This Week in Microbiology
With Vincent Racaniello, Michael Schmidt, Elio Schaechter, and Michele Swanson
Episode 162: Intracellular bacteria with flagella
Aired October 13, 2017
Vincent: This Week in Microbiology is brought to you by the American Society for microbiology at asm.org/twim.
(music)
Vincent: From Microbe TV, this is TWIM, This Week in Microbiology, episode 162, recorded on October 12 2017. This episode is brought to you by the Defense Threat Reduction Agency, part of the US Department of Defense, the agency’s chemical and biological technologies department hosts the 2017 Chemical and Biological Defense Science and Technology Conference to exchange information on the latest and most dynamic developments for countering chemical and biological weapons of mass destruction. Find out more at cbdstconference.com. Hi everybody, I am Vincent Racaniello, you are listening to the podcast that explores unseen life on Earth. Joining me today from Small Things Considered, Elio Schaechter.
Elio: Well hello there, how are you?
Vincent: Hi, how are you?
Elio: I’m doing okay.
Vincent: We had a little hiatus there, but we’re back. Also joining us from Ann Arbor, Michigan, Michele Swanson.
Michele: Hello!
Vincent: Welcome.
Michele: Thank you.
Vincent: And from Charleston, South Carolina, Michael Schmidt.
Michael: Hello, everyone!
Vincent: And there we have it, the TWIM team all here today. Today we have a snippet, we have a paper, and we have some email for your listening pleasure. The snippet today was suggested some time ago by our listener named Hannah. And she wrote,
Dear TWIM hosts and associated microbiomes (laughter), I came across this heartbreaking News and Views article in Nature yesterday and thought it would be worth talking about on TWIM. She sent a link to that and the paper, which we will discuss today, and she gives a lovely summary. In short it is about the aptly named chytrid fungus Batrachochytrium salamandrivorans which in just a few short years has nearly obliterated fire salamanders, Salamandra salamandra, from a few regions in northern Europe. The fungal disease is 96% fatal. Salamanders are unable to develop an immune response, the spores persist in the environment for an extremely long time, virulence has not been decreasing over time, and there are several European reservoir hosts. The only good news is the fungus is a relatively new arrival and hasn’t spread far yet, but judging by this paper the prognosis is grim.
Elio: In the paper they call it the perfect storm.
Vincent: The perfect storm. I think this is my first time writing to TWIM, though I’ve written to TWIV and TWIP a few times and have been listening to all three podcasts religiously for years. She writes a bit about her which I will save till afterwards. Very interesting stuff, she is working on termites. But let’s first talk about this very interesting paper which is published in Nature as a letter. It’s called “Drivers of salamander extirpation mediated by Batrachochytrium salamandrivorans.” And the first two authors equally contributed, Gwiji Stegen and Frank Pasmans, the last author is Ann Martel. And they are from Ghent University, the University of Zurich, the Swiss Ornithological Institute and the University of Brussels.
So Hannah said the culprit here is a fungus, a chytrid fungus, so this is a member of the phylum chytridiomycota, these are considered the oldest types of fungi that we know about, and over 1,000 different chytrid fungi that live mostly in water or moist environments, and you may have heard about chytrid fungi because they are also wreaking havoc on frogs globally and causing mass extinctions. Now, in this paper we are talking about a chytrid B salamandravorans which has been around for a while. It originated in Asia many, many, many years ago but seems to have been transported to Europe with salamanders as part of the pet trade.
Michael: Oh my.
Vincent: So Asian salamanders, this was many many millions of years old, so Asian salamanders have become resistant to the fungus but in other parts of the world the salamanders have never seen it. When it was introduced into Europe, the fungus that is, it spread like crazy in wiping them out. And that is what happens when you put a pathogen into a new population that has never seen it before. We’ve seen this happen with viruses all the time. You have problems. So the pet trade, shipping salamanders, people love to have salamanders, they are very attractive, but it is a problem.
So this paper, it is a very nice study. What they have done here, it was first found in Belgium, I should say, after the first discovery of this fungus in Belgium which was April 2014, they monitored the fungus and its effect on salamanders for the next two years. Part of that monitoring is part of the study, and they also do some experiments. They show, basically, they monitor the population of the salamanders, and they show this incredible decrease in populations, and there is a figure that shows that, where the number of salamanders from 2014 to 2015 has hugely declined after the introduction of this fungus. They do a series of infection experiments, you can grow these salamanders in the laboratory, you can grow the fungus of course, and you can infect and see what happens. But basically, in the lab, this infection in this species, Salamandra salamandras, is that it? It’s close. It’s almost 100% lethal.
Michele: What I found striking about that, too, is that it wasn’t dependent on just a high dose of infection. Even if they did a very low dose of infection, it took longer but still 95% death, yeah. Even at different temperatures. They tried to give the salamander every chance to fight back and they could not.
Vincent: These are fire salamanders, by the way. Also, the lethality is independent of temperature. The optimum growth temperature for the fungus is 15 C. If you infect at 4C it takes longer but it will eventually kill them, as well. And here is the thing that is very scary. If any salamander survives infection, they are not immune, they can be killed again by reinfecting them. There doesn’t seem to be any immunity built up against this fungus. Salamanders do have innate immune systems, but apparently they don’t have what it takes to fight off this infection.
Michael: They need good God fearing T cells in order to get rid of this.
Vincent: maybe that is the problem here. The reason why this fungus is wiping out the population is it disproportionately infects sexually mature animals, so you get rid of all the salamanders that can give rise to new salamanders and of course the population disappears. Older animals who don’t reproduce anymore are less susceptible but that doesn’t matter. Eventually they are going to die anyway, so this is a real problem. They have a photo here of two salamanders mating, and this fungus causes skin lesions and when they mate, they transfer the fungus to one another. That’s what happens, that is how it is transferred. This fungus has not shown any decrease in virulence over the time of the outbreak in Europe, and it makes environmentally resistant spores.
Typically this fungus makes motile spores which are not as resistant, and they can be transmitted by aerosols, but they also make what they call an infectious insistent spore, which is incredibly resistant. The other spores, the motile spores, can swim, and that may be how they get to their hosts, but they are not very stable. These insistent spores are extremely stable in the environment and they last for long periods of time. In fact, in this experiment they last at least 31 days in pond water.
Michael: And they are floating on the water air interface, and if you think about the life history of the salamander, it has to go into the water and as it breaks that surface, it is obvious that the salamander has to encounter those insistent spores. So even though it is a different mode of transmission, it is as efficient because of the life history of the animal that the spore is infecting. It’s a really remarkable adaptation of that insistent spore.
Vincent: Spores also stick to the skin of the salamander and they also stick to the feet of water birds, so they can be transmitted longer distances as the birds move around. It’s amazing, really.
Michael: This reminded me a lot of how influenza moves so rapidly around the globe with birds, and the other parallell I drew as I was reading this is how influenza is so universally lethal to a naive population that doesn’t have any inherent or intrinsic immunity to it, so in many ways, if you are thinking about it, this is a pandemic that is affecting the salamanders of Europe.
Vincent: Absolutely. Michele, you were gonna comment.
Michele: Yeah, these little spores are also more tolerant to prey in the water, so zooplankton that would normally feed on spores, they can tolerate that, as well. Boy, I just don’t know what methods we can use to get this under control.
Vincent: It’s going to be tough. They also looked at two other hosts of this fungus, toads, for example, can be infected. They don’t show signs of disease but they can transmit the fungus to salamanders, so they can actually infect them in the lab. Infect the toads in the lab, mix them with the salamanders, they will transmit infection. In addition, newts, alpine newts, which occur in the environment with the fire salamanders, they get disease and death at a high dose, but at low doses they survive and they can transmit the fungus to the salamander as well. So the newts also could be a pathogen reservoir.
In addition, the fungus is in forest soil, they show that they can transmit the infection to salamanders via contaminated forest soil, and the contamination of the soil occurs from the newts. The newts are infected, they shed it into the soil, and they found fungal DNA after 200 days in forest soil. So they write the presence of a resistant spore with the ability to persist environmentally, transmit through contaminated water and soil, combined with long term infected and pathogen shedding amphibian hosts creates the potential for extensive environmental reservoirs and hampers any efforts to eradicate the fungus from an infected ecosystem. No options to halt the spread in any way. We should point out that many parts of the world are free from this chytrid fungus, like the Americas, but who knows.
Michael: We love to import pets, especially exotic pets.
Vincent: If someone brings in the wrong salamander, this could introduce it here, because we certainly have salamanders here. So I don’t know what to do about that. You have to have rules but people always break the rules and bring in things when they are not supposed to. Maybe just a matter of time before it reaches the Americas.
Michael: It begs the question, how are the Asian salamanders resistant?
Vincent: That is a good question and that should be studied. Obviously it is something that happened over many many years. They point out here that over the 2 year period in Europe, the fungus has not decreased in virulence for the salamanders, but it is probably too soon, right? It takes a lot longer for these things to occur. Both the fungus and the host probably coevolved so they both persist. But of course if the fungus wipes out all of the hosts, then that’s the end of the fungus, too, right?
Michele: Yeah, but it can survive as a dormant spore for so long. It just seems like the odds are it can still come roaring back if a host comes along.
Vincent: That could very well be, sure. So that’s not a good story, as Hannah points out.
Michael: No, it’s a bad story.
Vincent: Unfortunately, probably doing research on this fungus and this salamander is not very easy to do and is not very easy to get funded, right? You can imagine that people are, who cares about a salamander, right? Let’s worry about people. But salamanders are a part of the ecosystem.
Michael: In many ways it is very reminiscent of how HIV wreaked havoc on the human population. Unfortunately, salamanders don’t have pharmaceutical companies working for them to try to eradicate this and HIV wreaks havoc because it destroys the immune system, and the poor salamander it appears doesn’t have a sufficient immune response to combat this disease or force natural selection on itself as well as the fungus to adapt.
Vincent: Having 100% lethality is bad, because that means no one is left who might be even partially resistant to carry on, right?
Michael: Yeah. And the reason HIV can persist is because it is such a slow acting death, but this is the opposite of that, it’s pretty fast.
Vincent: Go ahead, Michele.
Michele: I really appreciated this paper in that it is a great way to learn some of the basic principles of pathogenesis. They talked about what makes the perfect pathogen and for example, its ability to infect the reproductive age host drives the population dynamics, etc. So I recommend the paper as a teaching vehicle.
Michael: Michele, that was the question I was going to ask of you since you have the freshmen. Are you going to share with them the Nature summary or are you going to ask them to dig into the paper? I think freshmen would just love the salamander story.
Michele: Yeah, so of course I wrote my syllabus and chose papers and podcasts several months ago, so I would have to rearrange my syllabus to include this, but I will keep it in mind for next year.
Vincent: Elio, the bottom line is that there are reservoir hosts for the fungus in Europe, there is 100% lethality, and it is not yet here in the Americas, this fungus.
Michele: And it can persist in water and in soil for a very long time.
Vincent: Pretty grim for the salamanders, if the fungus came to the Americas via the pet trade, this would be a problem.
Michael: And the fungus got really clever and makes 2 variants of spores, both of which attack the life history of the animal.
Vincent: I guess the good news is that Asian salamanders are resistant or don’t all die, so there is some hope that in time, maybe European salamanders would become the same.
Michael: The biggest danger is that it can be spread by birds. A duck or a waterfowl lands in the pond where the fungus happens to be floating on the surface and the spore can literally attach itself to the bird who flies away and lands in another pond, and you literally have the fungal spread independent of the salamander.
Michele: Right.
Vincent: Alright, thank you Hannah for that. I will get back to Hannah’s email later on when we do some email, because she tells us some interesting things. In the meantime, I want to take a short break and tell you about the sponsor of this episode, the Defense Threat Reduction Agency. Imagine an everyday inexpensive drone you could buy online modified by terrorists to spread chemical or biological weapons over a crowded football stadium or a holiday parade. Plague, VX, sarin, weaponized flu, how can we prevent a scenario like this happening? How can we treat the victims? What could we do to counteract the effects?
Well, for answers to some of these questions, join us in Long Beach, California, November 28-30thfor the 2017 Chemical and Biological Defense Science and Technology Conference to examine information on the latest and most dynamic developments for countering chemical and biological weapons of mass destruction. Collaborate with over 1,500 scientists, subject matter experts, military service members, industry partners and academic leaders from across the globe who are committed to making the world safer by confronting chem bio defense challenges. Part of the US Department of Defense charged with safeguarding our war fighters and our nation, the Defense Threat Reduction Agency’s Chemical and Biological Technologies Department hosts this important conference and brings together the best and brightest from around the world. Please join us to share your important ideas. For more information and to register for this conference, you can go to cbdstconference.com and you can also get updates on Twitter or Facebook, on twitter it is cbdstconference and on Facebook just search for DODDTRA. The 2017 CBDST Conference, today’s innovation, tomorrow’s war fighter capabilities.
And now we will hear from Elio about a very different but nonetheless very interesting subject.
Elio: Yeah, I don’t know if there is much of a connection except we will talk about pathogens and hosts. In this case, I am going to talk about chlamydia. The reason I picked chlamydia is because there is a slight paradox, practically everybody has heard of chlamydia because it is the most common sexually transmitted disease. So who hasn’t heard of it? And that is true not just for the general public but for microbiology. On the other hand, most microbiologists and probably most of the public don’t know the rest of the story which is chlamydia is not just a human pathogen but not necessarily pathogens but are associated with a huge variety of animals and plants. In fact, you can, they seem to be ubiquitous and do not cause disease except in some species, like humans. They are all over the place, okay? So that, the view of chlamydia are sexually transmitted diseases and that is very narrow and inappropriate.
Now, I am going to end up someplace else, namely chlamydia have been found to have the genes for flagella, like bacterial flagella they seem to be very much the same as the flagella genes found in other bacteria. So what is the story? Why would a strict intracellular parasite, I didn’t say that but the chlamydia like a number of other organisms are strict intracellular parasites that cannot grow outside of cells or on agar plates or someplace like that. So why would a beast which is destined to live inside the cell be motile? I don’t have the answer, but that is where we are going. Let me start out, though, with chlamydia. So they say they are all over and in addition is limited because proving Koch’s postulates is not always easy as Michael always points out. It is not an easy thing to do. So we don’t know a great deal about most of the chlamydia in the world.
There is one called Chlamydophila pneumoniae which is called chlamydia pneumonia which causes pneumonia and is said not just to cause pneumonia but to be associated, who knows how, with such diseases as atherosclerosis, asthma, and Alzheimer’s. You name it. So this chlamydia has been associated with all kinds of other diseases. What I’m saying is chlamydia matter, they are interesting. They undergo a complex life cycle, they have sort of an extracellular component called the alimentary body which is likened to a spore in the sense that it is environmentally very tough, and a stage inside of cells where it expands, gets quite a bit bigger, and that’s called the reticulate body. Anyhow, they tend to have small genomes, some are larger than one million bases, but most of them are about one million bases. And they lack a lot of genes for survival such as amino acid biosynthesis and making nucleotides. They do not make their own energy, the acquire it readily, they have ATP/ADP translocases so they can import it.
Vincent: Elio, can I ask you, do they provide anything for the cell in which they reside?
Michele: Interesting.
Elio: That’s a phenomenal question. The answer is, I have no idea.
Michael: The traditional way of thinking about them is they are the ultimate parasite. And parasites traditionally don’t actually confer any benefit that human beings have figured out, but there’s gotta be something.
Vincent: They say in the abstract, chlamydia are obligate intracellular bacteria comprising important human pathogens and symbionts of protists.
Elio: Yes.
Vincent: So maybe in the protists they are endosymbionts.
Elio: They are seen as symbionts only because they don’t seem to cause any disease and are found in abundance in many protists. Symbionts are defined as it’s there. What it does, what good it does, I haven’t run into it. Maybe somebody knows, but I don’t. However, let me go into something quite different, which is surprising, namely that chlamydia are said to have participated in the establishment of plastids, of chloroplasts in plants. The reason for saying that is because they have proteins which are remarkably like those of both cyanobacteria which are supposed to be the ancestors of the plastids, bacteria which became plastids like rickettsia became mitochondria, and of plants themselves.
So then they have some characteristics which are really typical of the plastids and not of bacteria like having a 23s ribosomal RNA intron. For those who know what that means, it is a signature that is characteristic of lower eukaryotes, archaea, but it is in algal plastids but is absent in most bacteria. The question is, are chlamydia motile?
So this recent paper that we have that we are discussing, and the paper is by Astrid Collingro, Stephan Kostlbacher, Marc Mussman, Ramunas Stepanauskas, Steven Hallam and Matthias Horn, and these are folks from the University of Vienna, University of British Columbia, that’s it. Different units in the University of British Columbia. So what they find is that chlamydia have genes which are practically the same as the genes that code for bacterial flagella. So that is a good question, why do they have it? Why would they have that? And nobody knows, this is all genomics, by the way. It’s all finding genes.
Vincent: These are marine chlamydia, right?
Elio: That’s right, nice of you to point out these are not found throughout the world of chlamydia, it is found in marine chlamydia of which we know relatively little. So this is not a general attribute of all chlamydia, doesn’t seem to be, but they are found in three different isolates in three different parts of the world. So.
Vincent: These marine chlamydia are within protists in the oceans, right?
Elio: Undoubtedly, but we don’t know anything about it, all they know is when they do metagenomics, no they do single cell isolates of protists, that’s right. Single cell isolates and in it they find genes for motility, for flagella formation. Well, what else can I say? The only thing I can tell you is that they are, there is an analogy in the world of different strict intracellular parasites, namely the rickettsia. Rickettsia and chlamydia sometimes are lumped together in the minds of microbiologists but they are not, they belong to different phyla. And rickettsia which causes a disease like typhus, a variety of typhus diseases, are also widespread in nature and not only do they have the genes for flagella, they have flagella.
The reason you can isolate them and see them but with chlamydia you have problems. You can’t, in the case of the marine chlamydia we are talking about, you can’t just go and take them and look at them and say are they motile or not. Nobody has done that. But in the case of rickettsia it is possible, and when you look at rickettsia they are motile, and they are motile only inside of cells. Let me clear something up. There is a different kind of motility in rickettsia and in other organisms like listeria and shigella which have besides having flagella are capable of moving inside of cells by being pushed around by actin filaments. This is not our story, okay? They move around that way and apparently they go from cell to adjacent cell that way. This seems to be a mechanism for transferring from one cell to another.
Michael: Without being exposed to the immune system through those actin rockets, and that is the beauty of that type of motility inside a cell.
Elio: That’s right. These guys, the rickettsia here, move in a different way. They move by flagella, flagellar motility, inside of cells and in one case they move around in nucleus of the cell, so in a circular motion, and in another they move in the cytoplasm in a linear motion. The interesting part is if you squash around the cell and release the rickettsia, they stop moving. This is peculiar. So anyhow, the reason I make that point is because in the case of chlamydia, you could make the following case that in outside of cells, chlamydia need to find their host. One way to find their host is by having motility. Nobody has shown yet that the chlamydia can do this outside of cells but it is plausible, unlike rickettsia which stop moving when they are outside of cells. Here the chlamydia possibly can move in the environment and move from cell to cell and find new hosts that way. So we don’t know a great deal about it yet but this is a peculiar situation and I think it was worth discussing.
Vincent: Do we actually know that the flagellar proteins are made in the chlamydia or is it just the DNA? It could be that the DNA is just there, right?
Elio: This is purely genomics.
Vincent: So it could be that there are actually no flagella on the surface of chlamydia. Someone needs to look, right?
Michael: Or the chlamydia flagella genes are morphing into the type III secretion system. They did comment on that that notably they contain orthologs for both the flagella system and the NFT3 secretion system. So it could be very similar to type III secretion, which makes a lot more sense for an intracellular parasite.
Michele: But but but, as a counterpoint, I believe they also found genes for chemosensing.
Michael: That too.
Michele: Which many motile organisms use to decide not just to swim but where to swim.
Elio: Thanks for making that point, that’s actually right.
Michele: That would suggest that it is a functional conservation.
Elio: The point that we made is if you find sets of whole genes in an organism like chlamydia, it is likely to be important because these have a reduced genome. You don’t have enough of a genome to make it in the environment let alone carry extra genes. So because of the parsimony of this organism, finding a set of genes suggests function.
Vincent: Of course the experiment still has to be done where someone looks for the flagellar proteins, right?
Elio: Exactly.
Michele: But it’s really tricky because as Elio said, the way they got these samples in the first place is they went to different locations, Vancouver Island, I forget where the other one was, got water, and then they used high tech methods to separate into single cell pools and then amplified from a single cell. So the idea of doing an experiment to look at flagellar proteins like that, they need to culture the organism first.
Vincent: They probably don’t have cultures at all, right. Yeah.
Michele: Yeah.
Vincent: The reason–
Elio: This extends in a way our view of parasitism, as a strict intracellular parasitism. What I’m saying is I always thought of chlamydia and rickettsia being something like a virus in the sense that they only grow and live and thrive inside of cells, but maybe there is something like motility outside of cells. That is the point I think is worth at least considering.
Vincent: But the rickettsia do not move.
Michael: They have no energy system.
Elio: That’s right, it does not work rickettsia, and so maybe there are two different rules, these are very different organisms of their own.
Vincent: So I have a little skepticism because from my view of viruses inside of cells, viruses always move in cells along the cytoskeletal elements, either naked or within vesicles, because the cytoplasm of a eukaryotic cell is incredibly crowded. So I don’t know how a rickettsia would move around with the flagellum unless it were hooked on to an actin filament.
Elio: Let me say something about that, I used to look when I was younger and I had been drafted into the army, one of the jobs I was given was to look at cells infected with rickettsia. Although cells are, these were cells in culture, fibroblasts, very flat, and the cytoplasm looks very crowded around the nucleus, that’s where all the mitochondria are, probably endoplasmic reticulum, who knows what else. Outside there is sort of, the cells spread out and they look quite empty, not many mitochondria there, so rickettsia could move around there with no problem at all.
Vincent: Yeah, but there are things you can’t see under light microscopy like ribosomes and filaments and vesicles of various sorts. I mean, this illustrator, David Goodsell, has drawn images of cells that in fact are in our textbook of virology, we have a lovely one showing it is just hard to move around. It is packed in the cytoplasm. We used to think that viruses diffused through the cytoplasm, but that can’t be. They have to be motored around, and whether, I think this rickettsia can’t just swim around by itself even if it had flagella. It would have to be attached to a cytoskeletal element. But then why would it stop moving outside of the cell?
Michael: As they speculate in the second to last paragraph of their paper, they point out that the flagella may just be something to stick to particles in the marine environment.
Vincent: Could be, sure.
Michael: They’ve lost the motility function and it is simply another means for them to move from cell to cell.
Vincent: Could be.
Elio: that’s right, flagella involved in signaling function as well.
Michael: As Michele brought up, we have to remember they also have the genes for chemotaxis, and they can chemically sense the environment that they are in, so I think the expression experiment to see whether or not these things actually express the flagella gene on the surface is really the cool thing that could come from this, to see if it is able to express when they detect a chemical gradient change and say, hey things are good, I can move to a new house.
Vincent: That would make sense, yep.
Michele: And the authors suggest that during their extracellular life out in the water, they may rely on glycogen, so a storage compound to drive the flagella and then once they get inside a cell they can just start feeding off of host goodies.
Elio: I think one of the things that the paper tells me is that you can find out a tremendous amount from genomics which here is the finding of the genes for flagella, but to figure out what these genes are doing and how they work, you really have to have the cells, the organisms themselves that genomics can only take you so far.
Michele: It is a neat way to look deep into the family tree, because they found some of the ancient ancestors of all the chlamydia that we think about. Apparently they arose from an ancestor that did have flagella. That’s the easiest explanation.
Elio: I think it is a good way of asking questions. It points towards, like all of metagenomics, tells you what questions to ask.
Vincent: For sure.
Elio: Anyhow, I had a good time with this because I got to love chlamydia (laughter)
Vincent: It is very interesting for sure.
Elio: Fancy that!
Michele: I was able to communicate with Astrid–
Elio: I can’t say I’ve had a personal experience with them but… (laughter)
Vincent: I’d hope not.
Michele: Too much information.
Michael: Too much information.
Michele: I was able to communicate with Astrid Collingro today, the first author. She was very generous in communicating with me when I didn’t give her much of a lead time, but I can tell you that she grew up in a small town in Bavaria, Germany, and then she studied microbiology at the Technical University of Munich. There she did a diploma thesis on the influence of facultative and obligate symbionts of a acanthamoebus species on their host. So she has been interested in these intracellular microbes for some time. She started her PhD also in Munich and then she went with Michael Wagner and Matthias Horn, her senior author on this paper, to the university of Vienna.
She got her degree there as a microbial ecologist studying the infection and genome analysis of these chlamydia symbiotes of amoeba. Since then she has been doing this comparative genome analysis and their evolution, but she is also interested in chlamydia diversity and their role in the environment. She also studies some other host microbe interactions in the lab. She says it was really exciting the first time they looked into this genome sequence and found the flagellar genes and found not just one or two but some 20 or more genes to make up the apparatus, and that set her on the path for this paper. Apart from her science, she and her husband have 3 daughters between the ages of 6 and 12, and when she is not working she likes to be outside with her family in nature enjoying hiking and mountain biking.
Vincent: Hopefully watching out for the chytrid fungi, where did you say she is?
Michele: Well, they are in Vienna now.
Vincent: Okay.
Elio: Which by the way is a hotbed of very good work in environmental microbiology these days.
Michele: They clearly have a lot of technology that they would have had to draw on for this single cell genome analysis.
Vincent: Great. Thank you, Michele. Let me read a few emails and let me resume Hannah’s email, if you recall, Hannah had sent us the salamander paper. A bit about me, she writes,
A bit about me: I’m a Canadian biology Master’s student studying at the Free University Berlin, and although I’m not doing microbiology per se, I’ve been working with Eastern subterranean termites (Reticulitermes flavipes) and the entomopathogenic fungus Metarhizium anisopliae, focusing on the mechanisms that termites use to protect their colonies from fungal infection. For decades, people have tried to use this fungus to control subterranean termites, but because termites are amazing and have something called social immunity, it hasn’t worked.
While I’m on this tangent, here are some more cool termite facts for a microbiology-inclined audience: R. flavipes, like other “lower” termites, has a specially adapted hind gut that’s PACKED with the biggest, most beautiful flagellates you’ve ever seen, plus loads of bacteria, some of which live as ectosymbionts on the flagellates and propel them around. The flagellates, and to a lesser extent the bacteria, help the termite digest wood.
Michele: Wow.
Vincent: Can you imagine? (laughs)
Michele: Bugs within bugs within bugs.
Vincent: So the flagellates, the bacteria are sticking to the flagellates, and that is how the bacteria get around. So there is a connection between the two stories, Elio. The flagellates and to a lesser extent the bacteria help the termite digest wood. Higher termites don’t have flagellate symbionts, just plenty of bacteria. But one group, the macrotermitinae, live in a special symbiotic relationship with another type of microbe, the fungus genus termitomyces. They build and tend fungus gardens inside their nests, a bit like leafcutter ants. We have one macrotermes species in the lab, but sadly I have not yet found an excuse to do anything with them. They are so cool. Okay.
Elio: One thing you could do with the termitomyces is eat them. They are among the most delectable fungi in places where you have termite colonies growing up.
Vincent: Really? Have you ever eaten any?
Elio: No, I haven’t but I have read about it.
Vincent: Okay.
Michele: Sauteed with a little butter, is that what you would do? (laughter)
Michael: You can eat anything if you put butter on it.
Vincent: You can eat any fungus once, right?
Elio: That’s it.
Vincent: That’s Elio’s thing, I stole that from him. Alright, okay, Hannah writes, I will sign off now before I get even more carried away. Thanks for all your hard work, I look forward to the next episode. Then we have an email from Joshua Weitz, who was one of the authors on a paper that we recently did.
Dear Vincent, Michael, Michele, and Elio,
My colleagues alerted me today to the TWIM podcast on our immunophage synergy paper in Cell Host and Microbe. Thanks for taking the time to reflect on our work. I found the conversation quite stimulating and hope our future efforts can address some of the questions raised.
Just to remind everyone, this was a paper where it was found that they used phage to control pseudomonas infections in mice, and the control of the infection requires an intact immune system in the mice. So Joshua continues:
At one point, the podcast raised a question on the details of the models. Given the access issues noted for CHM, we just posted the following github link on our group page, it should have all the relevant simulation code in case you are interested or know folks who want to see the details underlying the mathematical concepts:
https://github.com/WeitzGroup/Immunophage-synergy-in-vivo
Note that even more details on the proof of concept model are available in a related paper in J. Theor. Biol.:
http://www.sciencedirect.com/science/article/pii/S0022519317303235
Best, Joshua
Michele: I’ll get right on that.
Vincent: You better! (laughs) I think you were the one who wanted to know, Michele. Anyway, so Joshua puts a link to the mathematical model information. Note that even more details on the proof of concept model are available on a related paper in the Journal of Theoretical Biology. Joshua is a professor at Georgia Institute of Technology and of course was a co author on that paper. So I’m glad Joshua found out. Always interested to hear if people end up finding out that their work has been discussed on TWIM or any of our podcasts. Now, Anthony sends a link to an interesting article. It was published in a website called National Hogfarmer which is not something I read.
Elio: Say that again?
Vincent: National Hogfarmer. I don’t read this everyday.
Michael: That’s surprising given the extensive reading list that you have for your podcasts, Vincent.
Vincent: (laughs) Maybe I should add it. Anyways, he sends an article entitled “McDonald’s developing species specific antibiotic use policies.” So McDonald’s has a global vision for antibiotic stewardship, I didn’t realize this.
Michele: That’s great.
Vincent: And their goal is to preserve antibiotic effectiveness through ethical practice, so they have issued an update to that. They will develop specific policies and implementation timelines for suppliers because McDonald’s doesn’t grow animals themselves, but they get it from suppliers who provide chicken, beef, pork, dairy products, and eggs. So they are saying here is what you should be doing in the use of antibiotics in your animals. So that is good because they are a huge user of these animals, of course.
Michael: And the products, like eggs and other things.
Vincent: So it is good that they are being more responsible, right?
Michele: Terrific.
Michael: They along with many of the other fast food giants like in South Carolina we have Chick-a-Filet, and Chick-a-Filet is actively pursuing antibiotic free chickens and it is part of their marketing campaign. And so many companies are practicing good antibiotic stewardship in order to try and help us preserve the antibiotics that we currently have.
Vincent: Good for McDonald’s. They may have other problems but that is good at least. Alright, we have an email from Sarah, who writes:
Hello TWIXers!
I’m finally writing my first email – only took me 5 years… I’ve been listening since 2012 when in my second year of undergraduate studies at the University of Glasgow I encountered your series of podcasts through my courses in microbiology. At this point I was still on track for a degree in Anatomy, but after being spellbound by our Micro courses I decided to change and get my degree in Parasitology instead.
Elio: Yay!
Michele: Great!
Vincent: I was of course further inspired by your podcasts (of which, no offense to the others, TWiP remains my absolute favourite) and I quickly listened to the very long list of episodes I had missed in my ignorance. The TWiX podcasts have kept me entertained on train commutes, flights home to Sweden and on holiday travels with my husband (who has endured many long and somewhat one sided discussions on various topics). The podcasts have not only helped teach my husband more than he ever wanted to know about worms, bacteria and viruses, but they helped me tremendously with my studies by making lots of information more accessible and they of course kept up my motivation and science interest on those dark days when no experiments would work. Most recently the podcasts have taken on a new role of keeping me more widely informed (and entertained on my daily 40 min walk to- and from work) as I in my career focus on a slightly more narrow topic: after my getting my BSc Hons + MSci I gained employment as a research technician in a UoG CVR lab last November (Vincent may remember us, he was a recipient of the Stoker Price a few years back – sadly I wasn’t here!). It’s ironic but I now work on viruses (my least favourite of infectious agents – sorry Vincent!) instead of my beloved parasites, but I actually love it. Our area of research is what prompted this very lengthy first email as Vincent mentioned using Wolbachia endosymbionts in mosquitoes as a potential population control strategy and a method to reduce transmission of viral diseases like ZIKV and DENV. This is what we work on! I mainly spend my days in our insectary taking care of and experimenting on our many mosquitoes (with all the delightful TWiX-hosts as company), but I also do some cell work and once in a while even a plaque assay! It’s nice to have a cell break sometimes when you work with fussy, tropical mosquitoes that must be kept at 28°C and 80% humidity! Vincent might like the humidity, but for a northern Swedish person it takes some getting use to!
Anyways, sorry about the long email – I guess it’s what happens when you don’t write for 5 years – and my sincerest thanks to you all for your excellent work and dedication to these podcasts, they really are a treat to listen to and I recommend them to anyone who will listen (scientists or not!).
Sincerely,
Sara from Scotland
P.S. I subscribe on all of our devices, it’s dead easy and everyone should do it, if only so that Vincent can stop pleading
(laughter)
Michele: Thanks, Sarah!
Elio: So there!
Vincent: Thank you Sarah, very nice. Love to hear your stories. Anthony sends a number of links, he writes:
Small Things Considered recently had a post on stromatolites
http://schaechter.asmblog.org/schaechter/2017/09/in-the-beginning-there-were-stromatolites.html
These are found in NJ
http://www.state.nj.us/dep/njgs/enviroed/stromat.htm
They are in Central, NJ, too:
http://www.lehigh.edu/~fjp3/srt/srt_geology.html
You know about that, Elio?
Elio: Yeah, it was written by a graduate student.
Vincent: Yeah, Julian Belk. In the beginning, there were stromatolites. And I live in central New Jersey, so that is probably why he is sending it. He writes:
Stromatolites give us a peephole into a time billions of years ago when new developments were not McMansions but vast tracts of mats of microorganisms.
Michele: Well said.
Vincent: Very nice. And finally, our last email is from Mark, who writes:
Elio: Oh, thank you Anthony, I appreciate it very much.
Vincent: Mark writes:
The true purpose of microbiology.
Hello Elio, Michele, Michael, and Vincent,
Greetings from a long time listener from San Jose CA. The California harvest and winemaking season is underway. This Saturday we receive and will crush a few tons of Chardonnay from Alexander Valley. I am currently buying yeast and nutrients for its primary fermentation, and bacteria for secondary malolactic fermentation.
The true purpose of microbiology is to crest all those little bugs that make delicious beer, cheese, bread, and wine.
Enjoy the attached picture.
Mark
And he sent a photograph of (laughs)
Michael: Inoculum packages.
Vincent: Inoculum packages you can use to make wine. It’s called H2S Preventing Wine Yeast and you can get Vivace, Allegro, Adante, Maestoso, Brioso, Brio, Ossia. Strains for Pinot Noir, aromatic expression of wine variety, ah this is just great.
Michele: Renaissance Yeast, they call it.
Vincent: Isn’t that cool?
Michael: Now he’s making me hungry for some bread.
Vincent: The chardonnay sounds good to me.
Michael: That too.
Vincent: It’s a bit early, I guess. But 5 o’ clock somewhere.
Michael: I work in a state building, so I can’t speculate on chardonnay (laughter)
Vincent: Thank you Mark, good luck with your wine, hope it works out well. The microbes are wonderful for all these goodies. Alright, that’s TWIM 162, you can find it at asm.org/twim. You can also find it at Apple Podcasts. Please subscribe so you get every episode, just like Sarah said. Subscribe on all your devices and once you do that I will stop asking you to subscribe. If you like what we do, consider supporting us financially. Go to microbe.tv/contribute for the different ways you can do it. We do love hearing your questions, we love hearing your stories, how you found us, what we mean to you, and all that goes to twim@microbe.tv. Don’t be shy. Michele Swanson is at the University of Michigan, thank you Michele.
Michele: Thank you, it is a pleasure.
Vincent: Michele, this morning I was driving on the New Jersey turnpike, there was heavy traffic, the car in front of me had a sticker on the back. It was a football helmet with a big M on it. How about that? Here in New Jersey there are Michigan fans.
Michele: We’re all over the place.
Michael: You sure it wasn’t for Marhest College?
Elio: (laughs)
Vincent: It was a big blue M, you know?
Michele: That block M is, yeah.
Vincent: Marhest is red, I think.
Michael: Okay.
Vincent: And they don’t have a very good football team, I think. My son goes to Marhest, you know.
Michael: You’re gonna get letters!
Vincent: My son goes to Marhest! But he doesn’t listen to TWIM. Michael Schmidt is at the Medical University of South Carolina, thank you Michael.
Michael: Thanks, everyone.
Vincent: Is it still warm there, Michael?
Michael: 90 degrees today.
Vincent: Wow!
Michele: Ooh.
Michael: I’m hoping for October before November, but it’s turning to summer. We went from one beautiful week of fall to back to summer. Climate change is here, folks.
Vincent: Elio Schaechter is at Small Things Considered, thank you Elio.
Elio: My pleasure, of course.
Vincent: I’m Vincent Racaniello, you can find me at virology.ws. I’d like to thank the American Society for Microbiology for their support of TWIM and Ray Ortega for his technical help. I also want to thank the sponsor, the Defense Threat Reduction Agency. The music you hear on TWIM is composed and performed by Ronald Jenkees. You can find his work at ronaldjenkees.com. Thanks for listening everyone, we will see you next time on This Week in Microbiology.
(music)
Content on This Week in Microbiology (microbe.tv/twim) is licensed under a Creative Commons Attribution 3.0 License.
Transcribed by Sarah Morgan.