Speaker 1: Hey, everyone, just wanted to give you a quick content
Speaker 1: warning here that the first hand account for this episode
Speaker 1: does include the death of a parent, so if you
Speaker 1: would like to move past that, you can skip ahead
Speaker 1: to about eleven minutes and fifteen seconds in.
Speaker 2: Hi. My name is Denise, and I'm here today to
Speaker 2: talk about the story of my mom and what she
Speaker 2: went through with listeria. As a little backstory, my mom
Speaker 2: turned eighty years old in June of twenty twenty two.
Speaker 2: She was very, very vibrant. She still worked, she golfed,
Speaker 2: she was exceptionally active. She some more backstory. She had
Speaker 2: a regular, routine, normal colonoscopy in June that showed no
Speaker 2: ulcerations at all. This is important. A little later in August,
Speaker 2: she started having some excruciating headaches after she would eat,
Speaker 2: and when she saw her doctor, they diagnosed her with
Speaker 2: a condition called temporal arteritis and started her on high
Speaker 2: dose steroids and methotrex eight. At the same time, she
Speaker 2: had a long standing trip planned August eighteenth through October
Speaker 2: ninth to go up to Washington to visit some friends
Speaker 2: and escape the heat of the Palm Springs desert. I'm
Speaker 2: a nurse. I've been a nurse for twenty seven years.
Speaker 2: I talked to her about the risks of continuing to
Speaker 2: go on this vacation because of the immunosuppression that the
Speaker 2: steroids were causing, and I think because of the COVID
Speaker 2: fatigue for the past several years and not seeing her friends.
Speaker 2: She wasn't really interested in putting that off. She had
Speaker 2: people to see, things to do, and golf to play,
Speaker 2: and away she went fast forward up until September twenty fourth.
Speaker 2: She texted me that she had gained two pounds, She'd
Speaker 2: eaten a great big bowl of ice cream, and was
Speaker 2: having some macaroni and cheese for dinner. On the twenty eighth,
Speaker 2: she called because she said that she had started not
Speaker 2: feeling so good. So then the next day was Thursday,
Speaker 2: the twenty ninth, she called me in the morning and
Speaker 2: said that she was feeling worse, and she did go
Speaker 2: ahead and cancel her lunch date that day. So Friday,
Speaker 2: September thirtieth, I received a call at three o'clock in
Speaker 2: the afternoon from the people she was staying with. She'd
Speaker 2: been laying on the couch all day, had not eaten
Speaker 2: any food and only taken SIPs of water, had a
Speaker 2: low grade temp, negative COVID tests, and because I'm down
Speaker 2: here outside of Palm Springs, I said it was a
Speaker 2: good idea to take her to Virgin Care. So they
Speaker 2: did take her in. The blood work came back and
Speaker 2: showed that she had some impaired kidney function, borderlining on
Speaker 2: kidney failure. She also had a really high calcium level
Speaker 2: and a low potassium level. The doctor there, though, thought
Speaker 2: that she was stable enough that she could just come
Speaker 2: back in the morning and get some ivy fluids and
Speaker 2: repeat the labs the morning of October first, they went
Speaker 2: to the urgent Care straight away, where she got her fluids.
Speaker 2: The doctor did advise our friends to go ahead and
Speaker 2: take her over to the emergency department. She was checked
Speaker 2: in entriaged about three and then because of just how
Speaker 2: life in the er is these days, she got back
Speaker 2: to a room at like eight thirty at night, and
Speaker 2: the doctor saw her at ten o'clock at night. Luckily,
Speaker 2: our friends were able to stay. They rotated staying with
Speaker 2: her so that she wasn't just by herself, and at
Speaker 2: three point thirty in the morning, she had a sudden
Speaker 2: mental status change where she completely went lethargic, started reaching
Speaker 2: at the air, not communicative, not able to speak. So
Speaker 2: our friend Frank grabbed the nurse. They took her temperature
Speaker 2: rectally and it was one hundred and three point four.
Speaker 2: The staff came and drew blood cultures and she was
Speaker 2: started on an ivy antibiotic cocktail that they do for
Speaker 2: sepsis of unknown origin. I got on the plane to
Speaker 2: go up to Portland at like nine o'clock in the
Speaker 2: morning on Sunday. I arrived at the hospital at eleven am.
Speaker 2: She looked like she was going to die when I
Speaker 2: walked into the room. I worked eleven years in the
Speaker 2: emergency room, and I thought, oh, this is not good.
Speaker 2: It's not good at all. She was not responsive to
Speaker 2: people talking to her, she was not following commands, she
Speaker 2: was pulling at things. On Monday, the third, the infectious
Speaker 2: disease doctor came to me about noon and said that
Speaker 2: three of the four blood culture bottles were showing bacterial
Speaker 2: growth of some sort, but that the microbiology text that
Speaker 2: he knew and really trusted didn't I identify anything. So
Speaker 2: he was really concerned that it was contaminant, which would
Speaker 2: be really highly unusual in three out of four bottles.
Speaker 2: So they ran what they call an extended infectious disease panel.
Speaker 2: After she came back from her lumbar puncture, the infectious
Speaker 2: disease doctor comes down the hall towards me and kind
Speaker 2: of frantically gesturing at me and says, you're not going
Speaker 2: to believe this, but she's actually got listeria and it's
Speaker 2: her blood stream and it's also in her spinal fluid,
Speaker 2: and this is really really bad. And it's bad not
Speaker 2: just because, I mean, the mortality rate is exceptionally high,
Speaker 2: but also because the antibiotics that she had been getting
Speaker 2: are not the ones that are effective at all against lysteria.
Speaker 2: It took until eleven o'clock at night to finally get
Speaker 2: her started on the ampicillin. But I was still preparing
Speaker 2: myself that my mom was going to pass. So when
Speaker 2: I came in at six point thirty Monday morning, my
Speaker 2: mom had little restraint mittens on her hands, and I thought,
Speaker 2: oh my god, it's gone from bad to worse. And
Speaker 2: she was shaking those little mittens at me, and I said, Mom,
Speaker 2: if I take these off of you, you have to
Speaker 2: leave your things alone. You can't pull on things. And
Speaker 2: she made eye contact with me and she said okay,
Speaker 2: and I thought, oh my god, she's in there. This
Speaker 2: is a glimmer of hope. I think it could be.
Speaker 2: It could be okay, And over the course of the day,
Speaker 2: her mental status actually improved. She was answering yes and
Speaker 2: no questions. I was able to transfer her out of
Speaker 2: bed and get her on the little bedside commode to
Speaker 2: go to the bathroom. We also discovered at that time
Speaker 2: in her MRI that they had done of her brain
Speaker 2: that it showed that she had four areas that were
Speaker 2: possibly like septic ambolai from the infection. So to see
Speaker 2: her mental status also improving like that was really amazing.
Speaker 2: They had given her a medication called Erykstra to prevent
Speaker 2: blood clots, and they also gave her an aspirin because
Speaker 2: of the potential for cardiac strain. So I was a
Speaker 2: little worried about that when they started that the day
Speaker 2: before because of her platelet account was not super low,
Speaker 2: but it was low enough that I was concerned about it.
Speaker 2: So Wednesday morning, when she's talking and moving and she's
Speaker 2: doing great, she told me that she had just never
Speaker 2: felt so awful. And I explained to her that most
Speaker 2: people that get as sick as she is, don't even
Speaker 2: wake up. And she looked at me. She said, you
Speaker 2: mean I could have died And I said, yes, mom,
Speaker 2: it's that serious. You could have died. And she said, well,
Speaker 2: I'm not ready to die. And I said, well, that's great,
Speaker 2: because I'm not ready to be an orphan. Everybody was
Speaker 2: so excited, her doctor's, the hospitalist, and the infectious disease doctor.
Speaker 2: They were just amazed at how good she was doing.
Speaker 2: And then at three point thirty I got her up
Speaker 2: to the commode. As soon as she went to the bathroom,
Speaker 2: I knew right away that there was blood. When somebody
Speaker 2: has an intestinal bleed, it has in a past tool
Speaker 2: it has a very very distinctive smell, and I just
Speaker 2: knew that this was not good. And that was really
Speaker 2: the very beginning of the end. The doctor came back
Speaker 2: up and looked at it and he said, yeah, we're
Speaker 2: going to hold off on transferring her off the floor.
Speaker 2: So they did an upper endoscopy where they looked at
Speaker 2: her stomach on the seventh and that was negative, no ulcers.
Speaker 2: So they did do the colonoscopy and that showed that
Speaker 2: her large intestine and all throughout her large intestine and
Speaker 2: up into what they could see in her small intestine
Speaker 2: was just riddled with ulcers. On the fourteenth, she really
Speaker 2: started bleeding quite heavily and went into shock. And before
Speaker 2: she actually went into full blown shock from this, I
Speaker 2: had to call my daughter and tell her that if
Speaker 2: this scan that they had just taken her for did
Speaker 2: not show any bleeding that we could do anything about that,
Speaker 2: her grandma was most likely going to pass away. That
Speaker 2: was the hardest phone call I've ever had to make.
Speaker 2: The results of that scan came back and they finally
Speaker 2: did see that there was bleeding coming out of an
Speaker 2: artery in her small intestine, so interventional radiology was called
Speaker 2: in and off she went for procedure and off to ICU.
Speaker 2: That procedure we thought was good, but then in the
Speaker 2: morning it turned out that they had maybe stopped the
Speaker 2: bleeding a little too well and some of her small
Speaker 2: intestine was starting to die. So this led down the
Speaker 2: course of a bowel resection and then reattachment, which she
Speaker 2: did great came out of that very well. By the
Speaker 2: twenty sixth she had had twelve units of blood, two
Speaker 2: failed interventional radiology procedures, and three surgeries. Throughout this time,
Speaker 2: with her in Washington with when the bleeding would stop
Speaker 2: and it would start. Our only goal was to get
Speaker 2: her home, to get her back to California, and trying
Speaker 2: to navigate that when you're at a hospital system that
Speaker 2: so eleven hundred miles from your home is exceptionally difficult.
Speaker 2: But throughout the whole time that was our single focus,
Speaker 2: get her home so that she could pass at her
Speaker 2: home when it became obvious that she was not probably
Speaker 2: going to pull through this, and thankfully we were able
Speaker 2: to do that. On the second of November, I was
Speaker 2: finally able to get her on an air ambulance home
Speaker 2: to get her admitted down here at the hospital system
Speaker 2: that I work in. I was able to have hospice
Speaker 2: come out bring the bed and all of the equipment
Speaker 2: here on the fourth and my dear, dear friend Julie
Speaker 2: was with her at the hospital in the morning and
Speaker 2: she called me and she said she's ready. She was alert,
Speaker 2: and she knew she was in the hospital and she
Speaker 2: was ready to come home. She has a beautiful view
Speaker 2: at her condo here and.
Speaker 1: She was able to see that.
Speaker 2: And she passed away on the ninth. So we don't
Speaker 2: know what the source was we don't know what she
Speaker 2: ate or how she contracted this. It was a very
Speaker 2: long month of stops and starts where we would think
Speaker 2: the bleeding had maybe stopped, and then to have it
Speaker 2: start again. When I told her that we had gotten
Speaker 2: the air ambulance that we were going to be flying
Speaker 2: home to California, she said, oh, Denise, that's wonderful. And
Speaker 2: when she saw her sun set, she said, it's so
Speaker 2: beautiful and she's missed every day. And thank you for
Speaker 2: letting me share her story.
Speaker 1: Thank you so much, Denise, like I can't imagine, and
Speaker 1: we really appreciate you being willing to share that story,
Speaker 1: and we know it couldn't have been easy to do,
Speaker 1: so thank you. Yeah, thank you.
Speaker 3: I being able to hear a story of how this
Speaker 3: disease can really affect people and their families. It's just
Speaker 3: so powerful, and thank you so much for being willing
Speaker 3: to be so vulnerable and share that with us.
Speaker 2: Hi.
Speaker 3: I'm Aaron Welsh and I'm Erin Alman Updike and.
Speaker 1: This is this podcast will kill you.
Speaker 3: Today's a heavy duty topic. M hm, listeria.
Speaker 1: Yeah, more heavy duty than I realized. It is so gnarly,
Speaker 1: so I feel like probably many other people can relate
Speaker 1: to this when I say that, until doing this episode,
Speaker 1: lysteria to me was just one of those things that
Speaker 1: pops up occasionally with like, oh, lysteria detected in this
Speaker 1: food or that food, and be careful if you are
Speaker 1: pregnant or you know. But it was just sort of
Speaker 1: another food born pathogen, which is, you know, they can
Speaker 1: be very bad. But I just sort of had lumped
Speaker 1: it all in together with some of the other culprits
Speaker 1: and I had no idea.
Speaker 3: Right, I did not know the extent of it either,
Speaker 3: even having been pregnant now twice and been like, I'm not.
Speaker 1: Allowed to eat turkey.
Speaker 3: I'm so upset about it. But that's what it was
Speaker 3: to me, right, It was just like, oh, I can't
Speaker 3: eat turkey and I'm annoyed. But I also did not
Speaker 3: realize the extent of why, just how scary it really is.
Speaker 3: So yeah, we're going to get into it today, we
Speaker 3: really are.
Speaker 1: But first things first, feels very strange to dive into
Speaker 1: like a cocktail or quarantin any time. But yet here
Speaker 1: we go. That's what time it is, It's what time
Speaker 1: it is, What are we drinking this week?
Speaker 3: We're drinking the Coldest of Cuts.
Speaker 1: We toyed with a lot of different names for this
Speaker 1: last episode was a dairy filled cocktail because we did
Speaker 1: vitamin D so we couldn't do dairy again. Although my
Speaker 1: second favorite name was don't you Dairy, which is very
Speaker 1: good by the way I do. And then there was
Speaker 1: like the Salami sling or the Salami sour or the
Speaker 1: cold cut Collins. But I think I like the coldest
Speaker 1: of cuts. I love it.
Speaker 3: I love it, Aaron, what is in the coldest of cut?
Speaker 1: It is a slushy or blended Arnold palmer with some
Speaker 1: rum in there, some spiced rum.
Speaker 3: Serve it alongside a nice turkey sandwich.
Speaker 1: Yeah, don't.
Speaker 3: We'll post the full recipe for that quarantini as well
Speaker 3: as the non alcoholic Plasy Brita on our website This
Speaker 3: podcast would kill You dot com and all of our
Speaker 3: social media channels, ah more.
Speaker 1: Podcast business, website stuff. We've got lots of website stuff.
Speaker 1: We have transfer, we have all of our references. We
Speaker 1: have links to merch to our music by bloodmobile, to
Speaker 1: our Goodreads list, to our bookshop dot org affiliate account.
Speaker 1: You know, we've got lots of stuff. Patreon, I think
Speaker 1: I should have impressed used it. It's not here anymore.
Speaker 1: I lost it in the break.
Speaker 3: I'm impressed that you went through a list at all,
Speaker 3: quite honestly.
Speaker 1: So you win. Yeah, yeah, well thank you?
Speaker 3: All right, well with that, shall we get into this episode?
Speaker 1: We shall okay, right after this break.
Speaker 3: So, the genus Listeria includes at least seventeen different species
Speaker 3: of bacteria, but the main one that we're focusing on
Speaker 3: today is Listeria monocytogenes because that's the main positive agent
Speaker 3: of listeriosis, which is the disease that we're talking about today.
Speaker 3: Listeria in general are gram positive. This is a gram
Speaker 3: positive rod shaped, so a little bacillus, or sometimes it's
Speaker 3: called a coxobacillus because it's like a short rod.
Speaker 1: I don't know.
Speaker 3: They are a facultative anaerobe, which means that they can
Speaker 3: grow both with and without the presence of oxygen. Already
Speaker 3: cool little bug. They can survive even at very low temperatures,
Speaker 3: like in the refrigerator or the freezer, and they can
Speaker 3: continue to grow under those conditions. And they're very resistant
Speaker 3: to other extreme environmental conditions like low pH very acidic environments,
Speaker 3: or high salt concentrations.
Speaker 1: So these are.
Speaker 3: Very hardy little bugs. Most of the time they're found
Speaker 3: living free living in soil or detritus or water. And
Speaker 3: they also readily form biofilms, right, so they can form
Speaker 3: this entire biofilm that's really hard to get rid of.
Speaker 1: Aaron, what other episode were we talking about biofilms in.
Speaker 3: I honestly have no idea. Okay, I would I would
Speaker 3: have to google through our transcripts. Yeah yeah, yeah, but yes,
Speaker 3: So that's a lot already that we've already talked about
Speaker 3: when it comes to this little bacterium. And because of
Speaker 3: all of these reasons, this bacterium poses a really big
Speaker 3: risk to the food industry because they can survive despite
Speaker 3: a lot of things that our food industry does to
Speaker 3: try to decontaminate everything, right, like refrigeration, like acidic cleaning
Speaker 3: solutions like high salt to preserve foods, et cetera. And
Speaker 3: then on top of that, you have this biofilm formation
Speaker 3: which can form on food production equipment and be really
Speaker 3: difficult to get rid of.
Speaker 1: First of all, it's really scary. Second of all, I
Speaker 1: just did a search through our transcripts and Legionnaire's disease.
Speaker 3: Ooh, yes, okay, that does make sense because they little
Speaker 3: biofilms in the like ac equipment.
Speaker 1: If any of you listeners got that without having to
Speaker 1: search our transcripts, you are better than us. You win. Okay.
Speaker 3: But this bacterium gets even cooler, or rather it gets
Speaker 3: even more terrifying, because while Listeria is a free living
Speaker 3: environmental microbe, it also can oscillate between being one of
Speaker 3: those something hanging out in the soil, living and replicating
Speaker 3: just fine, and then switch to being an intracellular bacterium
Speaker 3: that invades mammalian host cells and survives and replicates inside
Speaker 3: of our cells. So it's also found as a transient
Speaker 3: inhabitant of both animal and human guts. And so there's
Speaker 3: a lot of evidence that we are all probably exposed
Speaker 3: to Listeria monocytogenies on a relatively regular basis, and it's
Speaker 3: a really common pathogen in the environment because of this.
Speaker 1: Again, I had no idea. I know, I know, I know,
Speaker 1: I know.
Speaker 3: So the way that we get exposed to this in
Speaker 3: general is through our food. The way that this becomes
Speaker 3: a pathogen is it's a food borne pathogen, which means
Speaker 3: that we eat this bacterium we ingest it on our
Speaker 3: food and it travels through our guts. But from there
Speaker 3: it's actually quite different from most any other food born
Speaker 3: illness that we've talked about.
Speaker 1: Here's why.
Speaker 3: In general, and this really did surprise me, the symptoms
Speaker 3: either go incredibly severe disseminated infection that we're going to
Speaker 3: talk about in detail, or mild, if any symptoms, and
Speaker 3: we might never know that you had this as an illness.
Speaker 3: So let me explain when you ingest listeria on your food,
Speaker 3: let's say, on your turkey, or your cheese, or your lettuce.
Speaker 1: Even anything really, which is just adds to the scary column.
Speaker 3: If you have a fully competent immune system, fully competent
Speaker 3: gut lining, no major risk factors, you may or may
Speaker 3: not get exposed to enough bacteria a high enough bacterial
Speaker 3: load to cause an infection that's limited to your gastrointestinal
Speaker 3: tract a gastro enteritis. So that might mean that you
Speaker 3: have some diarrhea or some nausea vomiting. If that's the case,
Speaker 3: then those symptoms would generally start within about twenty four
Speaker 3: hours of exposure and last for about one to three days,
Speaker 3: which is a really common time frame, and set of
Speaker 3: symptoms for a food born gastroenteritis, but we have essentially
Speaker 3: no clue how often this happens or what's the likelihood
Speaker 3: that if you're exposed to contaminated food that you get
Speaker 3: this kind of infection in the absence of any other
Speaker 3: risk factors for invasive affection, which we'll get to because
Speaker 3: we just don't have data on it. Most of the
Speaker 3: people that are getting food borne illness of any kind,
Speaker 3: we're never detecting what that pathogen actually is, and they.
Speaker 1: Recover with issues.
Speaker 3: What we worry about with listeria, the disease we know
Speaker 3: of as listeriosis is an invasive infection, and when that happens,
Speaker 3: the symptoms are different entirely, which I think is one
Speaker 3: of the most interesting parts of the listeria story because
Speaker 3: it doesn't mean that it starts with this food born infection.
Speaker 3: Think of it as two different diseases entirely. Does that
Speaker 3: make sense?
Speaker 1: Yeah, so you don't have the one to three day
Speaker 1: GI symptoms, not necessarily, Okay, tell me why? Why?
Speaker 3: I don't know, But from what I can gather, there
Speaker 3: are three major disorders that we worry about that are
Speaker 3: all classified under this umbrella of listeriosis three like manifestations.
Speaker 3: One are maternal fetal infections, and this encompasses a lot
Speaker 3: of different possibilities that.
Speaker 1: We'll get into.
Speaker 3: Two bacteremia or septicemia, so infection of this bacteria in
Speaker 3: the bloodstream. And three neurolisteriosis or a meningitis picture infection
Speaker 3: of our central nervous system. We've talked about other food
Speaker 3: borne illnesses before, some of which can pose a risk
Speaker 3: of invasive infection, like E. Coli one, five, seven, for example.
Speaker 3: But with those, what we tend to see is a
Speaker 3: GI infection. You have these diarrhea, nausea, vomiting, fever, You're
Speaker 3: feeling crappy. With a GI infection, your guts are a mess,
Speaker 3: and then this leads to an invasive infection. But that
Speaker 3: is often not the case when it comes to listeriosis.
Speaker 3: So while we can see this gaster enteritis, nausea, vomiting, diarrhea,
Speaker 3: maybe fever, you're feeling crappy, but the cases that we
Speaker 3: worry about are actually separate entire and the incubation period
Speaker 3: for these is not twenty four hours. It's one to
Speaker 3: four weeks or more. Whoa, yeah, So it's separated in
Speaker 3: time entirely. And so that's why I say, was there
Speaker 3: a preceding diarrhea? Maybe would we even remember it? Maybe not?
Speaker 3: But most of the data that I see doesn't even
Speaker 3: mention whether or not there was a preceding gast or enteritis.
Speaker 1: Picture that makes things so difficult, I imagine for intervention
Speaker 1: because with something like ecola, it's clearly a gi bug
Speaker 1: that's then moving into disseminated infection and more severe infection.
Speaker 1: And this is like, suddenly, here's this disseminated infection, but
Speaker 1: we don't there's nothing that tips you off as to
Speaker 1: what it could be beyond the usual suspects, and listeria
Speaker 1: is not necessarily a usual suspect. Now that aaron one
Speaker 1: to four weeks, so is there like a threshold response
Speaker 1: where it's like the bacteria you know, replicate in high
Speaker 1: enough numbers, that's suddenly they're systemic Because it seems very sudden. Yeah,
Speaker 1: let's talk about it, Okay, getting like very excited, like
Speaker 1: not excited, but like intense about this, and I can
Speaker 1: dial it back. No, I love it.
Speaker 3: I love the intensity.
Speaker 1: It's it is.
Speaker 3: I was feeling honestly the exact same way, and that's
Speaker 3: I couldn't even wrap my brain around how interesting that
Speaker 3: that part of the listeria story is. So let's first
Speaker 3: talk about the three major manifestations of listeriosis perinatal infections, bacteremia,
Speaker 3: and the CNS, the nervous system infections. We'll talk about
Speaker 3: what those look like, how they present, how somebody would
Speaker 3: show that they have this infection, and what the results
Speaker 3: tend to be, which are spoilers not good, And then
Speaker 3: we'll talk about the path of physiology that kind of
Speaker 3: unites them about this bacteria. So when it comes to
Speaker 3: perinatal or neonatal infections, overall, on average, they account for
Speaker 3: an estimated ten percent plus or minus of all listeriosis cases.
Speaker 3: And again, when I say listeriosis, I just mean these
Speaker 3: three invasive infections. Think of the food borne illness as
Speaker 3: totally separate. Oh okay, m But perinatal infections are a
Speaker 3: huge cause of morbidity and mortality, especially of neonates. So
Speaker 3: I'm going to talk about that first. So, a perinatal
Speaker 3: infection means infection with listeria during pregnancy, and the symptoms
Speaker 3: here tend to be very non specific. It's often what's
Speaker 3: called a flu like illness. So fever, chills, malaise, muscle aches,
Speaker 3: your overall feeling really crappy. Some of the papers that
Speaker 3: I read described it as sometimes being mistaken for pylo nephritis,
Speaker 3: which is infection of the kidneys.
Speaker 1: So really that could.
Speaker 3: Just be like back pain along with a fever and
Speaker 3: evidence of an infection. Okay, but with infection during pregnancy.
Speaker 3: While the infection for the pregnant person is very rarely
Speaker 3: severe or life threatening, the problem is that for the fetus,
Speaker 3: infection almost inevitably eighty percent of the time or more
Speaker 3: leads to severe complications because this is a bacteria that's
Speaker 3: crossing over the placental barrier very easily infecting the fetus
Speaker 3: and can lead to early pregnancy loss or still birth,
Speaker 3: depending on how far along you are in pregnancy. It
Speaker 3: can lead to premature labor and delivery, which can have
Speaker 3: a whole host of complications arising from that prematurity, and
Speaker 3: it can also lead to a both an early neonatal
Speaker 3: infection right when that baby is born, they can become
Speaker 3: infected and have signs of either sepsis or meningite, or
Speaker 3: if infection happens around the time of delivery, it can
Speaker 3: lead to a late onset meningitis. So a few days
Speaker 3: or weeks after delivery, the baby can end up super
Speaker 3: sick from listeriosis as well.
Speaker 1: So this is another thing where we're seeing a delay
Speaker 1: between exposure and ramping up and then severe complications.
Speaker 3: Potentially, it all just depends on the timing of the
Speaker 3: infection during pregnancy.
Speaker 1: So, okay, speaking of the timing of infection during pregnancy,
Speaker 1: are their highest risk periods and how long is someone
Speaker 1: infected with listeria? And I guess that's such a that
Speaker 1: answer is probably super variable.
Speaker 3: Yeah, it's really variable and even variable in terms of
Speaker 3: the timing of infection. Infection at any point during pregnancy
Speaker 3: eighty percent of the time has severe complications. What those
Speaker 3: complications are going to be will depend on the timing
Speaker 3: of pregnancy. So more likely to lead to early pregnancy
Speaker 3: loss if you're earlier in the course of pregnancy, more
Speaker 3: likely to lead to a neonatal infection if you're very
Speaker 3: close to the end, et cetera. But at any time
Speaker 3: point we see severe complications for the fetus. Okay, so
Speaker 3: it's always super high risk, always super high risk, yeah,
Speaker 3: which is terrifying. Yeah, and again here we tend to
Speaker 3: see a delay of one to four weeks between exposure
Speaker 3: for the pregnant person and when they start to have
Speaker 3: these symptoms of fever chills, that mean that they have
Speaker 3: listeriosis and now the fetus is also infected.
Speaker 1: These symptoms are not super severe, like I'm sure that
Speaker 1: they are extremely uncomfortable and painful, but they're not necessarily
Speaker 1: something that's going to look like sepsis or whatever. So
Speaker 1: how does someone get tested for listeriosis?
Speaker 3: Yeah, that's a really good question, and it's likely when
Speaker 3: there's a complication with the pregnancy. That's when someone is
Speaker 3: more likely to seek care when something is going wrong
Speaker 3: with the pregnancy, if they haven't already sought care when
Speaker 3: they had these flu like symptoms. And I don't want
Speaker 3: to downplay how sick someone would likely feel when they
Speaker 3: have listeriosis during pregnancy. They're feeling really sick, so it's
Speaker 3: very likely that they may go in and seek care
Speaker 3: and you would see that they have signs of an infection.
Speaker 3: But it's generally not life threatening for the pregnant person, right, Okay,
Speaker 3: that's the big difference. Yeah, it is, though life threatening
Speaker 3: for adults who are not pregnant. In the other cases
Speaker 3: that we'll talk about. So let's get to that, shall
Speaker 3: we h. And by the way, when I'm talking about
Speaker 3: groups who are at highest risk for infection aside from
Speaker 3: during pregnancy, there are a few groups that we see
Speaker 3: that are at highest risk. Primarily it's those of older age,
Speaker 3: especially over age sixty five, whether or not they have
Speaker 3: any immunal compromising conditions, but especially if they do have
Speaker 3: things like diabetes or perhaps we're on steroids for one
Speaker 3: reason or another. So older age is the primary risk factor.
Speaker 3: We also see it like with neonatal infections in the
Speaker 3: very very young, as well as in people who are
Speaker 3: immunal compromised for one reason or another, which includes poorly
Speaker 3: controlled HIV infection or progression to AIDS, which we actually
Speaker 3: see as a really big risk factor for listeriosis. So
Speaker 3: what are these other infections look like outside of pregnancy.
Speaker 3: So in the case of a bloodstream infection with listeria,
Speaker 3: which by the way, accounts for anywhere from thirty to
Speaker 3: fifty percent of cases of listeriosis, which is a.
Speaker 1: Lot, a lot.
Speaker 3: Yeah, with this infection, the symptoms are incredibly nonspecific, and
Speaker 3: when you read them, they really are just the symptoms
Speaker 3: of sepsis, which we covered in detail in our sepsis episode.
Speaker 3: So it often starts with fevers, feeling overall really bad,
Speaker 3: like you're just not feeling like yourself. You often have chills,
Speaker 3: and because this is a cause of sepsis, then it's
Speaker 3: going to go on to develop the same severe complications
Speaker 3: and outcomes that we see in sepsis from any other
Speaker 3: bacterial organism, that is, multi organ failure and eventually death
Speaker 3: from an overwhelming bacterial load in the bloodstream. But what's
Speaker 3: interesting is that there often isn't like a single presenting
Speaker 3: organ that you might suspect as the ideology of this infection,
Speaker 3: because while you got infected through your guts several weeks
Speaker 3: prior to presenting with these symptoms of bacterymia or septicemia,
Speaker 3: you may not have ever even had gastroenteritis symptoms. So
Speaker 3: in that way, it's different than when we talked about
Speaker 3: sepsis and you're trying to think of like what is
Speaker 3: the source, This would probably be a case where you'd
Speaker 3: have a really hard time identifying what is the source
Speaker 3: of this infection. Yeah, and when it comes to bacteremia
Speaker 3: and septicemia, the mortality rate is twenty to thirty percent,
Speaker 3: and that is even with treatment.
Speaker 1: It's so scary, it's so awful, terrifying.
Speaker 3: Yeah. Finally, listeria can also cause a meningitis or, in
Speaker 3: some cases a new word, a rhomb encephalitis. Okay, we'll
Speaker 3: talk more about because that includes the disease known as
Speaker 3: circling disease in animals.
Speaker 1: Oh thank goodness. I had that written down in my
Speaker 1: notes and then it just stayed circling like that was
Speaker 1: all that I Yeah.
Speaker 3: Yeah, So meningitis or infection of the central nervous system,
Speaker 3: accounts for, by most studies that I saw, about thirty
Speaker 3: percent of cases of listeriosis in adults. So if you've
Speaker 3: been adding this up as we go, perinatal infection accounts
Speaker 3: for about ten percent, bacterymia about fifty percent, meningitis about
Speaker 3: thirty percent, and we're left with an extra about ten
Speaker 3: percent of cases that are very very rare, and we'll
Speaker 3: talk about in a minute.
Speaker 1: And are these mutually exclusive categories?
Speaker 3: Great question. No, okay, no they're not. You can certainly
Speaker 3: have a bacterymia and a meningitis picture at the same time. Okay, yep, yeah, yeah, yeah, definitely.
Speaker 3: So in adults who end up with a meningitis or
Speaker 3: a meningo encephalitis from listeria. Again, the symptoms are like
Speaker 3: another meningitis from a viral cause or a bacterial cause.
Speaker 3: So what that means is fever, headache, stiff neck. If
Speaker 3: it's infecting the brain itself, you might have things like
Speaker 3: confusion or even disruption in consciousness. Usually the onset is
Speaker 3: a little bit less abrupt than some other more common
Speaker 3: causes of bacterial meningitis like numacoccle or meninchoccle meningitis. And
Speaker 3: it's often harder to detect listeria in for example, a
Speaker 3: spinal tap, because this is an intracellular bacterium, so you
Speaker 3: have to wait until cell culture results because it's not
Speaker 3: gonna show up on a gram stain necessarily. Okay, But
Speaker 3: one thing that's also interesting and seems to happen with listeria,
Speaker 3: and I don't know the frequency because some papers were like,
Speaker 3: this isn't specific to listeria, and some were like, yes
Speaker 3: it is. But it's a specific and bizarre form of
Speaker 3: meningitis that infects the cerebellum, the back part of our brain,
Speaker 3: like the and you look at a picture of a
Speaker 3: brain it's like the two tiny balls on the back,
Speaker 3: and this is a romb encephalitis. You see similar signs
Speaker 3: as a typical encephalitis fever, headache, but more often you'll
Speaker 3: also see a lot of nausea and vomiting, and then
Speaker 3: signs of what we call cerebellar dysfunction, like not being
Speaker 3: able to walk in a straight line, what we call
Speaker 3: a taxia. You might see cranial nerve abnormalities because you're
Speaker 3: cranial nerves that innervate the muscles and sensory system of
Speaker 3: your face and neck come out in our brain stem
Speaker 3: near the cerebellum, and so you might see various palsies
Speaker 3: or abnormalities in the function of those nerves. And this
Speaker 3: is what we see in animals, especially ruminants who get
Speaker 3: infected with listeria. This exact same type of infection a
Speaker 3: romb encephalitis, and it can lead to very odd behaviors,
Speaker 3: including circling, where animals walk in unidirectional circle and they
Speaker 3: have like head and neck deviation to one side. And
Speaker 3: it's all because of this infection in the back part
Speaker 3: of the brain and the brainstem.
Speaker 1: Okay, so many thoughts. Number one, I remember seeing a
Speaker 1: video of circling ruminants of some kind. I can't remember
Speaker 1: what it was going around like last fall, and I
Speaker 1: think that's when we added lysteria as a topic or
Speaker 1: we were like, oh, for sure, what's going on here?
Speaker 3: So here's the thing. That video almost certainly not listeria.
Speaker 1: What is it? Don't know.
Speaker 3: There was a lot of explanations that I found online,
Speaker 3: and I am not a veterinarian, so I'm not going
Speaker 3: to try and delve into the nitty gritty of what
Speaker 3: those are. But the reason that it most likely was
Speaker 3: not listeria is because, first of all, you're right, I
Speaker 3: wouldn't expect that an entire herd is going to get
Speaker 3: infected in the exact same way at the exact same
Speaker 3: time with a pathogen that's an opportunistic pathogen that's not
Speaker 3: infecting everyone equally well.
Speaker 1: And so that's my other question about that, because ruminants,
Speaker 1: because livestock can be infected and be totally fine, and
Speaker 1: they just shed listeria into the environment just like us. Okay,
Speaker 1: So this would be a case this would be an
Speaker 1: individual more likely, okay, And this would be an individual
Speaker 1: that had something else going on that was you know,
Speaker 1: suppressed in some.
Speaker 3: Way exactly, Yes, And it wouldn't be walking in a
Speaker 3: perfect unidirectional circle with all of your friends like that
Speaker 3: video of the sheep that was going around virally. It
Speaker 3: would be a lot more of that a taxic gate.
Speaker 3: It would be a lot more like stumbling, kind of
Speaker 3: confused gait. Would it still be unidirectional?
Speaker 1: Likely?
Speaker 3: Yes, because it often what we see in animals is
Speaker 3: this asymmetric infection. So you're damaging one side of the
Speaker 3: brainstem more than the other, and that's why you see
Speaker 3: like a unilateral picture of infection.
Speaker 1: Okay, so let's talk about why the heck it happens there?
Speaker 1: Do you have an answer.
Speaker 3: That we don't have an answer to it?
Speaker 1: Okay?
Speaker 3: Like why that part of the brain? I don't know?
Speaker 1: And why one side? Yeah, I don't know. A great question. Okay.
Speaker 3: So those are all of the different ways that you
Speaker 3: can get listeriosis.
Speaker 1: I did mention.
Speaker 3: The remaining ten percent of cases are often localized infections.
Speaker 3: So you can actually see skin infections, especially maybe among
Speaker 3: people who get exposed from livestock, or rarely other specific
Speaker 3: organ infections like an endocarditis infection of the heart or
Speaker 3: a liver infection or infection of the wall of the abdomen,
Speaker 3: so we can also see potentially infection in specific organs,
Speaker 3: but this tends to be very, very rare compared to
Speaker 3: the other manifestations of listeriosis.
Speaker 1: Okay, so how does this happen? Why does this happen? Yeah,
Speaker 1: it's crossing the placenta, it's crossing blood brain barrier. This
Speaker 1: bacterium has a lot of tricks up its sleeve. You
Speaker 1: nailed it.
Speaker 3: I didn't realize something that I didn't realize at all
Speaker 3: before researching for this episode is that because of these traits,
Speaker 3: listeria has actually become a model organism of infection and
Speaker 3: invasion because it is so good at invading across our
Speaker 3: normal protective barriers. So in the case of a person
Speaker 3: who's immunocompromised and exposed to listeria, listeria can then cross
Speaker 3: three you named them, very important structures that we usually
Speaker 3: use to keep pathogens out. First, it's crossing over our
Speaker 3: intestinal epithelium, so it's no longer just limited to our guts.
Speaker 3: It has a really easy time penetrating these tight barriers.
Speaker 3: It makes its way into our lymph system and our
Speaker 3: blood stream, where It can then travel to our liver
Speaker 3: and our spleen and in theory any organ but primarily
Speaker 3: the liver and spleen, and continue to grow and progress
Speaker 3: to infection. It can then also, like you said, aaron,
Speaker 3: cross our blood brain barrier, so it can cross through
Speaker 3: these other really tight cell to cell junctions made to
Speaker 3: keep bacteria out, and then it very easily crosses the
Speaker 3: placental barrier and is able to infect a developing fetus.
Speaker 3: So how is it able to do this? How is
Speaker 3: it so easily able to cross these barriers? The truth
Speaker 3: is that it's largely because this bacterium has adapted to
Speaker 3: not just survive, but also divide, continue replicating, and thrive
Speaker 3: within the sidasol of our cells. Both cells like our macrophages,
Speaker 3: which which I talk about a lot, but these are
Speaker 3: the white blood cells whose job it is to go
Speaker 3: out and find and engulf and usually neutralize bacteria. So
Speaker 3: Listeria can survive that normal neutralization process that macrophasias do
Speaker 3: by actually hijacking those macrophasia's machinery and breaking out of
Speaker 3: the vacuoles that we've trapped it in and replicate inside
Speaker 3: of those macrophases. But Listeria can go one step further.
Speaker 3: They can then actually escape sell to sell.
Speaker 1: It is so wild, it's amazing.
Speaker 3: So they're able to spread directly from one of our
Speaker 3: cells to another of our cells without having to leave
Speaker 3: the cell that they've been replicating in. Most of the time,
Speaker 3: when I've talked about intracellular pathogens like viruses and other
Speaker 3: intracellulara I say they replicate and replicate, and then they
Speaker 3: burst out of our cells and they travel through the
Speaker 3: bloodstream to infect another cell. Listeria don't have to do
Speaker 3: that part. They can intentionally travel from cell to cell
Speaker 3: to sell without having to burst out and enter our
Speaker 3: bloodstreams or our lymphatics. And they can do this not
Speaker 3: just in our macrophases, our macrophases and other white blood cells,
Speaker 3: intentionally in gulf bacteria. So bacteria have an easy time
Speaker 3: getting inside of macrophasis. There's a lot of bacteria we've
Speaker 3: talked about on this podcast that can survive inside of macrophage.
Speaker 3: They've evolved to escape that one protective response. But Listeria
Speaker 3: take it one step further. They have a whole host
Speaker 3: of other receptors that allow for them to intentionally enter
Speaker 3: our other cells like our intestinal epithelium like other cells
Speaker 3: in our spleen and our liver and throughout our body
Speaker 3: and survive and replicate within those cells as well. It's
Speaker 3: it's incredible.
Speaker 1: It's incredible. So this bacterium is slowly invading our entire body, Yeah,
Speaker 1: hopping cell to sell or sneaking cell to sell to anthropomorphize,
Speaker 1: and most of the time it's doing this silently more
Speaker 1: or less.
Speaker 3: Right, Well, that's a really good question, Aron. That question
Speaker 3: has a lot to it because the question is what
Speaker 3: percentage of the time, if I'm exposed to listeria in
Speaker 3: my turkey sandwich, is it getting through my guts and
Speaker 3: replicating in my cells without me ever getting sick from it?
Speaker 1: Does that happen question mark?
Speaker 3: Or does it not? Do I have a gut barrier
Speaker 3: that doesn't allow it to penetrate, And in the case
Speaker 3: that it does penetrate, does it just take those one
Speaker 3: to four weeks for the bacteria to replicate to a
Speaker 3: point at which our body recognizes it and now is
Speaker 3: causing a response that is illness, right, and that is
Speaker 3: that overwhelming infection that now we're really sick from. I
Speaker 3: don't know which of those two my suspicion is that
Speaker 3: it is the latter, where in people who don't have
Speaker 3: any risk factors, who are not getting severely ill from
Speaker 3: this most of the time, this bacterium is not establishing
Speaker 3: an infection in our cells for a very long period
Speaker 3: of time.
Speaker 1: Okay, and when our body recognizes it as a pathogen,
Speaker 1: which happens, you know, at a certain point later on
Speaker 1: when things are real bad, what is that response like,
Speaker 1: because it's unusual.
Speaker 3: Right, Yeah, So it seems like one of the biggest
Speaker 3: risk factors for infection with listeria, for listeriosis, these invasive infections,
Speaker 3: is lack of a adequate T cell response. So it is
Speaker 3: T cells that are primarily the ones that are blocking
Speaker 3: this infection from happening and responding to this infection when
Speaker 3: it is established. And so for cases when you lack
Speaker 3: that response for one reason or another, that is when
Speaker 3: you actually see listeriosis manifest itself. And that is largely
Speaker 3: because of the way that it's an intracellular only pathogen.
Speaker 3: Our T cells are much more involved in that part
Speaker 3: of our immune response, like killing infected cells versus antibody
Speaker 3: responding to bacteria that are free floating in our bloodstream. Okay,
Speaker 3: So you don't see a lot of the more antibody
Speaker 3: mediated response with.
Speaker 1: Listeria, which is fascinating.
Speaker 3: It's interesting because it's still a bacterial infection.
Speaker 1: Yeah, yeah, And that means presumably that you know, is
Speaker 1: their sustained immunity to listeria. Probably not.
Speaker 3: I don't think we have any data on that whatsoever, though.
Speaker 1: Yeah.
Speaker 3: Yeah, because mortality is really high and because it's a
Speaker 3: very rare infection still, Oh thank goodness. But that is
Speaker 3: most of the biology of listeria and the disease that
Speaker 3: we know of as listeriosis.
Speaker 1: It's a bad one.
Speaker 3: It's a really bad one. It is treatable with antibiotics,
Speaker 3: and in general, antibiotic resistance has yet to be a
Speaker 3: huge concern in terms of like the normal antibotics that
Speaker 3: we would use to treat it. But it tends to
Speaker 3: respond better to specific antibiotics that maybe aren't used as
Speaker 3: commonly as like mineral antibiotics if someone comes in with
Speaker 3: bacterymia or stept to semia. So a lot of times
Speaker 3: we do see delays in appropriate treatment because it's a
Speaker 3: hard disease to diagnose.
Speaker 1: And which I would guess contributes to mortality rate.
Speaker 3: Absolutely contributes to mortality rate. Yes, definitely. So any other
Speaker 3: questions erin, I mean, I have a lot, but.
Speaker 1: Like I'm sure I'll come up with something again at
Speaker 1: some point.
Speaker 3: Yeah, well, can you tell me, like where this bacterium
Speaker 3: came from and how long it's been making us sick
Speaker 3: and everything that we know about it and how we
Speaker 3: got here.
Speaker 1: Oh yeah, everything, I'll just everything, all of it, all
Speaker 1: of it right after this break. In many ways, I
Speaker 1: think that the story of Listeria monocytogenies will sound like
Speaker 1: maybe fairly familiar to you, and especially you Aaron, but
Speaker 1: also you listeners, if you have listened to the podcast before.
Speaker 1: It involves the discovery of a new pathogenic microbe in
Speaker 1: the early twentieth century, and then it's followed by the
Speaker 1: realization that, hey, this pathogen is a lot more widespread
Speaker 1: than we previously thought, and then people tracing its spread
Speaker 1: not just in present day but also in the past.
Speaker 1: And it's a fascinating story of discovery, and it follows
Speaker 1: this common pattern. But what I think separates the story
Speaker 1: of Listeria from these other ones comes down to a
Speaker 1: few things. And by the way, when I say listeria,
Speaker 1: I am specific referring for the most part, unless I
Speaker 1: say otherwise to Listeria monocytogenies, I mean same. Yeah. But
Speaker 1: one of these things that separates this story out from
Speaker 1: some of the others is what I found to be
Speaker 1: a surprising delay between discovery and when people realized how
Speaker 1: it was commonly transmitted. And we'll get into that. And
Speaker 1: the other is just how well we can see the
Speaker 1: drivers of pathogen movement across time and space. Oh okay,
Speaker 1: and that's not just in hypothetical terms, but by looking
Speaker 1: at what this bacterium's biology can tell us about the past.
Speaker 1: It's I love this ooh okay. We'll get into all
Speaker 1: of it, but first let's start at the beginning. And
Speaker 1: I'm skipping right to the discovery side of things, because
Speaker 1: even though you asked where did this thing come from?
Speaker 1: Listeria is widely distributed in the environment, and it can
Speaker 1: infect a ton of different animals, and so I don't
Speaker 1: really know when or where it first emerged. There are
Speaker 1: some papers looking at the evolutionary relationships among some of
Speaker 1: the species within the Lasteria genus and some of the
Speaker 1: nonpathogenic ones compared to the pathogenic ones, and looking at
Speaker 1: when did they evolve virulence and so on and so forth.
Speaker 1: But I'm not going to get into it. Okay, okay,
Speaker 1: but when did we as humans first recognize it as such? Well,
Speaker 1: sometimes people look for a pathogen to match a known
Speaker 1: or an infamous disease, think like plague or cholera or something.
Speaker 1: Other times it's more of like a fishing expedition. You
Speaker 1: cast your net and you see what you pull up.
Speaker 1: There are some where people are just like, let's collect
Speaker 1: swabs from infants' throats and see what we find, or
Speaker 1: from pond water or this rabbit's foot or something.
Speaker 4: Oh okay, yeah, And sometimes it happens, I think, a
Speaker 4: bit more methodically, in a bit more of an expected fashion,
Speaker 4: as much as scientific discovery can be expected in any case.
Speaker 1: Listeria monocytogenies or Bacterium monocytogenies as it was first called,
Speaker 1: falls into this last category. And I'll tell you how.
Speaker 1: In nineteen twenty four, a researcher named Everett George Dunn
Speaker 1: Murray happened to be looking in the blood of lab
Speaker 1: rabbits when he found something new. And I say happened
Speaker 1: to be but it was really quite intentional, as you'll
Speaker 1: hear when I read a snippet of his paper, which
Speaker 1: I felt was like written in a surprisingly poetic way,
Speaker 1: and I love when that happens with older papers. Like
Speaker 1: it was lovely. So I have a lot of quotations
Speaker 1: here from it, hopefully not too many, but I think
Speaker 1: you'll enjoy it. I love it already, all right, prepare yourself.
Speaker 1: This is a long quote, okay quote. An important responsibility
Speaker 1: attached to the breeding of normal laboratory animals for the
Speaker 1: Department of Pathology was the routine autopsies on animals which died.
Speaker 1: This practice was rewarded by the control it exercised over
Speaker 1: the quality of the stock and by the interesting diseases
Speaker 1: it discovered. Foremost amongst these is the disease described in
Speaker 1: this paper. In May nineteen twenty four, six cases of
Speaker 1: rather sudden death in rabbits were observed to present strikingly
Speaker 1: similar lesions, though no direct cause of the evidently acute,
Speaker 1: toxic or infectious condition could be discovered in any of them.
Speaker 1: The interesting characters presented by the disease and the increasing
Speaker 1: mortality amongst our young rabbits caused us to watch carefully
Speaker 1: for any signs of illness and to investigate all cases
Speaker 1: which occurred. Although there seemed to be every reason to
Speaker 1: say suppose that the disease was of a septocemic nature,
Speaker 1: all cultures from the heart's blood remained sterile. During July
Speaker 1: nineteen twenty four, small gram positive basilla were found in
Speaker 1: films of the acidic fluid in a guinea pig and
Speaker 1: in smears from the omentum of a rabbit. Side note,
Speaker 1: I don't know what an omentum is, so I did
Speaker 1: look it up. I forgot to do. You want me
Speaker 1: to tell you? Yeah, yeah, I tell you.
Speaker 2: So.
Speaker 3: It's like this kind of like fatty layer that lays
Speaker 3: over our guts. It's like attached to the top of
Speaker 3: your guts, and it kind of lays over all of
Speaker 3: your intestines and it's a little cushing.
Speaker 1: There for you.
Speaker 3: Yes, nice, it's really nice.
Speaker 1: Omentum. Cool, all right, back to the quotes. I have
Speaker 1: just a few more lines, but little heed was taken
Speaker 1: of these, and the heart blood cultures remained sterile. In
Speaker 1: August nineteen twenty four, a pure culture of a small
Speaker 1: gram positive bacillis was a obtained from the heart's blood
Speaker 1: of an obviously acute case in a pregnant rabbit. These
Speaker 1: basilla closely resembled those seen in the two animals during July,
Speaker 1: and with their isolation in pure culture, our experimental work
Speaker 1: began and quote. So basically what happened here was that
Speaker 1: they found this disease, they found some sort of condition
Speaker 1: in these rabbits. They kept culturing and culturing, and then
Speaker 1: eventually they found this gram positive basilla. And after that point,
Speaker 1: once they were able to culture this, they conducted a
Speaker 1: bunch of observational and experimental work which included a combination
Speaker 1: of clinical observations of the young rabbits in the lab, autopsies,
Speaker 1: tissue preparations, experimental infection, culturing the organism, things that are
Speaker 1: not just the usual but like the usual, and then
Speaker 1: some This was a packed paper full of information. It
Speaker 1: was really quite impressive. What they found was that the
Speaker 1: infection seemed to hit the young rabbits particularly badly, causing
Speaker 1: some to die very suddenly and others to die over
Speaker 1: the course of weeks. The researchers remarked on how striking
Speaker 1: the disease was, like how distinguishable it was once you
Speaker 1: saw it in an animal. There was very little else
Speaker 1: that they felt it could be I thought was really
Speaker 1: interesting because we've talked about in the biology section, Like
Speaker 1: you talked about it's very difficult. You can't look at
Speaker 1: someone and go, oh, that's listeria for sure, right, but
Speaker 1: they evidently could do that, at least in the way
Speaker 1: it manifested in rabbits. And it was this characteristic nature
Speaker 1: of the disease that was part of the reason why Murray,
Speaker 1: the lead author on the paper, thought that this must
Speaker 1: be a new pathogen not yet described. Quote. Both the
Speaker 1: natural and experimental disease have interesting and characteristic features, and
Speaker 1: their consideration has forced us to the conclusion that the
Speaker 1: causative organism either has not been described previously or has
Speaker 1: been inadequately described, and so cannot be traced in the literature.
Speaker 1: In either case, we feel justified in naming it. Its
Speaker 1: salient character is the production of a large mononuclear leucocytosis.
Speaker 1: This is by far the most important and most striking
Speaker 1: character we have discovered, and we name the microorganism we
Speaker 1: shall describe in this paper Bacterium monocytogenes. I love that.
Speaker 1: I love it. We feel what was it? We feel
Speaker 1: justified in naming it. I love it. I mean they
Speaker 1: maybe they were justified in naming it, but they certainly
Speaker 1: weren't the first people to culture it, especially given its
Speaker 1: widespread prevalence in nature.
Speaker 3: I wonder if the really high monocyte peripheral monocytes that
Speaker 3: they were seeing were part of what they said. Once
Speaker 3: you see this, you know it can't be anything else,
Speaker 3: because that is true in rabbits, but it is not
Speaker 3: true in humans.
Speaker 1: Interesting. Yeah, yeah, that's interesting in and of itself. But yeah,
Speaker 1: why do different species respond differently to this? But yeah,
Speaker 1: so not only had other there's pretty strong evidence for
Speaker 1: like other people, other researchers having identified or at least
Speaker 1: isolated this bacterium before. But either they're being punished for
Speaker 1: the crime of not writing their paper in English, or
Speaker 1: they didn't describe it well enough, or it was classified
Speaker 1: as something else. But then also, retrospective analysis of old
Speaker 1: tissue sections seemed to indicate that people there were human
Speaker 1: infections at least before World War One. Okay, I mean
Speaker 1: all of this is just to say that, like, this
Speaker 1: bacterium has been around. There was no sudden rise necessarily
Speaker 1: or any sort of reason why Murray was in the
Speaker 1: right time and place for it was just a really
Speaker 1: well written paper, But unlike we've seen with other infectious
Speaker 1: diseases in the past, it didn't necessarily lead to this
Speaker 1: widespread recognition where everyone's like, oh my gosh, I see it.
Speaker 1: It's everywhere. Suddenly, here's Bacterium monocytogenies. It kind of laid
Speaker 1: low for a while. It was mentioned in textbooks. It
Speaker 1: got a genus name change along the way from Bacterium
Speaker 1: or whatever it was called to Listeria. And also side
Speaker 1: note Listeria, of course, is to honor Joseph Lister. Mister
Speaker 1: features in our Percepsist episode, so go check that episode
Speaker 1: out if you want to learn more about his story
Speaker 1: if you haven't already. Anyway, in the twenty five years
Speaker 1: or so since Murray first cultured this bacterium, it didn't
Speaker 1: really make itself known as a pathogen of public health importance.
Speaker 1: Took a while, which I find interesting. Mostly it was
Speaker 1: found in small rodents or in domestic animals like sheep,
Speaker 1: causing occasional outbreaks in those organisms. There were a handful
Speaker 1: of human cases reported in Denmark in nineteen twenty nine,
Speaker 1: and at the time it was thought to be related
Speaker 1: to infectious mononucleosis, but in general it was thought to
Speaker 1: be extremely rare in humans, so rare that it didn't
Speaker 1: merit a mention in bacteriology textbooks relevant to human health
Speaker 1: at the time. Wow, But it did merit a note
Speaker 1: from a researcher named Burns in nineteen thirty five who
Speaker 1: warned that Listeria monocytogenies could be a cause of granulomatis
Speaker 1: septicemia in infants and fatal meningitis in adults. But this
Speaker 1: warning by Burns was either forgotten about or never heard
Speaker 1: in the first place until nineteen fifty one when HPR
Speaker 1: Seliger at the University of Bonn, who wrote the textbook
Speaker 1: on Listeria literally and I think there's a species named
Speaker 1: after this researcher as well, when Seliger isolated the bacteria
Speaker 1: from lesions in newborns who had infections that resembled some
Speaker 1: that had just been written about from Germany had just
Speaker 1: been published about, and so researchers there in Germany a
Speaker 1: couple of years before had isolated the same bacteria from
Speaker 1: various tissues of eighty three newborns and stillborn infants who
Speaker 1: had been diagnosed with quote unquote Granulomatis in fantaseptica, which
Speaker 1: was thought to be a never before described infection. Oh okay,
Speaker 1: but these researchers thought that the bacteria they had found
Speaker 1: was a kind of Krina bacterium, And it was only
Speaker 1: realized that it was Listeria monocytogenies after Seliger recognized it
Speaker 1: as such a couple of years later. So, like I said,
Speaker 1: this was certainly not the first time that Listeria had
Speaker 1: infected humans. And some researchers have looked back at case
Speaker 1: reports from the late eighteen hundreds and early nineteen hundreds
Speaker 1: and hypothesized that listeriosis may have previously been diagnosed or
Speaker 1: described as quote unquote pseudo tuberculosis or quote unquote neonatal septicemia.
Speaker 1: And I saw a reference to a paper that I
Speaker 1: couldn't access where the author speculates that Queen Anne, who
Speaker 1: lived from sixteen sixty five to seventeen fourteen, had repeated
Speaker 1: pregnancy losses, still births, neonatal deaths, and post natal meningitis
Speaker 1: seventeen pregnancies overall with no living offspring. Oh, and some
Speaker 1: people have speculated that it was due to listeria. I
Speaker 1: don't know. That's a lot of lasteria, it's a lot
Speaker 1: of lysteria. So even though we know that listeria probably
Speaker 1: infected people throughout history, there's no way to make precise
Speaker 1: estimates of past prevalence for something like listeriosis. But infections
Speaker 1: did seem to start rising in the second half of
Speaker 1: the twentieth century. This could be due in part to
Speaker 1: the increase in microbiology techniques and the fact that people
Speaker 1: knew about listeriosis, but or I think it could be
Speaker 1: the large scale changes in food production and the lag
Speaker 1: in food safety policies that had been taking place and
Speaker 1: continued to take place throughout the twentieth century. Yeah uh huh.
Speaker 3: Okay, big chicken, Big chicken all over again.
Speaker 1: Big chicken. Yeah, I mean, and this goes back even further.
Speaker 1: I love talking about the Industrial Revolution and how it
Speaker 1: changed so much in terms of health and disease. The
Speaker 1: rise of cities, the growth of hospitals, the commercialization of medicine,
Speaker 1: the poor air quality, the limited diets, the mass produced foods,
Speaker 1: et cetera, et cetera. Many pathogens, as we know, as
Speaker 1: we've talked about, absolutely flourished in these new settings, including listeria.
Speaker 1: We now think of listeria as a pathogen that is
Speaker 1: primarily associated with food. Many outbreaks have been traced to
Speaker 1: food like milk, cheese made with raw milk, deli meats,
Speaker 1: hot dogs, fruits and veggies contaminated with manure containing listeria,
Speaker 1: but the link between listeria and contaminated foods was only
Speaker 1: made in nineteen eighty three after an outbreak of listeriosis
Speaker 1: among pregnant people and infants, with an extremely high mortality
Speaker 1: rate of twenty seven percent of the infants born alive
Speaker 1: despite aggressive supportive care and forty seven percent overall nineteen
Speaker 1: eighty three nineteen eighty three. So this particular outbreak was
Speaker 1: linked to coalslaw that had been contaminated by sheep manure
Speaker 1: containing listeria. So before then, before this this outbreak, researchers
Speaker 1: suspected that humans got infected with listeria from some kind
Speaker 1: of indirect transmission from animal sources, especially given its widespread
Speaker 1: prevalence in domestic and wild animals, but this was the
Speaker 1: first time that it was actually demonstrated. Epidemiologists went to
Speaker 1: the farms or went to the food production facilities where
Speaker 1: this coal slaw had been processed, and they were like, oh,
Speaker 1: it's in the everything, yeah, yeah, And later on I'm
Speaker 1: going to pick back up on some of these food
Speaker 1: born outbreaks of listeria and lessons learned and so on,
Speaker 1: But first I want to head back into the Industrial
Speaker 1: Revolution where I started this whole like topic. So, during
Speaker 1: this time, as more and more people began to move
Speaker 1: to live and work in cities, food production had to
Speaker 1: change to accommodate these increasing population densities. There was more
Speaker 1: of a demand for mass produced foods and process foods
Speaker 1: as the time from harvest to table grew longer and longer.
Speaker 1: And of course, as we've talked about on the podcast,
Speaker 1: before food safeties or technology allowing for analysis of food
Speaker 1: and food safety, it lagged tremendously far behind these new
Speaker 1: food production practices, especially in the US, where the giants
Speaker 1: and food industry, who were more concerned with profit than
Speaker 1: the health of their consumers actively discouraged any safety legislation
Speaker 1: from being passed in the US for years, years, decades.
Speaker 1: Person surprised, Oh, oh, it's even though it's not surprising,
Speaker 1: its shocking somehow, still just appalling. Maybe milk was diluted
Speaker 1: with pond water, it was preserved with formaldehyde and adulterated
Speaker 1: with plaster of Paris to get rid of the murky
Speaker 1: blue tint because it had been diluted with like pond water,
Speaker 1: and you could see horse hair worms swimming in and
Speaker 1: of it and stop it. But the plaster of Paris
Speaker 1: made it look farm fresh and straight from the utter.
Speaker 1: Stop it.
Speaker 3: Oh, this is worse than the Arsenic. I feel like
Speaker 3: you talked about similar things.
Speaker 1: Yeah, yep, I mean meat production, Like, don't even get
Speaker 1: me started. It was. It was equally appalling, if not
Speaker 1: more so. There's a reason that Upton Sinclair's The Jungle
Speaker 1: caused such a stir. No food was safe to eat.
Speaker 1: Spices were like cinnamon was mostly just brick dust, for instance.
Speaker 1: If you want to learn more about this, stay tuned
Speaker 1: to the podcast for a bonus episode later this season
Speaker 1: where I interview Deborah Blum about her fantastic book The
Speaker 1: Poison Squad, which goes into the fascinating history of food
Speaker 1: safety in the US. Oh, will read the book now
Speaker 1: if you don't feel like waiting for the upper Yeah,
Speaker 1: it's such a jaw dropping book. Oh my gosh, that's yeah. Okay. Anyway,
Speaker 1: it's easy to see how these practices with essentially no
Speaker 1: oversight for food safety, mass processing of milk based products
Speaker 1: and meats, longer times between production and purchase, no refrigeration.
Speaker 1: How these things would have led to a massive increase
Speaker 1: in listeria, both in terms of prevalence as well as geographically.
Speaker 1: But this time we don't have to settle for speculation.
Speaker 1: A paper from twenty twenty one by Maura at All
Speaker 1: traced the global spread of listeria, particularly one clonal group
Speaker 1: LMCC one, if anyone's interested, and this clonal group commonly
Speaker 1: causes infection in humans and is often found in cattle
Speaker 1: and dairy products, if you remember from our Anthrax episode.
Speaker 1: The clonal aspect of this really helps with being able
Speaker 1: to more closely trace diversification and rates of evolution and
Speaker 1: so on. And when these researchers looked at the genetic
Speaker 1: diversity of this group, what they found was that around
Speaker 1: the mid nineteenth century Industrial Revolution time, this group, this
Speaker 1: clonal group, underwent a big period of expansion both in
Speaker 1: overall diversity as well as geographic expansion, particularly in Europe.
Speaker 1: If you overlay this with what was going on in
Speaker 1: the global food trade, you would find that in eighteen
Speaker 1: seventy the North Atlantic Meat Trade Agreement was passed, which
Speaker 1: allowed for excess cattle in North America to be shipped
Speaker 1: to Europe, whose cattle population had dwindled due to things
Speaker 1: like contagious bovine plural pneumonia and foot in mouth disease.
Speaker 1: It's all about diseases, like I always everything.
Speaker 3: It's just always about diseases.
Speaker 2: Erin.
Speaker 1: We're not biased or anything, uh huh, but this trade
Speaker 1: agreement isn't just a matter of a few head of cattle.
Speaker 1: According to this paper, it led to a one thousandfold
Speaker 1: increase in the amount of cattle moved from North America
Speaker 1: to Europe. Wow. And right around this time, the researchers estimate,
Speaker 1: is when this particular clonal group of listeria arrived in Europe,
Speaker 1: after which it spread across the continent, helped along by
Speaker 1: railroad expansion which was currently going on both in Europe
Speaker 1: and North America, and it continued to diversify along the way.
Speaker 1: A drought in Oceania from eighteen ninety five to nineteen
Speaker 1: oh three led to cattle and their listeria being transported there,
Speaker 1: and then subsequent decades saw the continued global spread of
Speaker 1: this pathogen from North America to Asia to Oceania, from
Speaker 1: Europe to Africa, basically all over the world, and the
Speaker 1: pattern in genetic diversity of Listeria supports this increasing during
Speaker 1: this time of widespread cattle movement. And then this is
Speaker 1: the part I find so interesting, slowing down during the
Speaker 1: Great Depression, when countries such as the US and many
Speaker 1: other countries stopped exporting cattle and other foods for a while,
Speaker 1: so we're like, we need to food our people in
Speaker 1: this variety or whatever.
Speaker 3: Oh my gosh, that's really really cool that they had
Speaker 3: enough data to be able to see.
Speaker 1: That, right, And then it keeps going when trade resumed
Speaker 1: and cattle farming and food industrialization intensified around the mid
Speaker 1: twentieth century. Boom. You can see that these changing practices
Speaker 1: are reflected by what's happening also with this clonal group,
Speaker 1: which is so amazing and has also been seen for
Speaker 1: a few other food borne pathogens with a zonotic reservoir
Speaker 1: like E. Cola one five, seven, seven. Sooo, it seems
Speaker 1: pretty likely to me that the apparent rise in Listeriosis
Speaker 1: around the mid twentieth century may not have been just
Speaker 1: because people knew what to look for. Seems like it
Speaker 1: could be tied to the widespread global expansion of this pathogen.
Speaker 3: Yeah, and changes in food production that just like favor Yeah,
Speaker 3: this pathogen's growth.
Speaker 1: Just favor contamination, Like yeah, like actively promotes contamination. But
Speaker 1: I mean it certainly did help once people knew what
Speaker 1: they were looking for. It wasn't until the nineteen eighties
Speaker 1: that another change was made that we can see in
Speaker 1: these clonal groups, which is the stabilization of the clonal population.
Speaker 1: And that happened around the mid nineteen eighties, which is
Speaker 1: after people realized that it was tied to food production
Speaker 1: and certain food practices, and so they started to institute
Speaker 1: these safety measures. Oh my gosh, how interesting. It is
Speaker 1: so cool And I really hope that I interpreted this
Speaker 1: paper correctly. And granted, this study did look at just
Speaker 1: one clonal group, and there are others that are known
Speaker 1: to cause disease in humans. But I think it's just
Speaker 1: so cool because usually on the podcast, I feel like
Speaker 1: I'm talking about the spread of this or that pathogen
Speaker 1: in purely hypothetical terms. It's likely that this period of
Speaker 1: history led to the proliferation of this pathogen because more
Speaker 1: people were going to hospitals or as we know, war
Speaker 1: always leads to increased infectious disease because of crowded and
Speaker 1: unsanitary conditions, Like it's not very often that we can
Speaker 1: actually trace the impact that certain political practices I think
Speaker 1: had on a disease that we know about so much
Speaker 1: more recently than I don't know. I just think it's
Speaker 1: so cool.
Speaker 3: Yeah, And to be able to track like pathogen diversity
Speaker 3: like that, I really that's very cool.
Speaker 1: Yeah, it's beautiful. But not only is it interesting or beautiful,
Speaker 1: it also helps us with control or prevention today, since
Speaker 1: Listeria is not transmitted human to human and mostly comes
Speaker 1: from contaminated food sources, even if we don't necessarily always
Speaker 1: or even often know the source of the contamination, and
Speaker 1: because of the biology of this pathogen it's clonal nature,
Speaker 1: the fact that at the local level, certain genotypes dominate,
Speaker 1: we can use all this information to trace persistent sources
Speaker 1: of infection, like whether it be from a particular herd,
Speaker 1: maybe there's a really high prevalence and a certain herd
Speaker 1: on a farm or within a certain farm, or within
Speaker 1: a certain processing facility, and that's where public health officials
Speaker 1: can sort of target or put resources to eliminate the
Speaker 1: bacterium there. And on that front, We've made a lot
Speaker 1: of progress since the nineteen eighties, in large part thanks
Speaker 1: to the outbreaks of listeriosis that highlighted just how deadly
Speaker 1: it could be, sparking these public health and food safety responses.
Speaker 1: So earlier I mentioned that nineteen eighty three listeria outbreak
Speaker 1: in Canada tied to contaminated coalslaw and that was the
Speaker 1: one that really solidified food as a source of the pathogen.
Speaker 1: But that was really only the beginning in terms of
Speaker 1: food associated outbreaks of listeria. That same year, another outbreak
Speaker 1: of listeriosis involving forty nine people, primarily infants and aminosuppressed adults,
Speaker 1: and a fatality rate of twenty nine percent was detected
Speaker 1: in Massachusetts, this time linked to milk, not raw milk,
Speaker 1: but pasteurized milk, which pointed towards dairy products as a
Speaker 1: source of listeria minus cytogenies, because remember the first one
Speaker 1: was Coleslaw, and so this one really put dairy on
Speaker 1: the map. And sure enough, a couple of years later,
Speaker 1: soft cheese was the culprit, and a large outbreak of
Speaker 1: listeriosis in California involving at least one hundred and one
Speaker 1: human cases and fifty or more deaths.
Speaker 3: Oh my, that's massive.
Speaker 1: Massive. Ice Cream was next on the chopping block. When
Speaker 1: the bacterium was found in large quantities of a well
Speaker 1: known brand, they didn't name it in the paper, and
Speaker 1: there have been subsequent ice cream associated outbreaks as well.
Speaker 1: And one consequence of these outbreaks was that screening for listeria,
Speaker 1: especially in cheeses and other dairy products, ramped up significantly
Speaker 1: all over the world with the finding that listeria was
Speaker 1: so so much more prevalent in certain types of cheeses
Speaker 1: as well as in raw meat and meat products than
Speaker 1: anyone had guessed before. And of course, with this alarming news,
Speaker 1: at WHO and national public health authorities got involved and
Speaker 1: began to investigate how to best stop this bacterium from
Speaker 1: getting into the food supply, and how to raise awareness
Speaker 1: among medical professionals about potential outbreaks, and how to estimate
Speaker 1: or even begin to estimate the scope of this problem.
Speaker 1: Research into the ecology of this pathogen revealed how widespread
Speaker 1: it was, not just in livestock settings, but also in
Speaker 1: the wild, found in soil or infecting wild animals like
Speaker 1: I read one paper that found Listeria monocytogenies in nearly
Speaker 1: half of the black bears that they sampled in parts
Speaker 1: of the eastern US bears. Oh my god, I know.
Speaker 1: And also how different conditions in farms, things like herd
Speaker 1: size or livestock composition, like whether you have this many
Speaker 1: sheep or this many cattle, or whatever, grazing or housing practices,
Speaker 1: how all of these things could change the amplification or
Speaker 1: dispersal of the pathogen or select for certain strains that
Speaker 1: differ in their abilities to infect humans or livestock. Basically,
Speaker 1: there's been a lot of information that we have uncovered
Speaker 1: and are continuing to uncover. And while outbreaks did continue
Speaker 1: to happen and continue to happen today, these improved safety measures,
Speaker 1: along with this greater understanding of the ecology of this bacterium,
Speaker 1: led to a pretty substantial decrease and reported the stereosis
Speaker 1: cases in the nineteen nineties from eleven per million population
Speaker 1: in nineteen eighty eight to four cases per million in
Speaker 1: nineteen ninety eight. So it's like, that's a pretty substantial decline.
Speaker 1: In nineteen ninety nine, a US wide outbreak involving one
Speaker 1: hundred and one cases and twenty one deaths linked to
Speaker 1: hot dogs stopped lysteria from dropping further down on the
Speaker 1: food borne priority list as it kind of had been
Speaker 1: doing since. Like, Hey, the measures we're implementing are working,
Speaker 1: and this outbreak, in conjunction with other sporadic outbreaks as
Speaker 1: well as individual cases, has kept people searching for ways
Speaker 1: to stop this pathogen from invading the food supply chain.
Speaker 1: And I have to admit that when reading about all
Speaker 1: of these outbreaks and the subsequent response, like it's great
Speaker 1: that there seems to be a response, but it's also
Speaker 1: frustrating or I wish it could be different. That it
Speaker 1: has to be a response, it has to be reactive,
Speaker 1: and people have to experience these horrible things in order
Speaker 1: for change to be made, in order for or in
Speaker 1: order for people to go, hey, maybe we should re
Speaker 1: examine how often we're testing this particular machine for listeria,
Speaker 1: or what constitutes an acceptable level of listeria or so on.
Speaker 3: I wish that we could be relactable a whole another
Speaker 3: set of discussion, and that.
Speaker 1: Well, that being said, I think it is important to
Speaker 1: recognize that we have come a long way, not just
Speaker 1: in food safety practices, but also in our understanding of
Speaker 1: Listeria monocytogenies and as you mentioned, not just as a
Speaker 1: pathogen of public health importance, but also what it can
Speaker 1: tell us about things like cell signaling, surface proteins, and
Speaker 1: ad immunity. And my favorite mention was patho epigenetics. Ooh,
Speaker 1: but I don't want to step on your toes erin,
Speaker 1: So why don't you bring us up to speed on
Speaker 1: where we stand with listeriosis today and also why the
Speaker 1: heck cellular biologists are so fascinated with this bacterium.
Speaker 3: M hmm, I can't wait to We'll take a quick
Speaker 3: break and then get into it. In the US, annually,
Speaker 3: the CDC estimates that there are one thousand, six hundred
Speaker 3: cases of listeriosis, so again that means invasive infection, not
Speaker 3: just diarrhea. Oney six hundred cases and two hundred and
Speaker 3: sixty deaths annually, and as far as I can tell,
Speaker 3: that statistic does not include necessarily things like early or
Speaker 3: premature labor or other pregnancy complications that don't result in
Speaker 3: death of a neonate that would be counted as deaths.
Speaker 3: So that's not a massive number compared to most of
Speaker 3: the pathogens that we talk about on this podcast. But
Speaker 3: it's not an entirely small number either. When we try
Speaker 3: and look globally, unsurprisingly we don't have Greade numbers what
Speaker 3: but the World Health Organization estimates anywhere from point one
Speaker 3: to ten cases per one million people per year globally.
Speaker 3: So if we air in math that situation love it
Speaker 3: trademark air and math, that is anywhere from eight hundred
Speaker 3: to eight thousand cases globally every year, which is a
Speaker 3: huge range, but all together numbers that are significantly smaller
Speaker 3: than numbers that you mentioned, Aarin. And I think one
Speaker 3: thing that's really interesting about this is that I talked
Speaker 3: about the pathogenesis of this and how terrifying and how
Speaker 3: severe the disease listeriosis is when it causes this invasive
Speaker 3: infection in people who are susceptible, immuno compromised, or during pregnancy.
Speaker 3: But this is still a very rare pathogen and despite that,
Speaker 3: like you said, Aarin, it's still an incredibly important part
Speaker 3: of how we make our food safety regulations, which I
Speaker 3: think is fascinating and it really has sparked continued continues
Speaker 3: to be a big point of debate. The US actually
Speaker 3: has I learned, a zero tolerance policy for listeria monacytogenies
Speaker 3: in industry sampling, which I was shocked by.
Speaker 1: Yeah, me too.
Speaker 3: How often are we testing, et cetera. I don't know,
Speaker 3: but it does have a zero tolerance policy. Most other
Speaker 3: countries don't necessarily have a zero tolerance policy because that's
Speaker 3: really difficult to achieve. So deciding how do we balance
Speaker 3: risk of infection versus being able to feed a growing
Speaker 3: global population, it's really difficult. But I do think that
Speaker 3: it's really interesting that a pathogen that is as rare
Speaker 3: as listeria when you look at it compared to other
Speaker 3: food borne illnesses causing hundreds of millions of infections, it
Speaker 3: still has a really important role to play in making
Speaker 3: this kind of policy because of how severe it is
Speaker 3: when it does happen, right, and because like you mentioned it,
Speaker 3: and we do still see a lot of outbreaks food
Speaker 3: born outbreaks associated with specific types of foods, which means
Speaker 3: that this is a pathogen that could potentially cause quite
Speaker 3: a lot more morbidity and mortality if a large outbreak
Speaker 3: were to occur.
Speaker 1: In terms of the.
Speaker 3: Types of foods that are highest risk, I think you
Speaker 3: mentioned a lot of them already, but you can think
Speaker 3: of them as things that are already prepared and then
Speaker 3: refrigerated and then you eat them right because despite how
Speaker 3: heardy of a bacteria, Listeria monocytogenes is, it can't survive
Speaker 3: the cooking process. So foods that you take home and cook,
Speaker 3: like most meats that you're cooking thoroughly, even if they
Speaker 3: have listeria on them. If you're cooking them thoroughly, then
Speaker 3: that listeria is going to die. But foods like a
Speaker 3: deli turkey eat or deli ham, any deli meats that
Speaker 3: you don't cook when you bring home that are cooked
Speaker 3: and then processed and refrigerated and sold for immediate consumption, those,
Speaker 3: if contaminated with listeria, can pose a significant risk because
Speaker 3: that listeria can continue to replicate even if it's at
Speaker 3: very low levels in that food to begin with, and
Speaker 3: then can cause infection thereafter. The same thing is true
Speaker 3: for milks that are raw or unpasteurized, or cheeses that
Speaker 3: are not cured, so like soft cheeses that are made
Speaker 3: from milks that are unpasteurized. Those are some of the
Speaker 3: highest risk things that we've seen, but we see outbreaks
Speaker 3: in other things too, like one that's ongoing currently, as
Speaker 3: we record in Inenok mushrooms in the US often consumed
Speaker 3: raw those mushrooms. In twenty twenty two, in the US,
Speaker 3: we saw outbreaks in deli meats and cheeses like generically
Speaker 3: just meats and cheeses of deli counters across the country.
Speaker 3: We also saw outbreaks in some soft cheeses like Breeze
Speaker 3: and Camembers, and in ice cream. Like you mentioned, there's
Speaker 3: been outbreaks in various bad salads, things that again are
Speaker 3: prepared and ready to eat. So those are the kinds
Speaker 3: of things that tend to be highest risk, and that's
Speaker 3: why the recommendations tend to be that people who are
Speaker 3: at high risk, who are immunal compromised, or pregnant, try
Speaker 3: to avoid those foods.
Speaker 1: That's hard to do, Yeah, it's really hard. And it
Speaker 1: seems like it could also be an issue of access
Speaker 1: where where it's difficult to buy food to then prepare
Speaker 1: rather than getting like who has the time, or it's
Speaker 1: more expensive sometimes to buy food to then prepare, and
Speaker 1: so it's that's an interesting, I think component of it.
Speaker 3: Yeah, absolutely absolutely, But that's kind of where we stand
Speaker 3: with infections with listeriosis today across the globe, a lot
Speaker 3: left to be desired, I feel like, but I think
Speaker 3: we're in a very interesting place where it's definitely still
Speaker 3: a pathogen of big concern, especially for the food industry,
Speaker 3: and it's something that still shapes how our food industry
Speaker 3: operates and makes decisions globally. H Yeah, I do think
Speaker 3: in terms of even bigger picture, you know, future directions
Speaker 3: and research when it comes to listeria. The most exciting
Speaker 3: thing is all of the ways in which listeria serves
Speaker 3: as this model organism that I mentioned in the biology section,
Speaker 3: which again I had no idea, but I will post
Speaker 3: a few really great, incredibly detailed papers about the kinds
Speaker 3: of research being done on the pathogenesis of listeria and
Speaker 3: what the implications are for what we can learn about
Speaker 3: intracellular infection in general, as well as our understandings of
Speaker 3: cell to sell communication on a broad scale, because understanding
Speaker 3: listeria infection has implications for understanding the process of infection
Speaker 3: and dissemination and how pathogens not just evade our immune
Speaker 3: responses but also penetrate these supposedly impenetrable barriers that are
Speaker 3: meant to keep them out, but also the way that
Speaker 3: our cells actually talk and communicate with each other because
Speaker 3: Listeria hijacks a lot of these mechanisms in our own cells.
Speaker 3: So the things that we are learning from listeria are
Speaker 3: having and I think we'll continue to have implications that
Speaker 3: go far beyond this one food borne pathogen, which is
Speaker 3: just it fills me with thrill.
Speaker 1: Yeah, so.
Speaker 3: That's listeriosis, Listeria monocytogenies.
Speaker 1: There's a lot to it, there, really is.
Speaker 3: We probably missed a lot.
Speaker 1: We probably did, and you can check for us by
Speaker 1: taking a look through our references. Yes, so I have
Speaker 1: several I have a bunch, but I will shout out
Speaker 1: just a couple in particular, So the one that was
Speaker 1: tracing the spread of that one clonal group of Listeria
Speaker 1: monocytogenies by Mara at All from twenty twenty one. And
Speaker 1: then of course I want to shout out the classic
Speaker 1: discovery paper by Murray at All from nineteen twenty six
Speaker 1: and where I saw the phrase patho epigenetics I just
Speaker 1: want to shout out was in a paper looking at
Speaker 1: sort of this like new microbiology and understanding the cellular
Speaker 1: signaling aspects of Listeria monocytogenies by Cosart and le Breton
Speaker 1: from twenty fourteen.
Speaker 3: I have a paper by it sounds like one of
Speaker 3: the same authors. The two papers that were very detailed
Speaker 3: on where we stand with understanding this pathogen as more
Speaker 3: than just a pathogen. One was from twenty eighteen in
Speaker 3: Nature Reviews Microbiology called Listeria monocytogenies Toward a complete picture
Speaker 3: of its physiology and pathogenesis, and the other was from
Speaker 3: Cellular Microbiology in twenty twenty called Listeria monocytogenies a Model
Speaker 3: in Infection biology. And then I had a few older
Speaker 3: papers more specific to the symptoms and what we see
Speaker 3: with disease ats self, as well as the citations for
Speaker 3: the numbers of epidemiology and all of that. You can
Speaker 3: find the list of our sources for this episode and
Speaker 3: every one of our episodes on our website, This podcast
Speaker 3: will Kill You dot com under the episode's tap.
Speaker 1: A huge and heartfelt thank you again to Denise for
Speaker 1: sharing your story with us. It's we really can't thank
Speaker 1: you enough. Yeah really.
Speaker 3: Thank you also to Bloodmobile for providing the music for
Speaker 3: this episode and all of our episodes.
Speaker 1: And thank you to Leana Squalacci for the excellent audio
Speaker 1: mixing you're the greatest.
Speaker 3: Thank you to the exactly Right Network.
Speaker 1: And thanks to you listeners. We hope you liked this one.
Speaker 1: Hope you found something new.
Speaker 3: Yeah, and something I did, so did.
Speaker 1: I lots of new, lots of new.
Speaker 3: And as always, a special thank you to our patrons.
Speaker 3: Thank you so much for your support. It really means
Speaker 3: a lot.
Speaker 1: It does so much. Okay, Well, until next time, wash
Speaker 1: your hands
Speaker 3: You feel the animals