Rosa Rubicondior: Malevolent Designer News - How A Bacterium Is 'Intelligently Designed' To Spread Disease

Bacteria hijack tick cell defenses to spread disease | WSU Insider

Here we have yet another example demonstrating that, if we apply Discovery Institute fellow William A. Dembski's criteria for proving intelligent design — namely the presence of complex specified genetic information — then we must conclude that creationism's supposed intelligent designer is, in fact, a malevolent force devising ever more sophisticated ways to inflict suffering on the world.

Once again, honest creationists are left with a stark dilemma: either complex specified information is indeed evidence of design, in which case the designer is malevolent, or it is not, in which case a central tenet of Intelligent Design creationism collapses. The dishonest ones, of course, will simply dismiss the evidence, likely misrepresent the science, and continue to bear false witness against scientists. In neither case should we expect creationists to admit that the theory of evolution fully accounts for the appearance of "malevolent" design, arising naturally without conscious intent or divine interference.

It’s a curious paradox that people who claim to worship the God of the Bible as an omnibenevolent, anthropophilic being are so often willing to see that deity cast in the role of a malevolent agent—so long as they can reject the theory of evolution. This strongly suggests that their opposition to evolution is not primarily theological, but political.

The latest example comes from the tick-borne pathogen Anaplasma, which causes anaplasmosis and contributes to Lyme disease. This bacterium hijacks the cellular machinery of ticks to ensure its own survival and transmission to new hosts, including humans. Although Dembski has famously avoided providing a rigorous, testable definition of "complex specified genetic information," any such definition would surely encompass genetic adaptations that promote survival and reproduction.

This discovery was made by researchers at the College of Veterinary Medicine, Washington State University (WSU). Their findings have just been published in Proceedings of the National Academy of Sciences (PNAS) and are explained in lay terms in WSU Insider, the university's online news outlet.

What information do you have on Anaplasma and the tick that transmits it? Anaplasma is a genus of bacteria that includes several species capable of causing disease in humans and animals. The most medically relevant species is Anaplasma phagocytophilum, which causes anaplasmosis—a tick-borne disease that affects both humans and various mammals.

Overview of Anaplasma

Anaplasma are obligate intracellular bacteria in the family Anaplasmataceae.
They primarily infect white blood cells (especially neutrophils in the case of A. phagocytophilum).
Disease is often seasonal, peaking during the months of high tick activity (late spring to early autumn in temperate zones).

Disease in Humans

Caused mainly by Anaplasma phagocytophilum.
Known as Human Granulocytic Anaplasmosis (HGA).
Symptoms include:

Fever, chills, headache
Muscle aches
Malaise
Occasionally gastrointestinal symptoms (nausea, vomiting)
In severe cases: respiratory failure, organ failure, neurological symptoms

Incubation period: ~5–14 days after a tick bite.
Treatment: Responds well to doxycycline, especially if started early.
If untreated, it can lead to complications, especially in the elderly or immunocompromised.

Tick Vectors

The primary vector in the United States is the blacklegged tick (Ixodes scapularis), also called the deer tick.
In Europe, the main vector is the castor bean tick (Ixodes ricinus).
These are the same ticks that transmit Lyme disease (Borrelia burgdorferi) and Babesia (babesiosis), leading to frequent co-infections.

Hosts and Reservoirs

Main animal reservoirs include:

White-tailed deer
Rodents
Small mammals

Ticks acquire the bacteria when feeding on an infected host and then transmit it during subsequent feedings.

Biological Strategy of the Pathogen

Recent research (such as the 2025 WSU referenced) shows that Anaplasmacan:

Hijack the tick's cellular defence mechanisms, particularly its oxidative stress response, allowing the bacteria to survive within the tick's gut.
Manipulate the cell death pathways of tick cells, suppressing apoptosis (programmed cell death) to extend the viability of the cells it infects.
Modify gene expression in the tick to enhance its own survival and transmission potential.

These mechanisms qualify as highly sophisticated biological strategies—precisely the sort of adaptations that Intelligent Design proponents would struggle to explain without appealing to either special pleading or malevolent intent.

Ecological and Public Health Impact

Geographic spread is increasing, partly due to climate change, which expands the habitat range of ticks.
Public health monitoring is challenged by co-infections and misdiagnosis (HGA is often confused with Lyme disease or viral infections).
Preventative strategies include tick checks, repellents, and public awareness campaigns.

Bacteria hijack tick cell defenses to spread disease
Washington State University researchers have discovered how the bacteria that cause anaplasmosis and Lyme disease hijack cellular processes in ticks to ensure their survival and spread to new hosts, including humans.
Based in the College of Veterinary Medicine, the team found that the bacteria can manipulate a protein known as ATF6, which helps cells detect and respond to infection, to support its own growth and survival inside the tick. The findings, published in the journal Proceedings of the National Academy of Sciences, could serve as a launching point for developing methods to eliminate the bacteria in ticks before they are transmitted to humans and other animals.

Most research has looked at how these bacteria interact with humans and animals and not how they survive and spread in ticks. What we have found could open the door to targeting these pathogens in ticks, before they are ever a threat to people.

Kaylee A. Vosbigian, lead author
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.

Vosbigian and her advisor, Dana Shaw, the corresponding author of the study and an associate professor in the Department of Veterinary Microbiology and Pathology, focused their research on Ixodes scapularis, also known as the black-legged tick, which is responsible for spreading both Anaplasma phagocytophilum and Borrelia burgdorferi, the causative agents of anaplasmosis and Lyme disease. Both diseases are becoming increasingly common and can cause serious illness in humans and animals.

The team discovered that when ATF6 is activated in tick cells, it triggers the production of stomatin, a protein that helps move cholesterol through cells as part of a normal cellular processes. The bacteria exploit this process against their tick hosts, using the cholesterol — which they need to grow and build their own cell membranes but cannot produce themselves — to support their own survival and success.

Stomatin plays a variety of roles in the cell, but one of its key functions is helping shuttle cholesterol to different areas. The bacteria take advantage of this, essentially stealing the cholesterol they need to survive.

Kaylee A. Vosbigian

When the researchers blocked the production of stomatin, restricting the availability of cholesterol, bacterial growth is significantly reduced. The researchers believe this shows targeting the ATF6-stomatin pathway could lead to new methods for interrupting the disease cycle in ticks before transmission occurs.

As part of the study, Vosbigian also developed a new research tool called ArthroQuest, a free, web-based platform hosted by WSU that allows scientists to search the genomes of ticks, mosquitoes, lice, sand flies, mites, fleas and other arthropod vectors for transcription factor binding sites — genetic switches like ATF6 that control gene activity.

There aren’t many tools out there for studying gene regulation in arthropods. Most are built for humans or model species like fruit flies, which are genetically very different from ticks.

Kaylee A. Vosbigian

Using ArthroQuest, the team found that ATF6-regulated control of stomatin appears to be prevalent in blood-feeding arthropods. Since the hijacking of cholesterol and other lipids is common among arthropod-borne pathogens, the researchers suspect many may also exploit ATF6.

We know many other vector-borne pathogens, like Borrelia burgdorferi and the malaria-causing parasite Plasmodium, rely on cholesterol and other lipids from their hosts. So, the fact that this ATF6-stomatin pathway exists in other arthropods could be relevant to a wide range of disease systems.

Assistant Professor Dana K. Shaw, corresponding author.
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.

Publication:
K.A. Vosbigian,S.J. Wright,B.P. Steiert,K.L. Rosche,E.A. Fisk,E. Ramirez-Zepp,J.M. Park,E.A. Shelden,& D.K. Shaw
ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics
Proc. Natl. Acad. Sci. U.S.A. 122 (25) e2501045122, https://doi.org/10.1073/pnas.2501045122 (2025).

Significance
Infection dynamics for tick-borne pathogens like Anaplasma have primarily been studied in mammals. Comparatively less is known about tick–pathogen interactions. We found that Anaplasma activates the stress response receptor, ATF6, in ticks. Activated ATF6 functions as a transcriptional regulator. Using a custom script in R, we identified stomatin as an ATF6-regulated target that supports Anaplasma by modulating cholesterol trafficking. Our custom tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to arthropods. Given that lipid hijacking is common among arthropod-borne microbes, ATF6-mediated induction of stomatin may be exploited in many vector–pathogen relationships. In addition, our findings predict that there are many ATF6-regulated genes unique to ticks, highlighting that there is still much to be uncovered.

Abstract
How tick-borne pathogens interact with their hosts has been primarily studied in vertebrates where disease is observed. Comparatively less is known about pathogen interactions within the tick. Here, we report that Ixodes scapularis ticks infected with either Anaplasma phagocytophilum (causative agent of anaplasmosis) or Borrelia burgdorferi (causative agent of Lyme disease) show activation of the ATF6 branch of the unfolded protein response (UPR). Disabling ATF6 functionally restricts pathogen survival in ticks. When stimulated, ATF6 functions as a transcription factor, but is the least understood out of the three UPR pathways. To interrogate the Ixodes ATF6 transcriptional network, we developed a custom R script to query tick promoter sequences. This revealed stomatin as a potential gene target, which has roles in lipid homeostasis and vesical transport. Ixodes stomatin was experimentally validated as a bona fide ATF6-regulated gene through luciferase reporter assays, pharmacological activators, RNA interference transcriptional repression, and immunofluorescence microscopy. Silencing stomatin decreased A. phagocytophilum colonization in Ixodes and disrupted cholesterol dynamics in tick cells. Furthermore, blocking stomatin restricted cholesterol availability to the bacterium, thereby inhibiting growth and survival. Taken together, we have identified the Ixodes ATF6 pathway as a contributor to vector competence through Stomatin-regulated cholesterol homeostasis. Moreover, our custom, web-based transcription factor binding site search tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to blood-feeding arthropods. Collectively, these findings highlight the importance of studying fundamental processes in nonmodel organisms.

The North American deer tick, Ixodes scapularis, can transmit up to seven different pathogens that impact human and animal health including Anaplasma phagocytophilum (causative agent of anaplasmosis) and Borrelia burgdorferi (causative agent of Lyme disease) (1). The continuous rise in reported cases of tick-borne disease (2–10) underscores the need for novel intervention strategies. Although the intricacies of mammalian host–pathogen interactions have been well studied, comparatively little is known about tick–pathogen interactions.

Recently we have shown that A. phagocytophilum and B. burgdorferi activate the unfolded protein response (UPR) in ticks, which influences microbial colonization and persistence in the arthropod (11, 12). The UPR is a cellular response network that is initiated by three endoplasmic reticulum (ER) transmembrane receptors IRE1α, PERK, and ATF6. Each branch of the UPR initiates a signaling cascade and coordinates gene expression networks by activating specific transcription factors. We have shown that the IRE1α-TRAF2 pathway leads to microbe-restricting immune responses in arthropods by activating the NF-κB-like molecule, Relish (11). We have also demonstrated that stimulating PERK activates the antioxidant transcription factor, Nrf2, which facilitates pathogen persistence in ticks (12). Out of the three UPR receptors, ATF6 is the least understood (13). When activated, site-1 and site-2 proteases cleave the cytosolic portion of ATF6, which allows it to translocate to the nucleus and act as a transcriptional regulator (nATF6) (14). The role of ATF6 has never been explored in arthropod vectors.

Here, we demonstrate that Ixodes ATF6 is activated by tick-borne pathogens and supports A. phagocytophilum colonization in ticks. To determine how ATF6 impacts vector competence, we used protein modeling and a custom transcription factor binding site query to probe the ATF6 regulatory network in I. scapularis. Gene ontology (GO) and Reactome analyses identified Stomatin, a lipid homeostasis and vesical transport protein, as a potential gene regulated by ATF6 in ticks. Using pharmacological manipulations, RNA interference (RNAi), quantitative fluorescent assays, and immunofluorescence microscopy, we found that Stomatin supports pathogen colonization in ticks by facilitating cholesterol acquisition by the bacterium. These findings demonstrate that stomatin is induced during the arthropod-phase of the pathogen life cycle to enable survival and persistence in the vector.

Programs that predict transcription factor regulatory networks are generally restricted to model organisms, leaving out many arthropod vectors. We used our custom R script to develop a publicly available, web-based tool termed “ArthroQuest” that currently allows users to query 20 different arthropod vector genomes, in addition to Drosophila and humans. Queries with ArthroQuest revealed that the ATF6-regulated nature of stomatin appears to be unique to arthropods. Given that lipid hijacking and cholesterol incorporation is common in many arthropod-borne microbes (15), ATF6-mediated induction of stomatin may be a shared phenomenon among many vector–pathogen relationships that is exploited for the survival and persistence of transmissible pathogens.

K.A. Vosbigian,S.J. Wright,B.P. Steiert,K.L. Rosche,E.A. Fisk,E. Ramirez-Zepp,J.M. Park,E.A. Shelden,& D.K. Shaw
ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics
Proc. Natl. Acad. Sci. U.S.A. 122 (25) e2501045122, https://doi.org/10.1073/pnas.2501045122 (2025).

Copyright: ©2025 The authors.
Published by the National Academy of Sciences of the USA. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

This discovery poses a significant problem for proponents of Intelligent Design (ID) creationism because it challenges one of their core assertions: that complex specified information (CSI) within genetic material is a reliable indicator of an intelligent, purposeful designer. If we accept this premise, then we are compelled to ask why such intelligence would devote itself to crafting mechanisms that cause suffering, disease, and death—such as the ability of Anaplasma to hijack tick cell defences and ensure its own propagation at the expense of both ticks and mammalian hosts, including humans.

The usual ID response is to insist that their designer is benevolent — typically equated with the God of the Bible. But here, we are faced with a biological system so well-adapted to spreading infection that it must either be acknowledged as a product of evolutionary processes or attributed to a designer with malevolent intent. This is not a fringe example; it is one of many cases where nature reveals a level of intricate adaptation that ID advocates would normally cite as evidence for design, were it not so profoundly disturbing.

What this ultimately reveals is the theological inconsistency at the heart of ID creationism. The refusal to acknowledge the explanatory power of evolution, even when confronted with examples like Anaplasma, indicates that ID is not a scientific theory but a religious or ideological stance. The selective application of their own criteria — applauding "design" in butterflies but ignoring it in parasites — exposes the intellectual dishonesty behind the movement. Evolution, by contrast, provides a consistent and naturalistic framework that explains both the beautiful and the brutal features of the living world — without invoking a morally compromised designer.

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