Speaker 1: On the first day of August fifteen seventy six, Coco
Speaker 1: Litsli began extremely strongly in Tekemachalco. It could not be resisted.
Speaker 1: For this reason, many people died, young people, married people,
Speaker 1: old people, men and women and children. In two or
Speaker 1: three days. They died of hemorrhage. Blood emerged from their noses,
Speaker 1: from the ears, from the eyes, from the anus, and
Speaker 1: women bled between their legs. And for us men, blood
Speaker 1: emerged from our members. Others died from diarrhea, which took
Speaker 1: them suddenly. They died quickly from this awful Oh yeah,
Speaker 1: it's this episode is loaded with quotes, Karen. That particular
Speaker 1: quote was from an anonymous Nahua, author of the anal
Speaker 1: state Techamachalco from the epidemic of Coco Leeseley in fifteen
Speaker 1: seventy six. Okay, hi, I'm Aaron Welsh.
Speaker 2: And I'm Erin Allman Updyke.
Speaker 1: And this is this podcast will kill.
Speaker 2: You And today we are doing a medical mystery.
Speaker 1: We are. It's a first one in many episodes. It's
Speaker 1: been the years, yeah, I think definitely over fifty episodes.
Speaker 1: The last one was Sweating Sickness.
Speaker 2: Sweating Sickness, yep yeah, no, no, dancing Pike.
Speaker 1: I don't know. I don't know, could be either, It's
Speaker 1: one of those. But yeah, this has been on our
Speaker 1: list for a while, which I feel like we say
Speaker 1: about every topic. But I'm really excited that we're covering
Speaker 1: it because there is so much to get into. And wow,
Speaker 1: like once I started pulling the string on this, I
Speaker 1: just couldn't stop.
Speaker 2: Like a sweater just came all the way unraveled.
Speaker 1: Yep, I can't wait.
Speaker 2: I am thrilled because so listeners, you may recall or
Speaker 2: you may not, because again it's been a number of years.
Speaker 2: We are going to do this episode in a different way,
Speaker 2: and the way that Aaron and I have researched for
Speaker 2: this episode is very different than.
Speaker 1: Are you usual.
Speaker 2: I know nothing about this story about Coco Elitesley at all,
Speaker 2: but I have been given a list of contenders of
Speaker 2: possible pathogens that may have caused this, and then we're
Speaker 2: going to try and solve it, you know, in just
Speaker 2: like the next hour and a half. Medical mystery that's
Speaker 2: been going on for hundreds of years.
Speaker 1: I mean, I hope that people aren't looking for full
Speaker 1: resolution like I always do when I watch Unsolved mysteries,
Speaker 1: and then at the end, I'm upset like that, what
Speaker 1: a you solved in the name of the show. But
Speaker 1: so brace yourselves. You'll know a lot more and maybe
Speaker 1: be able to come to some conclusions yourself. But yeah,
Speaker 1: this will be an unsolved mystery at the beginning, middle,
Speaker 1: and end.
Speaker 2: I can't wait. I'm really excited about it and to
Speaker 2: get us started. I believe that it's quarantining time.
Speaker 1: It certainly is. What are we drinking this week?
Speaker 2: It's Anyone's Guess. That's the name of the name of it.
Speaker 1: Thanks to John for that title. Appreciate it so creative
Speaker 1: and in It's Anyone's guess. It's delicious, and it's got
Speaker 1: a lot of ingredients, which is you know, I think
Speaker 1: sometimes can be fun. It's got some dark rum, it's
Speaker 1: got pineapple juice, orange juice, lemon juice and passion fruit juice,
Speaker 1: tropical and lots of juices. Yeah, it's delicious.
Speaker 2: We'll post a full recipe for that quarantine as well
Speaker 2: as the non alcoholic and equally delicious plus Ebrita on
Speaker 2: our website, This podcast weekili dot com and our social media.
Speaker 1: We certainly will. On our website you can find all
Speaker 1: sorts of things, such as transcripts, links to bookshop dot
Speaker 1: org and goodreads lists. You can find music by Bloodmobile merch.
Speaker 1: We've got some cool new merch coming out for you.
Speaker 1: You know. There's more stuff sources for our episodes.
Speaker 2: That's enough, right, it's a lot. There's a lot there.
Speaker 2: Check it out O this podcast.
Speaker 3: Weicill you dot com.
Speaker 1: Can we get started? Please please?
Speaker 2: I can't wait, all right, primed to take notes while
Speaker 2: we talk. I'm so excited.
Speaker 1: Let's just take a quick break and then we can
Speaker 1: get right to it.
Speaker 3: Okay.
Speaker 1: In the year fifteen eighty four, seventy five years after
Speaker 1: Hernando Cortes first arrived in what is now Mexico, Antonio
Speaker 1: Sioux dad Reale and Frey Alonzo Ponce, both Spanish, traveled
Speaker 1: through much of Mexico and wrote what they saw of
Speaker 1: this once densely populated and vibrant land. Quote in times
Speaker 1: past that town had a large population, according to the
Speaker 1: older people, and now it just seems like ruins of houses,
Speaker 1: and for the many fruit trees there are in the
Speaker 1: surroundings among which the Indians usually have their towns, especially
Speaker 1: being in the hot lands like it is, but with
Speaker 1: the coco Litli. There was such a very large pestilence
Speaker 1: and mortality in that land that everything was destroyed and
Speaker 1: now there are scarcely two hundred inhabitants whoa yeah. And
Speaker 1: while they name drop cocolitle specifically there, it was far
Speaker 1: from the only factor in the tremendous population losses and
Speaker 1: cultural devastation experienced by indigenous populations in Mexico following first
Speaker 1: contact with European colonizers in the sixteenth century. And if
Speaker 1: you'll just allow me to get on a soapbox for
Speaker 1: a little bit. Even though the focus of today's episode
Speaker 1: is on just one of those factors, cocoliteslei, which we'll
Speaker 1: spend a lot more time about, I don't want to
Speaker 1: lose sight of that fact that this cultural and population
Speaker 1: devastation was multifactorial. That we can't take this disease cocolitsli,
Speaker 1: or these epidemics out of their historical context without considering
Speaker 1: everything else that was going on at the time. Retrospective
Speaker 1: diagnosis is a tricky enough business as it is, and
Speaker 1: ignoring all of the social and political factors that played
Speaker 1: a role in the spread of disease, it's only going
Speaker 1: to further limit our ability to say anything about whether
Speaker 1: Cokolitsli was rodent associated or waterborn. For way too long,
Speaker 1: many historians have over emphasized the effects that pathogens alone
Speaker 1: had on the population declines of indigenous peoples living in
Speaker 1: the America's following European contact. The concept of quote unquote
Speaker 1: virgin soil epidemics, as in the idea that these pathogens
Speaker 1: that Europeans were more acquainted with and brought with them
Speaker 1: to the New World, that these pathogens were more devastating
Speaker 1: to immunologically naive populations. This concept has been overly used
Speaker 1: in the construction of these like Eurocentric Jared diamond esque histories,
Speaker 1: where the strong conquered the weak and took what was
Speaker 1: rightfully theirs because nature i e. Pathogens determined that they
Speaker 1: were the victors. Right.
Speaker 2: No, oh, no no.
Speaker 1: Focusing on the role that germs alone played in mass
Speaker 1: mortality events in the Americas ignores the decisions that European
Speaker 1: colonizers made to subjugate and oppress the indigenous populations, forced
Speaker 1: labor overburdensome taxation, complete upheaval of everyday life, and repression
Speaker 1: of traditional cultural practices. Germs weren't acting alone here in
Speaker 1: more ways than one, Like, yes, there were devastating smallpox
Speaker 1: epidemics that cannot be ignored, that cannot be debated, and yes,
Speaker 1: there were also horrific measles outbreaks and influenza epidemics and
Speaker 1: so one and so forth. But it's not like in
Speaker 1: those like eighties action movies where the bad guys take
Speaker 1: turns fighting the one good guy. It's like multiple pathogens
Speaker 1: were all circulating at the same time, all the bad
Speaker 1: guys were fighting all at once. And this isn't to
Speaker 1: downplay the enormous mortality rates that we see during these epidemics,
Speaker 1: upwards of sixty to eighty percent of the entire population
Speaker 1: in some cases, but it's just to try to present
Speaker 1: a more nuanced view you of where those numbers, those
Speaker 1: mortality rates might be coming from. Death from disease absolutely
Speaker 1: maybe increased by malnutrition or coinfection with another pathogen, or
Speaker 1: weakened health from forced labor or fewer people to care
Speaker 1: for the sick, like societal collapse. The layers of protection
Speaker 1: from getting sick or dying from illness in many cases
Speaker 1: had been entirely stripped away, and I think sometimes that
Speaker 1: can get lost in looking at these epidemics from like
Speaker 1: a purely biological microbiological epidemiological focus, I guess, and I
Speaker 1: think this is especially important to remember when we're trying
Speaker 1: to go through and guess which pathogen might be responsible
Speaker 1: for Coco litesle and be like, wow, there's no known
Speaker 1: pathogen that causes such high mortality rates. Like well, of course,
Speaker 1: because it's not just one loan pathogen. But anyway, keeping
Speaker 1: all that in mind, LAO, let's turn to Coco Leathsley.
Speaker 1: What were the Coco Leitsli epidemics? In short, they were
Speaker 1: a series of epidemics of undetermined cause that swept through
Speaker 1: much of Mexico and the rest of meso America during
Speaker 1: the sixteenth, seventeenth, eighteenth, and possibly even the nineteenth centuries. Huh.
Speaker 1: At least thirteen distinct epidemics according to one paper I read.
Speaker 1: But today I'm only going to be focusing on the
Speaker 1: two most devastating Coco Leathsley epidemics, one that began in
Speaker 1: fifteen forty five and the other in fifteen seventy six,
Speaker 1: since they have the most documentation and had the most
Speaker 1: apparently impact on the population. But to better understand how
Speaker 1: these epidemics happened when they did and the impact they had.
Speaker 1: Let's do a little bit stage setting. In fifteen nineteen,
Speaker 1: the Spanish conquistador Hernando Cortes and his crew landed in Mexico,
Speaker 1: where they claimed the land for the Spanish crown and
Speaker 1: proceeded to travel inland until they reached toto che Lan,
Speaker 1: the massive capital of the Aztec Empire, or specifically the
Speaker 1: Mashka people. Aztec is kind of a political term I
Speaker 1: learned that means really just the three tribes that controlled
Speaker 1: a lot of Mexico at the time, and one of
Speaker 1: these tribes, the most powerful, was the Meshika. Anyway, shortly
Speaker 1: after arriving in to notche Chielan and being showered with
Speaker 1: please go away gifts of silver and gold and textiles,
Speaker 1: the Spanish then took the Meshika emperor of the city
Speaker 1: as prisoner, Montezuma for a year until he was killed.
Speaker 1: And skipping over a whole lot of history here, that
Speaker 1: really sort of kicked off the beginning of Spanish colonial
Speaker 1: rule in Mexico. Like that is not even beginning to
Speaker 1: get into that's not even surface level. There's so much
Speaker 1: more history there. But basically things changed very quickly in
Speaker 1: that Aztec Empire, from political organization to wealth distribution, cultural
Speaker 1: practices to daily life. Agriculture shifted under Spanish rule as
Speaker 1: domestic animals were introduced and the dominant crops switched from maize, squash, amorants, beans,
Speaker 1: and peppers to wheat so that the Spanish could make
Speaker 1: European style bread. Lakes were drained to prevent flooding or
Speaker 1: to provide more arable land for farming. Taxation or tributes
Speaker 1: grew enormously in demand, pretty much beyond anyone's means, and
Speaker 1: as a result, nutrition really suffered, especially since there were
Speaker 1: a series of droughts throughout the sixteenth century that we'll
Speaker 1: talk maybe a little bit more about later on. Many
Speaker 1: indigenous people were enslaved or forced to do labor, or
Speaker 1: displaced from their homes and land. Even clothing changed, apparently
Speaker 1: with an emphasis on European style clothing, along with fewer baths,
Speaker 1: since it was the Spanish belief at the time that
Speaker 1: bathing daily was bad for your health. Now, all of
Speaker 1: these changes did not take place everywhere or at the
Speaker 1: same time throughout Mesoamerica, but life certainly changed for everyone,
Speaker 1: and I came across a paper about Coco Lethsley by
Speaker 1: mar and Kirakoff from two thousand, where the authors wrote that,
Speaker 1: quote certainly, the policies of the Spanish colonial regime were
Speaker 1: harsh in many ways, but no more so than those
Speaker 1: of the Aztec imperial regime had been end quote I
Speaker 1: mean wrong, and I think to claim that is to
Speaker 1: kind of undermine the drastic effects that the Spanish regime
Speaker 1: had on life for indigenous peoples. So anyway, when Cortes
Speaker 1: and his crew landed in fifteen nineteen, Mexico was home
Speaker 1: to a population of around twenty two million people, and
Speaker 1: the major city, ten Ochtreetlan had approximately two hundred and
Speaker 1: fifty thousand to three hundred thousand occupants, which was five
Speaker 1: times the size of London at the same time. Oh wow,
Speaker 1: with an incredibly intricately connected society. But within the century,
Speaker 1: millions upon millions of people would be dead from a
Speaker 1: combination of disease and the major upheaval of Spanish rule.
Speaker 1: And the first disease to make itself felt with smallpox,
Speaker 1: which began to spread in fifteen twenty, only a year
Speaker 1: after Cortes arrived. Eight million people died during the smallpox epidemic. Oh,
Speaker 1: out of a population of twenty two million.
Speaker 4: Yeah, that's.
Speaker 1: Unfathomable.
Speaker 4: Yep.
Speaker 1: And again this was not just from smallpox alone, but
Speaker 1: also from the general collapse of their society. Measles epidemic, typhus, influenza,
Speaker 1: and other diseases all followed, described by witnesses as distinct diseases,
Speaker 1: even though they may co occur. And although the fifteen
Speaker 1: twenty smallpox epidemic has probably received more attention historically because
Speaker 1: of how it affected the transition of power from Aztec
Speaker 1: to Spanish rule, the Coco Leesle epidemics that followed were
Speaker 1: no less terrifying or devastating. So finally getting to Coco
Speaker 1: Ltsley in fifteen forty five, Coco Lethsley struck for seemingly
Speaker 1: the first time. Over a dozen early Spanish and indigenous
Speaker 1: contemporary accounts describe a deadly disease that swept through Mexico
Speaker 1: and the rest of meso America. Bernardino des Sahagoon, Franciscan
Speaker 1: scholar who witnessed this epidemic, wrote, quote, in the year
Speaker 1: fifteen forty five, there was a huge and universal pestilence
Speaker 1: where in all of New Spain most of the people
Speaker 1: who lived there died. At the time of this pestilence.
Speaker 1: I was in Mexico City, in the part of tlate Loco,
Speaker 1: and I buried more than ten thousand bodies. And at
Speaker 1: the end of the pestilence, I became ill and almost
Speaker 1: died end quote hm. Importantly, Sahogoon also lived to see
Speaker 1: the second epidemic of Cocolitsli in fifteen seventy six, which
Speaker 1: he described as being very similar to the one in
Speaker 1: fifteen forty five, and he ultimately died in a third
Speaker 1: Cocolitsi epidemic in fifteen ninety.
Speaker 3: Okay, okay, yeah.
Speaker 1: The symptoms of the illness were described as quote acute
Speaker 1: onset of fever, vertigo, and severe headache, followed by bleeding
Speaker 1: from the nose, ears, and mouth. It was accompanied by
Speaker 1: jaundice and severe abdominal pain and thoracic pain, as well
Speaker 1: as acute neurological manifestations end quote.
Speaker 2: I'm I'm listening so intently.
Speaker 1: I can hear you typing. I love it.
Speaker 5: I know.
Speaker 2: I'm sorry I doesn't pick up in the mic, but
Speaker 2: I'm taking notes. Fever, verdio, headache, bleeding, okay, jaundice, okay, And.
Speaker 1: We can go over all of this at the end.
Speaker 1: Oh we will also.
Speaker 2: Yeah.
Speaker 1: In general, the duration of the disease was described as short,
Speaker 1: about three to four days okay, and was said to
Speaker 1: have mainly affected the indigenous population. However, sources vary on
Speaker 1: that point, which is maybe something that we'll get into
Speaker 1: later when going through the possible pathogens. Children and young
Speaker 1: adults were said to be the most affected, although again
Speaker 1: sort of sources are not entirely consistent on this point,
Speaker 1: but this is supported by evidence from burial grounds in
Speaker 1: southern Mexico where the Mishtek peoples lived, and these burial
Speaker 1: grounds show that a young people were disproportionately buried and
Speaker 1: b bodies were stacked vertically, suggesting that the deaths happen
Speaker 1: too quickly for individual graves to be dug which is
Speaker 1: the norm. So definitely like this is considered an epidemic graveyard.
Speaker 2: Okay, okay.
Speaker 1: And the bleeding seems like a key feature of this
Speaker 1: disease since it shows up in many of the contemporary
Speaker 1: illustrations of the epidemic. So one features a man in
Speaker 1: a full body rash as blood or vomit flows from
Speaker 1: his face, and others also feature bleeding from the face,
Speaker 1: and written descriptions also mention in the blood quote a
Speaker 1: pestilence in which blood poured from the nose end quote.
Speaker 1: And someone who was writing about the fifteen forty five
Speaker 1: Cocleaedsli epidemic like sixty years after it happened, wrote that
Speaker 1: quote blood flowed from the mouth, eyes, nose, and anus
Speaker 1: end quote of all people poor and noble alike, and
Speaker 1: that the bodies were eaten by dogs and coyotes. Okay,
Speaker 1: I think just like emphasizing the speed with which this
Speaker 1: killed and how many people are killed. Another Franciscan friar
Speaker 1: and eyewitness to both the fifteen forty five and fifteen
Speaker 1: seventy six coco Leedes epidemics used the term pujamiento de sangre,
Speaker 1: meaning abundant bleeding or full bloodiness, and said it was
Speaker 1: characterized by blood fevers. Notably, though, this same author used
Speaker 1: the Spanish word for Typhus Tabardillo for the fifteen seventy
Speaker 1: six epidemic, and remember he saw both of them. But
Speaker 1: in general, this fifteen forty five Cocolitsi epidemic was described
Speaker 1: by most eyewitnesses as distinct from other European introduced diseases
Speaker 1: including smallpox, measles epidemic, typhus, pertussis, and malaria. So in total,
Speaker 1: an estimated five to fifteen million people died, said to
Speaker 1: be about eighty percent of the indigenous population.
Speaker 2: Is that in these two outbreaks combined or just in
Speaker 2: the fifteen forty five outbreak.
Speaker 1: Just fifteen forty five? Holy uh huh. Yeah, there's a
Speaker 1: lot more detail on the fifteen seventy six one, so
Speaker 1: we'll get into that one in a second. Oh my, yeah,
Speaker 1: eighty percent is what most estimates say, eighty percent of
Speaker 1: the indigenous population at the time.
Speaker 2: Yep, okay, I'm I'm I want to ask a million questions,
Speaker 2: but I want I feel like you're going to answer them.
Speaker 1: It's possible, but it's also possible that I won't at all.
Speaker 1: But yeah, this this fifteen forty five epidemic lasted. It's
Speaker 1: it's kind of unclear. It probably varied from region to region,
Speaker 1: but it seems like I've read one and a half
Speaker 1: years to four years as the total length of time,
Speaker 1: more often four years.
Speaker 2: And that's okay, So like from fifteen forty five till
Speaker 2: fifteen forty nine, basically, yeah, so over that time period,
Speaker 2: eighty percent of the population died presumably from this or
Speaker 2: related to it, right for you know, there's co morbid
Speaker 2: et cetera.
Speaker 1: Co morbid and also just sort of like societal collapse,
Speaker 1: like because this was such an intricately connected society. When
Speaker 1: you don't have let's say, people who are sick can't
Speaker 1: then harvest food, and then people who get sick who
Speaker 1: can't turn that food into ingredients, and then people who
Speaker 1: can't turn ingredients into meals, and then people who can't
Speaker 1: you know, it's just like becomes this thing where if
Speaker 1: you're sick, then who's caring for you? So I think
Speaker 1: that's where we have to kind of remember where those
Speaker 1: mortality numbers are coming from.
Speaker 2: Right, because it's not necessarily all directly attributable to disease,
Speaker 2: right exactly, and or to this one specific disease.
Speaker 1: Right and you can't assume care, even like palliative or
Speaker 1: supportive care or something.
Speaker 2: Yeah, and then this but despite that, that is the
Speaker 2: number that's attributed to this outbreak which took place over
Speaker 2: four years.
Speaker 1: It is what is the population losses during this epidemic?
Speaker 2: Yes? And can I ask a question? Yeah, when it
Speaker 2: like sporadic, like evenly distributed across those four years. Do
Speaker 2: we know was it like mostly at the beginning or
Speaker 2: mostly at the end. Was it like every spring for example,
Speaker 2: or something like that, or is it just like it
Speaker 2: was these four years? And that's the most resolution that
Speaker 2: we have.
Speaker 1: So for the fifteen forty five one, more or less,
Speaker 1: that's the most resolution that we have. I think it
Speaker 1: probably started out very strong, and it seems to have
Speaker 1: sort of swept through towns very quickly and very dramatically.
Speaker 1: But we do have more information in general for the
Speaker 1: fifteen seventy six one. Okay, so let's get into that, okay, please.
Speaker 1: But also I will say that the fifteen forty five
Speaker 1: to one did start in August.
Speaker 2: It started in August, Okay, Yeah, in Paris, in Mexico, Okay, Okay.
Speaker 1: So there would be other appearances of cocolitesli in the
Speaker 1: years following that fifteen forty five epidemic, but it really
Speaker 1: came back with a vengeance in fifteen seventy six. Quote,
Speaker 1: in the year fifteen seventy six, a great mortality and
Speaker 1: pestilence that lasted for more than a year overcame the Indians.
Speaker 1: It was so big that it ruined and destroyed almost
Speaker 1: the entire land. The place we know as New Spain
Speaker 1: was left almost empty. It was a thing of great
Speaker 1: bewilderment to see the people die. Many were dead and
Speaker 1: others almost dead, and nobody had the health or strength
Speaker 1: to help the diseased or bury the dead. In the
Speaker 1: cities and large towns, big ditches were dug, and from
Speaker 1: morning to sunset the priests did nothing else but bury
Speaker 1: the dead bodies and throw them into the ditches without
Speaker 1: any of the solemnity usually reserved for the dead, because
Speaker 1: the time did not allow otherwise. At night they covered
Speaker 1: the ditches with dirt. It lasted for one and a
Speaker 1: half years and with great excess in the number of deaths.
Speaker 3: End quote wow okay.
Speaker 1: That is a quote from Freewan de Torkumata, who was
Speaker 1: a Franciscan historian, and he was describing the epidemic in
Speaker 1: Mexico City. The epidemic. This epidemic began in June in
Speaker 1: central Mexico and quickly made its way across the land,
Speaker 1: reaching as far north as parts of what is now
Speaker 1: the Southern US and as far south as the Peruvian Andes.
Speaker 1: But the vast majority of cases were concentrated in like
Speaker 1: a four hundred mile radius in Mexico, where it spread
Speaker 1: from the dry plains of the north to the densely
Speaker 1: populated subtropical valleys of central Mexico, leaving almost no place
Speaker 1: unscathed except for perhaps the coastal areas. According to some,
Speaker 1: the spread seemed to slow by October fifteen seventy eight,
Speaker 1: so it's like two years after, but then increased again
Speaker 1: in August fifteen seventy nine, ending finally in the middle
Speaker 1: of fifteen eighty one. The effect was truly devastating in Mexico.
Speaker 1: More than two million people died during this epidemic, half
Speaker 1: of the population fifty one point three six percent to
Speaker 1: be precise. And we can be so precise because censuses
Speaker 1: were conducted a few years before the epidemic and a
Speaker 1: few years after.
Speaker 2: Wow.
Speaker 1: Yeah, this epidemic in general, like I mentioned, is much
Speaker 1: better documented, So get ready for lots of quotes.
Speaker 4: Okay.
Speaker 1: The mortality rate was not consistent across all areas, so
Speaker 1: one region southwest of Mexico City, Tepeyaka, lost eighty six
Speaker 1: point six percent of its population of sixty thousand, while Chilula,
Speaker 1: east of Mexico City lost only forty percent of its
Speaker 1: fifteen thousand inhabitants. Only forty percent, right.
Speaker 2: An unbelievable number.
Speaker 1: Yeah yeah. One eyewitness described its erratic spread. Quote, it
Speaker 1: appears as if it is a living thing, and that
Speaker 1: it goes in search of towns so that none remain
Speaker 1: end quote. The Bishop of Mishoa Khan wrote, quote, almost
Speaker 1: half of the natives of this province have been taken.
Speaker 1: When the pestilence enters a town for ten months or
Speaker 1: a year, it jumps from barrio to barrio and from
Speaker 1: house to house. And it was without order, even though
Speaker 1: divine disposition would have had it well ordered, because it
Speaker 1: struck one neighborhood and then jumped to another far away,
Speaker 1: sparing the one closer by, and in the same home.
Speaker 1: It took some and spared others, only to return four
Speaker 1: or six months later to claim the healthy. This was
Speaker 1: observed by all end quote hmmm. He added that quote,
Speaker 1: these poor indios are half what they were in number,
Speaker 1: and the half that return are wasted, weary, and miserable
Speaker 1: because everyone has either succumbed to the pestilence or escaped it.
Speaker 1: And even today the sorrowful ones who survived are still
Speaker 1: preoccupied with their loved ones who continue to suffer. End quote.
Speaker 1: So the Spanish, who seem to be less affected by
Speaker 1: the disease, although ASTERISK did keenly feel its impacts in
Speaker 1: other ways, namely economical. The accountant of the Royal Treasury
Speaker 1: of New Spain wrote, quote, the illness and death of
Speaker 1: the natives have been so great that they have been
Speaker 1: completely diminished, so much so that in many pueblos in
Speaker 1: this great land, fewer than half the population remains, and
Speaker 1: in others less than a third, And so our profits
Speaker 1: are less than they were. The absence of natives in
Speaker 1: these lands is so great that it seems unfathomable that
Speaker 1: they could have been brought to this point. The profits
Speaker 1: are far less, and our expense is ever greater because
Speaker 1: of the tremendous hardship, and the whole land is in misery,
Speaker 1: affliction and need end.
Speaker 5: Quote that quote, like, you're a tremendous hardship because your
Speaker 5: profits are down. That's yeah, gross, I know this tremendous hardship.
Speaker 5: If I need care for people, my goodness, and this
Speaker 5: is truly.
Speaker 1: Astounding, right, yeah, I mean, I know, I just keep
Speaker 1: saying it. Over and over again. But it's just like
Speaker 1: it's unfathomable, and it's there's so much here, and I
Speaker 1: think it's it's also fascinating how number one, how well
Speaker 1: this is documented too, how much more is still being
Speaker 1: uncovered because for a long time, the main accounts that
Speaker 1: were used were from were written by Spanish colonizers. And
Speaker 1: only more recently do we have people the Nahua people
Speaker 1: who's who also wrote down histories like those are being
Speaker 1: translated and then taken into account in these retellings, and
Speaker 1: so it's interesting, very interesting. Yeah. Yeah, but cocolitesle, this
Speaker 1: epidemic especially threatened Spanish rule and colonial order because of
Speaker 1: sheer population loss, not just economically but also culturally, fewer
Speaker 1: people to convert to the new religion and to rule over.
Speaker 1: And so okay, at this point we've established that this
Speaker 1: is a pretty deadly disease. Now let's go through how
Speaker 1: this one was described. Yeah. Again, the Nahwat word cocolitesli
Speaker 1: or hue cocolitsli was used to mean pestilence or great pestilence,
Speaker 1: and the Spanish also used malpestillencia, pestilencia universal bad or
Speaker 1: universal pestilence. It was discussed as distinct from the other
Speaker 1: known epidemic diseases, and was generally seen as something new,
Speaker 1: something unfamiliar. Some reports describe young people being disproportionately affected,
Speaker 1: while others say it attacked all ages. No animal deaths,
Speaker 1: domestic or wild were mentioned. When it comes to symptoms,
Speaker 1: there's actually a medical description by doctor Fernando Hernandez, who
Speaker 1: is the physician in chief of New Spain. It's very long,
Speaker 1: so brace yourself, but I think you're going to find
Speaker 1: it very interesting.
Speaker 2: And yes, I'm going to try and memorize it.
Speaker 1: Yeah. Quote. The fevers were contagious, burning, and continuous, all
Speaker 1: of them pestilential, in most part lethal. The tongue was
Speaker 1: dry and black, enormous thirst urine of the colors sea, green, vegetable, green,
Speaker 1: and black, sometimes passing from the greenish color to the pale.
Speaker 1: Pulse was frequent, fast, small, and weak, sometimes even null.
Speaker 1: The eyes and the whole body were yellow. This stage
Speaker 1: was followed by delirium and seizures. Then hard and painful
Speaker 1: nodules appeared behind one or both ears, along with heartache,
Speaker 1: chest pain, abdominal pain, tremor, great anxiety, and dysentery. The
Speaker 1: blood that flowed when cutting a vein had a green
Speaker 1: color or was very pale, dry and without serocity. In
Speaker 1: some cases, gangreen and Sphacilus aka necrosis invaded their lips,
Speaker 1: pudental regions and other regions of the body with putrefact members,
Speaker 1: blood flowed from the ears, and in many cases blood
Speaker 1: truly gushed from the nose. Of those with recurring disease,
Speaker 1: almost none was saved. Many were saved if the flux
Speaker 1: of blood through the nose was stopped in time. The
Speaker 1: rest died. Those attacked by dysentery were usually saved if
Speaker 1: they complied with the medication. The abscesses behind the ears
Speaker 1: were not lethal if somehow their size was reduced, either
Speaker 1: by spontaneous maturation or given exit by perforation with catteries.
Speaker 1: The liquid part of the blood flowed or the puss
Speaker 1: was eliminated, and with it the cause of disease was
Speaker 1: also eliminated, as was the case of those with abundant
Speaker 1: and pale urine. At autopsy, the liver was greatly enlarged.
Speaker 1: The heart was black, first draining a yellowish liquid and
Speaker 1: then black blood. The spleen and lungs were black and
Speaker 1: semi putrefacted. The bile was observed in its container, the
Speaker 1: abdomen dry, The rest of the body anywhere it was
Speaker 1: cut was extremely pale. This epidemic attacked mainly young people
Speaker 1: and seldom the elder ones. If old people were affected,
Speaker 1: they were able to overcome the disease and save their lives.
Speaker 1: The epidemic started in June fifteen seventy six and is
Speaker 1: not over in December when I am writing these lines.
Speaker 1: Very few with abdominal distension were saved. At the beginning,
Speaker 1: the blood was expelled by some without severe disease, then
Speaker 1: by very few. Vital energy was consumed quickly. End quote
Speaker 1: A lot to unpack.
Speaker 2: There was there a time frame in that description that
Speaker 2: I missed.
Speaker 1: There was not, but again in general, three to four days,
Speaker 1: three to.
Speaker 3: Five wow, okay okay, okay yeah.
Speaker 1: Other symptoms that I saw mentioned or key observations by
Speaker 1: other eyewitnesses include the fact that it was puss that
Speaker 1: would drain out of those swollen lymph nodes if cut,
Speaker 1: and that bloodshot eyes were common and insatiable. Thirst was
Speaker 1: also mentioned. Lung hemorrhage was seen at autopsy, but again
Speaker 1: bleeding does seem to be a main feature and the
Speaker 1: phrase blood emerged from our noses, and variations on that
Speaker 1: appeared many times throughout accounts of this epidemic. Epidemics of
Speaker 1: coco Elitzley continued, possibly until as recently as the early
Speaker 1: nineteenth century, although the name used in these later epidemics
Speaker 1: was mala zowat netlike rash, and it's unclear if the
Speaker 1: new name meant new disease, or was used in recognition
Speaker 1: of a new symptom, or was just something else like
Speaker 1: it's People don't know, but in any case, coco Elitzley,
Speaker 1: especially the sixteenth century epidemics, has stumped researchers for decades.
Speaker 1: The symptoms described, along with the high mortality rate, don't
Speaker 1: seem to match any known pathogen today, but don't worry,
Speaker 1: there are still plenty of hypotheses to go around. Historically,
Speaker 1: epidemic typhus has been a popular guess, and more recently,
Speaker 1: heemorrhagic fever possibly associated with rodents. This rodent association is
Speaker 1: because both the fifteen forty five and fifteen seventy six
Speaker 1: epidemics occurred during brief intense rainfall preceded by long periods
Speaker 1: of megadrought, which is very similar to the Four Corners
Speaker 1: nineteen ninety three huntavirus outbreak, where dear mice proliferated after
Speaker 1: that same drought rainfall cycle. Others that have been proposed
Speaker 1: include plague specifically mnemonic anthrax, sleptosporosis, malaria, diphtheria, Tessis lausborn
Speaker 1: relapsing fever, and malaria. All of these I just mentioned
Speaker 1: were proposed based on epidemiological characteristics or descriptions of symptoms,
Speaker 1: not physical evidence. Not yet for those anyway. But there
Speaker 1: is one candidate pathogen for cocolitesle that has gotten a
Speaker 1: lot of attention recently, and that is Salmonella in Enterica
Speaker 1: subspecies Enterica saravar paratipee s longest name for an organism
Speaker 1: ever maybe, but a few years ago, researchers detected Salmonella
Speaker 1: in Enterica paratifec DNA in ten individuals that were buried
Speaker 1: during the fifteen forty five coco leisle epidemic in Wahaka
Speaker 1: in southern Mexico. Now, the researchers who publish this paper
Speaker 1: are not claiming that this pathogen was solely responsible for
Speaker 1: the coco lee epidemics, but instead suggests that it may
Speaker 1: have acted in concert with other circulating pathogens at the time.
Speaker 1: But before we start debating which pathogen is the best candidate,
Speaker 1: if any, let's maybe learn a bit more about the
Speaker 1: ones proposed, keeping in mind number one what these diseases
Speaker 1: looked like, number two, how they're transmitted, number three, case
Speaker 1: fatality rates, number four, environmental factors, number five old World
Speaker 1: versus New World origins, and number six that this could
Speaker 1: have been the work of many factors acting simultaneously. And now, Aaron,
Speaker 1: I turn it over to you.
Speaker 2: Oh yeah, so let's take a quick break and then
Speaker 2: let's get into some of these candidate pathogens. I have
Speaker 2: so many thoughts already, so let's take a beat and
Speaker 2: then get real deep into it, shall we.
Speaker 1: Let's do it right after this break.
Speaker 2: I am bursting right now, and part of what I
Speaker 2: think I am bursting with is how much I can
Speaker 2: understand how this has stumped everyone because nothing, nothing fits.
Speaker 1: No.
Speaker 2: When we did dancing Plague, I remember feeling like, oh,
Speaker 2: at least some of these definitely fit, and some of
Speaker 2: them like kind of fit a little bit. Maybe yeah this,
Speaker 2: I'm like, uh mmmm, So let's let's get into all
Speaker 2: of these different proposed I have feelings about it, and
Speaker 2: I'm gonna have some more questions for you to be
Speaker 2: able to try and like parse out some of this.
Speaker 1: Okay, great, let's let's dig in.
Speaker 2: So the list that you told me, Aaron, or at
Speaker 2: least the ones that I definitely researched, included hantavirus, epidemic typhus,
Speaker 2: pneumonic plague, leptosporosis, barton elosis, measles, smallpox, malaria, an unknown
Speaker 2: hemorrhagic fever virus.
Speaker 1: My personal favorite is just like choose your own adventure,
Speaker 1: like just attribute traits that have not been observed in
Speaker 1: one virus. But that's fun.
Speaker 2: Yeah, And of course salmonella enterica paratyphe. See some of
Speaker 2: these I think we can very quickly and very easily discard.
Speaker 1: As the main contributor, Yeah, as.
Speaker 2: The main contributor, because they not only just don't match
Speaker 2: symptoms wise, but like you importantly mentioned, these were things
Speaker 2: that circulated and were described very differently.
Speaker 4: Right.
Speaker 2: So that includes something like smallpox where one of the
Speaker 2: predominant symptoms of smallpox and something aarin that you really
Speaker 2: didn't mention at all in that list of symptoms is
Speaker 2: a rash.
Speaker 1: Yeah, okay, rash. Interesting, So there was that one illustration
Speaker 1: of the fifteen forty five epidemic that did depict someone
Speaker 1: with a full body rash, but in general it was
Speaker 1: not consistently mentioned. And in fifteen seventy six there was
Speaker 1: that Franciscan scholar who used the word tabardio, which I
Speaker 1: think means like cloak rash or something like that, Like
Speaker 1: it refers to the rash from typhus from epidemic typhus,
Speaker 1: but that long quote from the physician didn't describe it,
Speaker 1: and in general it was not like it didn't seem
Speaker 1: to be.
Speaker 2: A main feature of the disease, right, Yeah, So I
Speaker 2: feel like based on that, like smallpox is just all
Speaker 2: the way out, like it just doesn't fit.
Speaker 1: It doesn't fit.
Speaker 2: Same thing with measles, quite honestly. And on top of
Speaker 2: that measles, which okay, side note. One of my favorite
Speaker 2: things about researching for this episode is that we have
Speaker 2: covered all of these things. Do we do Bartonella, we
Speaker 2: did bartnella erin, we did the literal because there's a
Speaker 2: few more things that I have on my list that
Speaker 2: you gave me, and literally the only ones that we
Speaker 2: haven't covered are unknown hemorrhagic fever, okay, and parvovirus B nineteen,
Speaker 2: which like it's not that either, right, right, but we'll
Speaker 2: get there. Everything else we've talked about, So this is
Speaker 2: really fun and most of my sources are c our
Speaker 2: previous episode NICs. But okay, smallpox is out. Measles. We
Speaker 2: did measles a very very long time ago. Now, measles,
Speaker 2: while it spread through populations and absolutely caused a lot
Speaker 2: of morbidity and mortality, the mortality rate is nowhere near
Speaker 2: what we're seeing with cocoa eatsle. The mortality rate of
Speaker 2: measles was far far lower. And on top of that,
Speaker 2: the symptoms really are just nothing like these symptoms that
Speaker 2: are being described.
Speaker 1: I do remember from our measles episode they're being in
Speaker 1: entirely naive populations, measles having a much higher mortality rate.
Speaker 1: But a again, like I still think that the symptoms don't
Speaker 1: like where's the hemorrhage? Is there a hemorrhagic form of measles?
Speaker 2: Not that I know of? Yeah, yeah, And like so
Speaker 2: much of measles is a very characteristic measles rash right, right,
Speaker 2: I think the things that make it seem like measles
Speaker 2: are just the rapidity, which it seems to have swept
Speaker 2: through a population, except that, like the duration of disease
Speaker 2: with measles also tends to be longer.
Speaker 1: Yeah. Well, and I think it's interesting that you say
Speaker 1: the pattern of spread, because I think that keeping that
Speaker 1: in mind for transmission root.
Speaker 2: So that's what I wanted to get. I wanted to
Speaker 2: ask you a little bit more questions. Okay, but let's
Speaker 2: knock a few more off this, Yeah, first, because I
Speaker 2: think there's some other easy ones. Okay, So it's not smallpox,
Speaker 2: it's not measles, it's not malaria.
Speaker 1: No cyclical fevers. Yeah, I mean, and like not to
Speaker 1: mention a lot of other things, a lot.
Speaker 2: Of other things. The mortality is not happening within a
Speaker 2: number of days. It's not like that's just not how
Speaker 2: measles works.
Speaker 1: It doesn't seem mosquito born like that just doesn't match
Speaker 1: the pattern of spread. Yeah.
Speaker 2: Hepatitis B was one that you mentioned to me via
Speaker 2: text message, Aaron.
Speaker 1: I saw that mentioned in like last minute in a
Speaker 1: paper that I came across.
Speaker 2: Yeah, it was like yesterday evening and I was like, great,
Speaker 2: more word. I love it. So hepatitis B again, we
Speaker 2: did this episode, y'all, hepatitis B causes chronic illness, and
Speaker 2: it absolutely accounts for, even to this day, hundreds of
Speaker 2: thousands of debts every year. But it's a chronic infection.
Speaker 2: It's not something that is acutely killing people, at least
Speaker 2: not at this scale. So it's not hepatitis B. It's
Speaker 2: not parvovirus B nineteen. It seems to me this is
Speaker 2: one that we haven't covered, so I'll just briefly mention
Speaker 2: it and even just doing this little dive on it
Speaker 2: for this episode. Maybe you want to do parvovirus I do.
Speaker 1: I definitely want to do parvoviruses.
Speaker 2: Yeah, yeah, So parvovirus B nineteen is one specific parvovirus.
Speaker 2: These are DNA viruses. They're transmitted person to person by
Speaker 2: respiratory droplets. They can be quite infectious and tend to
Speaker 2: infect kids more than adults, mostly because you develop immunity
Speaker 2: to it. But the disease that we tend to see
Speaker 2: in majority is a pretty mild illness, though it can
Speaker 2: cause an aplastic anemia, and I think maybe that is
Speaker 2: where there is this potential. Looks like there's a connection
Speaker 2: because a lot of the symptoms that you described not
Speaker 2: necessarily with regards to hemorrhage. But in that fifteen seventy
Speaker 2: six description of everything being pale and the blood being
Speaker 2: pale and et cetera, to me, that means we're not
Speaker 2: having enough red blood cells for one reason or another.
Speaker 2: A plastic anemia means that your body stops making red
Speaker 2: blood cell else and that's because in the case of
Speaker 2: parvovirus B nineteen, it's replicating and destroying your red blood
Speaker 2: cell precursors. Replicating in and destroying your red blood cell
Speaker 2: precursors interesting, and so it can cause this transient usually
Speaker 2: anemia where you basically can't make any more red blood cells,
Speaker 2: which can be really dangerous. But again, it doesn't happen
Speaker 2: in everyone. It's not killing people outright, it's not causing
Speaker 2: this massive amount of hemorrhage, et cetera, et cetera.
Speaker 1: Right, And it does like it does make me think,
Speaker 1: based on that description and the amount of hemorrhage that
Speaker 1: was happening, that the paleness may have been doue to
Speaker 1: that more than a plastic anemia. But I like that.
Speaker 2: That's interesting, Yeah, And it sounds to me like there's
Speaker 2: multiple things going on in the description. So I want
Speaker 2: to get into like my thoughts on it, and then
Speaker 2: talk about the more likely candidates. Okay, what were some
Speaker 2: of the others that you told me? That seem easy
Speaker 2: to say. I don't think it's that.
Speaker 1: Bartonella. Do we already talk about that one.
Speaker 2: We haven't talked about bartonella yet. Let me scroll through
Speaker 2: my nine.
Speaker 1: Page tablesporosis and protessis and diphtheria.
Speaker 2: Oh my gosh, Aaron, you did not tell me diphtheria
Speaker 2: and protessis.
Speaker 1: Okay, well, we can rule those out, like there were
Speaker 1: no respiratory symptoms described.
Speaker 2: There were no respiratory symptoms described. So because of that,
Speaker 2: I actually think that mneumonic plague is not likely to
Speaker 2: be a cause of this. And it's interesting because some
Speaker 2: of what was described in that fifteen seventy six outbreak
Speaker 2: sounded a little bit like bubonic plague.
Speaker 1: Oh, with the lymph nodes, with the lymph.
Speaker 2: Nodes and these ulcerated nodes behind the ears, like you have,
Speaker 2: you know, a pretty decent chain of lymph nodes back there.
Speaker 2: And pneumonic plague, which is a form of plague caused
Speaker 2: by your Cinia pestis. See season one for more details.
Speaker 2: Bubonic plague would cause these very inflat aimed lymph nodes,
Speaker 2: these boobos, though generally throughout the body and not necessarily
Speaker 2: only in one place. And it was pneumonic plague that
Speaker 2: was the most deadly. And with pneumonic plague, generally the
Speaker 2: symptoms very much were pneumonia, like you had symptoms predominantly
Speaker 2: in the lungs, and people tended to die from respiratory
Speaker 2: failure and not from hemorrhage like it sounds like happened here. Yeah,
Speaker 2: I will say that mneumonic plague is something that killed
Speaker 2: people very rapidly when it happened, often in as little
Speaker 2: as twenty four hours. And the untreated fatality rate for
Speaker 2: pneumonic plague is nearly one hundred percent. Yeah, So is
Speaker 2: it possible that there was plague going on that was
Speaker 2: causing bubonic, mneumonic, even septoscemic plague. I mean, it certainly
Speaker 2: seems possible that that was circulating me.
Speaker 1: And this is what I find interesting though, because it
Speaker 1: wasn't like plague was a known entity that was going to.
Speaker 2: Be My question is how much And I would have
Speaker 2: to go back and listen and re remember how much
Speaker 2: plague was kind of already well described and well known
Speaker 2: during the kind of Spanish conquista or takeover.
Speaker 1: Well, okay, it's a good question, and this is me
Speaker 1: grasping at wisps of memories from season one. The Black
Speaker 1: Death happened in the middle of the fourteenth century, and
Speaker 1: it didn't just go away like it remained in pockets.
Speaker 1: It would rear up every now and then. You know,
Speaker 1: there were epidemics of plague that happened on a regular basis,
Speaker 1: And so I think given its sort of like formative
Speaker 1: impact on medicine, Yeah, I would think that it would
Speaker 1: have been described or recognized as plague, like it was
Speaker 1: well known, it was familiar, and the other thing too.
Speaker 1: And maybe this is a little unfair, but like most
Speaker 1: papers seem to also kind of discard it or like
Speaker 1: you mention it as this was one of the ones
Speaker 1: considered or has been suggested, right, So like maybe we
Speaker 1: should be giving it a more fair shake, but I
Speaker 1: think that we have.
Speaker 2: Yeah, I don't think it fits.
Speaker 1: I don't think it fits.
Speaker 2: Yeah, I don't think it fits. Bartonellosis is an interesting one.
Speaker 2: So Bartnellosis, we did this aarin in a very non
Speaker 2: traditional episode way because we covered all of the different
Speaker 2: kinds of Banella.
Speaker 1: I remember that because we were like, what have we done?
Speaker 2: Yes, yeah, I still feel that way. But what's interesting
Speaker 2: is that because there are so many different bacteria, so
Speaker 2: many different species of Bartonella, that a pretty wide variety
Speaker 2: of disease, including so Bartonella bacilliformis is what causes Carrion's disease.
Speaker 2: Carrion's disease today is limited to the Andean Valleys of
Speaker 2: South America, but there are many other species of Bartanella
Speaker 2: that cause things like trench foot basilari angeomatosis. Of course
Speaker 2: Bartanella hensley, which causes cat scratch disease. And the symptoms
Speaker 2: don't quite fit, especially this hemorrhage. I really just keep
Speaker 2: coming back to the hemorrhage part of it.
Speaker 1: Yeah, it's hard to ignore.
Speaker 2: It's really hard to ignore. But the high fevers, the headaches,
Speaker 2: the jaundice that was mentioned in both of those descriptions,
Speaker 2: and the pallor, which could, in addition to being from
Speaker 2: just blood loss, be from a hemolytic anemia, which can
Speaker 2: definitely be seen with bartonellosis, especially with bartonellosis from Bartnella bacilliformis,
Speaker 2: which causes the most severe Bartnella that we see today.
Speaker 2: So could it be that there was a different species
Speaker 2: of Bartnella perhaps or the same species but causing infection
Speaker 2: in a slightly different way during that time.
Speaker 4: I don't know.
Speaker 2: Maybe the things that make me feel like it's less
Speaker 2: likely to be Bartnella is really that this was a
Speaker 2: more protracted illness. So while the mortality rate can be
Speaker 2: very high, according to some studies, at least Carrion's disease
Speaker 2: has an estimated mortality rate of anywhere from forty to
Speaker 2: eighty percent, although some studies suggest that the infection rate
Speaker 2: in a lot of these outbreaks was actually much higher,
Speaker 2: which means that the mortality rate comparatively was lower. Okay,
Speaker 2: But it also is just a more protracted illness. This
Speaker 2: was something taking place over the course of one to
Speaker 2: four weeks, and people were dying at the end of
Speaker 2: this very protracted illness, which is not what was described okay,
Speaker 2: and cocoletes.
Speaker 1: One interesting thing about Bartnella is that it's a bacterium,
Speaker 1: and I don't know, like I'm just not up to
Speaker 1: speed on how DNA analysis is done on like ancient specimens,
Speaker 1: So I don't know if they would have been able
Speaker 1: to look for Bartnella or if it would have come up.
Speaker 1: But definitely, I know that they mentioned in the paper
Speaker 1: that the techniques that they used could detect bacteria, many
Speaker 1: bacterial species as well as DNA viruses, but not RNA viruses,
Speaker 1: and so I do wonder if it was there they
Speaker 1: would have been able to find it and that. But
Speaker 1: you know, that doesn't mean at all that it's not
Speaker 1: Bartonella just because they didn't find it. Like again, these
Speaker 1: are very few samples in one specific region. That doesn't
Speaker 1: mean that that is what happened all over Mexico. But anyway,
Speaker 1: just thought that's interesting. But yeah, I think based on
Speaker 1: the duration, like I don't know, it.
Speaker 2: Just seems less It just seems less likely. I think
Speaker 2: that one is one that's maybe not like, not quite
Speaker 2: as easy of a just dismiss.
Speaker 1: It, Yeah, because that interesting.
Speaker 2: Yeah. Another one that I think based on symptoms is
Speaker 2: worth talking in a little bit more detail about, but
Speaker 2: I still think is very less likely more based on
Speaker 2: kind of epidemiological data is leptosporosis. Okay, so leptosporosis is
Speaker 2: caused by the spirokey Leptospira many different species. This is
Speaker 2: a water borne illness. In general, it's comes to us
Speaker 2: from the urine of other animals, and symptom wise, it
Speaker 2: seems like some things really do seem to fit. Fever
Speaker 2: is one of the first symptoms. There's generally a lot
Speaker 2: of GI symptoms like nausea and vomiting and diarrhea. Rashes
Speaker 2: tend to occur only pretty late in the course of disease,
Speaker 2: so they're definitely not like an everyone feature, and they're
Speaker 2: not like a predominant feature, I guess. But what does
Speaker 2: tend to be, especially in severe disease, is signs of
Speaker 2: organ dysfunction like jauntice because of damage to the liver,
Speaker 2: like kidney dysfunction, which tends to be what ends up
Speaker 2: killing people, okay, like hemolytic anemia. Okay, right, So a
Speaker 2: lot of things are kind of ticking boxes. We do
Speaker 2: also see in leptosperosis when it's severe disease, signs of bleach,
Speaker 2: signs of hemorrhage, and this is usually because of a
Speaker 2: decrease in platelets. But in general, it's mild bleeding. It's
Speaker 2: petikia like little pinpoint purple spots. You can, however, see
Speaker 2: more severe bleeding like massive gastrointestinal or pulmonary hemorrhage, and
Speaker 2: pulmonary hemorrhage tends to be what kills people in the
Speaker 2: case of leptosporosis. But this is not something that happens
Speaker 2: for everyone who gets leptosporosis.
Speaker 1: Yeah.
Speaker 2: The time course of leptosporosis is generally pretty long, and
Speaker 2: it's usually not until a kind of biphasic second round
Speaker 2: of disease that people get very very sick, okay, where
Speaker 2: they actually end up dying from the disease.
Speaker 1: Whereas this was like clearly seemed to be happening over
Speaker 1: the course of a couple of day, four days.
Speaker 4: Yeah.
Speaker 1: Yeah.
Speaker 2: And the other thing that I think makes leptos sporosis
Speaker 2: so much less likely is that you specifically mentioned that
Speaker 2: no animals seem to have died, right. Leptosporosis is something
Speaker 2: that infects lots and lots of different animals, and humans
Speaker 2: are dead end hosts. And so I mean, on the
Speaker 2: one hand, could it be that this, like I just
Speaker 2: wouldn't expect for it to be something that could spread
Speaker 2: across an entire region so easily and so rapidly without
Speaker 2: having some kind of animal involvement.
Speaker 1: Uh huh, Yeah, I feel like it would have to
Speaker 1: have been transmitted human to human, and since sleptosporosis humans
Speaker 1: are a dead end host, you would have to have
Speaker 1: a like continuous reintroduction of the pathogen into the water supply. Yeah,
Speaker 1: that's harder to imagine happening, YEP. I agree.
Speaker 2: I agree.
Speaker 1: All right, So now are we left.
Speaker 2: With We're left with, oh, epidemic typhus. Yeah, that's our
Speaker 2: last one besides the other three. So epidemic typhus you
Speaker 2: mentioned a number of times, and I think part of
Speaker 2: the reason that makes me think it's not epidemic typhus
Speaker 2: is just that epidemic typhus was known, it seems.
Speaker 1: Yeah.
Speaker 2: But in addition to that, symptom wise epidemic typhus, which
Speaker 2: is caused by Ricketzia prawaz echii, so a ricketzial intracellular
Speaker 2: bacterium spread by lice. So not quite person to person,
Speaker 2: but person to person in that you're transmitting lice person
Speaker 2: to person.
Speaker 1: I mean, and like we in historical epidemic typhus outbreaks,
Speaker 1: we see massive spread of course of mortality and mortality
Speaker 1: associated with malnutrition.
Speaker 2: Yeah, we talked about, YEP, I remember talking about that
Speaker 2: in a lot of detail. Yeah, pre antibiotic mortality rates
Speaker 2: were as high as sixty percent in epidemic typhus, which
Speaker 2: fits with this. A sudden onset of fever and headache
Speaker 2: and abdominal pain are the kind of key symptoms, along
Speaker 2: with central nervous system dysfunction, which could include seizures like
Speaker 2: you mentioned, and could include delirium and a lot of
Speaker 2: other things. But that's kind of where the overlap seems
Speaker 2: to end. There's really not a lot of description of
Speaker 2: hemorrhage at all when it comes to epidemic typhus. There's
Speaker 2: not the hemolytic anemia, there's not the jaundice. There does
Speaker 2: often tend to be a rash, and rash is something
Speaker 2: that is often described as associated with epidemic typhus, and
Speaker 2: we talked in that Typhus episode about the difficulties with
Speaker 2: those historic descriptions of rash because rash appears very differently
Speaker 2: on different colored skin, and so it's thought that maybe
Speaker 2: rash was actually less common or maybe more common, et cetera.
Speaker 2: But in any case, rash is definitely something that is
Speaker 2: described as associated with typhus, and the disease here tends
Speaker 2: to last for two to three weeks, So again we're
Speaker 2: talking about something that tends to have a much longer
Speaker 2: course of illness. Yeah, so I think less likely to
Speaker 2: be epidemic typhus. Okay, so we're almost done with this
Speaker 2: long list, and we've come to the few that I
Speaker 2: think are either the best contenders or that we, like
Speaker 2: you said, maybe have a little bit of evidence to
Speaker 2: suggest maybe. Okay, so let's go through these last couple
Speaker 2: and then we'll regroup, shall we. H. So one of
Speaker 2: the last is hauntavirus hantavirus. There are many different hauntaviruses.
Speaker 2: Hantaviruses are RNA viruses, so, like you mentioned, we would
Speaker 2: never know, at least not as of this point. Yeah,
Speaker 2: and they're generally spread by aerosolized rodent excrement, so like
Speaker 2: rodent p has to get in your face in order
Speaker 2: to get a hanted virus symptom. Wise, because there are
Speaker 2: many different types of hantaviruses that have been found in
Speaker 2: different parts of the globe, some of the symptoms do
Speaker 2: seem to fit fairly well. And certainly snombree virus has
Speaker 2: a mortality rate of like forty to fifty percent or
Speaker 2: even higher than that in some outbreaks that we've seen.
Speaker 2: The symptoms tend to be fevers, headaches, dizziness, body ache,
Speaker 2: so it can present kind of like more like the
Speaker 2: flu than what it sounds like. The descriptions of this
Speaker 2: particular outbreak of coco eatsy work, but it can also
Speaker 2: have nausea, vomiting, abdominal pain, diarrhea, And when hantaviruses cause
Speaker 2: severe disease, there's a couple different forms or a couple
Speaker 2: different manifestations that they can take. One, which is what
Speaker 2: tends to be caused by synombree virus, is a cardiopole
Speaker 2: lemonary disease which causes death within twenty four to twenty
Speaker 2: eight hours, like within a day usually, and the symptoms
Speaker 2: are caused by vascular permeability, by your blood vessels just
Speaker 2: leaking everywhere and fluid and blood just leaking out of
Speaker 2: these leaky blood vessels. So while we don't necessarily tend
Speaker 2: to see like pure hemorrhage, we certainly see leaky blood
Speaker 2: vessels in hantavirus infections in syndome brain infection, specifically in
Speaker 2: other hantaviruses like Hatan virus and Pumla virus, we do
Speaker 2: see more hemorrhage potentially, and we tend to see a
Speaker 2: cardio renal syndrome more than a cardiopulmonary syndrome because I
Speaker 2: know cocoliti, we didn't really see pulmonary. We didn't really
Speaker 2: see lung involvement described, but we did see potentially kidney
Speaker 2: involvement described, and so we do see that in a
Speaker 2: cardiorenal form of a hantavirus. But what we tend to
Speaker 2: see is just that your kidneys stop working and you
Speaker 2: stop making pee and then you die because of kidney failure.
Speaker 2: So I don't know, it doesn't it doesn't.
Speaker 1: Fit that well, okay, but it's something.
Speaker 2: It's something also though this is something that is spread
Speaker 2: by rodents.
Speaker 1: Right so far, for the most part, with like one
Speaker 1: possible exception or two, we do not see human to
Speaker 1: human transmission of hauntaviruses correct, which doesn't mean that it
Speaker 1: can't happen or didn't happen in the past.
Speaker 2: Yeah, but.
Speaker 1: Based on the ones that circulate that we recognize today, no.
Speaker 2: No, So that brings us to Salmonella paratype or rather
Speaker 2: Salmonella enterica subspecies and Enterica there of are paratyphee.
Speaker 1: See, there are multiple paratypees, there.
Speaker 2: Really are, and it's shockingly difficult to get information on
Speaker 2: symptoms of salmonella and Enterica subspecies and Enterica seraphar paratype
Speaker 2: see because all of the papers describe say, you can't
Speaker 2: tell the difference between Salmonella typhi and Salmonella paratyphe when
Speaker 2: it comes to the symptoms of disease, at least insofar
Speaker 2: as we know today. Okay, so we did typhoid relatively recently,
Speaker 2: and the classic description of symptoms of typhoid start with
Speaker 2: a fever. But there's a few things about typhoid that
Speaker 2: really stick out to me as not fitting with your
Speaker 2: description of Coco Latsle. Some of them include the fact
Speaker 2: that this fever you mentioned in those descriptions that the
Speaker 2: fever was constant, but the fever of typhoid is usually
Speaker 2: described as not which just constant, but getting progressively worse, Okay,
Speaker 2: day after day and rising over the course of a
Speaker 2: couple of weeks. Right, So already we don't quite fit. Also,
Speaker 2: classic typhoid, and we talked about this in our typhoid
Speaker 2: episode has a relative bredacardia, which means that your heart
Speaker 2: rate does not increase with that fever, and the description
Speaker 2: from the fifteen seventy six outbreak very nicely specifically said
Speaker 2: that you see really high heart rates, and in typhoid
Speaker 2: it's less likely for that to happen. Additionally, rash is
Speaker 2: a really common description of typhoid infection, and this rash,
Speaker 2: it tends to be salmon colored little spots starting on
Speaker 2: the trunk and then kind of spreading outwards from there.
Speaker 2: And then it's usually not until the third of this
Speaker 2: illness that you start to see GI symptoms like abdominal
Speaker 2: pain or diarrhea, and that is when we can see
Speaker 2: some bleeding from the intestinal tract, we can see bloody diarrhea,
Speaker 2: and potentially this infection spreading to the bloodstream where you
Speaker 2: can get hepatosplenomegaly, which is again where your liver and
Speaker 2: your spleen starts to swell, and that seems to have
Speaker 2: been described in that fifteen seventy six outbreak, where you
Speaker 2: have your liver and your spleen becoming abnormally large and
Speaker 2: all of your organs just getting super messed up. But
Speaker 2: other than that, we don't really see a lot of bleeding.
Speaker 2: We don't really see a lot of neurologic manifestations, so
Speaker 2: we don't really tend to see the delirium, we don't
Speaker 2: really tend to see the seizures. That kind of thing
Speaker 2: is much less likely in typhoid, but certainly mortality rate
Speaker 2: ranged from ten to thirty percent, so the most part
Speaker 2: if untreated with typhoid. But it is spread fecal oral,
Speaker 2: so easily spread person to person. And there's of course
Speaker 2: the carrier state i e. Typhoid mary yep, meaning that
Speaker 2: it would be really easy for this to be something
Speaker 2: that could spread across a country because people could be
Speaker 2: carrying it an asymptomatic for a really long time. But
Speaker 2: in general, I feel like it's interesting and we'll talk
Speaker 2: I know a little bit more about this that this
Speaker 2: happens to be the pathogen that has been found in
Speaker 2: people who likely died during this outbreak, because it seems
Speaker 2: to me like the least good fit in terms of symptoms.
Speaker 1: So okay, I definitely think and the authors also acknowledged
Speaker 1: the possibility that this is just a circulating pathogen that
Speaker 1: was there that people had. I did a bit of
Speaker 1: digging I can't wait, a little bit of Google scholaring,
Speaker 1: and one thing that I think is interesting and that
Speaker 1: this sort of reminded me of, is that a paper
Speaker 1: from even like the nineteen eighties or up to the
Speaker 1: two thousands that describes typhoid fever is going to, I think,
Speaker 1: look at a case of typhoid fever in a very
Speaker 1: different setting than historically. And this also applies to typhus,
Speaker 1: to hauntaviruses, etc. Another thing that I also wonder about
Speaker 1: is like virulence plasmids how and I don't remember this
Speaker 1: from our typhoid episode, Like whether there are different subspecies
Speaker 1: or seravars that contain different virulence plasmids and some are
Speaker 1: much more deadly or can cause different weets of symptoms
Speaker 1: or whatever. But yeah, okay, let's talk to me about
Speaker 1: hemorrhagic fever viruses and then we'll sort of do like
Speaker 1: a compare and contrast.
Speaker 2: Okay, okay, okay. So the last kind of group of
Speaker 2: possible infections would be a viral hemorrhagic fever of like
Speaker 2: unknown type. I guess just one of these other ones.
Speaker 2: And what's interesting about this is that like hantavirus is
Speaker 2: considered a viral hemorrhagic fever, like it's under this class
Speaker 2: of viral hemorrhagic fevers. There's a great paper that I'll
Speaker 2: link to that kind of groups all of these into
Speaker 2: a few different categories. So we have feloviruses, which include
Speaker 2: of course Marberg and ebolaviruses we've talked about both of those.
Speaker 2: We have flavaviruses, which we've talked about many of these.
Speaker 2: This includes the dengay viruses and yellow fever virus, as
Speaker 2: well as a few other born and mosquito born viruses.
Speaker 2: The bunia viruses which include rift valley fever that we
Speaker 2: have not yet covered, Crimean congo hemorrhagic fever virus, and
Speaker 2: of course the hantaviruses, which includes Nombavirushton virus, et cetera,
Speaker 2: et cetera, as well as a virus called it a
Speaker 2: really great name, severe fever with thrombocytopenia syndrome virus that
Speaker 2: is a tickborn virus found in China.
Speaker 1: That's not all one word, is it. No?
Speaker 2: No, no, it's literally just like the name of the
Speaker 2: syndrome virus.
Speaker 1: Okay, okay okay.
Speaker 2: And then there are arenaviruses, and we have not covered
Speaker 2: any arenaviruses on this podcast.
Speaker 1: Are you serious though?
Speaker 2: I know, but these include matupovirus, which is the causative
Speaker 2: agent of Bolivian hemorrhagic fever, right guanarito virus which causes
Speaker 2: venezuela and hemorrhagic fever, Sabia virus, loss of virus, Luho virus,
Speaker 2: chop a virus, a lot of different viruses that have
Speaker 2: been found across the globe in different specific regions that
Speaker 2: have caused haemorrhagic fevers of various types. Most of these,
Speaker 2: especially when it comes to arena viruses, we really don't
Speaker 2: have a good handle on huh okay. We don't have
Speaker 2: a good handle on their reservoirs. We don't have a
Speaker 2: good handle on infection, like how things are spread. So
Speaker 2: just like in my pocket, I'm banking on an arena virus.
Speaker 1: Okay for cocoa, yes, okay, okay, Yeah, but that's just me,
Speaker 1: and I still have a lot of questions for you, Aarin.
Speaker 2: So how about we pause here, we take a break,
Speaker 2: and then we get into some more of the details
Speaker 2: about the epitymiology of these outbreaks so that we can
Speaker 2: try and parse this apart, shall we, Yes, let's do it.
Speaker 2: Can I just start by asking you a question.
Speaker 1: I was going to start by asking you a question.
Speaker 2: Oh okay, okay, okay, I who asked first?
Speaker 1: You could ask.
Speaker 2: Okay. I feel like I should have asked this earlier,
Speaker 2: but like when you were going through the symptoms and
Speaker 2: this outbreak. So I know that the outbreaks themselves lasted
Speaker 2: for a number of years, like a year and a half,
Speaker 2: couple of years, four years, and people when they got
Speaker 2: infected were dying incredibly rapidly. People were dying in a
Speaker 2: number of days. But how quickly did this spread, say
Speaker 2: through a family or through a town. What was the
Speaker 2: estimated incubation period?
Speaker 1: Here? Great question? I don't know. Ugh, maybe there are
Speaker 1: more accounts out there, but none of the papers that
Speaker 1: I read mentioned in incubation period or like a possible
Speaker 1: estimated incubation period.
Speaker 2: Wow, that was a whole entire column of my table,
Speaker 2: and I really thought it was going to help parsing
Speaker 2: support Aaron.
Speaker 1: I know, I know. So it's difficult too, because I think,
Speaker 1: you know, the movement of it seemed really erratic. It
Speaker 1: didn't seem to move in like an outward spreading radius.
Speaker 1: It would be like all of a sudden it was there.
Speaker 1: But also let's consider the time and communication and limitations
Speaker 1: in terms of like did that town get hit before
Speaker 1: this town? If there was there's two days difference or
Speaker 1: even a week difference, would that have been something detected
Speaker 1: or like even able to be observed. I guess right, Yeah,
Speaker 1: I know, I wish I had that answer. Okay, but
Speaker 1: let me ask you a question real quick. Okay, what
Speaker 1: causes nose blade? What's happening in a nose bleed?
Speaker 2: There's potentially a lot of different things that can cause
Speaker 2: a nose bleed, but there's two different places in your
Speaker 2: nose that you tend to bleed from. Because your nose,
Speaker 2: your nasal mucosa, essentially the skin is very thin and
Speaker 2: there's a lot of vasculature there. So most nose bleeds
Speaker 2: come from the anterior vessels, the vessels that are like
Speaker 2: closer to where your nose opening is. Okay, yeah, and
Speaker 2: you have this like plexus of vessels that if that
Speaker 2: mucosa gets dried out or if there's any trauma to it,
Speaker 2: can just very easily start to bleed from that plexus
Speaker 2: of vessels. This can also happen if you have say thrombocytopenia,
Speaker 2: that is, you don't have any platelets to be able
Speaker 2: to clot any bleeding that happens there. So there's a
Speaker 2: lot of different things that can potentially cause that anterior bleeding.
Speaker 2: There's also posterior nose bleeds that happen farther back in
Speaker 2: your nose, and those tend to be more commonly from
Speaker 2: that type of bleeding disorder or like disease in the
Speaker 2: blood vessels, say, from like atherosclerosis or something like that. Okay,
Speaker 2: And those posterior nose bleeds can be massive and like
Speaker 2: really difficult to stop.
Speaker 1: Interesting, And so a lot of these nose bleeds and
Speaker 1: I feel like I'm a little bit hung up on
Speaker 1: the nosebleed thing, and maybe I shouldn't be, but like
Speaker 1: they do seem to be massive hemorrhaging out the nose.
Speaker 1: So could that be a combination of like some type
Speaker 1: of clotting issue combined with like what disease could do
Speaker 1: that or would do that? How? What's about the genesis?
Speaker 2: I feel like we have talked about a number of
Speaker 2: diseases that can cause nose bleeds. Generally, when we see
Speaker 2: nose bleeds, it's not isolated nose bleeds. If it's caused
Speaker 2: from say a hemorrhagic virus of some kind or something
Speaker 2: that's causing thrombocidepenia. But that would be one of the
Speaker 2: major things that I would think about. Thrombaside opinia is
Speaker 2: when we don't have enough platelets, And we've talked in
Speaker 2: a number of our episodes now about how essential our
Speaker 2: platelets are to be able to stop bleeding when it starts.
Speaker 2: So because your nose just happens to be a place
Speaker 2: much like your gingiva, like in our vitamin C episode
Speaker 2: way back when we talked about how you get bleeding
Speaker 2: from the gums because you just don't have like any
Speaker 2: collagen left. And so it's not even about in that
Speaker 2: case not being able to stop bleeding. It's just that
Speaker 2: that's a place that's really easy to bleed from. Okay,
Speaker 2: your nose is very similar. Same thing with your eyes,
Speaker 2: and you described maybe seeing bloodshot eyes. So the mucosa
Speaker 2: of your eyes is just another place where things are
Speaker 2: very thin and there's a lot of really small blood vessels.
Speaker 2: So if you have a tendency towards bleeding because you say,
Speaker 2: don't have any platelets to stop bleeding, then little tiny
Speaker 2: blood vessels breaking can lead to large amounts of bleeding.
Speaker 1: Okay, interesting, that makes sense.
Speaker 2: It's the same thing in your GI tract.
Speaker 1: Yeah, So it's not necessarily an indicator of any particular disease.
Speaker 1: It's just like this is maybe already when things have
Speaker 1: gone well wrong.
Speaker 2: Yeah, I would say it's an indicator that your coagulation
Speaker 2: state is totally screwed up.
Speaker 1: Okay, yeah, Okay.
Speaker 2: We saw it in you can see it in DIC,
Speaker 2: which we talked about so DIC is disseminated intravascular coagulation.
Speaker 2: We talked about it in our Sepsist episode. We talked
Speaker 2: about it in our Snake Bite episode. We've talked about
Speaker 2: it in a few other episodes. But basically, just anything
Speaker 2: that's going to like completely screw up your body's ability
Speaker 2: to clot properly, you could potentially see nosebleeds. Now that
Speaker 2: being said, there are a lot of diseases that are
Speaker 2: considered like hemorrhagic diseases of some kind we don't usually
Speaker 2: see described like actual and we've talked about this in
Speaker 2: a few episodes, Like it doesn't usually mean that you're
Speaker 2: just bleeding out of places like hemorrhagic doesn't often mean
Speaker 2: the way that you think of hemorrhage with where like
Speaker 2: blood is just gushing out of orifices.
Speaker 1: All right, this is not Richard Preston's the hot zone.
Speaker 2: Exactly, but it sounds like it is in the case
Speaker 2: of cocolitesly I mean.
Speaker 1: Yeah. And it's interesting too because this does appear in
Speaker 1: both Spanish accounts as well as indigenous Nawa accounts of
Speaker 1: the disease. Yeah, all right, so let's before we get
Speaker 1: into more questions, let's just do a quick recap. So
Speaker 1: I have a list of the symptoms. This is in
Speaker 1: not any specific order, but these are the ones that
Speaker 1: were mentioned primarily in that account by that physician. So
Speaker 1: excessive thirst, continuous and high fever, headache, confusion, delirium, rapid pulse,
Speaker 1: nasal hemorrhage, bleeding from mouth, eyes, ears, genitals, tongue black
Speaker 1: and dry, swollen lymph nodes in neck, jaundice, chest pain,
Speaker 1: bloody stool, stomach pain, sometimes rash. Autopsy showed enlarged liver,
Speaker 1: black heart, dry stomach, black lungs urine green or black,
Speaker 1: then pale, and no notable respiratory symptoms. The disease seemed
Speaker 1: to have a three to five day duration, incredibly high
Speaker 1: case fatality rate with the overall mortality rate of like
Speaker 1: fifty to eighty percent, again not necessarily attributable to one
Speaker 1: pathogen alone, and there was actually that. One Franciscan scholar, Sahagoon,
Speaker 1: wrote that quote many died of hunger and because no
Speaker 1: one was able to care for them. In many cases,
Speaker 1: every member of a household fell ill without a single
Speaker 1: person left to give them even a cup of water
Speaker 1: to the sick end quote. So it has also been
Speaker 1: described as disproportionately attacking young adults and adolescents, and it
Speaker 1: also has been said to have disproportionately affected the indigenous population.
Speaker 1: Not all accounts describe this, and I do kind of
Speaker 1: want to get into this in a little more detail
Speaker 1: because I think it can help maybe resolve the question
Speaker 1: of Old World versus New World pathogen. If this disproportionate
Speaker 1: impact on indigenous populations was a true phenomenon, where was
Speaker 1: that coming from? Was it socioeconomic factors? So one person
Speaker 1: described that people who were quote rich, well dressed, and
Speaker 1: with a comfortable living were not affected by the disease
Speaker 1: end quote. So was it just socioeconomic factors? And so
Speaker 1: it was a New World disease that everyone was in
Speaker 1: theory immunologically susceptible to But it was just that the
Speaker 1: indigenous population, who had been suffering the greatest losses due
Speaker 1: to forced labor and minds, ridiculous taxation, et cetera. Spanish
Speaker 1: witnesses did recognize this disproportion impact and the living conditions
Speaker 1: and how it affected the rate of disease. Quote. The
Speaker 1: reason why so many Indians die of pestilence is a
Speaker 1: god secret. I do not find any better answer than
Speaker 1: that in the past, the Indians were not as badly
Speaker 1: mistreated and oppressed as they are today. With heavy workloads.
Speaker 1: They are skinny and delicate. The disease finds them overworked
Speaker 1: and without resistance, so they are finished. End quote. Okay,
Speaker 1: so if we do New World, then for the most part,
Speaker 1: socioeconomic factors and living conditions would explain the difference in
Speaker 1: susceptibility or attack rate or mortality rate. If it's an
Speaker 1: old world pathogen, it's probably a combination of those things.
Speaker 1: Socioeconomic factors are still there, they're not going away. But
Speaker 1: it also might be something about if it's an old
Speaker 1: world pathogen quote unquote more familiar to the immune systems
Speaker 1: of the Spanish colonizers, and there is a little bit
Speaker 1: of evidence in this respect, because if socioeconomic status meant
Speaker 1: that you were not only protected from getting super sick
Speaker 1: if you did get infected, but that it also prevented
Speaker 1: you from getting infected, then we would still see high
Speaker 1: death rates among those who were exposed to disease, if
Speaker 1: that makes sense. And so you have a bunch of
Speaker 1: these Spanish members of these religious orders who did a
Speaker 1: lot of the caring for the ill and a lot
Speaker 1: of the burying of the bodies, these priests and so on,
Speaker 1: and they are not described as having high death rates,
Speaker 1: nor are the Spanish physicians that performed so many autopsies
Speaker 1: without the slightest bit of ppe. So one author also
Speaker 1: suggested that maybe the reason for the disparity in these
Speaker 1: mortality or attack rates is that the root of transmission
Speaker 1: was somehow unique to the indigenous populations. We don't know
Speaker 1: what the root of transmission was, but given that the
Speaker 1: Spanish colonizers and indigenous populations lived pretty similar day to
Speaker 1: day lives at that point, or at least not terribly
Speaker 1: drastically different in terms of like completely separate lives, it
Speaker 1: doesn't necessarily seem like it was that I don't know,
Speaker 1: because if the disease was transmitted through direct contact lice, fleas,
Speaker 1: blood or other bodily fluids, respiratory droplets, mosquitoes, or water,
Speaker 1: there's really no way that the Spanish would have just
Speaker 1: been completely spared if they had been as susceptible. So okay,
Speaker 1: that was my sort of new world, ole world thing.
Speaker 1: Root of transmission we don't know. We can compare the
Speaker 1: spread of cocolites to the other epidemics that were happening
Speaker 1: in the sixteenth century, and it seems very similar to
Speaker 1: those that were spread person to person, like smallpox, chicken pox,
Speaker 1: and measles. We can go over some of the other
Speaker 1: possible roots of transmission too, like waterborne or lousborne, or
Speaker 1: like a rodent reservoir. We kind of already touched on
Speaker 1: that geography. Again, we only have a few accounts to
Speaker 1: rely on, but it seems like everywhere was impacted, with
Speaker 1: the possible exception of some of the coastal areas. There
Speaker 1: are many different reasons why that could be. Maybe a
Speaker 1: less ferrulent variant of the disease made it there, people
Speaker 1: were more immune, or the vector or reservoir wasn't as
Speaker 1: prevalent or just something else interrupted transmission, could be a
Speaker 1: whole lot of things going on.
Speaker 2: Yeah, but was that trend like persistent across the years.
Speaker 1: I guess, I don't know. I don't know. Yeah.
Speaker 4: Yeah.
Speaker 1: And then there's the environmental factors, which this mega drought
Speaker 1: and then period of intense rainfall, and so some researchers
Speaker 1: have suggested that as evidence for rodent associated it's like
Speaker 1: this proliferation of rodents. But could it also be contaminated
Speaker 1: water supply because we know that you know, drought, excessive rainfall,
Speaker 1: and just in general, like disruption and chaos in everyday
Speaker 1: life is water supply is one of the first things
Speaker 1: to get all screwed up. And so I think it's
Speaker 1: an interesting question about like the symptoms, Does whatever disease
Speaker 1: that actually cause this have to include every one of
Speaker 1: those symptoms? Which symptoms do we concentrate on first? Which
Speaker 1: accounts are reliable? Like what if this physician never actually
Speaker 1: performed an autopsy and he's just hearing word of mouth.
Speaker 1: Then you have a physician who's looking at someone and saying,
Speaker 1: these are the things you're experiencing, versus someone who's like,
Speaker 1: this is what I'm experiencing, Like it's an interesting, I
Speaker 1: don't know, interesting questions, but but yeah, let's sort of
Speaker 1: get into a few of these things. So I feel
Speaker 1: like the New World versus Old World discussion plays a
Speaker 1: role in the hemorrhagic fever virus potential.
Speaker 2: Yeah, because I think when I would think about a
Speaker 2: hemorrhagic fever virus as the causative agent, it doesn't seem
Speaker 2: likely that it would have been a hemorrhagic fever imported
Speaker 2: from the Old World to the New World for a
Speaker 2: few reasons. One because then I would expect I don't know,
Speaker 2: something similar to have been reported somewhere else first, right,
Speaker 2: But I think that that argument stands for like any
Speaker 2: pathogen that was brought over, right, if it was something
Speaker 2: that was brought over, how could it be something brand
Speaker 2: new that hadn't been seen by the Spanish conquistadors beforehand. Yeah, right,
Speaker 2: And that is the part that I think makes it
Speaker 2: so hard to think could it have been anything that
Speaker 2: was brought over, right, unless it was something that was
Speaker 2: brought I don't.
Speaker 1: Know, brought over and then mutated into a more virulent strain.
Speaker 2: Or something perhaps not brought from Europe but brought from
Speaker 2: Africa during slave trade that maybe we was happening, but
Speaker 2: we don't have as great of records on it. Perhaps,
Speaker 2: but that also still doesn't explain why Spanish colonizers seem
Speaker 2: to have been less affected.
Speaker 1: Yeah, per se, unless it's just again down.
Speaker 2: To socioeconomics and exposure and things like that.
Speaker 1: Yeah, right, But so many of these hemorrhagic fever viruses
Speaker 1: that we do know are transmitted direct contact through bodily fluids,
Speaker 1: right many, And that happens a lot, not all the time,
Speaker 1: but a lot during caring for the sick and also
Speaker 1: taking care of the bodies of people who have succumbed
Speaker 1: to disease, And we don't see records of like the
Speaker 1: Spanish priests dying at higher rates.
Speaker 2: Right Well, And what's interesting is that that's the problem
Speaker 2: I think with lumping all of the hemorrhagic fever viruses together. Yes,
Speaker 2: the fela viruses like Marbourg and Ebola, Yes, are spread
Speaker 2: direct person to person through contaminated bodily fluids. The flavaviruses
Speaker 2: are often spread by mosquito vectors. So could this be
Speaker 2: something that was a hemorrhagic flavavirus of some kind that
Speaker 2: we don't know of? Because I don't think that it
Speaker 2: was dang gay or yellow fever, but.
Speaker 1: It doesn't seem mosquito born.
Speaker 2: I mean, I feel like I don't have a good
Speaker 2: enough handle on the spread of this thing.
Speaker 1: Yeah, I mean rapid, rapid is rapiden.
Speaker 2: Right, rapid and sudden, which I would say probably goes
Speaker 2: against the mosquito born because in general, you're going to
Speaker 2: need time for it to be in the mosquito and
Speaker 2: then causing more infection, et cetera.
Speaker 1: Well, and then like where did it come from.
Speaker 2: And why would it Why I would expect to be
Speaker 2: more infection at the coasts because if you have like
Speaker 2: a new mosquito coming in, or even honestly even a
Speaker 2: new infection coming in, you're gonna it's gonna come into
Speaker 2: the ports. So any kind of imported infection, how did
Speaker 2: it not come through the ports and cause more disease
Speaker 2: in the coasts than in inland.
Speaker 1: Yeah, yeah, I don't. I don't know.
Speaker 2: But there's a lot of other hemorrhagic fever viruses as well,
Speaker 2: the arena viruses and the bunia viruses, a contavirus. Many
Speaker 2: of those, well, the arenaviruses can be transmitted a lot
Speaker 2: of different ways, including person to person, but some of
Speaker 2: them maybe not so much. A lot of them are
Speaker 2: from rodent vectors. So could it be that it was
Speaker 2: a rodent vector disease that's somehow mutated to be able
Speaker 2: to be transmitted person to person. Sure, Sure, I mean,
Speaker 2: I mean maybe it seems possible.
Speaker 1: Yeah, But I.
Speaker 2: Think that what that comes back to is how to
Speaker 2: prioritize when we're thinking about this hundreds of years ago
Speaker 2: outbreak or outbreaks. Is which of these symptoms do we trust?
Speaker 2: Which of these symptoms were definitely caused by the pathogen
Speaker 2: that we think killed people in this case, versus which
Speaker 2: of them were a secondary bacterial infection on top of
Speaker 2: something else. Yep, although that seems less likely given the
Speaker 2: time course of this illness. I just can't get over
Speaker 2: how rapid this was.
Speaker 1: Yeah, And to be honest, I don't know, And I
Speaker 1: think it also probably would have been worth me looking
Speaker 1: into what predominant understanding of disease there was, so like,
Speaker 1: was it the humoral theory of disease? Are certain symptoms
Speaker 1: emphasized over others given those sorts of biases?
Speaker 4: Right?
Speaker 1: Like if someone has a fever, is that a primary symptom?
Speaker 1: Or is that like Okay, it's just a low grade fever.
Speaker 1: Is the bleeding, I mean, that's just seems so stark
Speaker 1: and so dramatic, But then there's stuff like rapid pulse
Speaker 1: abdominal pain. A lot of these symptoms are very general
Speaker 1: general can be severe manifestations of many different types of infections.
Speaker 2: But there's also I think enough descriptions that tell us
Speaker 2: that whatever this was, it was a pathogen that was
Speaker 2: very rapidly affecting a wide variety of our organs, and
Speaker 2: that was certainly causing a significant degree of what sounds
Speaker 2: like hemolytic anemia, because in all of the descriptions there
Speaker 2: was jaundice, in all of the descriptions, there was some
Speaker 2: amount of bleeding, be it bloody diarrhea or bleeding from
Speaker 2: the mucus membranes. And was it truly trauma level hemorrhagic
Speaker 2: We don't know, but it's very likely that if you're
Speaker 2: having this degree of hemolytic anemia, that you're also having
Speaker 2: issues with your other blood cells, including your platelets, which
Speaker 2: means that you're going to be at risk of bleeding,
Speaker 2: even if it's just the like your nose is constantly
Speaker 2: dripping and not truly a faucet coming out of it,
Speaker 2: right yeah.
Speaker 1: And I mean the illustrations show gushing, gushing, right yeah.
Speaker 2: But is that gushing like in combination with vomiting or
Speaker 2: or is.
Speaker 1: That like this is the degree with which we suffered exactly? Yes,
Speaker 1: good point.
Speaker 2: And so I think that all of those symptoms, including
Speaker 2: you know, the changes in the color of the urine,
Speaker 2: to me, that says this is affecting the kidneys in
Speaker 2: addition to affecting the liver and the spleen, the pulse
Speaker 2: being high, and the fevers. That just means you're sick. Right,
Speaker 2: that could be from anything, but all of these and
Speaker 2: the rapidity of the infection just sounds so viral to me.
Speaker 1: Okay, before we go further, can I just do a
Speaker 1: little bit of a dive into the other end of things,
Speaker 1: the bacterial side of things, okay, please, okay, because I
Speaker 1: wanted to do a little bit of research about typhus
Speaker 1: and typhoid. Okay, So, Epidemic typhus was one of the
Speaker 1: earliest diseases to be proposed as the cause of Cocolitzli.
Speaker 1: Hans Censer wrote about it in that book Rat'slice in History.
Speaker 1: During the Cocolaitzlei epidemics. Typhus was a recognized disease, but
Speaker 1: most people did not use the name for typhus to
Speaker 1: describe what was happening. But there is a precedent for
Speaker 1: typhus being described with more superlative or extreme names, like
Speaker 1: those that emphasize the severity of infection, and there exists
Speaker 1: at least one description from the late fifteenth early sixteenth
Speaker 1: centuries of typhus causing a severe nosebleed. The Italian physician
Speaker 1: Frakastorius wrote, quote, I have often seen cases where three
Speaker 1: pounds of blood burst from the nostrils, yet the patient
Speaker 1: died soon after end quote. And so I got a
Speaker 1: little bit curious about typhus and nose bleeds, and so
Speaker 1: I just put the words nose bleed and typhus into
Speaker 1: Google scholar and what I actually got were primarily results
Speaker 1: for typhoid. And that's something I remember from doing those episodes.
Speaker 1: Typhus and typhoid weren't really distinguished as separate diseases until
Speaker 1: like the early to mid eighteen hundreds or so, because
Speaker 1: they do have similar courses of disease and would also
Speaker 1: tend to proliferate during similar times of like chaos or
Speaker 1: unrest or war, even though they're transmitted differently. Epidemic typhus
Speaker 1: via lice, typhoid, fecal oral Also, I kept coming across
Speaker 1: the phrase abdominal typhus that actually means typhoid, which was
Speaker 1: very confusing for me. I was like, but what is it? So?
Speaker 1: But I don't entirely know whether or not tabardillo, the
Speaker 1: Spanish word for typhus, was also historically used for typhoid,
Speaker 1: or whether it was distinguished from typhoid, I don't know.
Speaker 1: But in any case, so going back to my Google scholaring,
Speaker 1: what I found were a bunch of historical reports of
Speaker 1: nosebleed in people with this abdominal typhus aka typhoid. A
Speaker 1: report of a typhoid outbreak associated with oysters that was
Speaker 1: published in nineteen thirty nine describes nosebleed as a cardinal
Speaker 1: symptom of typhoid and says that in that particular outbreak,
Speaker 1: it was the most common symptom observed and in young kids.
Speaker 1: Delirium also seems to be a common symptom that we
Speaker 1: found in a different paper, but in this oyster paper,
Speaker 1: hemorrhage happened to be the most common complication. Another paper
Speaker 1: from nineteen thirty four describes a case study of typhoid
Speaker 1: fever with hemorrhagic onset. Quote. In August nineteenth, nineteen thirty three,
Speaker 1: at about three am, the patient suffered a sudden, profuse nosebleed.
Speaker 1: A physician was consulted, who packed her nose. The bleeding, however, continued,
Speaker 1: and the patient was admitted to the hospital end quote.
Speaker 1: And typhoid, as we talked about, can be transmitted by
Speaker 1: asymptomatic carriers. I know that they're different diseases, but paratife
Speaker 1: C DNA has been found in an eight hundred year
Speaker 1: old skeleton of a woman in Trondheim, Norway, so that
Speaker 1: suggests an old world origin of at least paradifec. So
Speaker 1: I think that, you know, like I said, there's a
Speaker 1: lot that historically may have been reported and may have
Speaker 1: been attributed falsely to some of these diseases like typhoid,
Speaker 1: and searching for typhus and nose bleeds or typhoid and
Speaker 1: nose bleeds is certainly cherry picking Google scholar, But I
Speaker 1: just find that interesting because I was curious whether there
Speaker 1: had ever been something like that reported before. And then
Speaker 1: also I came across when I was looking for nose bleeds,
Speaker 1: I came across the fact that black tongue is often
Speaker 1: another characteristic of typhus slash typhoid people. I've seen it
Speaker 1: in both.
Speaker 2: So what he other?
Speaker 1: I mean? And maybe you could do this for literally
Speaker 1: any of the diseases, right, countavirus, nosebleed.
Speaker 2: Oh, I'm sure you would find it exactly. Oh, I
Speaker 2: kind of can I try it?
Speaker 1: Sure?
Speaker 2: Yeah, it exists, Saren.
Speaker 1: Yeah, So maybe all we learned from that whole dive
Speaker 1: was that nosebleed is not as specific a symptom as
Speaker 1: we thought, and that these diseases can take on many
Speaker 1: different forms.
Speaker 2: Definitely, I think that's definitely true. And again it's going
Speaker 2: to you what symptoms you have and what symptoms predominate
Speaker 2: are also going to vary depending on what the underlying
Speaker 2: immune state of a person or a population is. Yeah,
Speaker 2: but I still can't get over the rapidity aspect of it.
Speaker 1: Well, I mean that could be influenced by immune state as.
Speaker 2: Well, definitely, But it just seems like everything at least
Speaker 2: that we know about typhoid and typhus today our longer
Speaker 2: courses of.
Speaker 1: Disease, Yeah, for sure. So is it something that changed.
Speaker 1: Was it a virulence plasmid, was it a different serov
Speaker 1: art or was it just acting, you know, sort of
Speaker 1: swooping in opportunistically when the person's immune system was suppressed
Speaker 1: from another pathogen, right, or just was there in the
Speaker 1: background not doing anything right?
Speaker 2: I mean, because what I think is interesting is in
Speaker 2: the paper where they found the paratyphee in the dental pulp.
Speaker 1: Uh huh.
Speaker 2: I did read that paper. That's the only paper about
Speaker 2: actual coca leads together read. But one of the things
Speaker 2: that they said is that finding it in the dental
Speaker 2: pulp does suggest that the person or the people died
Speaker 2: with high levels of this bacterium in their bloodstreams.
Speaker 1: Specifically, Uh huh.
Speaker 2: Okay, because my first reaction was, well, we know that
Speaker 2: Salmonella enterica subspecies enterica blah blah blah blah, paradifee and
Speaker 2: typhe both can very easily establish asymptomatic infections and live
Speaker 2: within us predominantly in our gallbladder for weeks, if not months,
Speaker 2: if not years, and so finding it in a person
Speaker 2: isn't that interesting right on its own? Because this is
Speaker 2: something that circulates and can be present in people. But
Speaker 2: knowing that it's not likely to end up in someone's
Speaker 2: dental pulp upon death unless it was in their bloodstream
Speaker 2: is very interesting.
Speaker 1: In an epidemic graveyard.
Speaker 2: In an epidemic graveyard, however, it's still I mean, I
Speaker 2: just it. It's so interesting to me how much the
Speaker 2: symptoms and the time course don't seem to fit. Not
Speaker 2: to mention, and I think this is where I really
Speaker 2: wish that we had a little bit more data, like
Speaker 2: granular data on how rapidly this was spreading through homes
Speaker 2: and through families, right, because when you get down as
Speaker 2: well to the incubation period of something like a typhoid,
Speaker 2: we're looking at a much longer incubation period than we
Speaker 2: are for many of the viral hemorrhagic fevers, and again
Speaker 2: viral hemorohagic fevers. This is really really broad. But thinking
Speaker 2: of more of the bunya viruses or the viruses which
Speaker 2: seem more likely candidates than the flavaviruses and the filoviruses
Speaker 2: in this case, right, I think that the time course
Speaker 2: fits a little bit better. Not to mention the mortality rate.
Speaker 2: I mean, again, we would likely be looking at something
Speaker 2: that is causing a disproportionately high mortality rate because of
Speaker 2: the population that it's affecting, or because it was a
Speaker 2: particularly virulent strain or sero of VR or sub subsero VAR.
Speaker 2: But it still just seems to me to fit better
Speaker 2: in terms of the time course, in terms of how
Speaker 2: rapid the disease was, in terms of how it seems
Speaker 2: to have spread. But we don't know. We don't have
Speaker 2: that granular of data.
Speaker 1: You know. Erin I think I could be convinced of anything,
Speaker 1: Like I feel like I don't, I know so much more,
Speaker 1: and I'm just like, yep, I still have no idea.
Speaker 2: Yeah, I feel like I just want for it to
Speaker 2: be a viral hemorrhoagic fever, and I don't know why
Speaker 2: I can feel it being a bias for me right now.
Speaker 1: And I feel slightly similarly about typhoid. I think only
Speaker 1: because of my Google scholaring and nosebleed and the fact
Speaker 1: that it was mentioned in many papers as being a
Speaker 1: cardinal sign of early disease. I don't understand that.
Speaker 2: For times, I don't either, especially because like I definitely
Speaker 2: don't remember reading it.
Speaker 1: At all, and so it's like, again, there is so
Speaker 1: many grains of salt. This is like my salt shaker
Speaker 1: that it's shake it everywhere, right, And I do love
Speaker 1: a salty dish, so it's all always full. But we
Speaker 1: have to consider the sources yep, for these accounts, who's
Speaker 1: writing these symptoms, what emphasis are they placing on them?
Speaker 1: How accurate are these symptoms, How accurate is the translation,
Speaker 1: How accurate is everything? How much evolutionary gap there is
Speaker 1: between what pathogens exis then and what they look like today.
Speaker 1: How much is our care of these pathogens today influenced
Speaker 1: by the hospital systems by being able to give someone iv,
Speaker 1: antibiotics whatever. For these conditions that we're treating. We're going
Speaker 1: to do the best we can at putting ourselves in
Speaker 1: that time period, but we are super limited by both
Speaker 1: that time period as well as our own biases.
Speaker 2: Also the like nodules behind the ears that were full
Speaker 2: of us.
Speaker 1: Back to Google scholar, we go.
Speaker 2: I mean, that doesn't sound like a virus at all.
Speaker 2: I'm about to talk myself out of a viral hemorrhotic
Speaker 2: fever because that symptom doesn't make sense. I wonder how
Speaker 2: many people that physician examined to say that that was
Speaker 2: a symptom that was seen in all of them.
Speaker 1: That's a good question, no idea.
Speaker 2: So many of our episodes where we actually deep dive
Speaker 2: on an individual pathogen, we still have so much like
Speaker 2: sometimes the symptoms are this, or sometimes it's that. Sometimes
Speaker 2: the incubation period is two days, sometimes it's three weeks,
Speaker 2: and that's usually comes from a lack of clear data, right,
Speaker 2: And so in this case, I think it really just
Speaker 2: highlights how difficult it is to try and make these
Speaker 2: retrospective diagnoses when there's such limited data and such difficulty
Speaker 2: in interpreting that data. What it makes me feel like
Speaker 2: is it's amazing that we've been able to identify the
Speaker 2: causative agent of any outbreaks.
Speaker 1: Ever, It's true, you know, it's true. Yeah, But it
Speaker 1: also I.
Speaker 2: Think does like because we have for a lot of things,
Speaker 2: it makes these kinds of ones that much more interesting
Speaker 2: because it's like, what is it about these outbreaks that
Speaker 2: have made them so difficult to pinpoint to a particular pathogen?
Speaker 3: Hm?
Speaker 1: Well, you know, we don't know. Turns out, but I
Speaker 1: had so much fun.
Speaker 2: I just want to read. Can you tell me where
Speaker 2: I can read more?
Speaker 1: I absolutely can. There is a whole lot here. So
Speaker 1: there are several papers by Akuna Soto at All that
Speaker 1: really go into a lot of these and do some
Speaker 1: great analyzes of drought and putting forth different hypotheses. And
Speaker 1: then there is the Nature, Ecology and Evolution paper from
Speaker 1: twenty eighteen titled Salmonla and Terika Genomes from Victims of
Speaker 1: a major sixteenth century epidemic in Mexico. Really fascinating. But
Speaker 1: I want to give a special shout out to the
Speaker 1: supplemental information. It was the best supplemental information I've ever read.
Speaker 1: Do not sleep on it. I absolutely really appreciated the
Speaker 1: amount of work that people put into that. And then finally,
Speaker 1: if you want to get a little bit more background
Speaker 1: on the history of the Aztec Empire and Mesoamerica, there's
Speaker 1: a great book called Fifth Son by Kamila Townsend that
Speaker 1: I really enjoyed.
Speaker 2: I actually didn't have that many papers for this episode
Speaker 2: because I mostly just read over my notes from all
Speaker 2: of our old episodes. How fun. But I do have
Speaker 2: a few additional sources on Salmonella paratyphe. I now want
Speaker 2: to read the supplemental material for that one paper, but
Speaker 2: they did not read it. And I also have a
Speaker 2: couple of really great papers on the pathogenesis and the
Speaker 2: like molecular pathogenesis of all of the different viral hamorrhagic fevers,
Speaker 2: so if you want to read more about all of those,
Speaker 2: and then a bonus one on parvovirus just as a
Speaker 2: teaser for a future episode. But you can find the
Speaker 2: list of our sources from this episode and all of
Speaker 2: our episodes on our website This podcast will Kill You
Speaker 2: dot com under the episode stap.
Speaker 1: Thank you to Bloodmobile for providing the music for this
Speaker 1: episode and all of our episodes.
Speaker 2: Thank you so much to Tom Bryfogel for the incredible
Speaker 2: audio mixing.
Speaker 1: And thank you to you listeners. We hope that you
Speaker 1: enjoyed this and learn something new.
Speaker 2: I know that I did, so I'm holding that everyone
Speaker 2: else did and isn't just like wtf did we even
Speaker 2: talk about in this episode?
Speaker 1: Right? Write in your thoughts please please do you want
Speaker 1: more of these?
Speaker 2: Because I bet there's more?
Speaker 1: Yes I do.
Speaker 2: And especial thank you as always to our patrons. Thank
Speaker 2: you so much for your support.
Speaker 1: Yes, it really means the world to us. Well until
Speaker 1: next time, wash your hands.
Speaker 4: You filthy animals. Ou