Malevolent Design News - The Superbug, Clostridium Difficile (C. Diff), May Be Developing Resistance to Vancomycin - Design or Evolution?

Clostridium difficile (C. diff)

Treatment for Deadly Superbug C. diff May Be Weakening - University of Houston

The latest rabbit hole Michael J Behe has driven the creation cult into is the daft notion of 'Genetic Entropy'. This was introduced following the failure of the Discovery Institute to trick the courts in the USA into declaring that 'Intelligent [sic] Design' is real science and so should be foist on impressionable children in science class at taxpayers’ expense.

The notion of 'Genetic Entropy' plays on what used to be presented as an anti-evolution argument - the Second Law of Thermodynamics, which says that a closed system tends to disorder (increased entropy), so evolution can't increase order and complexity. This ignores the fact that Earth is not a closed system, of course, and relies on the scientific illiteracy of its target marks. And it looks nice and sciencey - something that creationists all crave while purporting to reject science.

So, Genetic Entropy starts off with the assumption that every species was created perfect and then, because Adam and Eve allowed 'Sin' to enter the world, these 'perfect' genes have been getting progressively less perfect. Now, this isn't Bible literalism, obviously, because that would make 'Genetic Entropy' religion, not science! Got it!

I posted this in an Evolution Vs Creation Facebook group. Creationists appear to be pretending not to have seen it.

The problem then is, how can increasing 'entropy' lead to greater fitness in a given environment? It can't of course because unlike the random process of mutation, there is no selective element which can produce more descendants from a worse genome, and unless it is getting worse, in what possible sense of the word can it be getting less perfect?

So, faced with something like increasing bacterial resistance to antibiotics, creationists in Michael J Behe's latest rabbit hole have only two ways to go. They can't argue that increased entropy is leading to an improved genome (from the perspective of the bacterium) because that would mean 'genetic entropy' is leading towards greater perfection. That then leaves them with the unenviable choice of design or evolution, and for design, read 'malevolence' because increasing antibiotic resistance increases the ability of the bacterium to make us sick, and any omniscient designer would know that.

IOW, Michael J Behe's attempt to resuscitate the Discovery Institute's flagging 'Wedge Strategy' has resulted in his fundamentalist cult having to choose between the twin 'evils' of blasphemy or evolution!

The latest twist in the evolutionary arms race between bacteria and human medical science is in the increasing weakness of the antibiotic of choice for Clostridium difficile (C. diff), vancomycin, against which C. diff appears to be developing resistance. This was discovered by researchers at the University of Houston College of Pharmacy, Texas, USA, who have just published their findings in the Journal Clinical Infectious Diseases, sadly behind a paywall with only the abstract available. However, their work is described in a University of Houston news release:

Unintelligent Design - The Brilliant Way Bacteria Evade Our Immune System - Malevolent Design or Incompetent Designer?

Burkholderia thailandensis (purple) uses cellular components (yellow) to form membrane protrusions from one host cell to another (green).

Burkholderia pseudomallei, a Gram-negative rod, straight or slightly curved, with bipolar staining

The enemy within: How pathogens spread unrecognized in the body - Biozentrum

Here's a conundrum for intelligent [sic] design creationists. Scientists working at Biozentrum, University of Basel, Switzerland with colleagues in the Department of Biochemistry, National University of Singapore, have discovered how the bacterium, Burkholderia pseudomallei that causes the serious tropical disease, melioidosis, manages to evade our immune systems to make us sick.

What information do you have on the origins of the bacterium Burkholderia pseudomallei and what it causes in humans? Burkholderia pseudomallei is a Gram-negative bacterium that causes melioidosis, a potentially fatal infectious disease primarily found in Southeast Asia and Northern Australia. The bacterium is commonly found in soil and water in endemic regions. It was first identified by Alfred Whitmore and C.S. Krishnaswami in 1912 in Rangoon, Burma (now Yangon, Myanmar). The name "melioidosis" is derived from the Greek word "melis," meaning "distemper of asses," as the disease was initially identified in horses. B. pseudomallei can infect humans and a wide range of animals through various routes, including inhalation, ingestion, or through breaks in the skin. In humans, it can cause a spectrum of symptoms ranging from localized skin abscesses and fever to more severe forms of pneumonia, septicemia (bloodstream infection), and multiple organ abscesses. Melioidosis can be challenging to diagnose due to its diverse clinical manifestations and can mimic other diseases, making it important for clinicians in endemic areas to consider it when evaluating patients with febrile illnesses. Treatment of melioidosis typically involves prolonged antibiotic therapy with drugs such as ceftazidime, meropenem, or imipenem, followed by oral antibiotics such as trimethoprim-sulfamethoxazole to prevent relapse. However, antibiotic resistance in B. pseudomallei is a growing concern, particularly in regions where the disease is endemic. Prevention strategies include avoiding contact with contaminated soil and water, wearing protective clothing during outdoor activities, and practicing good wound care.

The conundrum is, was this malevolently designed or is it the result if incompetent design?

The problem for creationists is that they believe the human immune system was intelligently designed to protect us from the bacteria and other organisms their putative designer god had designed to make us sick, and yet not only does it not work as intended but many of the harmful parasites from which we suffer seem to have been designed to avoid our immune system, some of them by ingenious ways, like the bacterium in question, B. pseudomallei.

It's hard to reconcile the difference between a designer who can't design a functional immune system and one who is genius enough to design some of the extremely clever and sophisticated mechanisms for evading our immune system. The idea that these could be one and the same entity is almost laughable unless the answer is that the inadequate immune system and the ingeniously designed parasites are all part of the same malevolent plan to make us sick.

What B. pseudomallei does to avoid being detected by the immune system, once it gets inside a cell, is cause the cell to make special tubes connected to other cells, through which it can pass without going outside the cell again, where it would be recognised as a pathogen. In this way it spreads throughout a tissue without the victim's immune system even being aware of it.

The research team have published their findings, in the open access, online Cell Press journal, Cell Host & Microbe and explain it in a press release from The University of Basel, Biozentrum:

Evolution in Action - New Study Finds Evidence for Evolution Of A New, Nitrogen-Fixing Cell Organelle

Composite of catalized reporter deposition fluorescence in situ hybridization (CARD-FISH) images showing the range of sizes of the different UCYN-A sublineages.

Cornejo-Castillo, F.M., et al (2024)

Transmission electron micrograph images of the C. parkeae stage of B. bigelowii. Light microscopy images (A,C) and corresponding TEM images are shown (B,D) for strain MK90-06. Usually, one endosymbiont is found per cell in the posterior of the cell (A,B); however, some of the cells had two endosymbionts per cell during cell division (C,D). Scale bars represent 5 μm in (A and C), and 2 μm in (B and D). E, endosymbiont; G, Golgi apparatus; M, mitochondrion; N, nucleus; P, plastid; and Py, pyrenoid.

Suzuki, Shigekatsu, et. al, (2021)

Evolution in action? New study finds possibility of nitrogen-fixing organelles – Rhody Today

Most biologists now accept the Endosymbiosis Theory which explains how simple prokaryote cells became complex eukaryote cells by a single-celled prokaryote such as an archaea incorporating other single-celled prokaryotes inside its cell membrane. This may have been by engulfing them as prey or by being parasitised by them. Whatever the mechanism, a symbiotic relationship ensued which progressed to the extent that the incorporated cell's DNA was transferred to the host genome and the incorporated cell became a cell organelle.

This explains the origin of cell organelles such as the mitochondria which metabolise glucose to turn adenosine diphosphate (ADP) into adenosine triphosphate (ATP) which can then be used to power metabolic processes within the cell. Mitochondria have some similarities with rickettsia bacteria which strongly suggests they have evolved from free-living rickettsia.

Likewise, chloroplasts in plant cells were once free-living, photosynthesising cyanobacteria which became incorporated in what was to become algae, so giving rise eventually to almost all plant life.

And now we have evidence that another incorporation is evolving, in the form of nitrogen-fixing bacteria being incorporated as organelles into a marine alga, which gives the algae the ability to create ammonia and so nitrates directly from atmospheric nitrogen. This was discovered by researchers from the University of Rhode Island, the Institut de Ciències del Mar in Barcelona, the University of California at Santa Cruz and the Massachusetts Institute of Technology. They have published their findings, open access, in the journal Cell.

Although nitrogen is abundant, comprising about 79% of Earth's atmosphere, it exists as the diatomic gas dinitrogen (N₂) which is notoriously stable making molecular nitrogen almost an inert substance and requiring a lot of energy to break the N-N bond. However, some bacteria, the nitrogen-fixing bacteria, have evolved the ability to do this using the enzyme nitrogenase:

Malevolent Designer News - New Discovery Unravels Malaria Invasion Mechanism

Malaria-infected red blood cells

Photo: AdobeStock

Plasmodium falciparum in a blood smear.

New Discovery Unravels Malaria Invasion Mechanism

Medical science just took a step forward in the continuing arms race between it and creationism's divine malevolence to try to prevent its parasite, Plasmodium falciparum from killing 600,000 people, mostly children, a year, mostly in Africa.

Creationists who use the traditional excuse that it's not their god who designs parasites but another intelligent designer - Sin - should refresh their memories of Michael J Beh's 'proof' that their god exists by falsely claiming that anti-malarial drug resistance in P. falciparum must have been intelligently designed because the (wrong) mathematical model he used gave the infinitesimally small probability it was intelligently designed to give, so could not have evolved.

So, they can't have it both ways: if evidence of design in parasites, no matter how spurious, is evidence for their god then their god is responsible for the design of those parasites. If not, then Michael J Behe's carefully concocted 'proof' is nothing of the sort.

The alternative is the blasphemous claim that there is another supernatural deity with powers to create living things, over whom their god has no power or authority.

So, while creationists are struggling with trying to hold two mutually exclusive views simultaneously, biomedical scientists are trying to unravel the devilishly clever way this parasite overcomes our defences to do what creationists must believe it was designed to do - make us sick and increase the suffering in the world.

This is the latest breakthrough medical science has just announced.

It was made by researchers from by the Swiss Tropical and Public Health Institute (Swiss TPH) and Griffith University’s Institute for Glycomics, led by Professor Gerd Pluschke of Swiss TPH. Their discovery concerns the way the parasite gains access to the red blood cells to begin their destruction. It is published, open access, in Cell Reports and is explained in a Swiss PTH news release:

Creationism's Heath-Robinson Designer - Muddling Through With Even More Ramshackle Complexity

Bacteria abundant in the newborn gut may supply the neurotransmitter needed to shape the immune system and prevent food allergies.

Shutterstock

Gut Bacteria Make Neurotransmitters to Shape the Newborn Immune System | Newsroom | Weill Cornell Medicine

The story so far, according to the Creationists Gospel:

Once upon a time, just a few thousand years ago, a magic man in the sky magicked a small flat planet with a dome over it in the Middle East, and then made some people to live on it.

It also made lots of harmful bacteria and other parasites to live in them and make them sick, but luckily, it also gave the humans an immune system to stop the parasites it made to make them sick, from doing what it designed them to do.

The only problem was that the ramshackle immune system it designed, which often doesn't do what it was designed to do, is also a little hypersensitive and prone to treating other things like the body it should be protecting as a parasite and mounting an attack on it so we suffer from all sorts of 'autoimmune' diseases that require another layer of complexity to keep in check. The other thing about it is that it needs training and until that's complete, it will treat all manner of things as parasites, including the food babies eat - and that could result in food allergies that would make life miserable!

But rather than do the simple thing and design the immune system to be able to tell the difference between food and harmful parasites, creationism's version of William Heath-Robinson went for one of the most bizarre solutions you can imagine. Rather like William Heath-Robinson's solution to an every-day problem, it co-opted things in the baby's environment to perform functions they were never intended to perform, like an upright piano being used to stand a step-ladder on to give it enough height, or a stick and some string being used to mend a broken spoke in a wheel, creationism's designer co-opted some of the bacteria that live in a baby's gut.

How it did this is explained in a free access paper in Science Immunology by a team of researchers from the Department of Pediatrics at Weill Cornell Medicine, led by Assistant Professor Dr. Melody Zeng of the Gale and Ira Drukier Institute for Children's Research. Their work is described in a Weill Cornel Medicine news item:

Malevolent Designer News - Creationism's Divine Malevolence Is Still Victimising Frogs

Foothill yellow-legged frog, Rana boylii

Photo Credit: Brome McCreary

Foothill yellow-legged frog, Rana boylii

Photo: Rebecca Fabbri/USFWS

Scientists assemble a richer picture of the plight and resilience of the foothill yellow-legged frog | The Current

Almost unnoticed by the general public and noticed only by biologists and wildlife conservationists, is a pandemic far more deadly than the Covid-19 pandemic, or even the Medieval Black Death.

It kills a very high percentage of its victims, has already exterminated whole populations of frogs and other amphibians, and has contributed significantly to the global mass extinction currently underway.

It is, of course, the chytrid fungus Batrachochytrium dendrobatidis, which, along with a closely-related fungus, B. salamandrivorans, causes the fatal disease, chytridiomycosis, in frogs and other amphibians.

As an example of the work of creationism's divine malevolence, it takes some beating for its sheer malevolent nastiness. It infects the skin of these amphibians, through which they breath, and causes it to thicken and fail as a respiratory organ, leading to suffocation, multiple organ failure and death. Here is how I described it in my illustrated book, The Malevolent Designer: Why Nature's God is not Good:

Exterminating Frogs with a Fungus.

Most of the examples I’ve talked about so far have been organisms and viruses that affect humans, but we are far from being the only species that Creationism’s putative intelligent designer seems to have taken an intense dislike to. For example, the world’s frogs and other amphibians are currently being decimated by chytridiomycosis, caused by a couple of related Chytrid fungi, Batrachochytrium dendrobatidis and B. salamandrivorans. It has been estimated that over 500 different species have been severely reduced in number by this fungal plague, with over 90 extinctions.

These fungi seem to have originated in an area of Southeast Asia by modification of a common, harmless, soil fungus. In that part of the world, the local population of amphibians seems to be resistant to the pathogenic forms of the fungi, suggesting that these fungi frequently become pathogenic and the local population have built up resistance to it.

According to research carried out by a team from the Fenner School of Environment and Society, Australian National University, ACT, Australia, it was resistance in the local population which probably kept the disease from spreading more widely, until human agency intervened to change the environment. They have related the increased trade in amphibian species to the spread of the fungi all over the world where they found species with no evolved resistance (42).

Figure 5 Frog Victims of Chytrid Fungus

Illustration: Catherine Webber-Hounslow

Recently, another team found that one of the factors that could have made these fungi so successful is that the frog’s immune response seems to have worked against it. Researchers from the University of Central Florida and the Smithsonian Conservation Biology Institute (SCBI) found that, in the frog Rana yavapaiensis, a species known to vary in its ability to survive attack by these fungi, those which showed an elevated immune response had a worse outcome that those with a lower response (43). Somehow, the frog’s ‘designed’ immune system was working against it and the fungi had been ‘designed’ to exploit this.

ID advocates would have us believe that, for reasons unknown, their putative intelligent designer has deliberately redesigned a soil fungus so it can overcome the immune system it designed to protect frogs from infections, and so exterminate over 90 species of amphibians that it designed earlier and severely endanger some 500 species in what has been described as the biggest single loss of biodiversity, albeit, aided and abetted by humans in this endeavour. Creationism’s intelligent designer must really hate the frogs it designed. Maybe a private definition of the word ‘intelligent’ is being employed here.

Now a team of researchers from multiple American wildlife and conservation agencies have looked in detail at the spread of this fungus in one particular frog which has declined so rapidly it is now an endangered species - the foothill yellow-legged frog, Rana boylii. This small frog's range once extended from Oregon to Baja California.

They have shown that human agency is implicated in the spread of this fungus by not only spreading it around the world in trade, as the earlier Australian study found (42), but with regard to the foothill yellow-legged frog specifically, by global warming, climate change and habitat destruction as more land is converted to agriculture. They have published their work, open access, in Royal Society Open Science. It is also explained in a University of California Santa Barbara, news release:

Up to only a few inches in length, with a lemon-hued belly, the foothill yellow-legged frog may seem unassuming. But its range once stretched from central Oregon to Baja California. In 2023, it was listed under the federal Endangered Species Act. Its rapidly decreasing range is due in part to a fungal pathogen called Batrachochytrium dendrobatidis, or Bd, that has devastated amphibians around the world.

A team of researchers, including UC Santa Barbara’s Andrea Adams, has conducted the most comprehensive study to date of disease dynamics in foothill yellow-legged frogs. The team’s data — sourced from both wild frogs and specimens in museum collections — enabled them to track patterns of infection across a large geographic range. In a study published in Royal Society Open Science, the researchers reveal that drought, rising temperatures and the increasing conversion of land for agriculture appear to be the largest factors driving Bd infection in this species.

The researchers aimed to assemble as much data as they could, both in space and time. They surveyed in the creeks and rivers of California and Oregon, where they swabbed wild yellow-legged frogs for the presence of Bd. It also led them into fluorescent-lit museum collections to sample specimens from as far back as the 1890s.

The team leveraged a large network of people and institutions to amass this wealth of samples.

Many foothill yellow-legged frog field researchers had data that they weren’t actively analyzing, and so we were able to bring all of this data together and get it into a usable format that we could use to paint a much bigger picture of what is, and was, going on with Bd in this species.

Andrea J. Adams, co-author.
Earth Research Institute
University of California, Santa Barbara, CA, USA.

The researchers swabbed each frog’s skin to determine if the animal was infected. To test for Bd, they used a PCR test, similar to some tests for COVID. By searching for Bd DNA from thousands of samples, the researchers were able to identify infection rates and severity. Co-lead author Ryan Peek ran this information through statistical models, which accounted for climatic, geographic, biologic and land use variables. This enabled the team to track disease patterns across a large geographic range over roughly 120 years.

The team discovered that disease patterns of Bd aligned with historical frog declines. The pathogen began to spread in the 1940s from the southern coast of California, moving northward and eventually affecting nearly the entire region. The biggest factors driving infection seem to be drought, increasing temperatures and the use of ever more land for agriculture.

Bd is a fungus that is spread through spores in the water, but that spread may occur differently in foothill yellow-legged frogs in different regions and climates, the researchers found. In some places, drought increased infection, while in others, it did not, possibly because of the presence or absence of other species that can carry Bd and share the same water, such as American bullfrogs, a species introduced from eastern North America.
“

If you combine the fact that there are bullfrogs building up the number of spores that these frogs are exposed to, and then they’re all kind of stuck in these small pools together, that explains why drought matters. They are suddenly getting hit with a really large number of spores and getting sick and dying.

These findings open more questions about what was stopping transmission and what allowed it to happen later.

Dr. Anat M. Belasen, co-first author
Department of Integrative Biology
University of Texas at Austin, Austin, TX, USA
And Department of Ecology and Evolutionary Biology,
Cornell University, Ithaca, NY, USA.

What’s more, foothill yellow-legged frogs live exclusively in streams and rivers, not ponds and lakes. So the species is already stressed when these waterways shrink into isolated pools.

The progression of Bd in the foothill yellow-legged frog also differed from its course in other western amphibians. In many other species, the disease radiated from urban centers, rather than this clear south-to-north trend. What’s more, the disease showed up later in the foothill yellow-legged frog than in other species in its range.

Frogs switch from herbivores as tadpoles to carnivores as adults, which means they connect different nutrient cycles together in the food web. Their position at the center of the food chain also influences the ecosystem.

When you remove frogs from an ecosystem, what you get is less control of insects, things that the frogs would eat. There is also less food for things that eat the frogs, like snakes, birds and small mammals. It really throws things off and makes the ecosystem less stable and less functional.

“There are areas that have wet soils that would be alongside suitable habitat. In areas where more of those lands have been converted to agriculture, we see a higher risk of frogs being infected with the fungus.

Dr. Anat M. Belasen.

Co-author Jamie Bettaso swabs a wild foothill yellow-legged frog to test for fungal infection.

Photo Credit: Jamie Bettaso

The conversion of land for agriculture was another major factor influencing the spread of Bd. for these frogs.

In addition to disease hotspots, the team also identified a number of cold spots — areas where the pathogen is present but less influential. The existence of so many cold spots in different areas is a good sign, as it may mean that many areas have conditions suitable for keeping disease rates low, even as climate change increases temperatures and patterns of drought.

The authors are curious what might explain this clustering, especially when cold spots appear in unexpected locations: for example, places with similar habitat, land-use and climatic impacts as hotspots. It suggests there may be some genetic basis for the differences, whether on the pathogen side or the host side. Adams is currently researching the feasibility of reintroducing foothill yellow-legged frogs to Southern California.

The results of this paper shed a lot of light on the dynamics of where Bd occurs, what drives its spread and how the pathogen and frog may interact in the future.

We took a big snapshot of this species’ disease relationship through time. Earlier studies provided the researchers with glimpses into disease patterns in smaller geographic regions, “but now we have a much larger dataset that further confirms many of these patterns, and expands on them.

Andrea J. Adams.

More detail is given in the team's open access paper in Royal Society Open Science:

Abstract

Species with extensive geographical ranges pose special challenges to assessing drivers of wildlife disease, necessitating collaborative and large-scale analyses. The imperilled foothill yellow-legged frog (Rana boylii) inhabits a wide geographical range and variable conditions in rivers of California and Oregon (USA), and is considered threatened by the pathogen Batrachochytrium dendrobatidis (Bd). To assess drivers of Bd infections over time and space, we compiled over 2000 datapoints from R. boylii museum specimens (collected 1897–2005) and field samples (2005–2021) spanning 9° of latitude. We observed a south-to-north spread of Bd detections beginning in the 1940s and increase in prevalence from the 1940s to 1970s, coinciding with extirpation from southern latitudes. We detected eight high-prevalence geographical clusters through time that span the species' geographical range. Field-sampled male R. boylii exhibited the highest prevalence, and juveniles sampled in autumn exhibited the highest loads. Bd infection risk was highest in lower elevation rain-dominated watersheds, and with cool temperatures and low stream-flow conditions at the end of the dry season. Through a holistic assessment of relationships between infection risk, geographical context and time, we identify the locations and time periods where Bd mitigation and monitoring will be critical for conservation of this imperilled species.

1. Introduction

Threatened species with large geographical ranges often require unique, regional conservation strategies to combat stressors such as infectious disease. Pathogen surveys and reporting have become standard for North American wildlife diseases [1,2]; however, relative risk across a landscape and among populations within species remains difficult to anticipate, especially when data are collected by separate research groups [3]. Central reporting databases [4], synthetic analyses and retrospective surveys can help assess disease threats and identify high-risk populations.

Among the most significant wildlife diseases, amphibian chytridiomycosis caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd) has contributed to declines of hundreds of species worldwide [5]; but see [6]. In North America, notable Bd-associated declines have occurred across the west including the southern Rocky Mountains [7,8], Arizona and New Mexico [9,10], Nevada [11] and California [12–14]. In several of these cases, infection outcomes varied widely among populations due to host-related and environmental factors including genetics, prior Bd exposure and abiotic conditions [15–17].

For the stream-dwelling foothill yellow-legged frog, Rana boylii, Bd's role in the species' changing abundance across its endemic range (California and Oregon, USA) is not well-understood. The species has declined for at least the last half-century, with extirpations reported from xeric lower latitudes [18], at the wetter northern range limit [19] and downstream of large dams range-wide [20]. A mix of abiotic and biotic factors influence Bd infection risk and disease dynamics in many systems, including elevation, latitude, climate, habitat quality and host characteristics [21]. The relative importance of these factors remains unclear in rivers with winter flood/summer drought flow regimes typical across R. boylii's geographical range. Bd is considered a significant potential threat to R. boylii [22] because it is implicated in the species' disappearance from rivers of California's South Coast [23] and in recent autumn die-offs of R. boylii in Central Coast streams [24,25]. A large-scale assessment of Bd infections is needed to clarify how infections relate to historical declines in some regions' rivers and persistence in others, identify clusters of increased infection risk across the species’ range, and evaluate how infection incidence and severity changes with the seasonality of the Mediterranean climate and across the diverse ecoregions that R. boylii occupies.

Here, we leverage data from over 2000 field and museum samples covering 124 years to synthesize knowledge and evaluate patterns of Bd infections in R. boylii. We use a combination of modelling approaches and spatial scan statistics to ask: (i) how are Bd detections in R. boylii are distributed over space and time, (ii) whether watersheds with high versus low Bd infection risk clustered historically and today, and (iii) how Bd infections are related to biotic and abiotic factors. Our results highlight priority populations for Bd mitigation, regions that are data-deficient and warrant further sampling and monitoring, and remaining gaps in our knowledge about Bd susceptibility in R. boylii. Our study serves as a resource for wildlife managers implementing disease mitigation and species recovery projects, such as re-introductions, and as an example of collaborative research to address conservation challenges in wide-ranging imperilled species.

Figure 1.
Distribution of R. boylii samples assayed for Bd infection. Diamonds show museum samples (collected 1897–2005), circles show field samples (2005–2021). Filled symbols indicate Bd-positive samples. (a) Sampling locations across California and Oregon, USA. Symbols overlap in some localities; see inset barplots for sample sizes. Rana boylii clades are outlined and labelled, with California Endangered Species Act status abbreviated in parentheses: SSC = Species of Special Concern, TH = Threatened, EN = Endangered. (b) Spatio-temporal spread of Bd detections. Symbol size indicates sample size at the HUC-12 (sub-watershed) level. Generalized additive model (GAM) of latitude∼capture year + sample size in Bd-positive samples is shown with black curved line (R² = 0.133).

Photo of R. boylii in Napa County, CA by Marina De León.

Belasen A. M., Peek R. A., Adams A. J., Russell I. D., De León M. E., Adams M. J., Bettaso J., Breedveld K. G. H., Catenazzi A., Dillingham C. P., Grear D. A., Halstead B. J., Johnson P. G., Kleeman P. M., Koo M. S., Koppl C. W., Lauder J. D., Padgett-Flohr G., Piovia-Scott J., Pope K. L., Vredenburg V., Westphal M., Wiseman K. and Kupferberg S. J. (2024)
Chytrid infections exhibit historical spread and contemporary seasonality in a declining stream-breeding frog
R. Soc. Open Sci.11. 231270. 231270 DOI: 10.1098/rsos.231270

Copyright: © 2024 The authors.
Published by The Royal Society. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

It must be thrilling for devotees of the putative divine malevolence to see the stunning success it is having exterminating so many species of frog, but one can't help but wonder what the ancestral frog did to incur this wrath. Did it maybe eat a forbidden mosquito or spawn out of wedlock?

---

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The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

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Creationism in Crisis - A Multicellular Organism 1.63 Billion Years Before 'Creation Week'

1.63-billion-year-old multicellular fossils from North China
The oldest record of a multicellular eukaryotes

(Artist’s concept.)
Credit: SciTechDaily.com

Fig. 1. Transmitted-light (TL) photomicrographs of Q. magnifica from the Chuanlinggou Formation.
(A to D and K) Filaments with cells of varying length and width. (E) Four-celled filament with hemispherical terminal cell. (F and G) Filament with notably decreasing cell width toward one end. Note that (F) and (G) represent the same specimen; (F) lost the narrowest part of the filament as shown in (G). (H to J) Filaments displaying more uniformity of cell dimensions. (L) Two-celled filament with ovoid terminal cell. All specimens were handpicked from organic residues of acid maceration and photographed in wet mounts, except for (K), which was photographed from a permanent strew mount. Solid and empty gray triangles in (A), (C), and (K) indicate the longest and the shortest cells, respectively, within single filaments. tb, transverse band (interpreted as cross wall); tr, transverse ring (interpreted as partially preserved cross wall). Scale bar, 50 μm [(A) to (E), (I), (J), and (L)] and 100 μm [(F) to (H) and (K)].

Fossils from North China indicate eukaryotes first acquired multicellularity by at 1.63 billion years ago---- Nanjing Institute of Geology and Palaeontology Chinese Academy of Sciences

As though the abundant evidence of life on earth before about 10,000 years ago wasn't bad enough for creationists who believe the Universe and everything in it were was magicked out of nothing in 6 days around about then, a team of scientists led by led by Professor ZHU Maoyan from the Nanjing Institute of Geology and Palaeontology, Chinese Academy of Sciences (NGIPAS), has now pushed the date of oldest-known multicellular, eukaryote organism back another 70 million years to a whapping 1.63 billion years before the supposed 'Creation Week'.

This would mean, if their superstition had any merit that creationists believe Earth has been around for just the last 0.0006% of the time that multicellular eukaryotes have existed on it.

And they wonder why people laugh!

The fossils were discovered in the Yanshan area of North China in the late Paleoproterozoic Chuanlinggou shale Formation which is about 1,635 million years old. The age of the fossils is constrained by a layer of volcanic ash ~40 m above the fossil horizon in the Kuancheng area, which has yielded a U-Pb zircon age of 1634.8 ± 6.9 Ma (23).

All complex life on Earth, including diverse animals, land plants, macroscopic fungi and seaweeds, are multicellular eukaryotes. Therefore, multicellularity is key for eukaryotes to acquire organismal complexity and large size, and often regarded as one major transition in Earth’s life history by scientists. However, it is still poorly understood when eukaryotes first evolved this innovation in their deep evolutionary history.

Fossil records with convincing evidence show that eukaryotes with simple multicellularity already appeared at 1.05 billion years ago, including red and green algae, and putative fungi. Older records claimed to be multicellular eukaryotes, but most of them are controversial due to their simple morphology and lack of cellular structure.

Malevolent Designer News - How Bacterial Pathogens Are Cleverly Designed to Invade Their Victim's Body

The exceptional secretion mechanism of Tc Toxins.

MPI MOPH

Functional model for Yen-Tc toxicity. Following ingestion of the Tc, it is likely that the surface-bound chitinases bind to and/or degrade the chitin-rich peritrophic membrane of the insect midgut. Cell surface recognition is likely facilitated by motifs within the A subunits prior to internalization. Similarities to the well characterized bacterial binary toxin systems (e.g., anthrax, cholera, diphtheria) suggest a mechanism involving receptor-mediated endocytosis followed by pore formation and translocation of the B and/or C components into the cytosol (I), although alternative mechanisms (e.g., II, III) cannot be ruled out.

Landsberg, MJ., Jones, SA., Rothnagel R., et al (2011)

24-01-18 | Max Planck Institute of Molecular Physiology

Imagine you're in charge of an invading army laying siege to your enemy's outer defences. How do you neutralise them?

One way would be to send a small group of soldiers, packed with high explosives and deadly toxins on a kamikaze mission into the defences, with instructions to detonate their explosives and so spread the toxins when inside to destroy the defences and kill the defenders. You could improve on that by removing any temptation the suicide bombers might have to not detonate their defences by automating the trigger to fire as soon as they encountered the defender.

That's exactly what a team at the Max Planck Institute for Molecular Physiology (MPI MOPH), Dortmund, Germany, have found bacteria use to gain access to their victim’s body and make their hosts sick and die. The team, led by Stefan Raunser, Director of MPI MOPH, have published their findings, open access, in Nature Microbiology. Their work is described in a MPI MOPH press release:

Creationism in Crisis - When Creationists Believe The Universe Was Being Made From Nothing, People Were Chewing Gum and Eating Trout, Deer And Nuts In Scandinavia

Photo from the excavation site Huseby Klev at the Swedish west coast.

Photo: Bengt Nordquist

The plastelina casts for one of the chewing gums from Huseby Klev. The cast captures the teeth imprints from each side.

Photo: Verner Alexandersen.

Ancient chewing gum reveals stone age diet - Stockholm University

How could the Bible's authors possibly have known what people were doing in Scandinavia when they didn’t even know where Scandinavia was because they thought Earth was a small flat place with a dome over it to keep the water above the sky out, centred on the Middle East?

The answer is that they couldn't of course. Had they done so, they would have concocted much less parochial tales about the things they didn't understand and would have known that Earth was much older than the few thousand years they imagined.

But now we know much better than they did. For example, modern science is able to take the resin people were chewing on (probably to make glue from it) and analyse the DNA in it to see what they had been eating and what organisms they had living in their mouths. It turns out that just about the time when the Bible's authors were setting their creation tale, people in Scandinavia were eating trout, deer and hazelnuts, and suffering from pathogenic bacteria, oblivious of the creation allegedly going on far away in the Canaanite Hills.

Although creationists now tell us that pathogens and other parasites didn't exist before the supposed 'Fall' and must have been made since by a thing called 'Sin', there is no biblical support for this modern invention which has been hurriedly cobbled together to defend the alleged creator god from the charge of malevolence in the design of pathogens which do nothing other than make more copies of themselves and add to the suffering in the world.

Embarrassingly for those creationist apologists, the same study presents compelling evidence of commensal and pathogenic organisms in the mouths of these Scandinavians, just as there are today in modern humans, including bacteria that cause teeth to fall out.

How scientists discovered this is the subject of an open access paper in Scientific Reports and a news release from Stockholm University:

Malevolent Design - No Fun For Creationists As The Candida Family of Fungi Are Evolving To Keep Infecting Us

A Candida albicans cell forming a hyphal extension

Candida auris causes multidrug-resistant infections that can result in organ failure

Credit: Kateryna Kon/Science Photo Library

Candida evolution disclosed: new insights into fungal infections | IRB Barcelona

The Candida genus of fungi are related to yeasts (i.e., single-celled fungi) but are specialists at living in or on our bodies and are common infections in body cavities such as the mouth, anus, vagina and urethra and the genito-urinary and respiratory tract, and other moist areas like armpits, inner surfaces of joints like the elbow and knee, groins and fold beneath breasts and buttocks.

They can also become systemic infections causing organ failure and death, especially in people who are immune compromised for any reason. So, they are a threat to people who are in generally poor health, who have had transplants and need to take immunosuppressive drugs, or people receiving chemotherapy for cancer.

And, like some bacterial pathogens, they are good at evolving immunity to anti-fungal medication.

One species, Candida auris, has evolved multiple drug resistance and is now a serious threat to people in hospital for other conditions.

Now, a research group from the Institute for Research in Biomedicine (IRB Barcelona) and the Barcelona Supercomputing Center - Centro Nacional de Supercomputación (BSC-CNS), led by the ICREA researcher Dr. Toni Gabaldón, has identified hundreds of genes subject to recent, clinically-relevant selection in six species of the fungal pathogen Candida. In other words, the genes that have given Candida species their clinically-relevant drug resistance.

First a little AI background to the Candida genus:

Unintelligent Design - The Heath-Robinson Contraption In A Western Honey Bee's Gut

Western honey bee,
Apis mellifera

Study shows western honey bee synthesizes food for its intestinal bacteria

A feature of creationism’s putative intelligent [sic] designer's designs is that they are almost always ingenious but overly complex for the task and often cobbled together from components designed for other purposes.

Just like a William Heath-Robinson contraption, where everyday objects such as a coal-scuttle full of coal, is a counterweight, every piece of string is made from short pieces of string knotted together and a simple task is made far more complicated than it need be.

And yet it works, just about, no matter how inefficiently, and removing just one component would make the whole thing fail - what creationists call 'irreducible complexity' but what a proper intelligent designer would probably call, 'bloody stupid'. Creationism's 'intelligent' [sic] designer wouldn't have lasted a term in design school.

Just such a Heath-Robinson machine has recently been discovered in the gut of the Western honey bee, Apis mellifera. Its purpose is to solve the problem of digesting the food the bee eats, for which it needs the help of 8 species of bacteria and other microorganisms that live in the bee's gut. Some of these bacteria are needed just to clean up the waste produced by other bacteria. 8 species is low compared to other species; humans, for example, need about 20 different species.

Apparently, giving bee's the same enzymes the bacteria use was far too simple and not nearly complex enough for the divine Heath-Robinson designer.

But even that wasn't complicated enough because one of the bacteria can't live on sugar alone, even though honey bees can, so the honey bee manufactures nutrients to feed to this bacteria.

How this was discovered was the subject of a recent paper in Nature Microbiology by a team of researchers led by Professor Philipp Engel in the University of Lausanne's Department of Fundamental Microbiology (DMF) in Dorigny. Their research is explained in a news release from the University of Lausanne (translated from French):

Malevolent Designer News - The Brilliance of Creationism's Divine Sadist

Scanning electron micrograph of Salmonella typhimurium invading a human epithelial cell.

New insights into what helps Salmonella cause infections | Carl R. Woese Institute for Genomic Biology

Salmonella

The brilliance of creationism's favourite sadist was on display again recently, when researchers from the Department of Microbiology, University of Illinois at Urbana Champaign, Urbana, Illinois, USA, showed how the pathogen, Salmonella, is designed to not only survive being engulfed by the macrophages in our blood that are supposedly designed to protect us, but positively thrives and multiplies inside them. Although rarely fatal, Salmonella infection can be distressing and unpleasant with vomiting and diarrhoea, as I can attest from my childhood in rural Oxfordshire at a time when food and water hygiene left much to be desired.

So, it looks like creationism’s intelligent [sic] designer won that particular arms race with itself, in favour of the nasty pathogen designed to increase the suffering in the world. At least, that's the sort of nonsense creationists needs to believe to retain the childish belief that living things are made by a magic man in the sky.

The fact that salmonella can live happily inside a macrophage supposedly designed to kill pathogens has been known for some time, but what the University of Illinois researchers have discovered is just how it manages the trick. It's all down to the structure and function of the bacterium's surface membrane which detects and adjusts to the conditions in which the organism finds itself.
First, a little AI background on the pathogen:

Creationism in Crisis - Eukaryote Fossils Were Highly Evolved 1.6 Billion Years Before 'Creation Week'

A soft summer evening in the Paleoproterozoic, as envisioned by DALL-E.

Photo Credit: DALL-E, prompt by Harrison Tasoff.

Limbunyasphaera operculata is a new species that shows a small door opening into the cell.

Photo Credit Riedman et al.

Even the oldest eukaryote fossils show dazzling diversity and complexity | The Current

By 1.64 billion years ago, eukaryote organisms had already evolved out of prokaryote cells and had diversified into a range of complex organisms. For creationists, this was more than 1.6 billion years before the Universe existed and way back in the dim and distant past before humans were supposedly magicked out of dirt in 'Creation Week.

The prevailing scientific consensus was that eukaryotes only diversified significantly about 800 million years ago, but a paper published in the Paleaontological Society's journal Papers in Palaeontology throws this back to double that age almost to the beginnings of eukaryote evolution. The paper is the work of palaeontologists from the Department of Earth Science, University of California at Santa Barbara, Santa Barbara, California, USA and the Department of Earth & Planetary Sciences/Geotop, McGill University, Montreal, Quebec, Canada.

The team arrived at this conclusion by examining microfossils recovered from 430 samples from eight cores drilled by a prospecting company in Australia's Northern Territory. The cores used for this study spanned roughly 500 meters of stratigraphy, or 133 million years, with around 15 million years of significant deposition. They consisted of shale and mudstone: remnants of an ancient coastal ecosystem that alternated between shallow, subtidal mudflats and coastal lagoons.

The microfossils were extracted from the rock by disolving it in hydrofluoric acid, then examined under microscopes. The team recorded 26 taxa, including 10 previously undescribed species.

From the UC Santa Barbara news release: