Two new books take an unusual approach to music history and blues appreciation

TERRY GROSS, HOST:

This is FRESH AIR. I'm Terry Gross. What are the most devastating disease agents on the planet? Bacteria? Nope. Viruses. Uh-huh. I learned in a new book that the answer is fungi and fungus-like pathogens. They're collectively the most devastating.

The book is called "Blight: Fungi And The Coming Pandemic," by my guest, Emily Monosson. This year, the CDC reported that a deadly fungus, first identified in 2016, is an urgent public health threat that has spread at an alarming rate during the COVID pandemic. It's often resistant to go-to antifungal drugs. It's a threat, but it's not a pandemic.

Morrison writes about this fungus in her book. She also writes about how and why fungal diseases have led to the extinction or near-extinction of species of trees, bananas, bats, frogs, salamanders and more. Most fungi are harmless. Some are beneficial, which is good news considering fungi are all around us. Fungi even populated the Russian space station Mir, threatening the controls, and they were found on the International Space Station.

Monosson is a toxicologist who became a science writer. She's an adjunct faculty member at the University of Massachusetts Amherst. "Blight" is her fourth book. She also edited the anthology of essays called "Motherhood, The Elephant In The Laboratory."

Emily Monosson, welcome to FRESH AIR. Let's start with the CDC's alarming report this year about candida auris, aka C. auris, the deadly fungus that the CDC called an urgent public health threat. Why is it so deadly?

EMILY MONOSSON: Well, it can go systemic, infecting the blood, and once it goes systemic, fungal infection can be lethal. And it can be very hard to treat some of these fungal infections. There are a limited number of antifungal drugs. And when candida auris came on the scene back in 2016 or earlier than that, many of the strains that began affecting people were also resistant to antifungal drugs. So it's hard to treat. So fungal infections in the first place are hard to treat. And then second, this one is resistant to many different antifungal drugs.

GROSS: Why did it spread so much during COVID?

MONOSSON: When the outbreak first happened, one of the things that really alarmed the medical community was that it seemed to - one, which is odd for fungus - be able to transmit from patient to patient or from surface to patient. So it seemed like there was a contact kind of transmission. And when someone had candida auris in a hospital room, it was really hard to disinfect the room after they'd had it. So when they used whatever disinfectants they would normally do when somebody with an infectious disease was in the room, that wasn't helping. But eventually they figured out what kind of disinfectants to use and how to clean up a room and how to, you know, practice a hygiene so that they weren't spreading candida auris - the medical workers weren't spreading Candida auris from patient to patient. So they did better on that.

Then COVID happened, and, you know, hospital workers were overworked. Hospitals were crowded. Hygiene kind of went out the window for candida auris. The specific focus on making sure that didn't spread kind of got pushed aside for just trying to reduce the spread of COVID. Also, some of the treatments for COVID, when people were on steroids - I mean, one of the things I guess I should mention is that candida auris is a really important disease. It's potentially deadly. It also tends to infect people who are immunocompromised or are already in the hospital or in long-term care facilities. So there's a very specific population of people who are already sick who tend to be most susceptible to candida auris.

GROSS: Yeah, and that's kind of one of the paradoxes of this, is that medical breakthroughs like organ transplants and cancer treatments that leave people immune compromised leave them more susceptible to other diseases such as C. auris.

MONOSSON: Yeah. You know, if there's a change in the human population, it's that more of us, because of these fantastic drugs, have become more susceptible to infections like fungal infections because of being immunocompromised. Steroids, other treatments can leave us more susceptible.

GROSS: And it also opens the door to certain pathogens because they have a breeding ground.

MONOSSON: Yes. So in humans, fungal infections tend to be relatively rare, compared to - in the beginning you mentioned bacteria and viruses, and those are more important infectious diseases in the big picture. And there's a reason for this, that, you know, we have defenses against fungal pathogens. One of them is our robust immune system. Another is our warm temperature. Fungi don't tend to like that. So yes, when we change these things, we are more susceptible.

GROSS: Now, candida - it will be familiar to a lot of people because candida albicans causes vaginal infections known as yeast infections and thrush, which is a fungal infection in the mouth. But that should not be confused with the candida that we're talking about.

MONOSSON: That's right. Those two - they're very distant relatives. I should say candida albicans, if it goes systemic, can also cause deadly infections.

GROSS: Thanks for that.

(LAUGHTER)

MONOSSON: Sorry.

GROSS: Now, pathogenic fungi are very resistant. Why are many fungal infections challenging to treat?

MONOSSON: To begin with, fungal cells are eukaryotes. That means that their cells are very much like our cells, unlike bacteria which are prokaryotes, so they're a very distant class from us. And so when we develop antibiotics or things to kill them or antifungals, you need antifungals that target parts of that fungus that are different from our cells. And so there aren't as many targets for a fungus, say, as there might be for bacteria, because bacteria have targets that are very different from our cells.

GROSS: And I think a lot of - most, maybe - fungi develop protective coatings around themselves.

MONOSSON: They do have some protective coatings that help them hide from our immune system. They can grow as things called biofilms on top of each other. Other microbes can do this too. But also the other thing that makes them hard to treat is that - so because their similarity to our cells, there aren't that many antifungal drugs. There aren't that many classes of antifungal drugs compared to antibacterial drugs. There are lots of different kinds of classes. And because fungi are microbes that reproduce rapidly, they can evolve resistance fairly quickly to those drugs. So here we have it's hard to make drugs. There aren't a lot of drugs. And then once the fungus becomes resistant to those drugs, kind of out of luck there.

GROSS: Let me add one thing to that wonderful list, and that is many kinds of pathogenic fungi can live a long time without a host. In other words, they can live a long time outside the human body. This isn't necessarily true of C. auris. I'm not sure if it is or not. But it's true of of some pathogenic fungi. How do they manage to live a long time without a body to feed on?

MONOSSON: Some of the other fungal pathogens that infect humans are - reproduce by making spores. And spores can be, depending on the kind of spore, highly resilient. Depending on the fungus, they could live for - you know, if you have a soil-borne fungus whose spores can infect us, like an aspergillus kind of fungus or the fungus that causes valley fever, those kinds of fungi produce spores, and spores can be depending on the kind of spore type, highly resistant and resilient and live in the soil for days, weeks, months, depending on the fungus. In plants, there's a spore that can live for decades in the soil. So this can make them a very long-term problem and very difficult to sometimes avoid, like valley fever, which is, you know, in the desert Southwest. It's a soil-borne fungus. And it's - if the soil is disturbed, those spores are released. And they could potentially live a long time, and they can travel.

GROSS: You mentioned fungi typically don't like our body temperature, which makes us immune to a lot of fungi because they live in cooler temperatures than the average 98.6 of human bodies. But you write that global warming might be changing it and that the fungi might be evolving to live in warmer climates. So tell us about the threat that this may pose and why.

MONOSSON: Yeah. So I interviewed a scientist, Arturo Casadevall, and he has been studying what he calls the mammalian fungal filter. So there's millions of fungal species. A very small proportion of them infect humans. It's believed that's because most of those fungi don't like our warm temperatures. He asked, why is that? You know, did that give us an advantage? And it seems that back in the day when the asteroid hit the Earth, you know, why did mammals emerge as sort of the dominant species rather than reptiles? And his hypothesis is that at the time the asteroid hit, lots of things died. There was dead stuff everywhere. Fungi love dead stuff. So fungi bloomed. And apparently this is in the fossil record. There's spores. And because the fungi couldn't live in our warm temperatures, mammals weren't as affected by all the fungi that were around. But maybe the amphibians and reptiles that were around who live at colder temperatures or whose bodies are colder became infected. And so that - this gave us an edge.

So Candida auris, some scientists think, is one of the first fungal sort of outbreaks potentially caused by climate change. The thinking is that it's a yeast that was probably living out in the environment, couldn't infect us because it just couldn't live at our body temperature. As environmental temperatures warmed, it kind of evolved to just be able to be more comfortable in warmer temperatures. Eventually it became more comfortable to live at what would be our body temperature. And so then it could begin to live in us and grow in us once it - you know, we became in contact with it. And fungi are - they're highly evolvable because they live in the environment, they're highly reproductive - especially spore-forming fungi - gives them a lot of opportunity to sort of evolve in response to a new pressure, like warmer temperatures.

GROSS: Let's take a short break here. If you're just joining us, my guest is Emily Monosson, author of "Blight: Fungi And The Coming Pandemic." We'll be right back. This is FRESH AIR.

(SOUNDBITE OF CHARLIE HADEN'S "EL CIEGO (THE BLIND)")

GROSS: This is FRESH AIR. Let's get back to my interview with Emily Monosson, author of the new book "Blight: Fungi And The Coming Pandemic."

So, you know, there's plant and animal species that have become extinct or are threatened with extinction because of pathogenic fungi. One example are a kind of bat that is - they're known as little brown bats, and some of them live in your neighborhood. So...

MONOSSON: Yeah.

GROSS: ...Let's start there since it's very close to home for you. What has killed so many of them?

MONOSSON: A fungal pathogen whose name - one of the few names that I will try to pronounce - is pseudogymnoascus destructans - nickname PD - and it's a fungus that causes a disease in bats called white-nose only because when it was first discovered in the dying bats - dead and dying bats, it appeared as a little puff of white fungus on the tip of the bat's nose. And it was one that we actually observed - we didn't see the disease in the neighborhood, but we actually observed the loss of the little brown bats in our neighborhood.

GROSS: Is there something about bats that have made them particularly vulnerable to this fungal infection?

MONOSSON: Yeah. So when I talked about humans having a high body temperature, all mammals have high body temperatures. And so typically, fungal infections would also be relatively rare across mammals. So what is it about bats? Why are they being killed off by a fungal pathogen? And it's because bats hibernate. And when they hibernate - it's amazing - they - their body temperatures actually drop to the level of the cave temperatures in the winter. So they can be just a few degrees above freezing. And when that happens, everything slows down. Their breathing slows down to, like, maybe, I don't know, one breath every 15 minutes or something like that. Their immune system is probably also kind of suppressed or slowed. And so they're there, but they're not at their very warm temperatures.

And when white-nose infects them, it is when they are hibernating during the winter in those caves. Scientists aren't totally sure about how the fungus is killing the bats, but one of the things they think is that it kind of rouses them from their hibernation or their torpor when they're down at these low temperatures and that they wake more. They typically, I guess, would wake during a normal hibernation every once in a while to drink or pee or, you know, flutter around a little bit, but then they'll go right back. But having the fungus causes this to happen more often. It might drain them of their energy. When they emerge in the spring and their body temperatures warm up, you know, if you were to look for white-nose in the bats that are in our local church in the winter, you probably wouldn't find it because the fungus can't live on them when they're at their warm temperatures.

GROSS: So they die off before emerging from hibernation or soon after?

MONOSSON: Yeah, that was how the disease was first detected was - I think it was in the early spring when people went to the caves because they found dead bats outside of the cave. And then when scientists started to go at the end of the spring, they found just horrendous scenes of dead and dying bats with fungus just at the end of their hibernation period.

GROSS: So do you miss the bats in your neighborhood?

MONOSSON: We do miss the bats. We used to go down to the church where they were up near the attic, and you would just sit there at dusk and watch streams of bats coming out of the church. And it was just a beautiful sight. So we would watch the bats come out of the church, and then they weren't doing that so much. And, you know, when you sit in your backyard at night and you see them flitting about, you know that they're eating insects, and that's a good thing. So not seeing them is a little sad. We are seeing a few more now and then, and there's some hope that bats might be able to - some bats in populations of bats might be able to overcome white-nose.

GROSS: So were the bats nesting in the church?

MONOSSON: They are roosting, yes.

GROSS: Roosting, OK.

MONOSSON: So what's so cool is that those - what I learned is that those bats in the church, especially in the early spring or, you know, maybe early summer, they're usually female bats. It's a maternity roost. So they roost there. They have their young. And sometimes, in the early part of the season when they're flying out, their young are clinging to them. So there's mother bats with babies clinging to them flying around.

GROSS: So let's talk about the banana plagues. I like bananas a lot, and I'm really worried about them. So the bananas that we eat now that are exported to America are largely Cavendish bananas. And they replaced a previous breed of banana, a breed that had died off because of a fungal plague. A lot of the bananas are grown by giant fruit companies. What did the giant fruit companies did wrong that left the previous breed of banana, the one that preceded Cavendish - that was called Gros Michel, G-R-O-S Michel - so maybe it's pronounced Gros Michel and not Gros Michel. But so what did the large banana growers do wrong that allowed this fungus to spread and make the Gros Michel bananas virtually extinct?

MONOSSON: I think one of the problems with the banana industry, which probably isn't unique to the banana industry, is the huge monocrops. So this is a soil-borne fungus, and it also spreads in the soil. So they grew huge monocrops, but bananas are also clones. And the way they grow them is they tend to take a - bananas are huge - are big herbs, and they'll have these shoots that come off, and they can just take the shoot and then plant it and make a new banana plant. So the plants are essentially clones of each other, so there's not a lot of genetic diversity in there. So you've got this huge monocrop of cloned plants. And so if you've got a fungus that can infect those plants, you've got a pretty happy fungus 'cause it's got zillions of plants that it can infect.

One of the problems today - so this one strain of fungus that impacted the Gros Michel called TR1 - and so it was so bad that they couldn't grow those bananas anymore, and they switched to the Cavendish, as you mentioned. And then today, there's a new strain, called TR4, of this kind of fungus that's now infecting the Cavendish plants. And it's swept across banana plantations, and it's sort of like - there's a writer that I quote in the book who basically says, you know, you could have seen this coming. But it's just - they found a new banana, and so they just did what they were doing before. And now they're having the same problem as they had before. The entire industry is under threat from this fungus.

One scientist who studies it has studied the movement and at first, you know, wondered about - it's the way that they're just moving soil. They move plants. They move farm equipment. People move. They've got - you know, you can carry this soil-borne fungus around in your feet, in the plant that's being moved and in the tread of tires. And so maybe that's how it's being moved around. But he now thinks that, you know, it can also spread if there's a flood or water in streams, anything that will pick up soil could potentially spread this fungus. And so he's now thinking that, you know, while probably growers were maybe to blame for moving this fungus around, in many cases, it might also be able to move around by forces that can't always be controlled. So it's a problem.

So the biggest problem is the huge monocrop of a single kind of banana. And so one of the solutions from some of the scientists that I spoke to is maybe we need to diversify our diet and enjoy different kinds of bananas, just like we enjoy different kinds of apples because then some might be more resistant to certain kinds of fungi, and we don't have to worry about the whole - one whole crop of a single kind of banana being wiped out.

GROSS: So just in looking ahead, do you have any idea how long the Cavendish bananas will exist?

MONOSSON: So I have some scientists that say we're not going to not have bananas. But I think what he's saying is we might have some other kind of banana. I don't know how long. I do know that, so far, that disease hasn't hit Costa Rica. They're trying very hard to keep it out, but it has hit a lot of other places. But we do have still Cavendish bananas. So I don't know how bad it's been in those places where it's hit. In the very beginning, I mentioned a fungus whose spore can live for decades. That's one of the fungi whose spores can live for decades, the TR4 kind of fungus, the soil fungus. So once that fungus gets in the soil, then they either have to grow a different kind of banana or move where they're growing bananas. So it is a big problem. I don't know how long.

GROSS: Well, let me reintroduce you here. If you're just joining us, my guest is Emily Monosson, author of the new book "Blight: Fungi And The Coming Pandemic." We'll talk more after a short break. I'm Terry Gross, and this is FRESH AIR.

(SOUNDBITE OF STEVE REICH'S "SECTION II")

GROSS: This is FRESH AIR. I'm Terry Gross. Let's get back to my interview with Emily Monosson, author of the new book "Blight: Fungi And The Coming Pandemic." It's about how fungi have killed off species of plants, animals, including trees, bananas, bats, frogs, salamanders and more. The CDC warned this year that a fungus that has spread in hospitals and nursing homes, a fungus that older people and people with compromised immune systems are particularly susceptible to, spread at an alarming rate during the pandemic and is an urgent public health threat. Emily Monosson is a toxicologist who has become a science writer.

Let's talk about trees, Emily - trees like chestnut trees, whitebark pine trees, elm trees which are close to extinction or have basically become extinct. You know, you point out in your book that, you know, lots of streets are named after chestnut trees. In Philadelphia, where I live, there's Chestnut Hill. There's Chestnut Street. I used to live in Buffalo, and I lived on Elmwood Avenue, but so many of the elm trees had died. And so how do trees become extinct or near extinct? What is responsible for them, you know, dying off in basically a fungal plague?

MONOSSON: Yeah. So I write about the chestnut trees and the whitebark pine trees. In both of those cases, the fungus that infected those trees and are killing off those trees is not a native fungus. And actually - I should say this - most of the fungi that I write about in this book are emergent diseases. So they're kind of relatively new. They're just kind of coming out. And what is new about them is that they traveled from one place to another and found a new host. So in both of the cases - in the whitebark pine and the chestnut - the fungus that infected them - in the case of the chestnut, the fungus probably came from Asia. It lives in Chinese chestnuts and Japanese chestnut trees, and it lives just fine. In those trees, the fungus and the tree have come to some kind of uneasy peace where they can live together.

About a hundred years ago, there was a lot of importation of - as there are now - trees from other places for exotic trees to - just 'cause they grow chestnuts that people wanted to eat, whatever. So when trees are imported, if they're carrying that fungus, it gave the fungus an opportunity to find a new host. And it did find a new host, in this case, in the American chestnut tree. And the American chestnut had never seen this fungus before. It had no resistance. And so it was just sort of a sitting host for this fungus. And apparently the fungus had a feast and killed all the chestnuts within a few decades up along the East Coast.

GROSS: There's a couple of different pathways scientists are trying to bring back chestnut trees. What are these approaches?

MONOSSON: So one of the longest ongoing approach was to breed resistant trees. So once scientists identified that there were chestnuts that were resistant to the fungus - Chinese chestnuts, Japanese chestnuts - you know, the obvious thought was, well, we just need to breed the resistance into the American chestnut tree. And if we could do that, if we can capture the resistance, whatever gene is, you know, imbuing that kind of resistance, then we can have American chestnut trees that are now resistant to the chestnut blight.

So there was a 30-year plan to breed resistant chestnuts. What the scientists would do would be that they would, you know, make a hybrid tree, capture the resistance gene from Chinese chestnut trees, and then, because they want a tree that has the American chestnut tree characteristics - the two trees grow kind of differently - if you see them, you can see the difference - to backcross, breed in American chestnut with their cross so that they would end up having a tree that had mostly American chestnut tree characteristics but the resistance of the Chinese chestnut trees.

These are trees, so it takes a long time to breed and then collect nuts and then breed. And so there was this 30-year plan that was taken over, basically, or they developed an organization that could oversee this 30-year plan, which was called the American Chestnut Foundation, which has done amazing work with chestnut trees and has taken charge of this breeding program. And so they breed the trees. Then they have to test to see if those trees are resistant. Then they take the resistant trees, and they breed those trees. So you can imagine it's a very long process, 30-year process. It started almost 30 years ago. So the foundation is coming to the end of that process.

The thing that happened over the years at the same time is genetics and the ability to do DNA sequencing, which - you know, in the beginning when this plan started, the thinking was that there was one or two genes that provided resistance. It turns out, which they only found out relatively recently, it's many genes, and they're spread across chromosomes. And so it would be very hard to capture those resistance genes. And so while they've bred trees that are kind of resistant, they haven't been able to reach their goal of a highly resistant chestnut tree that has most of the characteristics of the American chestnuts.

GROSS: So is there a more recent development in genetic engineering that is being applied to the chestnut tree or to other trees that are or are nearly extinct?

MONOSSON: Well, so around the same time, there was a scientist, William Powell, who wondered if he could use genetic engineering to develop a resistant chestnut tree. And in this case, there is a single gene that can make a chestnut tree able to resist the fungus. And so his idea was to take that gene - it's called an OxO gene - it produces an enzyme that can help the tree fend off the fungus - and to transfer that gene, the OxO gene, into the American chestnut. And so it's taken decades to do that successfully. And in the last few years, he's actually produced American chestnut trees that contain a gene that do give it resistance to the chestnut blight fungal infection. And so right now, that tree is going through all the federal approvals that it needs to go through, which I think is, like, FDA and USDA and EPA. So they have tested this tree every which way. So it's a genetically engineered chestnut tree. The goal is to put it out into - eventually - into the wild where chestnuts used to grow to restore a member of the forest ecosystem.

GROSS: Since so many of the fungi, the pathogenic fungi that have killed off, you know, plants or animals have come here from other countries, from importing animals or reptiles or trees, so what are the cautionary steps the U.S. government has taken so far to prevent the importation of any kind of, you know, plant or, you know, or animal or fish that may have a fungus that could spread here?

MONOSSON: So there's a fairly long history of plant inspections. And I spoke to our U.S. national mycologist, which I thought was kind of interesting that we have a national mycologist. So she is our national fungus expert for plant pathogens. And her job is when plants come in, they get kind of a cursory inspection at the ports they come into. If there's a problem, there's some kind of fungal identifiers, they take a closer look. And if they can't identify what's on those plants, they send a sample to her - this happens really quickly 'cause these are plants and they can't hold them too long - send them to her, and she looks at them under the microscope and tries to identify them. And she often sees new things. And so - you know, so that is one way that there's been movement to protect plants in our country from incoming diseases. That said, she is overwhelmed, and there's only two national mycologists, I think, who are doing this sort of final, you know, good look at a plant. So there is still a lot of potential for new pathogens to slip through even when they're doing this, but less than there was maybe 50, 60, 70 years ago.

For animals, it's a little bit different. There is no national mycologist kind of position for animals that come into our country, and we import them for various reasons by the many millions. So it's a huge industry. And one part of that industry is the pet trade. So pets - you know, importing animals for pets is a big deal. And I write about the frog-killing fungus, a fungus called Bd, which has killed frogs around the world. It was believed to be spread through the animal trade. And so these scientists - and that's one of the most catastrophic. So when, you know, talk about a fungal pandemic in animals - or a panzootic, which technically this is 'cause it's killing animals - the frog-killing fungus is sort of the poster example of how catastrophic fungi can be 'cause it's killed off dozens of whole species driven into extinction. So that was thought to be caused by the animal trade.

And so one of the things that's happened over the years is that there's - it has a cousin that's called Bd. There's a similar fungus that's called Bsal because it infects salamanders. And in the last decade or so, it's been killing off salamanders in Europe. So the scientists here who study Bd are terrified that if that salamander-killing fungus comes here, it will just take off. And we have some real hot spots for salamander diversity here. And so - especially in the Appalachians, I think. And so it's a real concern.

GROSS: We've talked about pathogenic fungi. Let's talk about good guy fungi for a second, 'cause not all - most fungi are not harmful. So let's briefly talk about what they're good for. First of all, you say, you know, fungi decompose things that are dead or dying, and without fungus, we'd be surrounded by the dead and there'd be no room for the living. I - that brought quite a picture to my mind. Can you elaborate on that?

MONOSSON: Well, yeah, they are the major decomposers of the planet, along with - there are other organisms that do that. But imagine, you know, when you walk through the woods and you see those logs decomposing and then you dig into them and you see the mycelia of fungus. There are fungal shrouds that people have made to bury people in. I mean, they are major, important decomposers. And what they do when they're decomposing, not only are they getting rid of a lot of the dead things, they're actually kind of turning the nutrients that are captured in those dead bodies - plant and animal - back into nutrients so that other animals can use those nutrients. So they're very important in recycling the nutrients of the world.

GROSS: And there's also penicillin, which comes from a mold.

MONOSSON: Yeah, and they provide us with antibiotics. Fungi are releasing chemicals, which people know. Mushrooms release certain kinds of chemicals that people like. And then there are also chemicals that are deadly. And some of those chemicals that fungi release are active against other microbes, which is useful for us to use as antibacterials.

GROSS: Emily Monosson, thank you so much for being with us.

MONOSSON: Thank you for having me.

GROSS: Emily Monosson's new book is titled "Blight: Fungi And The Coming Pandemic." After we take a short break, rock critic Ken Tucker will review two music-related books - one about blues pioneer Robert Johnson and the other about making music documentaries, including two related to Robert Johnson. This is FRESH AIR.

(SOUNDBITE OF MICHELLE LORDI SONG, "WAYWARD WIND")

TERRY GROSS, HOST:

This is FRESH AIR. Our rock critic Ken Tucker has been reading two unusual books about music history. Robert "Mack" McCormick's "Biography Of A Phantom: A Robert Johnson Blues Odyssey" is a long-awaited study of blues pioneer Robert Johnson's life, written during the 1970s but never published until now. And in Robert Mugge's "Notes From The Road: A Filmmaker's Journey Through American Music," Mugge reminisces about directing more than 25 music documentaries, his subjects including Robert Johnson, jazz great Sonny Rollins and soul singer Al Green. Here's Ken's review.

(SOUNDBITE OF SONG, "HELLHOUND ON MY TRAIL")

ROBERT JOHNSON: (Singing) I got to keep moving. I got to keep moving. Blues falling down like hail. Blues falling down like hail.

KEN TUCKER, BYLINE: Mack McCormick spent three decades trying to get to the bottom of the bottomless mystery of Robert Johnson, the blues innovator about whom little was known after his death in 1938 at age 27. McCormick's "Biography Of A Phantom" isn't a conventional biography. It's as much about McCormick's own journey. He speaks to the reader in the first person, taking you along with him as he visits small Southern towns, beginning in the late 1960s, sitting on dusty porches, eating in greasy spoons, interviewing anyone who'll talk to him about their memories of Johnson.

(SOUNDBITE OF SONG, "KIND HEARTED WOMAN")

JOHNSON: (Singing) I got a kind-hearted woman, do anything in this world for me. I got a kind-hearted woman, do anything in this world for me. But these evil-hearted women, man, they will not let me be

TUCKER: In part because McCormick kept tinkering with the manuscript until he died in 2015 at age 85, his work wasn't published until now and has been superseded in simple research by a couple of more recent biographies. But what they lack is something important, the feel, the atmosphere of McCormick's so-called blues odyssey. It's a completely engrossing exploration of the South, one that only elevates and deepens what Robert Johnson achieved as an iconoclastic musician who was said to have sold his soul to the devil for his mastery. McCormick's book also has the added gift of revealing how a great biography can be assembled.

(SOUNDBITE OF SONG, "STONES IN MY PASSWAY")

JOHNSON: (Singing) I got stones in my passway, and my road seem dark as night. I got stones in my passway, and my road seem dark as night. I have pains in my heart, they have taken my appetite.

TUCKER: In 1992, director Robert Mugge released "Deep Blues," a filmed road trip that explored the Delta blues via some then living and still vital musicians, including R.L. Burnside and Junior Kimbrough. Mugge followed this up in 1999 with "Hellhounds On My Trail: The Afterlife Of Robert Johnson," tracing the influence of Johnson on subsequent generations. Both films contain interviews that provide firsthand context that demystifies the creation of the blues, music that, at its best, can sting your soul and bring clarity to your darkest thoughts.

(SOUNDBITE OF SONG, "CROSS ROAD BLUES")

JOHNSON: (Singing) I went to the crossroad, fell down on my knees. I went to the crossroad, fell down on my knees. Asked the Lord above, have mercy, now - save poor Bob if you please. Yeah, standing at the crossroad. Tried to flag a ride.

TUCKER: In his new book, "Notes From The Road," Bob Mugge chronicles the making of these blues films, as well as ones exploring jazz, gospel and soul. But the stories he tells go well beyond anecdotes about musicians. He opens up the whole world of documentary filmmaking - how they're financed, how they're recorded and edited. He relates startlingly honest stories about unscrupulous producers and difficult artists, never sparing himself for his own flaws or naivete. "Notes From The Road" is the best thing I've read about what it's like to direct films since Sidney Lumet's 1996 classic "Making Movies." One thing these two new books prove is that it's not only hard to carve out a career as a musician, it's hard to carve out a career as a professional appreciator of musicians. Mack McCormick as biographer and Robert Mugge as filmmaker suggest it's not just artists who have to occasionally make deals with the devil.

GROSS: Ken Tucker reviewed the books "Notes From The Road," by Robert Mugge, and "Biography Of A Phantom: A Robert Johnson Blues Odyssey," by Robert Mack McCormick. Next month, Smithsonian Records will be releasing a boxed set of blues music called "Playing For The Man At The Door: Field Recordings From The Collection Of Mack McCormick, 1958-71." A new sequel to the series "Justified" premieres tomorrow. Like the original, it stars Timothy Olyphant. We'll hear our TV critic David Bianculli's review after we take a short break. This is FRESH AIR.

(SOUNDBITE OF GERALD CLAYTON'S "SOUL STOMP")

TERRY GROSS, HOST:

This is FRESH AIR. After starring as an 1870s Western lawman in HBO's "Deadwood," Timothy Olyphant played a modern-day marshal in the FX drama series "Justified." That show, based on writer Elmore Leonard's character, the quick-tempered, fast-shooting Raylan Givens, ran from 2010 to 2015. But now the actor, the character and the series are back in a new eight-part FX sequel called "Justified: City Primeval." It premieres tomorrow on FX. Our TV critic David Bianculli has this review.

DAVID BIANCULLI, BYLINE: "Justified," the original FX series, was one of the most underrated TV shows of the past decade. Graham Yost, who brought Elmore Leonard's vision and characters to television, did a great job with every aspect of the adaptation. The various writers and directors were electrifyingly original. And the stars and guest stars, from Walton Goggins to Margo Martindale, played at the highest possible level. This new sequel, called "Justified: City Primeval," is developed for TV by "Justified" veterans Dave Andron and Michael Dinner. And once again, it showcases what "Justified" did and still does best. It takes colorful and volatile characters, well-matched and equally unpredictable, and pits them against each other.

FX launches this eight-part sequel with a double feature consisting of the first two episodes. And if you watch them both, you'll witness the raw energy that "Justified" is capable of unleashing. And it's a daring, high-wire adaptation, a bold gamble that works only because this team knows the character of Raylan Givens, played magnetically by Timothy Olyphant, so, so well.

In Elmore Leonard's original "City Primeval" novel, U.S. Marshal Raylan Givens isn't even in it. The killer at the center of the story, Clement Mansell, is the same. But in the book, the hero is a detective named Raymond Cruz. But for TV, Cruz is demoted to a minor supporting character. And a plot twist early on finds a way to insert Raylan into the action and into the city of Detroit, along with his now teenage daughter, Willa, who figures in the story early on.

When we last saw Willa in the final episode of the original "Justified" in 2015, she was a preschooler. Now, at the start of this new series, years later, Willa is 15. And Raylan is driving her to summer camp, as the radio plays, but Willa doesn't want to go. This early scene is especially noteworthy because the actress now playing Willa, making her acting debut, is Timothy Olyphant's real-life daughter, Vivian. And just like her dad, she plays her role impressively without any artifice whatsoever.

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VIVIAN OLYPHANT: (As Willa Givens) Can we pull over at the next rest stop?

TIMOTHY OLYPHANT: (As Raylan Givens) You sound like every fugitive I ever transported - stalling, pleading, looking for their chance to give me a slip out the bathroom window.

V OLYPHANT: (As Willa Givens) The place you're shipping me off to might as well be a prison.

T OLYPHANT: (As Raylan Givens) Website made it look quite pleasant.

V OLYPHANT: (As Willa Givens) They won't let you leave, and they take your phone.

T OLYPHANT: (As Raylan Givens) Sounds like heaven.

V OLYPHANT: (As Willa Givens) You lost an hour without your phone. How else would you get the call?

T OLYPHANT: (As Raylan Givens) What call, your call? All you do is text, and you barely do that anymore.

V OLYPHANT: (As Willa Givens) Not my call, the call. Come on, Dad, I don't want to do this.

T OLYPHANT: (As Raylan Givens) I'm guessing you'll think about that the next time you consider punching a girl in the face.

V OLYPHANT: (As Willa Givens) I barely touched her.

T OLYPHANT: (As Raylan Givens) You broke her nose.

V OLYPHANT: (As Willa Givens) She deserved it.

BIANCULLI: And that happens to open this drama. And "Justified: City Primeval" has nothing but memorable performances and characters ahead. Central to this particular story are Mansell, the elusive killer played by Boyd Holbrook, and Carolyn Wilder, the defense lawyer who has represented him in the past and helped him avoid prison. She's played by Aunjanue Ellis from "Lovecraft Country" and "King Richard." And when the three of them meet in Episode 2, the tone is quiet, but the tension is high. Raylan, suspecting Mansell of a recent crime involving a local judge, confronts him in the lawyer's office. Mansell starts mouthing off to Raylan until she stops him cold.

(SOUNDBITE OF TV SHOW, "JUSTIFIED: CITY PRIMEVAL")

AUNJANUE ELLIS-TAYLOR: (As Carolyn Wilder) Not another word unless I ask you a question.

T OLYPHANT: (As Raylan Givens) Can I ask him a question?

ELLIS-TAYLOR: (As Carolyn Wilder) What is it?

T OLYPHANT: (As Raylan Givens) Was he driving around a Range Rover last night, license number 8...

ELLIS-TAYLOR: (As Carolyn Wilder) He's not going to answer that.

BOYD HOLBROOK: (As Clement Mansel) No, go on. I want to hear how you're going to lay the judge on me.

ELLIS-TAYLOR: (As Carolyn Wilder) Not another word.

HOLBROOK: (As Clement Mansel) He's dying. You got this idea of what happened to the judge, you just can't get nobody to - what's the word? - corroborate it.

T OLYPHANT: (As Raylan Givens) Corroborate. Hanging around courtrooms and county jails, you learn some words, don't you?

HOLBROOK: (As Clement Mansel) Yeah, you learn a few things about the lawman, too.

T OLYPHANT: (As Raylan Givens) This ought to be good.

HOLBROOK: (As Clement Mansel) Only two kinds of guys out in the street chasing bad guys at your age - the ones who got passed over for the big chair and the ones that just love it so much, they're going to have to be dragged off. Only question is, will they be breathing when it happens?

BIANCULLI: Other major players include Vondie Curtis-Hall and Adelaide Clemens as two of Mansell's associates. And smaller parts, served up like little treats, are played by David Cross, Terry Kinney and other familiar faces viewers should discover for themselves - and you'll be delighted when you do. I had forgotten how much I loved and missed "Justified," but this new miniseries sequel brings it all back home. The two installments shown as the premiere conclude with one of this year's best and most tense TV scenes. And the overall ending of this miniseries, when it finally arrives, is so tantalizing, the thought of FX making even more installments is entirely and inarguably justified.

GROSS: David Bianculli is a professor of television studies at Rowan University. He reviewed the new series "Justified: City Primeval." It premieres tomorrow on FX. Tomorrow on FRESH AIR, we'll hear from the star of "Justified" and "Justified: City Primeval," Timothy Olyphant. He recorded the interview last week before the actors went out on strike. I hope you'll join us.

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GROSS: Our interviews and reviews are produced and edited by Amy Salit, Phyllis Myers, Sam Briger, Lauren Krenzel, Heidi Saman, Ann Marie Baldonado, Therese Madden, Thea Chaloner, Seth Kelley and Susan Nyakundi. Our digital media producer is Molly Seavy-Nesper. Roberta Shorrock directs the show. Our co-host is Tonya Mosley. I'm Terry Gross.

(SOUNDBITE OF FLORATONE'S "SWAMPED")

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