Malevolent Designer News - How A Virus Turns Its Bacteria Hosts Into Zombies - And Reduces The Marine Food Supply

Sunset over the island of Helgoland, from where the researchers obtained their samples.

© Jan Brüwer/Max Planck Institute for Marine Microbiology

Under the microscope, scientists identified SAR11 zombie cells by their distinct lack of ribosomes. In an example comparing a live, infected SAR11 cell to an infected zombie cell: blue indicates bacterial DNA, yellow shows ribosomes, and purple highlights phage genes. The live cell (upper pictures) displays all three colors, while the zombie cell (lower pictures) lacks the yellow ribosome signal. The final column of images on the right merges these colors, clearly distinguishing the two cell types.

© Jan Brüwer/Max Planck Institute for Marine Microbiology.

Zombie cells in the sea: Viruses keep the most common marine bacteria in check

Aficionados of creationism’s malevolent designer will be interested to learn that researchers at the Max Planck Institute for Marine Biology in Bremen, Germany, have discovered a virus that seriously reduces the population of a marine microbe that is an essential part of the marine food cycle, so seriously depleting the food chain for other marine organisms.

The microbe is a bacterium, know to science as a Pelagibacterale or SAR11, and, as an added piece of nastiness, the virus doesn't just infect the bacterium, it turns it into something that is halfway between dead and alive. In other words, it keeps the essential processes working while it uses the parts it needs to make more copies of itself from the bacterium's mitochondrial DNA.

Malevolent Designer News - Has Creationism's Divine Malevolence Designed An Improved Version of Cholera?

Vibrio cholerae

Vibrio cholerae

Persistent Strain of Cholera Defends Itself Against Forces of Change, Scientists Find - UT News

One of the mysteries of microbiology and epidemiology, is why a virulent strain of Vibrio cholerae (the bacterium that causes cholera) has remained so stable ever since it emerged in 1961 in Indonesia, causing the seventh global cholera pandemic. this strain, known as 7PET, is now the predominant strain, out-competing the other strains and infecting an estimated 1.3 - 4 million people a year, of which between 21,000 and 143,000 die.

The reason for those wide-ranging estimates is because many of the deaths from cholera are in remoter areas of mostly third-world countries where sanitation is poor, health-care is hard to obtain, and many of the victims are children, so the cause of death is often not known with any certainty.

The traditional response of creationists to anything concerning the evolution of parasites like V. cholerae is to blame 'Sin'. The more sophisticated creationists who have realised that this is a blasphemy because it implies the existence of another creator over which their supposedly omnipotent, omni-benevolent god is powerless, so they simply blame this 'sin' thing for allowing 'genetic entropy' to cause an organism to 'devolve' (it would be a serious blasphemy to call it 'evolution' so Michael J Behe and the Deception Institute had put their heads together and come up with the term 'devolution' instead, which makes it look like the exact opposite of 'evolution'. Stupidly, this devise claims that everything was created perfectly and, when Adam & Eve 'sinned', somehow this opened the door to 'sin', which apparently took their 'omniscient' god by surprise, even though it had given its alleged creations immune systems in anticipation of the effects of 'Sin'.

But of course, we can dismiss that half-baked notion which no serious biomedical scientist would take seriously because there is no mechanism for a deleterious (i.e, 'devolutionarly' trait to accumulate in the species gene pool, and whatever it is about V. cholerae that gives it the edge over other strains, can't rationally be described as 'devolutionary', or a move away from some notional initial perfection, because there can't be anything better than perfect, and yet the 7PET strain of V. cholerae is better at doing the two things it appears to have been designed to do - making more people sick and making more copies of itself than the other strains.

Malevolent Design - How Creationism's Divine Malevolence Co-opted Red Squirrels To Spread Leprosy in Medieval England

Lepers having magic spells cast over them

Mycobacterium leprae

Ancient Mycobacterium leprae genome reveals medieval English red squirrels as animal leprosy host: Current Biology

Few places in Europe or elsewhere were more pious than Medieval England, but still creationism's pestilential malevolence continued to make people suffer with diseases such as bubonic plague, tuberculosis and the related leprosy. Even the extreme measures taken by believers to atone for imaginary transgressions that had brought about the Black Death had failed to assuage the putative designer god who was believed to be visiting this pestilence upon people.

The superstitious Bible-based belief in evil spirits and 'sin' as the cause of disease led to the social stigma that made the disease so feared and led to the isolation of sufferers in lepper colonies, and often reduced to begging to stay alive. Poor nutrition and poor sanitation led to a worsening of the condition and, although these counter-measures were visibly ineffective, such was the belief in the Bible that it was inconceivable that the disease could be caused by anything other than 'sin' and evil demons being permitted to enter the victim.

The modern equivalent of this victim-blaming superstition can be found in the modern creationist tactic of blaming 'Sin' and 'genetic entropy' for parasites, with demons being replaced by 'entropy' to make it sound sciencey. It is of course, Bible-based superstition without supporting evidence.

And now, if you believe that stuff, there is evidence that creationism's putative designer god designed M. leprae to also infect red squirrels so they would act as a repository to spread leprosy. Red squirrels were common in those days and were often captured in the wild for pets or pelts. Their skins, when used for clothing, would have carried M. leprae and infected anyone who wore them - a brilliant strategy, if you hate people and want them to be sick, suffer and die.

Malevolent Designer News - How Creationism's Favourite Pathogen Is Designed to Cause UTIs

Escherichia coli,
The usual cause of urinary tract infection (UTI)

UTI's will affect 50% of women at some time in their lives

How E. coli get the power to cause urinary tract infections | Michigan Medicine

Despite their protestations that their god doesn't create pathogens - some other creative entity does that, apparently - they have been in love with Escherichia coli, or E. coli ever since their guru and Deception Insitute flunky, Michael J Behe, persuaded them that he had 'proved' their god exists and designs things because he couldn't work out how the E. coli flagellum could have evolved - so God did it!

There problem then, courtesy of Michael J Behe is that they have accepted that, if there was a designer involved in E. coli's design, it is the god that Michael J Behe 'proved' designed it, so their god designs pathogens, and even designs clever way to make them good at making us sick.

With that in mind, which creationist is going to argue against Michael J Behe's clever 'proof' that their god designs things so must exist, and insist that it isn't also behind the newly discovered way it manages to cause urinary tract infections (UTIs)?

The discovery that they can live, reproduce, and do their nasty thing in the otherwise near-sterile urinary tract, was made by researchers at the laboratory of Professor Harry Mobley in the University of Michigan Medical School.

Having been filtered by the kidneys, while urine contains some chemicals such as metabolites, it is about as sterile as it gets, with anything in it entering through the urethral meatus, in women, stupidly placed near the anus and inside the vulva where it can become infected during sexual intercourse by a penis cleverly designed with a foreskin to harbour pathogens under.

It has now been discovered that E. coli is also cleverly 'designed' to grab the nutrients it needs but can't manufacture itself by have a highly efficient transport system for taking them from its victims at a rate of thousands of molecules a second. One of the genes responsible for this, codes for an enzyme known as ATP-binding cassette (ABC).

Typical of creationism's 'intelligent' [sic] designer, if you believe in such a thing, is the Heath-Robinson workaround for the lack of genes for manufacturing these amino acids, where the parasite needs an energy-intensive ATP-based transport system, complete with multi-layered back-up systems to keep them working - the needless waste and needless complexity, so typical of evolved systems and the antithesis of intelligently designed systems. The researchers have published their findings, open access, in the journal PNAS and explained them in a University of Michigan news release:

Creationism in Crisis - A Microorganism That Manipulates It's Host To Make The Nutrients It Needs

Electron microscopy showing the parasitic Candidatus Nanohaloarchaeum antarcticus: the small circular shape, attached to its host, Halorubrum lacusprofundi.

Image Credit: Joshua N Hamm

Another example of the parasitic Candidatus Nanohaloarchaeum antarcticus attached to its host, Halorubrum lacusprofundi.

Image Credit: Joshua N Hamm

Archaea can be picky parasites - NIOZ

The Bible is silent on the subject of microorganisms because they were unknown to the Bronze Age authors. But now we know better than them, we can see other ways in which they refute several basic creationist dogmas.

Firstly, there is the problem that creationists always struggle with when they don't avoid it altogether - that of parasites and how they fit into a world 'designed' by an omnibenevolent god who wishes to minimise the about of suffering in the world. More on this later…

Then the fact that archaea and bacteria could be different forms of life which arose independently showing that abiogenesis is not only possible but may have happened twice on Earth. And as they both have the same genetic 'code' this suggests that the 'code' was inevitable, not some special creation requiring a magician to produce it.

But that's a minority view; the consensus being that they have a common ancestor from which they diverged about 3.5 billion years ago.

Creationism in Crisis - Yeast Evolution - Not Whether But How

Electron micrograph of budding yeast cells.

Ira Herskowitz and E. Schabtach

Electron micrograph of budding yeast cells

Photo: Ira Herskowitz and E. Schabtach

Bioinformatics professor discovers surprising evolutionary pattern in landmark yeast study | Inside UNC Charlotte | UNC Charlotte

As I've remarked before, trying to debate with creationists is like boxing with a brain-dead opponent who lacks the cognitive ability to know when they're down and out. Their lumbering body keeps flailing around and like a defeated Donald Trump, insists that they’ve won, and are triumphing over all-comers in the ring.

Creationist frauds have been telling their willfully ignorant cult that they are winning the debate against science and science is about to convert to creationist superstition and abandon the materialist explanations. The science that has produced all of modern technology, including the computers and Internet that they use to inform the world that science is all wrong, and magic done by an unproven supernatural being is a better explanation for the observable facts, endearingly oblivious of the irony.

And yet not a single science paper has ever concluded any such thing and the small handful of pseudo-scientists that the creation cult employs to misinform the world never publish in peer-reviewed science journals. It's almost exactly like science just gazes bemusedly at the hopeless flailings of creationism, which has been on the canvas now for 50 years but still hasn't noticed. The trick has been to remain completely oblivious of real science by never reading anything that might make them wonder if being horizontal on the canvas is the best way of winning a boxing match.

Meanwhile real scientists do real science and science moves on.

An example of this was a paper published recently in Science which is the result on an AI assisted detailed analysis of the genomes of 1,154 strains of the ancient, single-cell yeast, Saccaromycotina, to discover how the different yeasts had evolved. Nowhere in the paper is there the slightest hint that the process that produced the different strains might be magic, not natural evolution. Instead, the research provides more understanding of how the evolutionary processes work.

The research by a team co-led by Professor of Bioinformatics Abigail Leavitt LaBella of the University of North Carolina at Charlotte, is explained in a University of North Carolina news release:

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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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.