Rosa Rubicondior: Malevolent Design - Creationists Plagued By Ancient Parasites

Two of the occupants of this grave were full siblings: a brother (aged 7-9 years old) and a sister (aged 9-11 years old) from whom plague DNA was identified. Not enough of the remains of the third individual were preserved to be able to be able to analyse them as well.

Photo: Vladimiri Bazaliiskii.

Oldest strains of plague caused deadly outbreaks 5,500 years ago – University of Copenhagen

For creationists who insist that biological complexity requires an intelligent designer, plague presents an awkward question: what, exactly, was the designer trying to achieve? A parasitic bacterium capable of causing fatal disease in children is certainly biologically impressive. Whether it is evidence of benevolent intelligence is another matter entirely, but it appears to conform to creationists 'proof' of intelligent design - irreducible complexity and complex specified genetic information, both of which ID proponents insist can only be created by an intelligent designer.

Research published in Nature reveals that early strains of Yersinia pestis, the plague bacterium, were already causing deadly outbreaks among hunter-gatherers around Lake Baikal in Siberia approximately 5,500 years ago. These were small, mobile communities: crowded agricultural settlements were evidently not a prerequisite for devastating plague outbreaks.

Researchers detected plague DNA in 18 of 46 individuals examined from four cemeteries. Combined with radiocarbon dating, burial evidence and reconstructed family relationships, the findings point to outbreaks that killed members of the same families, with a particularly striking impact on children. That detection rate is a proportion of the sampled dead, of course, not a measurement of the mortality rate in the living population.

The evolutionary details are especially revealing. These early strains lacked some of the adaptations associated with efficient flea-borne transmission in later plague. Nevertheless, they could cause lethal disease. They also possessed a gene locus encoding a superantigen — a substance capable of provoking excessive immune activation — which is absent from later plague strains. Its contribution to their lethality remains a hypothesis, but the changing genetic repertoire exposes a pathogen with an evolutionary history, rather than an organism equipped from the outset with one fixed set of features.

For intelligent design advocates, this creates a familiar difficulty. If useful biological machinery demonstrates a designer’s foresight, why should machinery that helps pathogens exploit their hosts be exempt from the same argument? Invoking a “Fall” supplies a theological explanation, but it does not establish a biological mechanism or account for the particular genetic changes revealed by ancient DNA.

Evolution requires no intention to harm, any more than it requires an intention to protect. It describes organisms whose inherited traits affect their survival and reproduction, with consequences that can be catastrophic for other species. These ancient graves make those consequences painfully concrete. They also show science doing what creationist dogma cannot: recovering evidence, testing competing explanations and revising its understanding when the evidence demands it.

How plague evolved^ a changing toolkit for infection. Yersinia pestis, the bacterium responsible for plague, has an evolutionary history written into its genome. Comparisons with its closest relative, Yersinia pseudotuberculosis, and with ancient plague DNA reveal changes in how it infected hosts and spread between them.

From an intestinal pathogen to plague

Y. pestis arose from an ancestral lineage of Y. pseudotuberculosis, a bacterium associated with gastrointestinal disease. This does not mean that today’s strains of the latter suddenly transformed into plague bacteria. Rather, one ancestral branch accumulated changes that established a different way of life.

Those changes involved both acquiring genetic material and losing or modifying existing functions. Bacteria can obtain DNA through horizontal gene transfer, including the acquisition of plasmids: DNA molecules separate from their main chromosome. Mutations can also change when genes operate or disable them altogether. Research has identified contributions from these processes to the emergence of flea-borne plague. [Research on plague’s genetic adaptations]

Why losing a function can be an advantage

Evolution does not necessarily mean becoming more complex. A function useful in one environment can become unnecessary, costly or obstructive in another.

In plague bacteria, the inactivation of particular regulatory genes helped increase biofilm formation inside fleas. A biofilm is a community of bacteria embedded in a protective matrix. In some infected fleas, this growth obstructs part of the digestive tract, interfering with feeding and promoting transmission during subsequent feeding attempts. Losing existing gene functions therefore contributed to a new ecological capability. [Experimental evidence]

Deadly before the later flea adaptations

The ancient Lake Baikal strains lacked some adaptations associated with efficient flea-borne transmission in later plague. One important gene, ymt, helps bacteria survive in the flea’s digestive tract. Nevertheless, the ancient DNA and burial evidence indicate that early strains could already cause lethal outbreaks.

The precise transmission routes remain uncertain. Contact with infected animals is a possibility, and the pattern of infections among relatives is consistent with spread between people. Absence of the later adaptations does not, by itself, prove that fleas played no role whatsoever. [Lake Baikal study]

When immune activation becomes dangerous

The early strains also carried a gene locus encoding a superantigen, absent from later plague strains. Superantigens can provoke excessive immune activation: instead of producing a controlled defensive response, the immune system can contribute to severe inflammation and tissue damage.

This provides a possible explanation for some of the ancient strains’ severity. However, finding the relevant DNA is not equivalent to demonstrating how much toxin an ancient infection produced, or establishing its contribution to an individual’s death. Its role in these outbreaks remains a hypothesis. [Study findings and interpretation]

Evolution has no target level of cruelty

Natural selection does not aim to make pathogens as deadly as possible. It favours heritable traits that improve reproductive success under particular conditions. Damage to a host may accompany successful infection, but killing the host can also restrict opportunities for transmission. The outcome depends on the pathogen’s biology and ecology.

The resulting history involves changing combinations of inherited, acquired and discarded functions, without foresight. Calling these features “designed” adds an intention that the biological evidence does not require — and leaves the advocate of benevolent design to explain the suffering they cause.

Glossary

Biofilm

A community of microorganisms embedded in a matrix they produce, often attached to a surface.

Gene regulation

Control over when, where and how strongly a gene is expressed.

Genome

The complete genetic material of an organism.

Horizontal gene transfer

Movement of genetic material between organisms other than through inheritance from parent to offspring.

Host

An organism in or on which another organism lives; here, an animal infected by a pathogen.

Locus

A particular position or region in a genome; plural: loci.

Mutation

A change in a DNA sequence. Its effects depend on the change and the circumstances.

Pathogen

An organism or infectious agent capable of causing disease.

Plasmid

A DNA molecule that replicates separately from the main chromosome. Some plasmids can move between bacteria.

Strain

A genetically distinguishable variant or lineage within a microbial species.

Superantigen

A substance that can trigger unusually widespread activation of immune cells, potentially causing harmful inflammation.

Virulence

The degree of harm a pathogen causes in a host; distinct from how readily it spreads.

Zoonosis

An infection naturally transmissible from non-human vertebrate animals to humans.

The paper in Nature was accompanied by a news item from Copenhagen University:

Oldest strains of plague caused deadly outbreaks 5,500 years ago
ANCIENT DNA A new study published in Nature reconstructs the earliest known plague genomes and for the first time shows that early forms of plague caused deadly outbreaks – long before the Black Death killed up to half the population of Europe.

"Whether the earliest forms of plague were mild or virulent has been a matter of debate, but our findings demonstrate that these ancient strains were already highly lethal."
Professor Eske Willerslev, co-senior author.

Photo: Vladimiri Bazaliiskii

Plague is commonly associated with rats, crowded medieval cities, and the epidemics that swept across Europe during and after the Middle Ages.

But a new study published in Nature shows that the disease was already lethal 5,500 years ago, where it killed humans in small, mobile hunter-gatherer communities – long before the rise of agriculture and cities created the conditions usually associated with plague epidemics.

An international group of researchers analysed ancient DNA from human remains found at four hunter-gatherer cemeteries in the Lake Baikal region of East Siberia. Using advanced DNA sequencing techniques, the researchers reconstructed ancient bacterial genomes preserved in teeth, revealing previously unknown early strains of plague.

Whether the earliest forms of plague were mild or virulent has been a matter of debate, but our findings demonstrate that these ancient strains were already highly lethal.

Professor Eske Willerslev, co-senior author.
Lundbeck Foundation Geogenetics Centre
Globe Institute
University of Copenhagen
Copenhagen, Denmark.

Mandibles from two individuals excavated at the burial ground in East Siberia. The mandible on the left is from an 18-24 year old man, found to have been infected with plague, based on DNA extracted from one of his teeth.

Photo: Angela Lieverse.

The study combines genetic, archaeological and radiocarbon evidence to reconstruct how the outbreaks unfolded within the prehistoric groups.

Based on the plague DNA, the genetic relationships between the victims, the archaeological analysis and the radiocarbon dating, we’ve built a really clear, complete picture of what happened during these outbreaks.

Dr Ruairidh Macleod, first author.
Lundbeck Foundation Geogenetics Centre
Globe Institute
University of Copenhagen
Copenhagen, Denmark.

In total, DNA from Yersinia pestis – the bacterium that causes plague – was detected in 18 of 46 individuals – nearly 40 percent. This is higher than the detection rate reported from some medieval plague pits.

More lethal than previously thought

Previous studies showed that early strains of Yersinia pestis lacked some of the genetic traits that later enabled bubonic plague to spread efficiently via fleas and rodent hosts. This led many researchers to believe that the earliest forms of plague were unlikely to have caused major outbreaks.

However, the new study challenges that assumption.

Whether the earliest forms of plague were mild or virulent has been a matter of debate, but our findings demonstrate that these ancient strains were already highly lethal.

Professor Eske Willerslev.

The mortality profiles at the two largest cemeteries show an exceptionally high number of children and young teenagers among the dead – something that had puzzled archaeologists working on the graves for decades.

The unusually high number of children and the short timespan was a real puzzle that we’ve been trying to solve since the 1990s. Finding out that plague was the cause is extraordinary, but it makes so much sense.

Andrzej Weber, co-corresponding author
Institute of Ethnology and Anthropology
Russian Academy of Sciences
Moscow, Russia.

Radiocarbon dating showed that many of the burials occurred within a very short time span. In several cases, siblings or parents and children appear to have died and been buried together.

Did superantigen cause lethality?

The ancient plague strains also carried a unique superantigen – a toxin-producing genetic factor not seen in historic plague strains. Superantigens can trigger extreme immune responses and are associated with severe inflammatory complications, likely increasing the severity of infection.

This finding changes our understanding of the earliest plague outbreaks: Even before the bacterium evolved efficient flea-borne transmission, these ancient strains appear to have carried a potent combination of virulence factors that could make infection highly lethal.

Associate Professor Martin Sikora, co-senior author.
Lundbeck Foundation Geogenetics Centre
Globe Institute
University of Copenhagen
Copenhagen, Denmark.

Two of the occupants of this grave were full siblings: a brother (aged 7-9 years old) and a sister (aged 9-11 years old) from whom plague DNA was identified. Not enough of the remains of the third individual were preserved to be able to be able to analyse them as well.

Photo: Vladimiri Bazaliiskii.

Together, the findings suggest that the earliest known plague outbreaks may already have been as deadly as later historical forms of the disease, especially for children, even without flea-borne transmission.

The study also supports the idea that plague may have originated in Central or North-East Asia before later spreading across Eurasia through wild rodent reservoirs. Archaeological evidence suggests these hunter-gatherers interacted closely with marmots – large burrowing rodents that still carry plague today – and researchers believe the outbreaks may have spread directly from infected marmots into humans.

Publication:
Macleod, R., Seersholm, F.V., De Sanctis, B. et al.
Lethal plague outbreaks in Lake Baikal hunter-gatherers 5,500 years ago. Nature 654, 697–705 (2026). https://doi.org/10.1038/s41586-026-10540-5

Abstract
Plague is among the most devastating diseases in human history¹. However, early strains of the plague-causing bacterium Yersinia pestis lacked virulence factors that are required for the bubonic form until around 3,800 years ago^2,3. Consequently, the morbidity and mortality of early plague strains remain unclear. Here we describe early plague strains that are associated with two phases of outbreaks among mid-Holocene hunter-gatherers near Lake Baikal in southeast Siberia, beginning from about 5,500 years ago. These outbreaks occur across four hunter-gatherer cemeteries, with a 39% detection rate for plague infection. By reconstructing kinship pedigrees, we show that small familial groups were affected, consistent with human-to-human spread of disease, and that the first outbreak occurred within a single generation. The infections appear to have resulted in acute mortality, especially among children (aged 8 to 11 years). We further note functional differences, including in the ypm superantigen locus, which is also present in present day Yersinia pseudotuberculosis. The new strains diverge ancestrally to known Y. pestis and constrain the timing of its emergence, indicating that this happened before approximately 5,700 years ago. These findings show that plague outbreaks happened earlier than previously thought and were indeed lethal. We contend that the occurrence of outbreaks among mid-Holocene hunter-gatherer communities well outside the sphere of Late Neolithic Europe challenges the notion that higher population densities and lifestyle changes during the Neolithic agricultural transition were prerequisites for plague epidemics.

Macleod, R., Seersholm, F.V., De Sanctis, B. et al.
Lethal plague outbreaks in Lake Baikal hunter-gatherers 5,500 years ago. Nature 654, 697–705 (2026). https://doi.org/10.1038/s41586-026-10540-5

Copyright: © 2026 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

What emerges from these ancient graves is a recognisable evolutionary history: a pathogen whose capabilities changed as genes were acquired, modified or lost. The early Lake Baikal strains did not need the complete repertoire of later flea-borne plague to cause lethal outbreaks. Evolution was not working towards the Black Death, or towards any other predetermined destination. Different combinations of traits enabled bacteria to survive and spread under different circumstances, with devastating consequences for their human hosts.

For advocates of intelligent design, the difficulty is not simply that this biological machinery exists, but that their own argument assigns responsibility for it. If complexity and functionality are evidence of deliberate design, then features that enable infection cannot be excluded merely because their effects are unpleasant. A designer credited with the immune system must also answer for bacterial products capable of turning immune activation into a source of harm. The proposed contribution of the ancient superantigen remains uncertain, but the broader problem requires no such uncertainty to be resolved: these infections were already killing people, including children, thousands of years ago.

Calling this the consequence of a “Fall” does not explain the bacterial family tree, the changing genetic repertoire or the particular adaptations involved. It adds an untestable theological story which adds nothing, where biological explanations can be tested against evidence. Nor does assigning every beneficial feature to design and every harmful one to corruption provide a consistent method for recognising either.

Science, meanwhile, can recover DNA from ancient teeth, reconstruct relationships between the dead and investigate how their pathogens evolved. Its explanations remain open to correction, including revisions to assumptions about how dangerous early plague could have been. These discoveries reveal neither foresight nor a concern for human welfare, but the consequences of evolution in which bacterial success and human well-being need not coincide.

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