No Rat Falls: The Founding Story of Pest Control and the Evidence For It

1. Introduction: one hundred articles later

This journal has spent ninety-nine articles asking whether the evidence supports the claim. For the hundredth we are going to ask it about the claim this trade was built on.

1.1 What this article argues

That the founding attribution of pest control is a mechanism observed in one pandemic and applied to another, that the physical evidence it should have left is absent, and that the leading alternative has a better fit and an unobserved mechanism. Sections 6, 12 and 15 are the case.

1.2 What it does not argue

That rats are innocent of plague generally. Section 19 is emphatic.

2. What is not in dispute

Establishing the common ground first, because a great deal of it is solid.

The pathogen. For decades historians debated whether the Black Death was caused by Yersinia pestis or something else, and ancient DNA studies have settled the question.¹⁰

The symptoms. Contemporaneous accounts are consistent with those of plague.¹

The scale. The disease killed an estimated one-third of the population by one account,¹ and nearly half of fourteenth-century Europe by another.⁹

2.1 Note that the sources disagree on the last one

A third against a half is a very large difference in absolute terms, and neither figure is presented with an uncertainty range.¹⁹

2.2 What is in dispute is only the vector

Which is the narrow question this article is about, and it is the question that concerns this trade.

3. The classical account

The story everybody knows, stated properly.

Fleas spread the infection through a rat population; when the rats began to die the fleas would search for other hosts.³

Stated in modern terms: most human plague cases today are bubonic, caused by spillover of infected fleas from rodent epizootics, or pneumonic, caused by inhalation of infectious droplets.¹

3.1 The mechanism depends on the rats dying

Which is the crucial structural feature. Fleas leave a host when the host dies, so the human infection is a consequence of a rat epidemic rather than of rats being present.

That distinction is ours to emphasise and everything in §§6 and 7 turns on it.

4. Where it came from

The provenance, which is the historiographic heart of this article.

The classical theory of rat transmission was based on observations of the disease in India and Hong Kong in the late 1800s.³

4.1 And the observation was overwhelming

Public health officials would find tens of thousands of dead rats during these outbreaks, but the number of human cases was relatively few.³

4.2 And note the ratio

Tens of thousands of rats against relatively few human cases, which tells you something about the mechanism's efficiency.³ Most of the dying was rodent dying, and the human outbreak was the overflow.

Which is the fact §9.1 turns into an argument about speed, and the observation is ours.

4.3 That is excellent evidence

Tens of thousands of carcasses is not an inference. It is a directly observed epizootic preceding a human outbreak, repeatedly, in multiple cities, recorded by trained observers.³

Nothing in this article suggests the third pandemic mechanism is wrong. It is among the better-established causal claims in the history of epidemiology.

5. The retrojection

And then the step that is worth examining.

The mechanism established in the 1890s was applied to a pandemic that began in the 1340s, five hundred and fifty years earlier, in a different continent, a different climate and a different urban form.

5.1 Which is a reasonable thing to have done

Same pathogen, same symptoms, and a demonstrated mechanism in hand. The inference that the earlier pandemic worked the same way is the obvious first hypothesis.

5.2 The question is what happened next

A first hypothesis is supposed to be tested. What this one appears to have received instead is six or seven decades as a settled fact, and that reading is ours.

5.3 And this journal has seen the pattern

Our article on a pesticide's history found a policy claim about an international ban that turned out to be a claim about pressure. Our article on a spider found a diagnosis applied thousands of times in places the animal does not live. A mechanism established somewhere travels more easily than the evidence for it does.

6. The missing rat falls

The central evidential problem.

While contemporaneous accounts of symptoms during the Second Pandemic are consistent with those of plague, there are no descriptions of rat epizootics, or rat falls, that often precede epidemics in the Third Pandemic.¹

6.1 A rat fall is conspicuous

Section 4.1 describes tens of thousands of dead rats being counted by officials. That is not a subtle phenomenon and it is not something a town would fail to notice.³

6.2 And the chroniclers were not inattentive

The same accounts that record no rat falls record symptoms in enough clinical detail to be judged consistent with plague six centuries later.¹

7. Why that absence counts

Because absence of evidence usually does not, and here it does.

The standard caution is that people fail to record what they do not consider notable. It applies to a great deal of historical argument and this journal has used it ourselves.

7.1 But the condition for the caution is not met

These observers were recording the same event in detail, from the same vantage, and describing the human disease carefully enough to be diagnostically useful. An epizootic producing carcasses in the streets would be within their field of attention.

7.2 And the comparison is internal to the same phenomenon

The third pandemic produced abundant rat evidence and the second produced none, for the same pathogen and, allegedly, the same mechanism. That is a difference between two records of one thing rather than a difference between recording habits.¹³

That reasoning is ours and it is the strongest form we can give the argument.

7.3 And the argument has a testable form

If rat epizootics occurred and were simply not written about, that is a claim about medieval observation habits which somebody could investigate: what else of comparable conspicuousness do these chroniclers record or omit?

We have not seen that done and it is the question we would want answered before treating the absence as decisive.

7.4 It is still not proof

Absence of a recorded epizootic is consistent with an unrecorded one, and we are describing a substantial evidential gap rather than a refutation.

8. Three further problems

The other lines of doubt, as one summary lists them.

There's a scarcity of rats in the archeological record; no masses of dead, infected rats found like there were discovered during the Third Pandemic; the climate of northern Europe could not have fostered their widespread distribution.⁶

8.1 The archaeology is independent of the chronicles

Which matters, because it is a different kind of evidence failing in the same direction. Excavated material does not depend on what anybody thought worth writing down.⁶

8.2 The climate argument is the weakest of the three

Black rats are a warm-climate commensal and northern Europe is at the edge of their range, but buildings create their own climate, which is the whole subject of our articles on indoor thermal refugia and overwintering.

We would not lean on that one, and that assessment is ours.

9. The alternative

What is proposed instead.

That the epidemics were driven by human ectoparasite vectors, such as human fleas (Pulex irritans) or body lice (Pediculus humanus humanus).²

Proponents argue that second pandemic epidemics differ from the rat-associated epidemics that occurred later, since the geographic spread and total mortality of the Black Death far exceeds that of modern plague epidemics.¹

9.1 The logic is about speed

A disease moving through a rat population first, and reaching humans only when those rats die, travels at the speed of a rodent epidemic. One moving directly between people via their own parasites travels at the speed of people.

9.2 Which is also why the mathematics can distinguish them

The patterns in how disease moves through a population are different for the rat-flea and human-parasite modes of transmission.⁵

10. The 2018 test

The study, and its design is good.

Nine outbreaks were examined: Givry, Florence, Barcelona, London, Eyam, Gdansk, Stockholm, Moscow and Malta, from 1348 to 1813, all of them known for the documentary evidence as to their weekly spreading.⁴

10.1 Three models, not two

Rat-flea transmission, human ectoparasite transmission, and pneumonic transmission by droplet.⁹

Including the third matters, because it is the other standing alternative and excluding it would have made the test a choice between two options rather than a comparison.

10.2 The construction

The rat model, based on a published metapopulation model, used 10 differential equations; the human ectoparasite model used seven.¹²

Fixed parameter values were taken from field, experimental, or epidemiological case studies when available, and unobservable parameters were estimated using Bayesian inference.²

10.3 And the span is the design's strength

Four hundred and sixty-five years, from a French village in 1348 to Malta in 1813, across nine cities of very different size and geography.⁴

A result holding across that range is harder to attribute to the peculiarities of any one place or period, and that assessment is ours.

10.4 Weekly mortality data is the input

Not a narrative account. The nine cities were chosen because their records permit a curve to be drawn, which is what the models are fitted against.⁴

11. The result

Stated by the authors in their own summary.

The results were surprisingly clear: in seven out of nine cities, the human ectoparasite model best explained the pattern of observed mortality.³

And the conclusion drawn: that plague transmission in European epidemics occurred predominantly through human ectoparasites, rather than the commensal rat or pneumonic transmission.⁴

11.1 And a reproduction number

The estimated basic reproduction number for the human ectoparasite model ranged from 1.48 to 1.91 across pre-industrial outbreaks, meaning each case generated roughly one to two additional cases.¹⁰

11.2 Which is a modest figure

And worth noting against the scale in §2. A pathogen with a reproduction number under two produced mortality of a third to a half of a continent, which says more about duration and recurrence than about explosive transmission.

12. And the concession

The detail we consider the most important in the whole study.

Although the expected ratio of urban rats to humans is about 1 rat to every 5 people, we allowed the prior in the model to have a maximum ratio of 1:1 rats to humans.¹

And the authors say why it matters: increasing the rat population in medieval cities allowed the simulated rat-borne plague outbreaks to more easily reach the mortality levels observed in humans during the Second Pandemic.¹

12.1 One rat per person is a lot of rats

It is roughly the density a modern reader imagines when they picture a medieval city, and it is five times what the literature actually expects.¹

12.2 They gave the rat model five times the rats

Knowing that doing so helped it, and said so.¹

13. Why that detail matters

Because of what it does to the strength of the result.

A test constructed to favour the hypothesis being challenged, which the challenged hypothesis then loses, is a stronger result than a test run on neutral assumptions.

13.1 It removes the obvious objection

Which would be that medieval cities were filthier and rattier than anybody can now estimate. The model was permitted to assume exactly that, up to a rat for every person, and the rat model still lost seven times out of nine.¹³

13.2 And it is disclosed rather than buried

Our article on resistance management strategy praised a modelling paper for reporting that an unfavourable result was an artefact of its own implementation. This is the same practice, applied in the other direction: a favourable result reported alongside the assumption that made it harder to obtain.

That is what a reader should look for and it is rarely there.

14. The caveat the authors state

And it is severe.

The study states that the transmission from body lice and human fleas to humans has not yet been documented, and thus the importance of human ectoparasite transmission in current and historic settings remains an open question.⁶

14.1 The winning mechanism has never been observed

Not in the medieval record, which is expected, and not in modern outbreaks either, where human fleas and body lice have been found present but their role in these outbreaks are not clear.⁶

14.2 The lead author's own framing

That such comparisons to mathematical models is not bulletproof evidence,⁷ and that there is room to improve their models with more experimental data.⁵

And on the dispute itself: in plague, there's a lot of hot debate. We have no dogs in this fight.⁷

15. Which leaves an unusual situation

The state of the question, which is the point of this article.

The rat hypothesis has a mechanism documented in detail, repeatedly, in modern outbreaks, and lacks the physical evidence it should have left in the medieval record.³¹

The human ectoparasite hypothesis fits the mortality curves better in seven cases of nine and describes a transmission route that has never been documented.³⁶

15.1 Each has what the other lacks

One is a mechanism without evidence in this setting. The other is evidence without a demonstrated mechanism anywhere.

That symmetry is ours and it is why we do not think either side of this should be stated as settled.

15.2 And it is an honest place for a question to be

Six hundred and fifty years on, with no witnesses, no specimens of the vector, and mortality curves as the principal quantitative record. That the answer is unresolved is not a failure of anybody's scholarship.

16. The flea prefers the rat

A biological detail that runs through the whole argument.

The fleas found on European black rats don't like to bite people much.⁸ And the researchers decided to focus on and distinguish human fleas due to the fact that rat fleas are known to prefer to bite rats.⁹

16.1 Which is why the researchers separated the two fleas

Not as a modelling convenience but because they are different animals with different host preferences, and lumping them would have hidden exactly the variable that matters.⁹

16.2 Which is why the rat has to die

A flea with its preferred host available does not seek an alternative. The mechanism requires the preferred host to be removed, which is §3.1 restated as behaviour.⁸

17. Which this journal has said before

Repeatedly, and this is the oldest instance.

Our article on boric acid found an industry association conceding low toxicity and arguing that lack of repellency compensates. Our article on a malaria vector found irritancy driving outdoor feeding. Our article on packaging found insects capable of chewing through film that mostly enter through seams instead. Our article on minimum risk pesticides found strongly repellent compounds that kill poorly.

17.1 The general form

What an organism can do and what it prefers to do are different facts, and outcomes depend on the second.

17.2 Here it is in the founding story

A rat flea can bite a person. Given a rat, it does not. Which makes the rat's death a necessary step in the mechanism and makes its absence from the record the thing that has to be explained.

That connection is ours.

18. The synthesis position

Which is probably where this lands.

This doesn't mean rats were irrelevant. The most likely scenario is that rats and their fleas introduced plague into human populations, and then human parasites took over as the primary driver of person-to-person spread within cities. The two mechanisms aren't mutually exclusive.¹⁰

18.1 Which the lead author's own comments support

Rats still spread a lot of plague, she says. Just probably not the Black Death.⁸

18.2 And it explains why both records look the way they do

An introduction event needs few rats and produces no conspicuous die-off. A propagating epizootic of the third pandemic kind produces tens of thousands of carcasses. If the second pandemic ran on introduction plus human spread, the absence of rat falls is what the synthesis predicts.¹⁰¹

Which is our reading and the reason we find the synthesis more persuasive than either single answer.

18.3 Introduction and propagation are different questions

And conflating them is what made the original attribution look stronger than it was. A vector that brings a pathogen into a city and a vector that moves it between households need not be the same animal.

That distinction is ours and it resolves most of the apparent conflict.

19. Modern plague is still rat plague

Emphatically, because this is the part that gets lost in the headlines.

In cases of plague since the late 1800s, including an outbreak in Madagascar in 2017, rats and other rodents helped spread the disease.⁵

And in 1994, for example, rats and their fleas spread plague through India, killing almost 700 people.⁸

19.1 Nothing here is an argument against rodent control

The rodent reservoir and the spillover mechanism are the established basis of modern plague epidemiology, and our articles on rodent-borne pathogens describe several other diseases where the case is not in question at all.

19.2 And the reservoir is the durable fact

Plague persists in wild rodent populations between outbreaks, which is why it cannot be eradicated and why the spillover mechanism remains relevant. That is not in dispute in any source we read.¹

19.3 The dispute is historical

About one pandemic, six centuries ago, and it has no bearing on why a building should exclude rodents today.

20. What the historians say

Because they have been making this argument longer than the modellers.

One medieval historian who has criticised the rat-flea theory: geneticists and modern historians were putting the rat into the position of spreading the plague and were straining bits of evidence.⁵

20.1 Straining bits of evidence

Which is a specific accusation: not that the evidence is absent but that what exists was worked harder than it would bear.⁵

20.2 And the alternative is not new

Some scholars have long toyed with the idea that fleas on humans spread the Black Death.⁵

The 2018 paper is a quantitative test of a position that existed before it, rather than a novel proposal.

21. And what the attribution cost

A point one source raises that we would not have thought of.

The historical attribution of plague's spread to rats was neither an incidental nor trivial occurrence; instead, it had important and serious sociopolitical consequences that should not be overlooked.⁹

21.1 We are not going to expand on that

The source does not develop it in the material available to us, and speculating about which consequences are meant would be us writing history we have not read.

21.2 But the structural point is recognisable

An explanation locating a catastrophe in an animal and in the conditions of poor housing does political work, and our articles on the social distribution of infestation describe the modern version of that.

22. What this means for the trade

Directly.

Pest control's public legitimacy rests substantially on one story: that controlling rats prevents catastrophic disease, demonstrated by the worst mortality event in European history.

22.1 That story is weaker than advertised

Not wrong, and not established. Sections 15 and 18 are where it sits.

22.2 It is also the wrong kind of argument

A claim about a catastrophe six hundred years ago cannot be checked by the person hearing it, and our credence goods article argued that unverifiable claims are exactly what this market already has too many of.

22.3 And the trade does not need it

Which is the useful conclusion. Modern rodent control is justified by modern evidence: the pathogens our rodent-borne disease articles describe, the structural damage, the contamination of food, and the allergen burden our threshold article quantified.

None of that depends on what happened in 1348. A trade that rests its case on a contested medieval attribution is choosing a weaker argument than the one available to it.

22.4 That is our position and it costs us a good story

The plague story is the most compelling thing anybody in this business can say, and we are saying it should be retired in favour of duller and better evidence.

23. The honest version of the story

What we would say if asked.

Plague is a rodent disease. That is settled, modern, and established.¹

Rats and their fleas cause plague outbreaks today. Documented repeatedly, including in the last decade.⁵

Whether they caused the Black Death is disputed. The evidence they should have left is missing, and the leading alternative is a mechanism nobody has observed.¹⁶

And the best current guess is both. Rats brought it; human parasites spread it.¹⁰

23.1 That is a more interesting story than the one it replaces

And it has the advantage of being what the evidence supports.

24. Our own position

The disclosure.

We sell rodent control. The plague story is a selling point and §22.3 says we are giving it up.

24.1 Why

Because this journal's entire premise is that a claim should be stated at the strength its evidence supports, and the first place to apply that is to the claims that favour us.

Ninety-nine articles of holding other people's evidence to a standard would be worth very little if the hundredth exempted our own founding myth.

25. The Manitoba position

Brief, because plague is not a local concern.

Sylvatic plague exists in rodent populations in parts of western North America and is not a meaningful risk in this province. Nothing in this article changes what a Winnipeg building should do about rodents, which our exclusion and rodenticide articles cover on entirely different grounds.

25.1 What we could not find

Any Canadian scholarship on this dispute, and any assessment of how the plague narrative functions in pest control marketing here, which would be an interesting piece of work for somebody with the right training.

26. One hundred articles

A short note, since this is the hundredth.

The recurring findings have been these. That the measurement usually does not exist. That a mechanism which is possible is routinely treated as an explanation that applies. That what an organism can do and what it does are different questions. That the half-measure is frequently worse than the omission. That the contamination outlives the organism. And that where confirmation is impossible, a well-built exclusion is the correct instrument rather than a consolation prize.

26.1 And one finding we did not expect

How often the researchers themselves say the careful thing. The paper disclosing that its own result was an implementation artefact, the packaging study reporting a standard deviation larger than its mean, the instrument reporting that no measurement was possible, and here a team explaining the assumption that made their own conclusion harder to reach.

The failures this journal documents are nearly always failures of transmission rather than of research. The caveats are in the papers. They do not survive the journey to the label, the syllabus or the sales conversation.

26.2 Every one of them appears in this article

Which we did not plan and which is not a coincidence. The subject was always going to be the same subject, because the problem is not entomology. It is what a person is entitled to assert on the evidence they have.

26.3 And the Manitoba gap has appeared in every one

One hundred articles, and we have not yet found a subject in this field where the local data exists.

27. Limitations and open questions

The primary paper was read as abstract and extracts. The model specifications, parameter tables and full results reach us through the published abstract, the article's opening sections and secondary accounts.¹²

Much of the detail is journalistic. Five of our ten sources are news or popular-science coverage, cited for quotations and summaries rather than findings.⁵⁶⁷⁸

We have not read the opposing literature. The rat hypothesis has active defenders and we located none of their responses to the 2018 paper, which means this article presents one side's case and its own authors' caveats rather than a debate.

That is a real gap and we flag it as the most serious one. An article arguing for evidential care should not rest on one side's evidence, and this one does.

The mortality figures conflict. Section 2.1.¹⁹

And the sociopolitical claim is unexamined. Section 21.1.⁹

Sections 1.1, 3.1, 5.2, 5.3, 7, 8.1, 8.2, 9.1, 10.1, 11.2, 13, 15.1, 15.2, 16.1, 17, 18.2, 22, 23, 24 and 26 are our reasoning. The framing of the retrojection, the argument for why the missing rat falls count as evidence, the reading of the rat-density concession, the symmetry between the two hypotheses, the introduction-against-propagation distinction and the position on what the trade should claim are ours rather than sourced positions.

28. Conclusion

The mechanism everybody knows was established by watching plague in India and Hong Kong in the 1890s, where public health officials counted tens of thousands of dead rats against relatively few human cases, and where the fleas left the carcasses and found people.³ It is among the better-established causal claims in epidemiology and it describes a pandemic that began five hundred and fifty years after the one it is usually used to explain. For the earlier pandemic, the chroniclers who described the symptoms in enough clinical detail to be diagnostically useful six centuries later described no rat falls.¹

When somebody finally tested it, fitting rat-flea, human-ectoparasite and pneumonic models to weekly mortality from nine outbreaks between 1348 and 1813, the human ectoparasite model explained seven of the nine best. And the rat model had been given a maximum of one rat per person against an expected urban ratio of one per five, a concession the authors disclosed and explained would make it easier for the rat-borne simulations to reach the observed mortality.³¹ It lost anyway. The same paper states that transmission from body lice and human fleas to humans has not yet been documented,⁶ so the winning model describes a route nobody has ever observed, which leaves one hypothesis with a mechanism and no evidence and the other with evidence and no mechanism.

Underneath it is a fact this journal has now met in five literatures: a rat flea can bite a person, and given a rat it does not, which is why the rats have to die first and why their absence from the record is the thing requiring an explanation.⁸ The likely answer is that both are true, rats bringing the pathogen into cities and human parasites carrying it between households.¹⁰ For our trade the consequence is that the best story we have is contested, and that we do not need it: rodent control is justified by pathogens documented this century, by structural damage, by food contamination and by measured allergen burden, none of which depends on 1348. Ninety-nine articles spent holding other people's claims to a standard would be worth nothing if the hundredth exempted our own.

References

1. Human ectoparasites and the spread of plague in Europe during the Second Pandemic. Journal article in a national academy proceedings, publisher page, read as abstract and opening sections. Used for the statement that today most human plague cases are bubonic, caused by spillover of infected fleas from rodent epizootics, or pneumonic, caused by inhalation of infectious droplets; for the note that little is known about plague transmission in Europe, the Middle East and North Africa during the Second Pandemic including the Black Death, when the disease killed an estimated one-third of the population; for the account that many studies have suggested human ectoparasites such as human fleas and body lice were more likely than commensal rats to have caused the rapidly spreading epidemics, and that proponents argue second pandemic epidemics differ from the rat-associated epidemics of the third pandemic since the geographic spread and total mortality of the Black Death far exceed those of modern plague epidemics; for the statement that while contemporaneous accounts of symptoms during the Second Pandemic are consistent with those of plague, there are no descriptions of rat epizootics, or rat falls, that often precede epidemics in the Third Pandemic; for the description of the rat model as based on a published metapopulation model for bubonic plague with transmission in a rodent epizootic and spillover to humans modelled by ten differential equations, assuming an initially entirely susceptible black rat population; and for the disclosure that although the expected ratio of urban rats to humans is about one rat to every five people, the prior in the model was allowed a maximum ratio of one to one, with the authors noting that increasing the rat population in medieval cities allowed the simulated rat-borne outbreaks to more easily reach the mortality levels observed in humans. https://www.pnas.org/doi/10.1073/pnas.1715640115
2. Portable document version of the above paper. Used for the significance statement that while it is commonly assumed that rats and their fleas spread plague during the Second Pandemic, there is little historical and archaeological support for such a claim; for the abstract's account that several studies have suggested human ectoparasite vectors, namely a named human flea and named body louse, caused the rapidly spreading epidemics, and that the authors describe a compartmental model for plague transmission by a human ectoparasite vector fitted by Bayesian inference to mortality curves from nine outbreaks in Europe; for the note that the human ectoparasite model is constructed from seven differential equations; and for the methodological statement that fixed parameter values were taken from field, experimental or epidemiological case studies when available while unobservable parameters were estimated using Bayesian inference, with the nine outbreaks identified by present-day location, date and pre-plague population size alongside recorded plague deaths. https://www.pnas.org/doi/pdf/10.1073/pnas.1715640115
3. Plague and human ectoparasites: a new model for an old disease. Authors' own account of the above study, published on a scientific publisher's community platform. Used for the statement that the classical theory of rat transmission was based on observations of the disease in India and Hong Kong in the late 1800s, during which plague spread by fleas through the rat population and the fleas searched for other hosts when the rats began to die; for the account that public health officials would find tens of thousands of dead rats during those outbreaks while the number of human cases was relatively few; for the note that in recent years an increasing number of studies have argued plague in Europe must have spread without rats, either by airborne pneumonic transmission or by human ectoparasites; and for the reported result that the final models were fitted in a Bayesian framework to historical human mortality records from nine outbreaks and that in seven out of nine cities the human ectoparasite model best explained the pattern of observed mortality. https://natureecoevocommunity.nature.com/posts/29629-human-ectoparasites-and-the-spread-of-plague
4. New research into the Black Death, medieval history news site. Secondary account, cited as attributed material. Used for the identification of the nine specific European outbreaks studied, namely Givry, Florence, Barcelona, London, Eyam, Gdansk, Stockholm, Moscow and Malta, spanning 1348 to 1813, all selected for documentary evidence as to their weekly spreading; for the description of the study as a theoretical analysis comparing what the result would have been if rats, droplets, or fleas and lice were the main vectors; for the finding that the model captures the dynamics of human ectoparasite transmission best in seven of the nine cases; for the quoted conclusion that the results suggest plague transmission in European epidemics occurred predominantly through human ectoparasites rather than the commensal rat or pneumonic transmission; and for the full author list and publication details of the underlying paper. https://www.medieval.eu/new-research-into-the-black-death/
5. Maybe rats aren't to blame for the Black Death, magazine science news article. Journalistic source, cited for quotations and summaries rather than findings. Used for the quoted criticism from a named university medieval historian that geneticists and modern historians were putting the rat into the position of spreading the plague and were straining bits of evidence; for the note that some scholars have long toyed with the idea that fleas on humans spread the Black Death, and that fleas and lice picking up plague by biting an infected human could hop onto another person in close quarters; for the statement that the patterns in how disease moves through a population are mathematically different for the rat-flea and human-parasite modes of transmission; for the description of the modelling approach as simulating the rise and fall of an outbreak based on how rats, fleas and body lice would behave; for the note that the authors acknowledge room to improve their models with more experimental data and anticipate controversy among plague scholars; and for the statement that in cases of plague since the late 1800s, including an outbreak in Madagascar in 2017, rats and other rodents helped spread the disease, with the bacterium passing to fleas that feed on infected rodents and the parasites abandoning the corpse when a plague-stricken rat dies. https://www.nationalgeographic.com/science/article/rats-plague-black-death-humans-lice-health-science
6. New study finds fleas from humans, not rats, spread the Black Death, online magazine science article. Journalistic source, cited for quotations from the study. Used for the quoted statement from the study authors that it has been difficult to assess how human ectoparasites contributed to historical plagues because while they have been found present during modern plague outbreaks their role in those outbreaks is not clear; for the quoted statement that transmission from body lice and human fleas to humans has not yet been documented, and thus the importance of human ectoparasite transmission in current and historic settings remains an open question; and for the summary of evidence casting doubt on the rat account, namely a scarcity of rats in the archaeological record, no masses of dead infected rats of the kind discovered during the Third Pandemic, and a northern European climate that could not have fostered their widespread distribution. https://www.inverse.com/article/40245-black-plague-human-flea-lice-rats
7. Are rats innocent of spreading the Black Plague? Museum magazine news article. Journalistic source, cited for quotations. Used for the report that for seven of the nine outbreaks studied the observed deaths most closely matched the model of disease spread by human parasites rather than rat-flea interactions; for the lead author's acknowledgement that comparison to mathematical models is not bulletproof evidence; and for her quoted remarks that in plague there is a lot of hot debate and that the authors have no dogs in the fight. https://www.smithsonianmag.com/smart-news/are-rats-innocent-spreading-black-plague-180967855/
8. Don't blame the rats for spreading the Black Death, science news publication for younger readers. Journalistic source, cited for quotations. Used for the statement that the fleas found on European black rats do not like to bite people much; for the report that in 1994 rats and their fleas spread plague through India, killing almost 700 people; for the lead author's quoted position that rats still spread a lot of plague, just probably not the Black Death; and for the quoted comment from a named university biologist that scientists have suspected rat fleas might not have played a big role and that it is useful to see a model showing how the alternative could happen. https://www.snexplores.org/article/dont-blame-rats-spreading-black-death
9. You've been lied to about rats and the Black Death, university science communication office article. Secondary source, cited as attributed material. Used for the statements that plague has killed over 200 million people throughout the past two millennia and that the Black Death is estimated to have resulted in the death of nearly half of Europe's fourteenth-century population; for the description of the pathogen as a named gram-negative bacterium with three disease forms; for the account that the 2018 study used mathematical models to compare three possible routes of human plague transmission, namely infected rat fleas biting people, infected human fleas biting people, and people directly infecting others; for the note that the researchers focused on and distinguished human fleas because rat fleas are known to prefer to bite rats; and for the position that the historical attribution of plague's spread to rats was neither incidental nor trivial but had important and serious sociopolitical consequences that should not be overlooked. https://www.mcgill.ca/oss/article/medical-critical-thinking-history/youve-been-lied-about-rats-and-black-death
10. How did rats spread the Black Death, or did they? Popular science site article. Secondary source, cited as attributed material. Used for the note that there is surprisingly little archaeological evidence for massive rat die-offs preceding many medieval plague outbreaks, something that would be expected if the rat-flea cycle drove every epidemic; for the reported estimated basic reproduction number for the human ectoparasite model ranging from 1.48 to 1.91 across pre-industrial outbreaks, meaning each case generated roughly one to two additional cases; for the position that this does not mean rats were irrelevant and that the most likely scenario is that rats and their fleas introduced plague into human populations after which human parasites took over as the primary driver of person-to-person spread within cities, the two mechanisms not being mutually exclusive; for the statement that ancient DNA studies have settled the decades-long debate over whether the Black Death was caused by the named bacterium or some other pathogen; and for the note that pneumonic plague can spread directly between people through respiratory droplets and likely accelerated transmission in crowded medieval households though it was probably not the dominant mode of spread across the continent. https://scienceinsights.org/how-did-rats-spread-the-black-death-or-did-they/