kind of at the same time. So

16:37

in twenty sixteen, there were these outbreaks in you

16:39

know, far flung places of this kind

16:41

of new pathogen, which

16:43

was kind of frightening. And one of the things that

16:46

the scientists that I spoke to

16:48

at CDC had said was, we wondered,

16:50

was it something we just couldn't detect before and now we

16:52

detected it, So was it something

16:54

that was just misdiagnosed and now we know that

16:57

it's something different? And so they could go back

16:59

into the archive. They'd had some programs

17:01

running where you know, physicians

17:03

were taking samples of fungi from

17:06

patients, and it wasn't that case.

17:08

It wasn't that they were detecting it now

17:11

and not before. They found a

17:13

few cases that had been misdiagnosed, but

17:16

most of them were really new cases, so

17:18

it really was an emergent fungus in

17:21

that case. So it's a very rare thing

17:23

to have a new disease like that just sort of emerge.

17:26

And this one was so deadly, and it

17:29

was resistant to a lot of the anti fungal medications,

17:32

and it was hard to clear from a room, although

17:34

they now you know, have learned

17:36

better how to you know, sterilize a hospital room.

17:38

Afterwards, let's

17:41

take a quick break and when we get back, there's

17:43

still so much to discuss.

18:01

Welcome back everyone. I've been chatting

18:03

with doctor Emily Monison about her

18:05

book Blight Fungui and the coming

18:08

pandemic. Let's get back into things.

18:11

I do want to take a moment because I feel

18:13

like I have to ask, even though I'm sure you get

18:15

this question a lot since writing this book,

18:17

to go into the fictional.

18:19

World a bit.

18:20

Have you ever played The Last

18:22

of Us or have you watched the show?

18:25

And if so, any thoughts.

18:27

I have not played the game, but I did

18:29

watch the show. So because it came out

18:31

right before the book came out.

18:35

So one thing was so it came out in

18:37

the in January twenty twenty

18:39

three. So one striking

18:42

thing was right after that came

18:44

out, there was so much about fungal

18:46

pathogens in the news, and

18:48

in the end of twenty twenty two,

18:50

the World Health Organization had just

18:53

made this big announcement of these nineteen

18:56

you know, priority fungal pathogens,

18:59

and so they were trying to get it out there in the news.

19:01

You know, here are some fung guy that we want you all

19:03

to be aware of. And that didn't really

19:06

make such a splash. There was maybe a couple

19:08

of weeks of the news that you know, World Health

19:11

Organization has these priority fungal pathogens.

19:14

Then Last of Us comes out, and you

19:16

know, fungal pathogens are everywhere. So it

19:19

was sort of like that show did an amazing thing

19:21

for awareness of fungal pathogens. The

19:25

one thing that I just cringed

19:27

from in the show is only mostly

19:30

that you know, they

19:32

had no concern about spores, you

19:34

know, so they'd be going in where they're

19:36

dead zombies and you could see the you

19:39

know, my cilia or whatever all over the

19:41

place, and you know, nobody's

19:44

worrying about breathing in the stuff. But

19:46

you know so, But I since

19:50

read you know that they didn't want to put masks on all

19:52

the stars. Would you can imagine why?

19:54

But yep, yep, okay,

19:56

that makes sense.

19:57

And speaking of masks, I read

19:59

that you worked on this book a lot,

20:02

or at least wrote a lot of this book

20:04

and researched for this book during the COVID

20:06

pandemic. What was that experience

20:09

like compared to previous books that you've

20:11

worked on, and another two parter,

20:14

how did writing about pathogenic

20:16

fungui during a pandemic shape

20:18

this book?

20:20

Yeah, So for this book, I had this, Like

20:23

the other books, I've just sat at home and read a lot

20:25

of papers, called up some scientists, and so

20:27

for this one, I'm like, I'm going to do a better

20:29

book. I'm going to go visit laboratories

20:32

and I'm going to go see bats and bat

20:34

caves and frogs and

20:36

the you know. So I had this I

20:38

was going to travel and be right there with the

20:40

scientists, and so that's what didn't

20:42

happen. I did get to Costa Rica

20:45

and we went to a banana plantation, which was really cool

20:47

and I'm glad I had that experience. But yeah, the rest

20:50

of it was sitting at home talking to science

20:52

except over zoom, so

20:55

that was different. I also felt that a lot of

20:57

them were kind of more relaxed because they're sitting in their living

20:59

rooms talk to me. And

21:02

I think the other thing was once

21:04

I realized that we were really in a pandemic,

21:08

I had this book called Blake in

21:11

the kind of pandemic, I asked

21:13

my editor, I'm like, do you really think people are going to read

21:15

this? Maybe I should stop writing it because you

21:17

know, And the last thing is that

21:19

it also since

21:22

it's come out talking

21:24

about the title, you know,

21:27

when I was before, when I proposed

21:30

it and was writing it, there hadn't been a

21:32

pandemic like this, and

21:34

so the time, you know, pandemic

21:36

wasn't such a hot button word. I don't think,

21:40

you know, And I chose it because I was trying to

21:42

say that, you know, some of these funky

21:45

are like, they're big outbreaks there,

21:47

not just an epidemic here. You know, small outbreaks

21:49

here and you're an epidemia. So you might

21:51

have thoughts on using the name a word

21:54

like pandemic. But I wanted people

21:56

to think about it in a large way. But

21:58

then we had this global viral pandemic

22:01

and I'm like, but not like that.

22:03

So right, right,

22:06

right, no, And I think I think

22:08

it's a completely apt term. I think that we tend

22:10

to, maybe in part because of COVID,

22:12

think about pandemics as in happening

22:15

to humans, especially very

22:18

human centric ideas of what a

22:20

pandemic is.

22:21

And that's not necessarily the case.

22:23

But anyway, so all that is to say,

22:25

is that I love the title, and

22:27

I think that it is something that

22:30

we are a little bit

22:32

in part, have this human

22:34

bias where we don't think about

22:36

fungi as much as we do, you

22:39

know, bacteria and viruses, things that we're more

22:41

familiar with, and humans

22:44

represent of course, only a small proportion

22:46

of organisms impacted by

22:48

fungal pathogens. You know, some frog

22:51

populations around the world have been absolutely

22:53

devastated by b D a cattrid

22:56

fungus that we did an episode on like years

22:58

back. At this point, can you talk

23:00

about why frogs are so susceptible

23:03

to this pathogen and what the

23:05

latest is on this fungal pandemic

23:08

and are there any glimmers of hope out

23:10

there?

23:11

Yeah, well, so I only

23:14

know what I've learned from the scientists, and I spoke to Karen

23:16

Lips, who is one of the lead scientists, and you

23:18

know, she sort of experienced this decline. It's

23:21

a good question about why frogs

23:23

are so susceptible. So part

23:26

of it is is that their skin they you

23:28

know, carotin and their skin just like we do, and it's

23:31

food for the Kittrids

23:33

are aquatic. So

23:36

that's one thing is that they'll spread their spores

23:38

into the aquatic ecosystem and then that can

23:41

spread easily move her on. Frogs

23:44

breathe, they're basically breathing through

23:47

their skin, and so this is a skin

23:49

pathogen and so once it infects

23:51

the skin, it you know, it will poke through

23:53

and send out its spores and when it does that, it's

23:56

completely ripping apart the frog skin. So

23:58

you've got this skin that's very important

24:00

for managing electrolytes

24:03

coming in and out, and then you've got all these it's

24:05

just being shredded by this fungus that's

24:07

eating the skin and then growing and

24:10

sending out its spores

24:12

through the skin. And so that

24:16

is what kills the frogs. They're

24:19

not I mean they are. So there's this

24:21

obviously, it's it's impacted

24:23

a lot of different species. So that's another thing

24:26

is that it's not species specific. It's impact

24:28

a lot of different frog species. There's

24:31

a very similar fungus and I do think that VD

24:34

I might misspeak, but I think BD can

24:36

also impact salamanders who

24:38

have a similar part of their lifestyle, but

24:43

it's not as problematic

24:45

in salamanders. But there is another

24:47

caterried fungus that has become

24:50

called B cell that

24:52

does impact salamanders,

24:54

and that outbreak for

24:57

that was in Europe, and there's a

24:59

lot of concern. We have some really

25:02

biodiversity hotspots here for salamanders,

25:04

and there's a lot of concern that if that B cell enters

25:07

the US. You know, what happened to

25:09

frogs around the world could happen to the salamanders

25:12

here.

25:13

It's alarming, especially because

25:15

there is so much global

25:18

exchange, global movement, global

25:20

trade of thousands of species

25:22

of plants and animals. And in your book

25:24

you use this great term conveyor

25:26

belt of disease. So what

25:29

role has this conveyor belt

25:31

of disease played in fungal

25:33

outbreaks?

25:35

So just about every fungal

25:37

pathogen that I wrote about was

25:41

an emergent disease, and it was emergent

25:43

in large part because of trade and travel.

25:46

So every fungus you

25:48

know that became emergent pathogen

25:52

is because it was brought to a new place

25:54

and it found something to infect that had

25:56

never seen it before. And that's

25:58

how why it became so devastating.

26:01

Those organisms had no defense. So

26:04

the movement of plants

26:07

and animals and us too, I mean there are

26:09

some outbreaks that you know, what happened

26:11

to the bats, which the white nose disease

26:15

is thought to have been kicked

26:17

off by cavers bats living caves.

26:20

That's a pathogen that has killed bats across

26:23

in the East and is moving across the country.

26:26

And it was discovered

26:28

also that that pathogen does

26:31

infect bats in Europe, but it

26:33

doesn't kill them, and it's

26:35

in the caves in Europe, and so it's believed

26:38

that you know, people tramping around those caves

26:40

then came here, tramped around in caves here, left

26:42

some spores disease.

26:44

So yeah, movement, movement,

26:48

I mean, it's a

26:51

real driver of the spread

26:53

of pathogens and fun guy,

26:55

especially because, like you've talked

26:58

about, the vast majority of the fungi we

27:00

encounter our or the pathogenic

27:02

fungui that we encounter, are stable

27:05

in the environment, and so they're

27:07

or long lived in the environment, and they're there,

27:10

they stay somewhere for a very long time.

27:12

They're they're very sticky in terms of

27:15

you know, not being able to get rid of them, and

27:18

that's I think one thing that makes them so I

27:21

don't want to say scary, but like kind of

27:23

alarming in that sense of like, once

27:25

it's here, it's here. But the other thing

27:27

that I find really both you know,

27:30

fascinating and terrifying

27:32

about some fungal pathogens of

27:34

humans, especially going back to the humans,

27:37

is that some of them can be incredibly

27:39

deadly even with treatment.

27:42

And I know that our treatments are

27:44

somewhat limited in in you know,

27:46

what they can do. But why are

27:49

some of these fungal pathogens so very

27:51

deadly?

27:52

Oh, that's a good question, and I'm not a

27:54

physician, and I

27:57

don't really have a good answer for that, except

27:59

that when we're thinking

28:01

about some of the people who are infected, that they're immunocompromised,

28:05

so that gives the fungus some advantage.

28:07

I think some fungi are also good at evading

28:10

the immune response, so

28:12

there's that, And I

28:15

do think part of it is just that some of them are hard

28:17

to treat because there aren't that many antifungal

28:20

medications. There are very few classes of antifungal

28:23

medications, and so once

28:26

of fungus can overcome all of them, there aren't

28:28

that many options after that for

28:31

treatment. So resistance to antifungal

28:34

medications is a real problem.

28:37

Most if not all countries have

28:39

regulations or laws that

28:42

limit the importation of plants

28:44

or animals into the countries

28:46

in part to try to prevent pathogens

28:49

from coming in and affecting these immunologically

28:52

naive populations.

28:53

But these laws aren't perfect.

28:55

And you pointed out one gap with like humans

28:58

just not knowing that we're transporting

29:01

the fungus responsible for white nose syndrome

29:03

on our boots. If we're cavers

29:05

and we're going from one airport to the next,

29:07

and what a cool cave. Let's pop

29:10

in that one and then go back home, pop in that one.

29:13

So there are some of these gaps

29:15

that we see, but there's also seems

29:17

to be sometimes resistance to stricter

29:20

laws or longer quarantine periods.

29:23

Why is there some resistance

29:25

And that's kind of a both a big

29:27

and simplistic question at the same time.

29:30

But yeah, to why

29:32

there's resistance, I mean, I think sometimes

29:35

it's just such a big ask

29:37

in many ways, and then some people would say it's not a

29:39

very big ask, and I think what I wrote

29:41

about was sort of. So there were two things,

29:43

and I have to say right up front, regulation

29:46

not my strong point. I find them very

29:48

complicated to even you know,

29:50

to try to dig into the history to understand the current

29:53

regulations. The biggest gap

29:55

that I came across, and I think that people

29:58

would point out, is that for play plants

30:01

since the nineteen hundreds, because there

30:03

were a lot of outbreaks in plant

30:05

diseases. The USDA,

30:08

I think it was, you

30:10

know, there was a lot there was a big fight between

30:12

a couple of different factions of people who want

30:15

to bring in plants from all over the world and people

30:17

who said no, no, no, those are bringing in pests and

30:19

pathogens, and so there was a big fight. But

30:21

in the early part of the nineteen hundred they actually

30:23

did eventually come up with some regulations

30:26

about quarantines and you couldn't bring soil in and you couldn't

30:28

do this to protect plants. So

30:31

plants there is, you know, there is some healthy

30:34

regulations. And we actually have a

30:36

national mycologist, we have two,

30:38

so that's a position and their

30:41

role is to identify odd things

30:43

that come in in plants that

30:45

can't be identified and that might be pathogenic.

30:48

And so they're sitting there in their labs

30:50

constantly looking and a lot of stuff comes in. They

30:52

look at a lot of different kinds of mostly

30:55

fungal spores, because that's how they can identify them.

30:58

So we have these people looking at for plants pretty

31:00

much, and still we get plant pathogens slipping

31:02

in. Okay, we don't have the same thing for

31:05

animals that are pet trade

31:07

animals, and you know, so for food

31:10

animals we do because we're worried about

31:12

humans and disease and

31:14

her food. But for other kinds

31:16

of animals that are in trade, there

31:18

is not. For a lot of them,

31:20

there is no you can't come

31:23

in with this disease. You know, they're not checked

31:25

for disease. Part of it

31:27

is a capacity thing, and part of it is

31:30

you know, I can't tell you

31:33

why not. So now we're talking about

31:35

millions of animals coming over and crates

31:37

of animals and things like that. How difficult

31:39

that is. So that's

31:42

a big gap, and it was almost shocking.

31:44

I had to ask a lot of times. I'm like, you mean,

31:46

there's no national mycologists equivalent

31:49

for animals because this seems so important and

31:52

there isn't. So

31:54

I will say one more thing, just about when I mentioned

31:56

the BD and the salamander, So this is something

31:58

that's kind of good that came out. I

32:00

mean the b seal in the salamander. So I

32:03

mentioned that there's concern that

32:05

this cattrid fungus that's in

32:07

Europe will come across to the US.

32:09

And so those scientists that were working

32:11

with frogs and knew how devastating

32:14

the disease could be of the

32:16

kittred BD could be in frogs

32:20

got together and they first

32:22

tried to have some

32:25

new regulations there's some enforcement about bringing

32:27

disease frogs into the country, and that really didn't

32:29

go anywhere because the response was, we already have the

32:31

disease here, so how are we going to stop it?

32:34

But when the B sal came along in the salamanders,

32:36

they got together again and they said, hey, it's

32:39

not here, maybe we can stop it. And

32:43

what happened and they worked with it was you know,

32:46

nonprofits and federal

32:48

agencies and you know, academics

32:50

all working together to do this. And what they did come up

32:52

with was in the end a list

32:55

of I think two hundred and maybe nine or something

32:57

salamanders that cannot come into the country

33:00

because they are known carriers of B

33:02

cell. So it's not exactly what they wanted,

33:05

which would have been, you know, you just can't

33:07

bring you have to be tested for diseased

33:09

or get a health certificate that says

33:11

you have no disease. But it's

33:14

a it's a step and so

33:16

and so far we haven't had b cell here. There

33:18

is monitoring for it, but so that's

33:20

kind of worked. But that's really you know, when

33:23

you ask about regulations, how

33:25

you do things, and you know that took a

33:27

lot of effort.

33:29

On this podcast, we're mostly talking

33:31

about animal diseases and animal

33:33

immune systems, but as

33:35

you discuss in blight, plants

33:38

especially trees are incredibly

33:40

impacted by fungal infections.

33:43

How do tree immune systems

33:45

work? And like why are they so susceptible

33:48

to some fungi?

33:50

So trees have they

33:52

do multiple things. So they grow,

33:55

they have you know when you look at bark, that's like our skin

33:57

first line. But they also do this thing

33:59

where they grow, you know, in layers,

34:03

right, so when you sometimes see the inside a

34:05

tree that looks kind of there's nothing

34:07

there, it's it's dead. And so they

34:10

grow and they can wall off pathogens.

34:13

It's just the way they grow. And so that's

34:16

one defense is that if you know, something

34:18

gets infected, they can kind of just grow around

34:20

it wallet off and don't need that part.

34:23

They don't need a branch or like

34:25

we need our arm. So that's one thing. But the other

34:28

thing they do produce a lot of chemicals. I mean, we know

34:30

this in plants, right because we

34:32

either use a lot of plant chemicals for drugs

34:34

or whatever, and a lot of these sort of secondary

34:36

chemicals that they're producing, including things

34:39

like alkaloids that might make foods

34:41

bitter, are defenses against

34:44

pathogens. So that's another thing that they'll

34:46

do is they can produce, you

34:49

know, different kinds of chemical

34:52

products to fend off disease

34:55

and in pests too, insecte

34:58

pests.

34:59

When that doesn't go according

35:01

to plan, it can be incredibly

35:05

dramatic and awful. So one of

35:07

the most tragic stories

35:09

of a fungal epidemic is

35:12

chestnut light And it's just so

35:14

hard to wrap my head around how different

35:17

some North American forests looked

35:19

like before this epidemic struck. So

35:22

can you take us through this tragedy,

35:24

you know, how it was first recognized

35:26

and then what led to this dramatic

35:29

and rapid change.

35:32

Yeah, so chestnut trees the American Because

35:34

a lot of people around me are like, wow, but I just got some chestnuts.

35:36

I'm like, yeah, but they're not American chestnuts. If you got

35:38

them from you know, the farmer down the road,

35:40

they're probably some hybrid. So American

35:43

chestnuts were huge

35:45

trees, beautiful trees, very productive. They

35:49

ranged along sort of the Appalachian Range

35:52

and up along the East Coast. There

35:54

were really important trees in many ways, both to humans

35:57

and ecosystems. And so

35:59

the story of the

36:01

demise of the American chestnut kind

36:03

of begins at the Bronx Zoo. So

36:06

when they were first developing

36:08

the zoo, the society

36:10

that wanted to bring these, you know, have these exotic

36:12

animals on show and everything, they were

36:14

also very interested in the trees

36:16

on their property. So they had a lot of

36:18

acreage and they had a lot of old trees, and

36:21

so they thought that those trees

36:24

were just as important almost as the animals

36:26

that they were going to bring in, and so they hired a

36:28

forester. He was in charge of the trees

36:31

and it was his job to make sure that all

36:33

the trees in the park were good, healthy,

36:35

whatever, and plant other stuff in

36:37

the park. And so he knew

36:39

all the trees in that park, and there were something

36:42

like over a thousand chestnut trees, and

36:44

they were some of them were, you know, the big, old, beautiful

36:46

chestnuts. And so I think it was in nineteen

36:49

oh four that Merkel noticed

36:52

on a couple of chestnut trees some of the leaves were

36:54

kind of curling and looked like they kind of looked like

36:56

it was fall. They were sort of dying at

36:58

a time when they shouldn't have been. So thought,

37:00

well, this seems like some kind of disease.

37:02

And he could see some little spots on

37:04

the trees, and he thought, you know, maybe it's

37:06

a fungal disease, but just a few trees,

37:09

maybe won't come back next year, so

37:11

you didn't worry about it. Nineteen

37:13

oh five, almost every tree in the park was infected

37:16

with this fungus and their leaves were

37:18

curling up and dying, and so

37:21

he at that point, you

37:23

know, got worried, called the USDA asked what to

37:25

do. One of the things that they did at the time

37:28

what to treat fungal pathogens,

37:30

which I thought was interesting because we still use this

37:32

to treat them with copper. So copper

37:35

is an organic fungicide

37:37

and it is effective against fungus,

37:39

but it's topical. And so the response

37:42

to him was, well, cut off the dead branches and

37:44

you know, treat the trees with copper. Well, you had

37:46

a thousand you know, big old trees that wasn't

37:48

really in you know, in early nineteen

37:51

hundred that he tried to do that, but that

37:53

was not that effective and it was just overwhelming.

37:56

He brought in a colleague from

37:58

down to the botanical gardens and he identified

38:01

as something different, and he identified

38:03

as what would become known as chestnut

38:06

light. By the time he figured

38:08

out what it was, you know, within that year

38:10

and identified that it was in fact

38:12

the organism that's infecting and killing the chestnut

38:14

trees, he predicted that

38:17

all the trees would probably be infected and dead

38:19

within a few years, and he was right. And

38:22

what happened from there is that the blight spread

38:24

from New York all the way down through

38:27

the Appellachians, killing chestnuts

38:30

just about every single chestnut tree, millions

38:32

of trees, maybe billions. Within

38:34

decades, there were no more American

38:37

chestnut trees growing. Now.

38:40

People also cut down the trees

38:42

in part to maybe make a fire break

38:44

of infection, you know, to stop the infection,

38:47

and also because chestnut wood was so valued,

38:49

and you know they

38:51

were going to try to stop this, and

38:54

nothing stopped it. One thing

38:56

we haven't talked about is spores. So you

38:58

know fungi makes except

39:01

for Last of Us, which didn't have spores, but

39:04

it could have, and I think

39:06

maybe in the game it does. I'm told that

39:08

they actually wear masks in the game. So anyway,

39:11

you know, fungi spread by spores. They can

39:13

put out hundreds of thousands or millions

39:16

of spores, and in the case

39:18

of the chestnut light, you know, these trees would

39:20

be infected the funguses putting out spores.

39:23

The wind can carry spores, and these spores

39:25

can be carried by birds and insects that you

39:27

know go to the trees and then go to the next tree,

39:30

and so you know it, it just

39:32

it spread rapidly and it was unstoppable.

39:36

As that was happening, as they were

39:38

realizing that they're losing these valuable

39:40

trees, they wanted to understand something about the fungus

39:43

and so there

39:45

were these people called agricultural explorers

39:48

around nineteen hundreds, which was part of that fight.

39:50

Remember when I said there was the argument about

39:52

you know, collecting and bringing in stuff from all over

39:54

the world, but so wrong with that. So

39:57

they had these and there were you know, dedicated

39:59

explorers who would do that. They'd go all over the world

40:01

looking for plants and fruits and you

40:03

know, crop plants and trees and bring

40:05

them back. And so they're happened to have an explorer

40:08

that was going to China or he was in China at the

40:10

time. They got in touch

40:12

with him and said, hey, you know, there's this

40:14

fungus on the chestnut tree.

40:16

We know there's chestnuts in China.

40:18

Can you see if this fungus is there, you

40:20

know, identify this fungus on those trees. And

40:23

he did, and what he also noticed is

40:25

that those trees weren't really impacted by the fungus.

40:29

He got word back and so you

40:32

know, in the end, what people figured is

40:34

that some of those trees that had been imported

40:36

from either China or Japan people, you

40:39

know, they're very popular. There's still we have neighbors

40:41

with Chinese chestnut trees. Still that

40:44

fungus probably came in on some of those imports

40:46

and then spread throughout the

40:48

country. But

40:50

that understanding that now

40:52

they know that the Chinese chestnut trees have

40:55

some kind of resistance against the fungus because

40:57

it co evolved with it, right, the

40:59

two of all over how many hundreds

41:01

of thousands of years together, that

41:04

maybe there might be some way to use the

41:06

resistance of Chinese chestnutrees and

41:09

breed it into the American chestnut trees. So that

41:11

started a whole new program

41:14

to try to bring back

41:16

American chestnutrees. One

41:18

thing that I haven't mentioned, because we are so

41:20

human centric, is that each

41:22

time you do this, you're changing the whole ecosystem.

41:25

And so you remove a key species

41:27

like that, you remove a frog or a

41:29

bat, and it changes things

41:32

and it's not you know, it doesn't always have to. Sometimes

41:35

it is still relevant to us that the ecosystem

41:37

has changed. But you know, you can just imagine

41:39

the changes that happen when this

41:42

occurs and you take a whole species out

41:45

of a.

41:45

System, instant, huge

41:47

transformation with unforseeable

41:50

consequences. And there

41:52

are some consequences I think that

41:54

are a bit more easily seen when it

41:56

comes to agriculture, and especially

42:00

a lack of biodiversity in

42:02

agricultural practice, so

42:04

monoculture basically, So,

42:07

could you take us through the story of bananas,

42:10

This fruit that we eat so

42:12

much of all the time around the world,

42:14

and maybe we don't ever give a second thought

42:16

to the banana that we hold

42:18

in our hands.

42:20

Yeah, So the banana

42:22

story which we did, you know, like I mentioned before,

42:24

it got to go to Costa Rica, went to

42:26

this place called Earth University, which is a really

42:28

cool place. They're growing bananas

42:31

sustainably because it's difficult to grow banana

42:34

sustainably for a couple of reasons.

42:36

One of them is fungus no

42:39

matter where you grow. But the story that I

42:41

focus on there is the story of a fungus

42:44

called tr ie. It's

42:46

an oxysporum, some kind of fungus.

42:49

And so back

42:51

in the thirties, forties and fifties, banana's

42:53

big business. They were grown

42:56

on these huge monocrop plantations

42:58

in Costa Rica and Swear Honduras,

43:02

and they at

43:04

that time there was this fungus that emerged

43:08

and it started killing those bananas.

43:11

And the bananas that we ate were called the

43:13

gross Michelle banana, and so

43:16

they call them dessert banas, the bananas that we

43:18

were all eating. So I should also clarify that

43:20

there are many there are different kinds of bananas.

43:22

We happened to eat one, as you mentioned,

43:25

that's grown in a big monocrop. Basically

43:27

clones, they're just clones of each other. They're

43:29

not even because banas don't have seeds, so

43:31

they're really really clones. A

43:34

lot of people eat other kinds of bananas,

43:37

So this particular fungus

43:39

impacted the banana that

43:41

we were all eating, the banana

43:44

that was grown, the growmy shell that was imported,

43:47

and it was devastating to those crops.

43:49

And interesting I didn't bother the other kinds

43:51

of bananas, but it was the industry

43:54

that got worried. And so basically at that time,

43:56

back in the fifties and sixties, there were concerns

43:58

that they might not have any more bananas because that's

44:01

a fungus that when

44:03

you talk about scary spores, that's

44:06

the one that makes spores and it

44:08

can make this kind of spore that

44:11

some scientists say has been

44:13

detected in soil. So it's a soil born fungus.

44:15

Means that it's in the soil, then it gets up

44:17

through the banana from the soil,

44:20

makes spores. It can last in the soil

44:22

for ten years or more so decades.

44:25

So this is a kind of thing that once it impacted

44:28

plantation, got in the soil, you just

44:30

can't grow bananas there anymore. And so

44:33

what the industry would do back then, because it was not

44:35

a great industry, would just be to move

44:37

to another place and grow

44:40

their bananas there, leave

44:42

behind the other land that they you know,

44:44

so they just kept moving. But it became clear

44:46

that they were going to be out of bananas, and

44:49

so around that time,

44:51

there was a you know, discovery that there

44:53

was another kind of banana called the cavendish

44:55

that was not susceptible to that fungus.

44:58

So that was a very you know, that fungus was very

45:00

specific for the gro michell banana,

45:02

and so they replaced the

45:05

gross michelle with cavendish, which is what

45:07

we eat. But they basically

45:09

did the same thing. So they just

45:11

planted huge monocrops of banana, same

45:13

kinds and cloned banana everywhere

45:17

wherever banas are grown for export.

45:20

I think it was in the seventies, maybe

45:23

slowly, a new kind

45:26

of fungus emerged called TR

45:28

four. So the first one was called tier one. The second round,

45:31

Tier four, similar kind of fungus,

45:34

causing the same kind of problem, and

45:36

it is frightening growers. It

45:39

was believed to be transported in soil, so

45:41

that would have been in boots of people or

45:44

farm machinery that was transported from one place

45:47

to another. But one of the scientists

45:49

I spoke to said, you know, even though we know that, I

45:51

don't think that that's the only way it spreads,

45:53

and that that would really stuck, you know that, even if

45:55

we were totally hygienic about this, But

45:58

there are you know, you used to be able to go in

46:00

Costa Rica. I think if you went

46:02

several years ago before TR four became a

46:04

problem, you could go take a tour of banana

46:07

plantation, which is just really it's fascinating

46:09

to see how much care the

46:12

bananas that we eat. We don't pay enough

46:14

for our bananas. Let's just say that they require

46:17

a lot of care. And so used

46:20

to be able to go there and see how they do that, and

46:22

that you're not allowed to do that anymore because there's

46:24

too much concern about TR four. So we're kind

46:26

of fortunate to be able to get a

46:29

tour of this smaller plantation. But

46:31

yeah, so there's TR fours out there

46:34

and there are concerns

46:36

about you know what will be next.

46:38

And so some of the banana breeders

46:41

and people who work with bananas have

46:43

said, you know, yeah, we might lose

46:46

this banana, but there are a

46:48

lot of other kind of bananas. And

46:50

so one thing to think about is that

46:52

when we you know, when I was growing

46:54

up, there are a few different kinds of apples

46:56

and that was it. And now it's I'm

47:00

boggling. I think just in the last

47:02

two years, how many different

47:04

kinds of apples there are out there. So

47:07

there's you know, that that different

47:09

kinds. If we are open to having

47:11

some diversity in our banana, that would

47:13

be great. And another thing is

47:16

is that growing these huge monocrops with

47:19

you know, so there are other ways. That was one of

47:21

the things that the scientists that I had

47:23

visited was doing was experimenting

47:26

with how to grow large crops, but not

47:28

in these big monocrops, to have them in blocks and

47:30

have other stuff planted, you know, agro

47:32

ecology or grow forestry whatever, have

47:35

other stuff growing in between, other crops growing

47:37

in between, so that the you know, a disease

47:39

can't spread so easily. So there are ways

47:41

of doing, you know, dealing with this, and it's

47:44

just that we you know, we we need

47:46

to either change what we want

47:48

and what we accept and also how we grow

47:50

things diversity. You had mentioned

47:53

diversity, So I'm glad you said that biodiversity before

47:55

because it reminded me that that's one of the most important

47:57

things for all of this is the

48:00

and that we need to understand

48:03

and do whatever we can to preserve biodiversity

48:05

across species, no matter what we're talking about.

48:09

It's it's amazing to me that we are provided,

48:12

you know, learning opportunities all of

48:14

the time, from fungal pathogens,

48:16

from other types of pathogens, from

48:19

don't you know maybe giant monoculture

48:21

is not a great idea, and that we have to

48:23

keep relearning those lessons over

48:26

and over again.

48:27

That's that's a problem. It Meanswediam

48:30

won't to learn them.

48:31

Yeah, exactly, because if we're

48:33

not, if we're learning them over and over again, we never learned them

48:35

in the first place. But so

48:39

for my last question, I want to go

48:41

back to the title of your book, blighte

48:43

Fungi and the Coming Pandemic, and

48:47

I want to ask you not about

48:49

like why we should be wary of fungal

48:51

pathogens, because I feel like we did a pretty good job

48:54

covering that so far. But I

48:56

want to ask about what should give

48:58

us hope in our ability to detect

49:01

or control or treat a possible

49:03

fungal epidemic in the future.

49:06

So one start is

49:08

awareness. So

49:10

just being aware when

49:13

we talk about you know, you go to the airport

49:15

and they ask you to not take any plants

49:18

or plant bits or whatever, pay

49:20

attention. There's a reason for that. There's

49:24

hope in new developments,

49:26

like we talked about better analysis,

49:28

faster analysis. You know, if you can you

49:31

know diagnosis, if you can have

49:33

rapid diagnosis that sorts of thing, there

49:35

is some hope there. You

49:37

know, I would hope that with trade

49:41

and travel, but trade, that we can

49:43

be more aware of sort

49:46

of what we want. There are some people that say, well,

49:48

why do we need to plant, you know, plant

49:50

plants from other countries. Why don't

49:53

we just you know, grow what's

49:55

native. So that's

49:57

why not, you know, really and

50:00

similarly, I think there are people who would like

50:02

to see less animal trade or and

50:05

you know, the flip side of that is that some people say, but then

50:07

when you do get to have a

50:09

salamander or some kind of odd lizard, you

50:12

develop an awareness for that animal and you

50:15

know some kind of you want

50:17

to save that animal. So there is you know, it goes

50:19

both ways to this kind of thing. I

50:22

think that just having

50:25

some greater awareness grow

50:27

things in different ways. I think, you

50:29

know, people in agriculture are beginning to understand

50:31

and think about how to grow crops differently

50:34

so that they're not so disease prone.

50:37

Just diversity in what

50:39

we eat and what we want. You know, why

50:41

do we just want one type of wheat? Maybe we could

50:43

be eating all sorts of different grains, which we're

50:45

just starting to do. But you

50:48

know, that's that's one

50:50

way. So there are those kinds of

50:52

things. Is that we just have to be open to more

50:55

diversity in what we want. We

50:57

also have to be aware of protecting a diversity

50:59

that's out there, and

51:02

just more cognizant of how

51:05

we all live in this one world. You know,

51:07

plants, animals, humans, we're

51:09

all together in this one world and we all impact

51:11

each other. We're not in our little human bubble.

51:14

Everything interacts with each other and

51:17

we really need to take that

51:19

seriously. And I think and if COVID didn't get

51:21

that us thinking that way, I don't know what will

51:24

which is kind of a sad note to end

51:26

it on, because I'm not sure, you know. I do think there's more

51:28

awareness of ecosystem health,

51:30

how important that is for diseases

51:32

and things like that. So we

51:36

just have such short memories. That's the problem,

51:57

you know.

51:58

This conversation just rein forced

52:00

how amazing and fascinating

52:02

fungi are. Doctor Monison,

52:05

thank you so very much for taking the time

52:07

to chat with me. We covered

52:09

so much ground in this convo, but

52:11

there is still so much more to the world

52:14

of fungal pathogens that I'm sure you

52:16

all want to learn about. If you find

52:18

yourself craving more fungi facts,

52:20

check out our website this podcast will kill

52:23

You dot com. We're all post a link to where

52:25

you can find blighte Fungi and the

52:27

Coming Pandemic, as well as a link

52:29

to doctor Monison's website. And don't

52:31

forget you can check out our website for

52:33

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52:36

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52:59

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53:04

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