Mallevolent Design - How Salmonella Sneaks Past Our Defences To Make Us Sick

Salmonella infects the small intestine and alters the colon environment

Intestinal lumen

New study shows how salmonella tricks gut defenses to cause infection

There is a simple paradox at the heart of creationism that I have never even seen an attempt to resolve. It all comes from two beliefs: there is only one designer god capable of designing living organisms and that designer god designed us complete with our immune system with which we can attempt to resist attack by pathogens, and that pathogens are not the work of this design, but are the result of 'genetic entropy' and 'devolution' since Adam & Eve let 'sin' into the world. The fact that Michael J. Behe, who invented that excuse, has let slip that ID Creationism is Bible literalism in a lab coat seems to be lost on his followers who still dutifully insist that it is a scientific alternative to evolution and should be taught in school science class (presumably now with the tale of Adam & Eve taught as real history and 'sin' as a real force in science).

The paradox is, did the designer god give Adam & Eve an immune system, or did it design an upgrade when 'sin' allowed pathogens to exist? If the former, it was anticipating and planning for the so-called 'fall'; if the latter, it lacked foresight so is not omniscient.

But however creationists resolve this paradox they still have to explain why the 'intelligently designed' immune system doesn't work very well and why whatever is designing pathogens seems to be able to overcome it.

The nonsense about 'sin', 'the fall', etc., is trivially easy to refute because any improvement in a parasite's ability to parasitise its host can't possibly be regarded as a devolution from some assumed initial perfection because an improvement can't be worse that what it's an improvement on. The whole nonsense of 'devolution' is biological gobbledygook, intelligently designed to appeal to scientifically illiterate simpletons who want to fit the Bible superstition somewhere in the reasoning without bothering too much about the logic or the biology.

So, the paradox boils down to why an intelligent designer would be having an arms race with itself so the parasites it creates can continue to parasitise the victims it creates complete with their immune system it created to stop them. Creationists normally flee in terror at the mere mention of arms races, which is why you'll never see them discussed in the cult literature apart from where pathogens are waved aside as 'caused by sin', blah, blah, blah...
So, it would be refreshing indeed to see a genuine attempt by an intelligent design creationist try to give some rational explanation, and hopefully without giving away the fact that ID creationism is merely Christian fundamentalism in disguise, for the discovery by a new UC Davis Health study that shows how the Salmonella bacteria, a major cause of food poisoning, can invade the gut even when protective bacteria are present.

As an added embarrassment for creationists, Salmonella is closely related to Escherichia coli (E.coli) that they usually cite Michael J. Behe as 'proving' it must have been designed by their god because its flagellum is 'irreducibly complex'.

First a little AI background information about Salmonella, where it came from and what it does to us:

Tell me all about Salmonella, please. Salmonella is a genus of bacteria that is commonly associated with foodborne illnesses in humans and animals. These bacteria are known for causing a range of conditions, from mild gastroenteritis to more severe diseases like typhoid fever. Here's an overview of Salmonella:

1. What is Salmonella?
   Salmonella are rod-shaped, Gram-negative bacteria belonging to the family Enterobacteriaceae. They are facultative anaerobes, meaning they can grow in both oxygen-rich and oxygen-poor environments.
   
2. Types of Salmonella
   Salmonella is classified into two broad categories based on the diseases they cause:
   
   
   1. Non-typhoidal Salmonella (NTS):
      • Causes salmonellosis, a common form of food poisoning.
      • Found in many animals, including poultry, cattle, reptiles, and amphibians.
      • Symptoms include diarrhea, fever, abdominal cramps, and vomiting.
   2. Typhoidal Salmonella:
      • Includes Salmonella Typhi and Salmonella Paratyphi, which cause typhoid and paratyphoid fever, respectively.
      • These infections are severe, systemic diseases primarily transmitted through contaminated water or food.
3. How is Salmonella Transmitted?
   
   • Foodborne: Consuming undercooked or contaminated meat (especially poultry), eggs, or dairy products.
   • Waterborne: Drinking contaminated water.
   • Contact: Handling animals or surfaces contaminated with Salmonella, such as pet reptiles or farm animals.
   • Person-to-Person: Rare but possible in cases of poor hygiene, especially among caregivers.
4. Symptoms of Salmonella Infection
   The symptoms vary based on the type:
   • Salmonellosis (non-typhoidal): Appears 6-72 hours after exposure; lasts 4-7 days.
     
     • Diarrhea
     • Fever
     • Abdominal cramps
     • Nausea and vomiting
   • Typhoid Fever: Develops gradually over 1-2 weeks.
     
     • High fever
     • Weakness
     • Abdominal pain
     • Rose-colored spots on the skin
     • Constipation or diarrhea
5. Risk Groups
   
   • Infants, young children, and the elderly.
   • People with weakened immune systems, such as those with HIV or undergoing chemotherapy.
   • Travelers to regions with poor sanitation.
6. Diagnosis
   
   • Laboratory Testing: Stool, blood, or urine samples are tested for the presence of Salmonella.
   • Serotyping: Identifies specific Salmonella strains, useful for outbreaks and epidemiological studies.
7. Treatment
   
   • Non-typhoidal Salmonella: Often self-limiting; hydration is crucial. Antibiotics are usually unnecessary unless the infection spreads beyond the intestines.
   • Typhoidal Salmonella: Requires prompt antibiotic treatment, such as ciprofloxacin or azithromycin. Severe cases may require hospitalization.
8. Prevention
   
   1. Food Safety:
      • Cook meat and eggs thoroughly.
      • Avoid cross-contamination between raw and cooked foods.
      • Wash fruits and vegetables well.
      • Store food at proper temperatures.
   2. Hygiene:
      
      • Wash hands frequently, especially after handling animals or raw foods.
      • Sanitize surfaces and utensils.
   3. Vaccination:
      • Vaccines are available for Salmonella Typhi for travelers to high-risk areas.
   4. Pet Precautions:
      • Avoid contact with reptiles or amphibians, especially for children under five.
9. Global Impact
   • Non-typhoidal Salmonella: A leading cause of foodborne illnesses worldwide.
   • Typhoid Fever: Endemic in many developing countries, with poor sanitation contributing to its prevalence.

Interesting Facts

• Salmonella is named after American scientist Daniel Elmer Salmon, though it was first discovered by Theobald Smith in 1885.
• These bacteria can survive on dry surfaces for weeks and in water for months.
  

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What is known about the evolutionary origins of the genus and their relationship to other genera?

The genus Salmonella has a fascinating evolutionary history that reflects its adaptation to a wide range of hosts and ecological niches. Here's an overview of what is known about its evolutionary origins and relationships with other genera:

1. Evolutionary Origins
   • Family and Order:
     • Salmonella belongs to the family Enterobacteriaceae and the order Enterobacterales. This group includes other genera such as Escherichia, Klebsiella, Yersinia, and Shigella.
     • These bacteria are believed to have a common ancestor that lived in the intestinal tracts of primitive animals hundreds of millions of years ago.
   • Divergence from Common Ancestor:
     • Genomic analyses suggest that Salmonella diverged from its closest relative, Escherichia coli, approximately 100–150 million years ago. This divergence was likely driven by adaptation to different ecological niches and hosts.
     • Salmonella has specialized in both intestinal and systemic infections, while E. coli primarily remained a commensal organism with occasional pathogenic strains.
2. Genomic Evolution
   • Horizontal Gene Transfer (HGT):
     • A significant driver of Salmonella's evolution has been the acquisition of genes through horizontal gene transfer. This process introduced:
       • Virulence genes (e.g., pathogenicity islands).
       • Antibiotic resistance genes.
     • These acquisitions allowed Salmonella to colonize new hosts and environments.
   • Pathogenicity Islands:
     • The genome of Salmonella contains specialized regions called Salmonella Pathogenicity Islands (SPIs) that encode genes crucial for infection.
     • SPIs are thought to have been acquired from other bacteria through HGT and are absent in its close relatives, such as E. coli.
   • Adaptive Evolution:
     • Salmonella has developed mechanisms to survive harsh conditions, such as the acidic environment of the stomach or macrophage phagosomes. Genes encoding acid resistance and intracellular survival are key to this adaptation.
3. Speciation and Lineage Divergence
   
   • The genus Salmonella is divided into two main species:
     1. Salmonella enterica: The most diverse and widespread species, with six subspecies and over 2,500 serovars.
     2. Salmonella bongori: Found primarily in cold-blooded animals, such as reptiles.
   • Host Adaptation:
     • Salmonella enterica has evolved to infect a wide range of warm-blooded and cold-blooded hosts, whereas S. bongori remains restricted to reptiles.
     • Within S. enterica, specific serovars have adapted to particular hosts (e.g., S. Typhi for humans and S. Dublin for cattle).
4. Relationship to Other Genera
   • Closest Relatives:
     • Escherichia coli: Shares a common ancestor with Salmonella. The two genera are highly similar at the genomic level but differ significantly in pathogenicity and host adaptation.
     • Shigella: Genetically very similar to E. coli but evolved independently to cause invasive infections.
   • Phylogenetic Placement:
     • Within Enterobacteriaceae, Salmonella is part of a subgroup that includes pathogens like Shigella and Yersinia.
     • Comparative genomics shows that Salmonella diverged from E. coli after acquiring genes enabling systemic infection and survival in macrophages.
5. Ecological and Evolutionary Pressures
   • Host-Pathogen Interactions:
     • The evolutionary success of Salmonella is linked to its ability to exploit host defenses. For example, genes enabling intracellular survival have allowed it to persist within macrophages.
   • Environmental Reservoirs:
     • While primarily associated with animals, Salmonella can survive in environmental reservoirs like water and soil. This versatility has helped it spread globally.
6. Evolutionary Insights from Genomics
   • Advances in genomic sequencing have clarified Salmonella's evolutionary trajectory:
   • Core Genome: Highly conserved genes related to metabolism and cell structure.
   • Accessory Genome: Includes mobile genetic elements like plasmids, transposons, and bacteriophages that contribute to virulence and antibiotic resistance.
7. Molecular Clock Studies:
   • Analysis of mutation rates suggests that Salmonella continues to evolve rapidly, especially in response to human interventions like antibiotics.

Key Takeaways:

• Salmonella evolved from a common ancestor with E. coli but adapted to systemic infections through gene acquisition and environmental pressures.
• Its genomic flexibility and ability to colonize diverse hosts have been critical to its evolutionary success.
• Relationships with other genera, like Escherichia and Shigella, reveal a shared evolutionary history with divergence driven by ecological specialization.

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Is there much evidence of host-specificity?

Yes, there is considerable evidence of host specificity in Salmonella, with some serovars adapting to infect specific hosts more effectively than others. However, the extent of host specificity varies among Salmonella serovars and is influenced by their evolutionary adaptations and ecological niches. Here's a breakdown:

1. Host-Specific vs. Broad-Host-Range Serovars
   
   • Host-Specific Serovars:
     • These serovars are restricted to specific hosts and often cause severe, systemic infections in their target species.
       • Salmonella Typhi: Human-specific, causing typhoid fever.
       • Salmonella Paratyphi: Human-specific, causing paratyphoid fever.
       • Salmonella Dublin: Primarily infects cattle but can occasionally infect humans, usually causing severe disease.
       • Salmonella Choleraesuis: Adapted to pigs and can cause systemic infections in swine.
   • Broad-Host-Range Serovars:
     • These serovars infect a wide range of hosts and typically cause gastroenteritis.
       • Salmonella Enteritidis: A leading cause of foodborne illness in humans, associated with poultry and eggs but can infect other animals.
       • Salmonella Typhimurium: Infects a wide variety of mammals, birds, and reptiles, and is a common cause of foodborne illness.
2. Mechanisms of Host Specificity
   The host specificity of Salmonella serovars is influenced by several genetic and molecular factors:
   • Pathogenicity Islands (SPIs):
     • Salmonella Pathogenicity Islands (SPIs) encode virulence factors like Type III Secretion Systems (T3SSs) that allow the bacteria to invade and survive in host cells.
     • Differences in SPI genes contribute to host specificity. For instance:
       • S. Typhi and S. Paratyphi have unique virulence factors (e.g., Vi antigen) that help evade the human immune system.
       • S. Dublin has genes that enhance its ability to persist in cattle.
   • Adhesins and Surface Proteins:
     • Host specificity is often mediated by adhesins, which enable the bacteria to bind to specific host tissues.
     • For example, S. Typhi expresses fimbriae and adhesins that preferentially bind to receptors found in human intestinal epithelial cells.
   • Immune Evasion:
     • Host-specific serovars have evolved mechanisms to evade or modulate the immune responses of their target hosts.
       • S. Typhi produces proteins that suppress human immune responses, facilitating systemic infection.
   • Metabolic Adaptations:
     • Host-specific serovars often exhibit metabolic pathways tailored to the nutrient environment of their host. For example, some serovars can utilize host-specific compounds as energy sources.
3. Evidence from Genomic Studies
   Genomic studies have revealed key differences between host-specific and broad-host-range serovars:
   
   • Unique Genes:
     • Host-specific serovars often have genes not found in broad-host-range strains. These genes may encode virulence factors, metabolic enzymes, or regulatory proteins specific to their host environment.
   • Pseudogenes:
     • Host-restricted serovars like S. Typhi often have many pseudogenes—nonfunctional remnants of genes. This suggests they have lost functions unnecessary for survival in their specific host, leading to a narrowing of their ecological niche.
   • Phylogenetic Insights:
     • Phylogenetic analysis shows that host-restricted serovars tend to form distinct clades, reflecting their adaptation to specific hosts.
4. Experimental Evidence
   • Animal Models:
     • Studies using animal models have demonstrated the inability of host-specific serovars to infect non-native hosts effectively.
       • S. Typhi does not cause disease in mice or cattle without genetic modification.
       • S. Dublin causes systemic disease in cattle but only sporadic, severe infections in humans.
   • Natural Observations:
     • Epidemiological data show strong associations between certain serovars and specific hosts. For example:
       • S. gallinarum and S. pullorum are highly adapted to poultry, causing fowl typhoid and pullorum disease, respectively.
5. Exceptions and Spillover Events
   
   While some Salmonella serovars are highly host-specific, spillover events can occur:
   
   • Broad-host-range serovars like S. Typhimurium can infect a wide variety of species, often leading to zoonotic transmission to humans.
   • Host-specific serovars can occasionally infect non-native hosts, sometimes leading to severe disease. For instance:
     • S. Dublin can cause life-threatening bacteremia in humans, particularly in immunocompromised individuals.
6. Implications for Public Health and Veterinary Medicine
   
   Understanding host specificity is crucial for controlling Salmonella infections:
   
   • Zoonotic Risks: Broad-host-range serovars pose significant zoonotic threats, especially in foodborne outbreaks.
   • Vaccination and Control Strategies: Vaccines and interventions can be tailored to target specific serovars in their primary hosts (e.g., poultry vaccines against S. Enteritidis).

Conclusion
Host specificity in Salmonella reflects a complex interplay of genetic, molecular, and ecological factors. While some serovars are highly specialized, others maintain the flexibility to infect a broad range of hosts, contributing to their global prevalence and significance as pathogens.

What the UC Davis Health study, led by Professor Andreas Bäumler of the Department of Medical Microbiology and Immunology found is the subject of a paper in Proceeding of The National Academy of Science (PNAS) and a UC Davis press release by Nadine A Yehya:

New study shows how salmonella tricks gut defenses to cause infection

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(SACRAMENTO) A new UC Davis Health study has uncovered how Salmonella bacteria, a major cause of food poisoning, can invade the gut even when protective bacteria are present. The research, published in the Proceedings of the National Academy of Sciences, explains how the pathogen tricks the gut environment to escape the body's natural defenses.

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The digestive system is home to trillions of bacteria, many of which produce short-chain fatty acids (SCFAs) that help fight harmful pathogens. But Salmonella manages to grow and spread in the gut, even though these protective compounds are present. The study asks: How does Salmonella get around this defense?

We knew that Salmonella invades the small intestine, although it is not its primary site of replication. The colon is.

Professor Andreas Bäumler, lead author
Department of Medical Microbiology and Immunology
School of Medicine
University of California at Davis, Davis, CA, USA.

Bäumler and his team discovered that the answer lies in how the pathogen changes the gut’s nutrient balance. When Salmonella enters the small intestine, it causes inflammation in the gut lining and disrupts the normal absorption of amino acids from food. This creates an imbalance in nutrients in the gut.

The imbalance gives Salmonella the resources it needs to survive and multiply in the large intestine (colon), where beneficial bacteria usually curb its growth. The study showed that salmonella causes inflammation in the small intestine in order to derive nutrients that fuel its replication in the colon.

Salmonella alters gut nutrient environment to survive

Using a mouse model, the team looked closely at how Salmonella changed the chemical makeup of the gut. They traced amino acid absorption in the small and large intestines.

They found that in mice that were infected with Salmonella, there was less absorption of amino acids into the blood. In fact, two amino acids, lysine and ornithine, became more abundant in the gut after infection. These amino acids helped Salmonella survive by preventing the growth-inhibiting effects of SCFAs. They did this by restoring Salmonella’s acidity (pH) balance, allowing the pathogen to bypass the microbiota’s defenses.

Our findings show that Salmonella has a clever way of changing the gut’s nutrient environment to its advantage. By making it harder for the body to absorb amino acids in the ileum, Salmonella creates a more favorable environment for itself in the large intestine.

Professor Andreas Bäumler.

In the study, the team showed that Salmonella uses its own virulence factors (disease causing molecules) to activate enzymes that break down key amino acids like lysine. This helps the pathogen avoid the SCFAs’ protective effects and grow more easily in the gut.

New insights could lead to better gut infection treatments

The new insights potentially explain how the gut environment changes during inflammatory bowel disorders , such as Crohn's disease and ulcerative colitis, and could lead to better treatments for gut infections. By understanding how Salmonella changes the gut environment, researchers hope to develop new ways to protect the gut microbiota and prevent these infections.

This research uses a more holistic approach to studying gut health. It not only gives us a better understanding of how Salmonella works, but also highlights the importance of maintaining a healthy gut microbiota. Our findings could lead to new treatments that help support the microbiota during infection. By learning how a pathogen manipulates the host’s system, we can uncover ways to boost the host’s natural defenses.

Dr. Lauren Radlinski, first author.
Department of Medical Microbiology and Immunology
School of Medicine
University of California at Davis, Davis, CA, USA.

The study’s results could inspire future treatments, including probiotics or dietary plans designed to strengthen the body’s natural defenses against harmful pathogens.

Coauthors of the study are Andrew Rogers, Lalita Bechtold, Hugo Masson, Henry Nguyen, Anaïs B. Larabi, Connor Tiffany, Thaynara Parente de Carvalho and Renée Tsolis of UC Davis.

Significance
The microbiota protects the host from microorganisms that cause disease in unprotected or immunocompromised individuals. Enteric pathogens such as Salmonella enterica serovar (S.) Typhimurium are adept at circumventing and weakening these protections and in doing so render the host susceptible to infection. Here, we identify a strategy by which S. Typhimurium uses its virulence factors to manipulate the host environment in the small intestine to trigger downstream changes in the environment of the large intestine that enable the pathogen to overcome microbiota-mediated defenses. The more general implications of our work are that ileitis-induced malabsorption causes downstream changes in microbial growth conditions in the large intestine, which can trigger compositional changes.

Abstract
The gut microbiota produces high concentrations of antimicrobial short-chain fatty acids (SCFAs) that restrict the growth of invading microorganisms. The enteric pathogen Salmonella enterica serovar (S.) Typhimurium triggers inflammation in the large intestine to ultimately reduce microbiota density and bloom, but it is unclear how the pathogen gains a foothold in the homeostatic gut when SCFA-producing commensals are abundant. Here, we show that S. Typhimurium invasion of the ileal mucosa triggers malabsorption of dietary amino acids to produce downstream changes in nutrient availability in the large intestine. In gnotobiotic mice engrafted with a community of 17 human Clostridia isolates, S. Typhimurium virulence factors triggered marked changes in the cecal metabolome, including an elevated abundance of amino acids. In an ex vivo fecal culture model, we found that two of these amino acids, lysine and ornithine, countered SCFA-mediated growth inhibition by restoring S. Typhimurium pH homeostasis through the inducible amino acid decarboxylases CadA and SpeF, respectively. In a mouse model of gastrointestinal infection, S. Typhimurium CadA activity depleted dietary lysine to promote cecal ecosystem invasion in the presence of an intact microbiota. From these findings, we conclude that virulence factor–induced malabsorption of dietary amino acids in the small intestine changes the nutritional environment of the large intestine to provide S. Typhimurium with resources needed to counter growth inhibition by microbiota-derived SCFAs.

The gut microbiota is a critical frontline barrier that precludes the expansion of invading microorganisms through the production of antimicrobial compounds and the depletion of essential nutrients (1). During homeostasis, obligately anaerobic bacteria dominate the microbiota of the large intestine and ferment unabsorbed carbohydrates to produce high luminal concentrations of the short-chain fatty acids (SCFAs) acetate, propionate, and butyrate. These SCFAs are weak acids that become protonated in mildly acidic environments (HAc), such as the lumen of the colon (pH 5.7 to 6.2) (2), as the pH approaches the respective negative base-10 logarithm of the acid dissociation constant (pKa) for each molecule (~pH 4.7). Protonated SCFA are membrane permeable, but exposure to a more neutral pH in the cytosol (pH 7.2 to 7.8) (3–5) results in their dissociation into the salt and a proton (Ac⁻ + H⁺). The consequent acidification of the bacterial cytosol results in growth inhibition and serves as a canonical, nonspecific defense mechanism against invading enteric pathogens such as Salmonella enterica serovar Typhimurium (S. Typhimurium) (3, 6–8).

S. Typhimurium uses its virulence factors, two type III secretion systems (T3SS-1 and T3SS-2) (9, 10) encoded by Salmonella pathogenicity island (SPI)1 and SPI2 (11, 12), respectively, to break colonization resistance through mechanisms that are not fully resolved (13, 14). T3SS-1 and T3SS-2 trigger intestinal inflammation (15–17), which boosts growth of S. Typhimurium by increasing the availability of host-derived respiratory electron acceptors, including tetrathionate (18), nitrate (19, 20), and oxygen (21). In addition, aspartate is liberated when phagocyte-derived reactive oxygen species lyse luminal bacteria (22), which fuels growth of S. Typhimurium through fumarate respiration (23). Tetrathionate respiration has been shown to promote growth of S. Typhimurium in the lumen of the murine cecum by utilizing ethanolamine (24), which is generated when taurine liberated during deconjugation of bile acids is used as an electron acceptor by Deltaproteobacteria. Oxygen and nitrate enable the pathogen to utilize host-derived lactate (25) or 1,2-propanediol (26), a microbiota-derived fermentation product of pentoses. However, growth during in vitro culture under conditions that mimic the cecal environment suggests that high concentrations of SCFAs and the acidic environment of the cecum counter the competitive edge that oxygen and nitrate respiration confer upon the pathogen (27). These data suggest that S. Typhimurium virulence factors act on the host to generate yet unidentified resources that enable the pathogen to overcome growth inhibition by SCFAs in the lumen of the large intestine.

Here, we used untargeted metabolomics to identify resources generated by S. Typhimurium virulence factor activity during gastrointestinal infection and investigated their role in countering SCFA-mediated intracellular acidification.

L.C. Radlinski, A.W.L. Rogers, L. Bechtold, H.L.P. Masson, H. Nguyen, A.B. Larabi, C.R. Tiffany, T.P.D. Carvalho, R.M. Tsolis, A.J. Bäumler
, Salmonella virulence factors induce amino acid malabsorption in the ileum to promote ecosystem invasion of the large intestine Proc. Natl. Acad. Sci. U.S.A. (2024) 121(47), e2417232121, DOI: 10.1073/pnas.2417232121.

Copyright: © 2024 The authors.
Published by the National Academy of Science. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

I wonder if a creationist would be brave enough to attempt to explain these advantageous abilities of Salmonella, which enable it to survive and overcome our natural defences in our intestines in terms of 'devolution' from an initially designed perfection, or, if not, explain why, if the E.coli's flagellum is proof of their designer god, as devotees of Michael J. Behe insist, it isn't also proof of their designer god's work in Salmonella.

Alternatively, perhaps they could talk us through the process by which 'sin' is able to redesign a pathological bacterium to make it better at making us sick and increasing the suffering in the world, and even tailor-making some serovars so they target specific species, one of which is human.

Common Ancestry - Ancient Choanoflagellates Genes Used To Make A Mouse

Electron micrograph of the choanoflagellate, Salpingoeca.

By Sergey Karpov - http://www.choano.org/wiki/Choanoflagellate_Gallery#Salpingoeca_sp._Gallery, CC BY-SA 3.0, Link

Choanoflagellates, singly and as a colony.

Scientists recreate mouse from gene older than animal life - Queen Mary University of London

If there is one thing designed to get creationists chanting 'Common Designer!' it's evidence of the same gene doing the same thing in lots of different organisms, no matter how distantly related they are.

But when that gene is needed because of a basic design blunder long ago in the evolution of multicellular organisms, that chant looks increasingly forlorn.

For example, scientists have just shown how SOX and POU genes isolated from a single-celled choanoflagellate can be used to convert a mouse cell to function as the stem cell to clone another mouse. The reason this works is because something needs to reset the epigenetic setting in specialised cells. In a multicellular organism like a mouse, this effectively means any cell produced after the first few cell divisions of the fertilised zygote.

But why would a single-celled organism like a choanoflagellate need to do that? The answer it that epigenetics originally evolved to make an organism more able to respond to environmental changes and stresses.

Refuting Creationism - How Eggs Evolved Hundred of Millions of Years Before Chickens

A cell of the ichthyosporean C. perkinsii showing distinct signs of polarity, with clear cortical localization of the nucleus before the first cleavage. Microtubules are shown in magenta, DNA in blue, and the nuclear envelope in yellow.

© DudinLab

Chromosphaera perkinsii resembles the early stages of animal embryo development during its multicellular life stage

DudinLab

The egg or the chicken? An ancient unicellular says egg! - Medias - UNIGE

Scientists believe they may have cracked the chicken and egg 'problem' that creationists have been fooled into thinking is a killer problem for the Theory of Evolution. With their child-like understanding of evolution, creationists can't imagine how species emerge over time from earlier species by a process of evolution and think that their mythical magic creation without ancestors is actually what happens, or at least what evolutionary biologists think happens. So, they imagine explaining how the first chicken hatched from the first egg before there was a chicken to lay it, is an insurmountable problem.

In fact, of course there never was a first chicken just as there never was a first human, and eggs are simply a phase in the life cycle of, in this case, chickens, so hens' eggs are chickens just as much so as adult hens are. The ancestral species that the Southeast Asian jungle fowl evolved from had been laying eggs ever since they diverged from the egg-laying avian dinosaurs that had evolved from the egg-laying theropod dinosaurs, etc, etc, back to the egg-laying tunicates and chordates in the Cambrian and their egg-laying ancestors...

Malevolent Design - How Chlamydia Is 'Designed' to Cause Maximum Sufferring.

Chlamydia pneumoniae

AI-generated image (ChatGPT4o)

Schematic representation of how a C. pneumoniae cell infects a human cell. The bacterium injects the protein SemD (green) into the cell, which activates the cell protein N-WASP, which in turn initiates vesicle formation.

Credit: HHU/Fabienne Kocher.

Universität Düsseldorf: Original or copy: How Chlamydia manipulate the host cell

The problem of parasites for creationists is one that, despite the best efforts of apologists like Michael J Behe of the Deception Institute, just won't go away.

Sadly, Behe shot himself in the foot with his original claim to have proven 'intelligent [sic] design in living organisms with his choice of the bacterial flagellum in E. coli, where he persuaded his willing audience that these nasty little pathogens had been intelligently designed - and by unspoken assumption, designed by the locally-popular god.

Now creationists wave his 'proof' of design as evidence for their creator god because only their god is capable of creating living organisms.

But, with characteristic double-think, creationists also argue that their god is omnibenevolent, so something else must have created parasites like E. coli, and, courtesy again of Michael J. Behe, they cite 'Sin' causing 'genetic entropy' and the absurd idea of 'devolution' this supposedly causes, as the cause of parasites and pathogens (but not the bacterial flagellum, obviously!).

The problem with that notion is that they need to do their double-think trick one more time and believe that a trait with improves a pathogens ability to live and reproduce in its host makes it somehow less perfect that one without that trait. So, in the creationist's world, an improvement is a move away from perfection!

But, with a cult that appears to believe learning is a move away from the 'perfection' of pristine ignorance (from whence comes expertise in all aspects of science), that's probably not too difficult a feat of mental gymnastics for a creationist to perform.

Refuting Creationism - Even More Signs of The Divine Malevolence's Obsessive Compulsive Disorder?

AI-generated image (ChatGPT4o)

Over 160,000 new virus species discovered by AI - The University of Sydney

This is the second paper today to show the apparent obsession creationism's putative designer has with creating viruses, if you believe that superstition.

The first paper dealt with the discovery that there are some 600 different viruses to be found on a used toothbrush and on the shower heads in US bathrooms; this one reports on a discovery that makes that finding pale into insignificance. It is the discovery, using the machine learning of AI, of 161,979 new viruses!

This is just tip of the iceberg as the authors say the method just scratches the surface of biodiversity and opens up a world of discovery with millions more to be discovered.

Refuting Creationism - Is Creationism's Divine Malevolence Sufferring from Obsessive-Compulsive Disorder?

Northwestern microbiologists found more than 600 viruses on samples collected from used toothbrushes and shower heads.

AI-Generated graphic (ChatGPT4o)

Structural model at atomic resolution of bacteriophage T4

By Dr. Victor Padilla-Sanchez, PhD https://www.drvictorpadillasanchez.com
Own work, CC BY-SA 4.0, Link

Viruses are teeming on your toothbrush, showerhead - Northwestern Now

Creationism's putative creator is nothing if not obsessive.

One of its obsessions appears to be designing ever-more exquisite ways to kill its creation as almost nothing in nature exists that doesn't have something that lives on or in it, often killing it in the process or at least weakening it in some way.

Its most visible obsession seems to be with designing beetles of which there are some 500,000 species with more being discovered almost daily. It's highly likely that there may be as many as a million different beetles in the world, many of which catch and devour other arthropods.

But it's in the field of virology that we find another obsession with designing variations on a general theme. Not only are there literally hundreds of thousands of viruses but every species has multiple variants - look at the number of different variants of the SARS-CoV-2 virus that have emerged since the initial wave of the COVID-19 pandemic!

Refuting Creationism - Living Bacteria Sealed Inside 2 Billion-Year-Old Rock

Microbial cells stained green

© Y. Suzuki, S. J. Webb, M. Kouduka et al. 2024/ Microbial Ecology

2-billion-year-old rock home to living microbes | The University of Tokyo

The Bushveld Igneous Complex (BIC), South Africa.
This picture shows a very famous outcrop where nearly horizontal black and white layers are observed. The BIC made of layers of igneous rock in a basin shape, formed over a period of about 1 million years, after which it seems to have barely changed.

© Y. Suzuki.

In today's incidental rebuttal of creationist dogma, archaeologists have discovered living colonies of microbes sealed within cracks in 2-billion-year-old rocks from South Africa.

The microbes became sealed in the cracks by tightly-packed layers of clay so effectively creating sealed chambers from which nothing could escape and, more importantly, nothing could enter. They have survived over geological time by firstly having an extremely low metabolic rate, with a generation time measured in thousands, even millions of years, compared to surface-dwelling microbes with generation times in hours or minutes, and by utilising sulphates as their energy source.

What they demonstrate, apart from the fallacy of Earth only being made by magic 10,000 years ago, is that in a highly stable environment, a plentiful source of energy and the ability to recycle their dead with almost no loss of energy, there is no environmental pressure to evolve, so the microbes have remained virtually unchanged for hundreds of millions, even billions of years.

Malevolent Design - A Newly-Discovered Gut Bacterium That Suppresses Immunity!

Drs. Thaddeus Stappenbeck, M.D., Ph.D., (left) and Qiuhe Lu, Ph.D., in the lab.

Cleveland Clinic Discovers Bacterium Causing Gut Immunodeficiency

The human gut, like that of other mammals, birds and vertebrates in particular and the gut of many insects and worms, in fact any organism with a moth and an anus, is an ideal environment for a whole host of other organisms, most of which will have co-evolved with humans and have been with us since our ancestors were small insectivores, skulking in the dark of the night to avoid dinosaurs and predatory proto-birds.

They for a complex and dynamic ecosystem of competing and cooperating bacteria, viruses, fungi and protozoa which exists in a more or less stable balance of arms races, predation and symbiosis.

Refuting Creationism - An Improved Method For Analysing Ancient Microfossils To Discover How Life Evolved

Research News - Unveiling Ancient Life: New Method Sheds Light on Early Cellular and Metabolic Evolution | Tohoku University Global Site

One of the clutch of science publications which casually and unintentionally refute creationism to be published today, comes in the form of a paper by a team from the University of Tokyo, Tohoku University and Kochi University, Japan, which describes a new method for analysing ancient microfossils, and so discovering more about how key processes evolved in early cellular life.

The purpose of this is to discover not whether (that is never in doubt) but the precise details of how and when these key processes evolved.

Malevolent Designer News - Why Cholera is So Good at Killing Us

Vibrio cholerae

AI generated image (ChatGPT4o)

Vibrio cholerae

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News - Experts discover the deadly genetics of cholera, which could be key to its prevention - University of Nottingham

Although good hygiene and safe drinking water have most brought cholera under control in developed societies, it is still a major kill, especially of children, in poor and technologically under-developed countries.

It was a cholera outbreak of 1849 in Soho, London, the John Snow famously showed was statistically linked to drinking water from a well in Broad Steet, eventually persuading the authorities to remove the pump handle from the well, so ending the epidemic, that Snow conformed the Germ Theory of disease and founded modern epidemiology.

The cause was later shown to be a leaking septic tank which was contaminating the water in the well, and more remotely to a baby which caught cholera elsewhere whose nappy (diaper) was washed into the sewer, introducing the Vibrio cholerae into the septic tank.

I was born and brought up in North Oxfordshire in a rural community where, a generation earlier, cholera had been the single most common cause of death of children. A perusal of the parish burial registers shows regular patterns of epidemics causing a sudden increase in child deaths.

Even in technologically advanced countries, natural disasters such as earthquakes and floods, and man-made conflicts such as those currently in Gaza and Ukraine can destroy the infrastructure and quickly lead to conditions in which cholera can further devastate an already weakened population.

It would be an especially despicable malevolence that designed an organism to exploit people in those situation to ensure there was even more suffering, but those subscribing to the intelligent design hoax are unwittingly attributing exactly that to their putative designer god.

Malevolent Designer News - What Was The Divine Malevolence Doing With Plague Bacteria 5000 years ago?

Spread of Yersinia pestis (Black Death)

AI generated

In the study, scientists performed a genetic analysis on the bones of 133 human individuals from late Neolithic megalithic graves near Warburg in North Rhine-Westphalia. The team discovered the genome of the bacterium Yersinia pestis in the bone samples of two independent individuals. Additionally, previously published genomic data from a bone sample of a Neolithic dog found in Ajvide (Sweden) suggested a potential infection route.

© Carsten Reckweg, CRC 1266/Uni Kiel

Neolithic plague bacterium did not cause mass mortality

What was creationism's divine malevolence up to with one of its most successful pathogens with which if killed hundreds of millions and changes society - the Yersinia pestis bacterium which caused the waves of black death and plague that regularly spread across the world?

It seems to have been experimenting, possibly trying to either perfect its virulence or work out the best delivery system to ensure it got to and killed as many people as possible. Sometimes, entire villages were wiped out. Not far from where I currently live are a couple of former villages that disappeared during the black death - the village of Woodperry near Oxford is an example, surviving now only in the name 'Woodperry Road' and a farmhouse later built on the site.

But 5000 years ago, Y. pestis doesn't seem to have been anything like a virulent as it became in the 12th Century. According to a recent discovery, it was capable of killing the occasional neolithic farmer but not of becoming a major pandemic able to kill hundreds of thousands and depopulate vast areas.

So, what changed, and more to the point, which explanation would a creationist prefer; the one which blames their god or the one which attributes it to evolution, climate change and cultural changes in human society? One thing we can be sure of though is the Michael J. Behe's biologically nonsensical religious apologetic of 'genetic entropy', causing the bacterium to 'devolve' away from an assumed created perfection (as though that were remotely possible), can be ruled out, because whatever the changes were, it led to a massive increase in the number of Y. pestis organisms, so was indisputably beneficial to it - in other words, in classical terms, it evolved.

Refuting Creationism - Co-Evolution Of Humans And Their Gut Microbiome

Development of the infant gut microbiome

AI generated image
(complete with spelling idiosyncrasies)

Natural probiotic discovered in UK newborns’ microbiomes

In a very nice example of how humans and their gut microbiome have co-evolved, researchers from the Wellcome Sanger Institute, University College London (UCL), and the University of Birmingham, have identified a bacterium that helps digest breast milk and protects the baby from harmful pathogens.

As an example of intelligent [sic] design, this comes as close to a Heath-Robinson solution to a problem of the designer's own making as it's possible to imagine.

No designer who designed a baby's digestive system so it is susceptible to the harmful pathogens that it also designed, and created the baby to feed on breast milk that is difficult to digest, then solved those problems by creating another bacterium to fight the pathogens and help digest the milk, and infecting the baby with it, doesn't deserve the adjective 'intelligent'. 'Bloody stupid' would be a more appropriate term.

It's almost exactly as though the designer of these systems is a mindless automaton, simply obeying the natural laws of chemistry and physics and working without a plan!

The researchers have completed the largest study of UK baby microbiomes to date, carrying out whole genome sequencing to analyse stool samples from 1,288 healthy infants, all under one month old from the UK Baby Biome Study^1.1.

Malevolent Designer News - How An Oral Bacteria Aggrevates Rheumatoid Arthritis

AI-generated image (ChatGPT4o)

Colorized image of a colony of Actinobacillus actinomycetemcomitans

Derren Ready/Wellcome Images
CC BY-NC-ND 3.0

Shedding Light on How Oral Bacteria Can Aggravate Rheumatoid Arthritis｜Tokyo Medical and Dental University, National University Corporation

Not content with the suffering that gum disease and dental caries cause, creationism's divine malevolence used at least one of the pathogens behind those problems to increase suffering a little more by aggrevating rhuematoid arthritis.

That's the inevitable conclusion honest creationist, who rejects the notion of evolution in which pathogenic parasites evolve naturally without intent, malevolent, benign or indifferent, should be drawing from the evidence from a Tokyo Medical and Dental University team of researchers led by Tokuju Okano and Toshihiko Suzuki of the Department of Bacterial Pathogenesis recently published in the International Journal of Oral Science.

This is not the first instance of creationism's divine malevolence multi-tasking its pathogens: in 2017 a team of researchers from The Chinese University of Hong Kong found a link between five oral bacteria, Peptostreptococcus stomatis, Streptococcus anginosus, Parvimonas micra, Slackia exigua and Dialister pneumosintes and the incidence of stomach and eosphageal cancer.

The oral bacterium which has been found to be aggrevating rheumatoid arthritis is Aggregatibacter actinomycetemcomitans.

Refuting Creationism - Selfish Genes Evolved Cooperative Alliances

Complex human gut microbiome

ChatGPT4o AI generated image

This article is best read on a laptop, desktop or tablet

Fish swimming past coral and marine sponge. The researchers are currently using the proposed framework to investigate microbes inside marine sponges.

Researchers create new framework to help understand how microbial communities emerge - Swansea University

One of the lines of attack against the science of evolutionary biology is the lie that Richard Dawkins was advocating selfishness with his seminal book, The Selfish Gene, so 'proving' that rejection of the Christian god as the explanation for biodiversity is because 'Evolutionists' just want to sin.

It is, of course, like other creationist attacks on science, utterly devoid of any factual basis and reflects badly both on those who seek to fool their target dupes with it and on their dupes who eagerly believe them in order to justify a pretense of moral superiority.

In fact, natural selection and differential success of different alleles within a selective environment is devoid of any moral contents because it is devoid of intelligent input and genes are passive in the process. In Dawkin’s analogy, the result is as though genes behave selfishly, not that they make moral decisions or have the ability to choose which environmental selectors act on them.

One of the predictable outcomes of this gene-centred approach is that in a competition, the result which suits all competitors is cooperation since in a cooperative alliance, all the genes are winners, just as with a human group, a cooperative group is invariably more successful than a group of competing individuals in perpetual conflict.

Malevolent Design - How A Human Mouth Bacterium Is 'Designed' For Super-Fast Proliferation

Corynebacterium matruchotii

Public domain

Open Wide: Human Mouth Bacteria Reproduce through Rare Form of Cell Division | Marine Biological Laboratory

Cellular elongation at the tips of the filamentous bacteria Corynebacterium matruchotii.

Credit: Chimileski et al (2024).

Most cells, either single-celled organisms like bacteria or the eukaryote cells of multicellular organisms, reproduce by simple division into two daughter cells. Under favourable conditions, this means a cell can produce a population of descendants that grows exponentially 1 → 2 → 4 → 8 → 16 → 32→64 … etc. (population = 2ⁿ; where n= the number of generations)

But the trick a bacterium, Corynebacterium matruchotii, that is only found in the human mouth uses is to divide into multiple new cells at each generation. For example, assuming it splits into 10 daughter cell at each generation, its growth rate from a single founder cell will be 1 → 10 → 100 → 1000 → 10,000 → 100,000 → 1,000,000 … etc., (population = 10ⁿ). But scientists have found it can do better than that, producing up to 14 new cells at each generation.

In 6 generations in favourable conditions, Corynebacterium matruchotii can produce 1 million or more offspring, against an 'ordinary' bacteria's 64, so rapidly out-pacing any other bacteria. C. matruchotii is an essential component of the plaque that quickly develops on teeth. It appears to have no other known function.

In some ways, C. matruchotii behaves more like fungal hyphae, growing at the tip to produce a long thin filament. It is this filament that then simply splits up into small sections, each of which becomes a new cell.

The filamentous bacteria C. matruchotii splitting into multiple cells at once, a rare kind of cell division called multiple fission.

Credit: Scott Chimileski, MBL

In 2020 a team of researchers showed how plaque is a highly structured and organised colony of different microorganisms which almost seems to be designed to allow Streptococcus mutans to get on with its job of dissolving the tooth enamel and causing caries. Creationists dogma insists that anything with a complex, organised structure must be intelligently designed because, so they assert, complexity and order can’t arise from disorder without intelligent intervention.

This latest discovery shows how the beginnings of this organised colony are established very quickly.

Creationism Refuted - A Marine Relative of Mycobacterium Tuberculosis Shares 80% Of Its Genome

Mycobacterium spongiae

Credit: Sacha J. Pidot and team

A new species of bacterium, related to Mycobacterium tuberculosis has been found living in a sponge on the Great Barrier Reef.

TB under the sea: A marine sponge microbe provides insights into the evolution of tuberculosis | Doherty Website

Tell a creationists that humans and chimpanzees have 98% of their genomes in common, and they'll tell you this doesn't prove common origins or 'macro-evolution', but show them evidence that two bacteria have evolved from a common ancestor because they have 80% of their genome in common and they'll tell you this doesn't mean they've evolved because they are both still 'bacteria kind'.

So, why doesn't 98% commonality mean humans and chimpanzees are both still 'ape kind'?

But the evidence that the two bacteria, Mycobacterium tuberculosis, and the newly-discovered M. spongiae is compelling, and gives a clue as to the origins of M. tuberculosis, one of the most deadly pathogenic bacteria, possibly from marine origins.

Malevolent Designer News - The Sneaky Way Chlamydia Is Designed To Get Round The 'Problem' of Antibiotics

Immunofluorescence staining of human gastric cells grown in a microplate and infected with Chlamydia trachomatis.
Blue: cell nuclei, green: C. trachomatis, grey: actin.

Image: Pargev Hovhannisyan / Universität Würzburg

Chlamydia doesn’t always cause symptoms, but when it does, these are some of the most common.

Everyday Health

Chlamydia Can Settle in the Intestine -

Chlamydia is a sexually-transmitted bacterial infection in which the bacteria are passed to a new victim during sexual intercourse. It caused few or no symptoms to begin with - usually nothing worse than mild itching - but if left untreated it can cause infertility and sometimes cancer. Fortunately, it can be treated successfully with antibiotics.

However, it is not unusual for people who have been successfully treated to develop a new infection with exactly the same strain as the previous infection, suggesting that the bacteria had somehow survived the antibiotic treatment although symptoms had disappeared, and traces of the bacteria had gone.

Researchers have now shown that chlamydia can take up residence in the gut where it can survive for some considerable time and develop increasing resistance to antibiotics with each course of treatment. The mechanism of this increasing resistance is a classic example of evolution as the antibiotic acts as an environmental selector which removes the non-resistant bacteria from the population gene pool, leaving the resistant form to become dominant in the gene pool.