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.

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.

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 - How A Respiratory Pathogen Manipulates Our Immune System.

Haemophilus influenzae (H. flu)

A microscopic view of Haemophilus influenzae bacteria.

Image: Adobe

Respiratory bacteria ‘turns off’ immune system to survive - UQ News - The University of Queensland, Australia

Regular readers may recall my recent article explaining how bowel cancer has been cleverly 'designed' to switch off our immune system to prevent the cancer cells from being detected and attacked.

Well, it seems this same technique has been employed by the malevolent designer to make a bacterial pathogen better at making us sick when it infects the lining of the respiratory system of vulnerable people.

Or at least that is what an intellectually honest intelligent [sic] design creationist has to believe (if there is such a thing) because, in rejecting the science that shows how organism's evolve by a mindless, unintelligent natural process without the involvement of supernatural magic, and attributing it all to their putative designer, they are tacitly accepting that it also designs parasites such as these bacterial pathogens.

And we can exclude Michael J. Behe's scientifically nonsensical notions of 'genetic entropy' and 'devolution' [sic] from some assumed created initial perfection - made possible by the religious dogma of 'The Fall', because an ability that conveys an advantage to a pathogen and makes it able to produce more offspring than what went before, can't logically be described as less perfect than something worse, and of course, there is no known mechanism which would cause a detrimental mutation to increase in the species gene pool, other than riding piggyback on a mutation that conveys a greater advantage.

Refuting Creationism - How A Common Bacterium Became A Dangerous Pathogen - By Evolution, Naturally

Pseudomonas aeruginosa

Pseudomonas aeruginosa

Scientists map how deadly bacteria evolved to become epidemic | University of Cambridge

Aficionados of creationism's putative intelligent designer will doubtless be thrilled to discover the imaginative lengths it's gone to to ensure as many people get sick as possible with its cleverly designed bacterium, Pseudomonas aeruginosa, which has gradually been modified over the last 200 years to make it more effective and more resistant to the antibiotics medical science has developed to protect us. There is even a strain specially 'designed' to infect children with cystic fibrosis, just to add to their suffering.

Since these modifications involve genetic mutations which improve the bacterium's ability to love and replicate, we can dismiss the scientific gibberish Michael J Behe invented to explain parasites away as 'devolutionary' and due to 'genetic entropy, since even Michael J Behe would be hard pressed to explain how an advantageous mutation can be less perfect that what went before it. Something better can't be less perfect than something less good, unless you invoke a private definition of 'perfect' that means something which can be bettered.

So, what are these changes in this dangerous pathogen that makes it a problem for people with other health conditions?

Refuting Creationism - More Evidence of Endosybiosis in Progress

A group of diatoms with their fluorescently-labeled symbionts.

© Max Planck Institute for Marine Microbiology Bremen/Mertcan Esti

The rhizobial nitrogen fixing symbionts (fluorescently-labeled in orange and green using genetic probes) residing inside diatoms collected from the tropical North Atlantic. The nucleus of the diatom is shown in bright blue.

© Max Planck Institute for Marine Microbiology Bremen/Mertcan Esti

Long-standing marine mystery solved: How algae get nitrogen to grow

Readers my remeber my article about how a team of scientists have discovered a new cell organelle in the process of transforming from a free-living nitrogen-fixing bacterium to becoming an endosymbiont of a marine alga, in much the same way that cyanobacteria became the chloroplasts of plant cells and rickettsia bacteria became the mitochondria of all eukaryote cells.

Now a different team, from the Max Planck Institute for Marine Microbiology, the Alfred Wegener Institute and the University of Vienna, have reported on a similar phenomenon in the form of a bacterium closely related to the Rhizobia that form a symbiotic association with leguminous plants such as peas and bean, which has teamed up with a marine diatom. This symbiotic relationship involves the bacterium living within the single cell of the diatom, unlike the relationship between Rhizobia and legumes in which the bacteria live in special nodes on the roots of the plants, but not inside the plant cells as such.

What is the chemical pathway by which nitrogen-fixing bacteria convert atmospheric nitrogen into ammonia and nitrates? Nitrogen-fixing bacteria play a crucial role in the nitrogen cycle by converting atmospheric nitrogen (N₂) into ammonia (NH₃), which can be further converted into nitrates (NO₃⁻) by other microorganisms. The chemical pathway for nitrogen fixation primarily involves the enzyme nitrogenase, which catalyzes the reduction of atmospheric nitrogen to ammonia. Here is an overview of the pathway:

1. Nitrogen Fixation
   Nitrogenase Enzyme Complex:
   • Components: The nitrogenase complex consists of two main proteins: the iron (Fe) protein and the molybdenum-iron (MoFe) protein.
   • Reaction:
     \[ \begin{equation*} \begin{aligned} \text{N}_2 + 8H^+ + 8e^- + 16ATP & \\ \rightarrow 2NH_3 + H_2 + 16ADP + 16Pi & \end{aligned} \end{equation*} \]
   • Steps:
     1. Electron Donation: Electrons are donated from ferredoxin or flavodoxin to the Fe protein.
     2. ATP Hydrolysis: ATP binds to the Fe protein and is hydrolyzed, providing energy for the transfer of electrons.
     3. Electron Transfer: Electrons are transferred from the Fe protein to the MoFe protein.
     4. Nitrogen Reduction: The MoFe protein reduces atmospheric nitrogen (N₂) to ammonia (NH₃) in a series of steps involving the binding and reduction of N₂.
2. Ammonia Assimilation
   Once ammonia is produced, it can be assimilated into organic compounds or further processed into other nitrogenous compounds.
   
   Conversion to Nitrates
   The conversion of ammonia to nitrates occurs in two steps involving nitrifying bacteria:
   
   
   Step 1: Ammonia to Nitrite
   Bacteria Involved: Ammonia-oxidizing bacteria (AOB), such as Nitrosomonas. \[ \text{NH}_3 + \text{O}_2 \rightarrow \text{NO}_2^- + 3H^+ + 2e^- \] Step 2: Nitrite to Nitrate
   Bacteria Involved: Nitrite-oxidizing bacteria (NOB), such as Nitrobacter. \[ \text{NO}_2^- + \frac{1}{2}\text{O}_2 \rightarrow \text{NO}_3^- \]

Summary of Pathway

1. Nitrogen Fixation: Atmospheric nitrogen (N₂) is converted to ammonia (NH₃) by nitrogenase enzyme complex in nitrogen-fixing bacteria.
2. Ammonia Assimilation: Ammonia can be incorporated into organic molecules or further processed.
3. Nitrification: Ammonia is first oxidized to nitrite (NO₂⁻) by AOB and then nitrite is oxidized to nitrate (NO₃⁻) by NOB.

This pathway is essential for making atmospheric nitrogen available to plants and other organisms in a usable form, thereby sustaining the nitrogen cycle in ecosystems.

This association in the oceans accounts for the supply of fixed nitrogen in the seas which is then available for plant and ultimately animal life.

Of course, any intelligent designer would have given the diatoms the necessary genes to fix nitrogen themselves, just as it would have given legumes the same ability, but evolution, in its haphazard, unplanned and unintelligent way often produces sub-optimal, overly complex solutions to problems simply because that solution was better than what went before; there is no intelligence to think about using processes designed earlier or of the elegance of the solution.

The discovery is the subject of an open access paper in Nature and a press release from Vienna University (Universität Wien):

Long-standing marine mystery solved: How algae get nitrogen to grow

Newly discovered symbiosis between Rhizobia and diatoms could also open new avenues for agriculture

In a new study, scientists from the Max Planck Institute for Marine Microbiology, the Alfred Wegener Institute and the University of Vienna shed light on an unexpected partnership: A marine diatom and a bacterium that can account for a large share of nitrogen fixation in vast regions of the ocean. This symbiosis likely plays a key role for global marine nitrogen fixation and productivity, and thus uptake of carbon dioxide. The newly-discovered bacterial symbiont is closely related to the nitrogen-fixing Rhizobia which live in partnership with many crop plants and may also open up new avenues for engineering nitrogen-fixing plants. The results were published in the current print edition of the renowned journal Nature.

Nitrogen is an essential component of all living organisms. It is also the key element controlling the growth of crops on land, as well as the microscopic oceanic plants that produce half the oxygen on our planet. Atmospheric nitrogen gas is by far the largest pool of nitrogen, but plants cannot transform it into a usable form. Instead, some crop plants like soybeans, peas and alfalfa (collectively known as legumes) have acquired Rhizobial bacterial partners that "fix" atmospheric nitrogen into ammonium, which can be used by plants. This partnership makes legumes one of the most important sources of proteins in food production.

Yet, how marine plants obtain the nitrogen they need to grow has not yet been fully clarified. Scientists from the Max Planck Institute for Marine Microbiology, the Alfred Wegener Institute and the University of Vienna now report that Rhizobia can also form similar partnerships with tiny marine plants called diatoms – a discovery that solves a long-standing marine mystery and which has potentially far-reaching agricultural applications.

An enigmatic marine nitrogen fixer hiding within a diatom

For many years it was assumed that most nitrogen fixation in the oceans was carried out by photosynthetic organisms called cyanobacteria. However, in vast regions of the ocean there are not enough cyanobacteria to account for measured nitrogen fixation. Thus, many scientists hypothesized that non-cyanobacterial microorganisms must be responsible for the "missing" nitrogen fixation.

For years, we have been finding gene fragments encoding the nitrogen-fixing nitrogenase enzyme, which appeared to belong to one particular non-cyanobacterial nitrogen fixer but, we couldn’t work out precisely who the enigmatic organism was and therefore had no idea whether it was important for nitrogen fixation.

Marcel M. M. Kuypers, lead author
Max Planck Institute for Marine Microbiology, Bremen, Germany

In 2020, the scientists travelled from Bremen to the tropical North Atlantic to join an expedition involving two German research vessels. They collected hundreds of liters of seawater from the region, in which a large part of global marine nitrogen fixation takes place, hoping to both identify and quantify the importance of the mysterious nitrogen fixer. It took them the next three years to finally puzzle together its genome.

It was a long and painstaking piece of detective work but ultimately, the genome solved many mysteries.

Bernhard Tschitschko, first author
Max Planck Institute for Marine Microbiology, Bremen, Germany Now: Department of Microbiology
University of Innsbruck, Innsbruck, Austria.

Based on the nitrogenase gene fragment we had seen in many marine samples before, one would have expected to find this gene in a Vibrio-related organism, but by carefully piecing together the genetic information it turned out that instead, it belonged to a genome closely related to known Rhizobia, which typically live in symbiosis with legume plants.

Daan R. Speth, co-author
Max Planck Institute for Marine Microbiology, Bremen, Germany Now: Centre for Microbiology and Environmental Systems Science
Division of Microbial Ecology
University of Vienna, Vienna, Austria,

Together with its surprisingly small genome, this raised the possibility that the marine Rhizobia might be a symbiont.

The first known symbiosis of this kind

Spurred on by these discoveries, the authors developed a genetic probe which could be used to fluorescently label the Rhizobia.

This allowed us to visualize the Rhizobia directly in their native habitat - the complex environmental samples collected in the Atlantic.

Katharina Kitzinger, co-author
Max Planck Institute for Marine Microbiology, Bremen, Germany
Now: Centre for Microbiology and Environmental Systems Science
Division of Microbial Ecology
University of Vienna, Vienna, Austria.

Indeed, their suspicions about it being a symbiont were quickly confirmed.

We were finding sets of four Rhizobia, always sitting in the same spot inside the diatoms. It was very exciting as this is the first known symbiosis between a diatom and a non-cyanobacterial nitrogen fixer.

Marcel M. M. Kuypers.

The scientists named the newly discovered symbiont Candidatus Tectiglobus diatomicola. Having finally worked out the identity of the missing nitrogen fixer, they focused their attention on working out how the bacteria and diatom live in partnership. Using a technology called nanoSIMS, they could show that the Rhizobia exchanges fixed nitrogen with the diatom in return for carbon. And it puts a lot of effort into it:

In order to support the diatom’s growth, the bacterium fixes 100-fold more nitrogen than it needs for itself.

Wiebke Mohr, co-author
Max Planck Institute for Marine Microbiology, Bremen, Germany

A crucial role in sustaining marine productivity

Next the team turned back to the oceans to discover how widespread the new symbiosis might be in the environment. It quickly turned out that the newly discovered partnership is found throughout the world’s oceans, especially in regions where cyanobacterial nitrogen fixers are rare. Thus, these tiny organisms are likely major players in total oceanic nitrogen fixation, and therefore play a crucial role in sustaining marine productivity and the global oceanic uptake of carbon dioxide.

A key candidate for agricultural engineering?

Aside from its importance to nitrogen fixation in the oceans, the discovery of the symbiosis hints at other exciting opportunities in the future. Kuypers is particularly excited about what the discovery means from an evolutionary perspective.

The evolutionary adaptations of Ca. T. diatomicola are very similar to the endosymbiotic cyanobacterium UCYN-A, which functions as an early-stage nitrogen-fixing organelle. Therefore, it’s really tempting to speculate that Ca. T. diatomicola and its diatom host might also be in the early stages of becoming a single organism.

Marcel M. M. Kuypers.

Tschitschko agrees that the identity and organelle like nature of the symbiont is particularly intriguing.

So far, such organelles have only been shown to originate from the cyanobacteria, but the implications of finding them amongst the Rhizobiales are very exciting, considering that these bacteria are incredibly important for agriculture. The small size and organelle-like nature of the marine Rhizobiales means that it might be a key candidate to engineer nitrogen-fixing plants someday.

Bernhard Tschitschko

The scientists will now continue to study the newly discovered symbiosis and see if more like it also exist in the oceans.

Original publication:
Bernhard Tschitschko, Mertcan Esti, Miriam Philippi, Abiel T. Kidane, Sten Littmann, Katharina Kitzinger, Daan R. Speth, Shengjie Li, Alexandra Kraberg, Daniela Tienken, Hannah K. Marchant, Boran Kartal, Jana Milucka, Wiebke Mohr, Marcel M. M. Kuypers (2024): Rhizobia-diatom symbiosis fixes missing nitrogen in the ocean. Nature (2024) DOI: 10.1038/s41586-024-07495-w

Participating institutions:

• Max Planck Institute for Marine Microbiology, Bremen, Germany
• Alfred Wegener Institute - Helmholtz-Centre for Polar and Marine Research, Bremerhaven, Germany
• University of Vienna, Vienna, Austria

Abstract
Nitrogen (N₂) fixation in oligotrophic surface waters is the main source of new nitrogen to the ocean¹ and has a key role in fuelling the biological carbon pump². Oceanic N₂ fixation has been attributed almost exclusively to cyanobacteria, even though genes encoding nitrogenase, the enzyme that fixes N₂ into ammonia, are widespread among marine bacteria and archaea^3,4,5. Little is known about these non-cyanobacterial N₂ fixers, and direct proof that they can fix nitrogen in the ocean has so far been lacking. Here we report the discovery of a non-cyanobacterial N₂-fixing symbiont, ‘Candidatus Tectiglobus diatomicola’, which provides its diatom host with fixed nitrogen in return for photosynthetic carbon. The N₂-fixing symbiont belongs to the order Rhizobiales and its association with a unicellular diatom expands the known hosts for this order beyond the well-known N₂-fixing rhizobia–legume symbioses on land⁶. Our results show that the rhizobia–diatom symbioses can contribute as much fixed nitrogen as can cyanobacterial N₂ fixers in the tropical North Atlantic, and that they might be responsible for N₂ fixation in the vast regions of the ocean in which cyanobacteria are too rare to account for the measured rates.

Main
Nitrogen is an essential component of all living organisms and limits life in the ocean. Atmospheric N₂ gas is the largest reservoir of freely accessible nitrogen, but it is biologically available only to microorganisms that carry the nitrogenase metalloenzyme and thus can fix N₂ into ammonia⁷. Even though a wide diversity of marine bacteria and archaea encode nitrogenase, the bulk of nitrogen fixation in the ocean has been attributed to cyanobacteria (ref. ⁴ and references therein). These phototrophs are capable of both free-living and symbiotic lifestyles, and can directly or indirectly contribute to carbon fixation and export production in the regions where they are abundant, such as oligotrophic coastal waters and margins of subtropical gyres⁸. Notably, in vast regions of the ocean, such as the centres of subtropical gyres, cyanobacterial N₂ fixers are too rare to account for the measured rates of N₂ fixation. Instead, a role of non-cyanobacterial N₂ fixers has been invoked, on the basis of the abundance of nitrogenase-encoding gene sequences (nifH), most of which belong to uncultured proteobacteria (for example, refs. ^3,5,9,10,11). So far, the most frequently detected non-cyanobacterial N₂ fixer is the so-called gamma-A, named after its nifH gene phylogeny that clusters within the Gammaproteobacteria¹². This enigmatic microorganism has been shown to be distributed in most world oceans, and its potential activity has been inferred from in situ nifH transcription^13,14. To date, however, there is no proof that gamma-A fixes N₂ in situ, and essentially all aspects of its physiology remain unknown.

An N₂-fixing rhizobial diatom endophyte We investigated the role of non-cyanobacterial N₂ fixation in the tropical North Atlantic during an expedition in January–February 2020. This region is responsible for around 20% of oceanic N₂ fixation⁸, and cyanobacteria can only explain approximately half of the rates measured in the region¹⁰. We detected high N₂ fixation rates of up to 40 nmol N l⁻¹ d⁻¹ in the surface waters (Extended Data Table 1), and the presence of both cyanobacterial and heterotrophic N₂ fixers—specifically, gamma-A—was confirmed by metagenomic sequencing (Extended Data Fig. 1a). Gamma-A nifH sequences were retrieved only from the large size fraction (greater than 3 µm) suggesting particle attachment or an association with a host organism (Extended Data Fig. 1a). We recovered a near-complete metagenome-assembled genome (MAG; 1.7 Mb, 37.8% GC, 98% completion with 0% redundancy) containing the gamma-A nifH gene, as well as a complete cluster of rRNA genes (Supplementary Table 1). Although the retrieved nifH sequence clustered within the Gammaproteobacteria as previously reported^3,14,15 (Extended Data Fig. 2), both 16S-rRNA-gene-based and whole-genome-based taxonomy¹⁶ firmly placed this MAG within the alphaproteobacterial family Hyphomicrobiaceae (Fig. 1a). This family belongs to the order Rhizobiales, which comprises the prominent rhizobial symbionts of nodule-forming terrestrial legumes^6,17,18. In addition to nifH, most other genes of the nif regulon are of gammaproteobacterial origin, including nifD and nifK, which encode the catalytic component of the nitrogenase; nifE, nifN and nifB, which encode the iron-molybdenum cofactor assembly proteins; and nifS, which is involved in metallocluster biosynthesis (Extended Data Fig. 2a). Almost all other genes in the gamma-A MAG are of alphaproteobacterial origin (Supplementary Table 1). On the basis of these results, we conclude that the gamma-A N₂ fixer is, in fact, an alphaproteobacterium that has acquired its nitrogenase genes through horizontal gene transfer from a gammaproteobacterial donor. Besides gamma-A, several other bacteria, including members of the order Rhizobiales, obtained their nitrogenase genes through horizontal gene transfer from a gammaproteobacterial donor (Extended Data Fig. 2b). Such horizontal gene transfer across classes, resulting in the acquisition of nitrogenase genes, has been reported previously for other N₂ fixers^19,20.

Fig. 1: Phylogeny and visualization of Candidatus Tectiglobus diatomicola and its diatom host.

a, Maximum likelihood phylogenetic tree of concatenated bacterial marker genes from the order Rhizobiales, showing the placement of Ca. T. diatomicola within the Hyphomicrobiaceae family (see Methods). The novel genus Ca. Tectiglobus, comprising Ca. T. diatomicola and its closest relative Ca. T. profundi, is highlighted in pink. Families within the Rhizobiales that contain known N₂-fixing legume symbionts and their exemplary host plants are shown. The order Parvibaculales was used as an outgroup. Black dots indicate more than 95% bootstrap support. Scale bar indicates amino acid substitutions per site. Plant icons were designed by Freepik (Neptunia oleracea) or created with BioRender.com. b,c, False coloured scanning electron microscopy (SEM) image (b) and confocal laser scanning microscopy image (c) of a Haslea diatom. Four Ca. T. diatomicola cells (pink, overlay of Hypho1147 and Hypho734 fluorescence in situ hybridization (FISH) probes; Extended Data Table 2) were detected next to the host nucleus (white; stained with DAPI). Scale bars, 5 µm.

We name the newly discovered species ‘Candidatus Tectiglobus diatomicola’ within a novel genus ‘Candidatus Tectiglobus’ (see Methods for etymology). One other marine MAG from the North Pacific, which we now name ‘Candidatus Tectiglobus profundi’, is affiliated with this novel genus, with 72% average amino acid identity with Ca. T. diatomicola (Supplementary Methods). Compared with their closest relative, a MAG from the Mediterranean Sea, both Ca. Tectiglobus species have a substantially reduced genome size (around 1.7 Mb versus around 5 Mb) and a strongly decreased GC content (around 38% versus around 54%) (Extended Data Fig. 3), which are features typical of endosymbionts²¹. Notably, a similar reduction in genome size and GC content is observed for the N₂-fixing cyanobacterial endosymbiont Candidatus Atelocyanobacterium thalassa, or UCYN-A, which lives in symbiosis with a haptophyte alga^22,23. Thus, the genome properties of Ca. T. diatomicola, together with its presence in the large size fraction, strongly indicate a host-associated lifestyle.

A couple of points here for creationists to ignore or lie about:

• The authors show no doubts that this is an evolutionary process and show no evidence of adopting creationist superstition as a better explanation.
• The endosymbionts have a much reduced genome compared to their free-living relatives, showing that their evolution has involved a loss of genetic information typical of both endosymbionts and endo-parasites, despite the creationist assertion that a loss of genetic information is either fatal or 'devolutionary' [sic]
• This process illustrates the processes involved in the earlier evolution of biodiversity which produced eukaryote cells from associations of prokaryotes, which itself illustrates how 'selfish' genes form co-operative alliances with other 'selfish' genes, despite creationists assertions that selfish genes can only produce selfish individuals.

Unintelligent Design - An Over-Complex, Heath-Robinson Solution To A Simple Problem

Antarctic landscape (Ross Sea)

Small Antarctic worms (zoom) rely on microbes to resist the chill of the frigid waters where they live.

Michael Tangherlini, Marco Lo Martire

Bacteria found to produce proteins that act like antifreeze, helping marine worms survive in polar waters

Imagine you're a designer with all the power you need and all the solutions you've designed earlier at your fingertips and your task is to redesign some marine worms that you designer earlier and put into an arctic environment, perhaps not realising they wouldn't survive if they got frozen.

So, what you have to do is give these marine worms some way to prevent this happening and so mitigating your earlier blunder.

At your disposal is the method you gave to some marine bacteria, and even some fish known as icefish, when you made similar blunders years earlier - you gave them some genes for making antifreeze to stop the contents of their cells freezing and the ensuing ice crystals from destroying them.

Do you give these marine worms the same genes you gave the bacteria?

Not if you're creationism's putative intelligent [sic] designer, you don't. That would be far too simple.

Malevolent Designer - How A Dangerous Pathogen Is Designed to Infect Our Lungs

Pseudomonas aeruginosa

The pathogenic bacterium Pseudomonas aeruginosa breaching through the respiratory epithelia of a human lung microtissue model, captured via Scanning Electron Microscopy.

Image: Benoit Laventie, Biozentrum, University of Basel.

Lung organoids unveil secret: How pathogens infect human lung tissue | University of Basel

A team at the Biozentrum of the University of Basel have shown how a dangerous pathogen gains access to tissues in the lungs, the better to infect them.

To an intelligent [sic] design creationist, there can only be one explanation for this - intelligent design.

To quickly dispense with the traditional excuse offered for this evidence of malevolence, if you subscribe to the intelligent design nonsense - to blame 'Sin' which was caused by 'The Fall', oblivious of the fact that this exposes the intelligent design argument as fundamentalist religion in disguise. Even given a spurious gloss of sciencey-sounding gibberish by Michael J Behe, with his 'genetic entropy' and 'scientifically nonsensical 'devolution' from some assumed created perfection, makes no sense and fails abysmally to rescue creationism from its obvious religious fundamentalism.

No mutation which conveys an advantage, and so progresses to fixation in the species gene pool, can possibly be regarded as 'devolutionary' or less perfect than what went before it, and of course, postulating some assumed initial created perfection simply underlines the religious fundamentalist and the intellectual contortions needed to try to shoehorn the facts into the superstition inherent in the notion.

So, we are left with malevolent intent as the only conclusion, if we subscribe to the intelligent design notion.

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.

Uninteligent Design - Bacteria Have A Defence Against The Viruses Designed To Infect Them

Bacterium infected by phage viruses

Illustration: Getty Images

Structural model at atomic resolution of bacteriophage T4

Dr. Victor Padilla-Sanchez, PhD via Wikimedia (CC BY-SA 4.0)

Study details a common bacterial defense against viral infection

Creationism's latest hobbyhorse, designed by Michael J Behe to revive the flagging fortunes of his Discovery Institute’s Wedge Strategy and the abysmal failure of his Intelligent [sic] Design ploy to get creationism inserted into the US public school science curricula at US taxpayers' expense, is the silly notion of 'genetic entropy' and 'devolution'.

This unintelligently designed strategy contains the seeds of its own failure at being regarded as a science because it starts off with the assumption that all species were created perfectly by a perfect creator, in compliance with Christian superstition, and so any mutation must be devolutionary away from that perfection. Mutations are called 'genetic entropy', so incorporating the idiotic notion that genetic 'information' is subject to the same law of physics as energy, so the Second Law of Thermodynamic make evolution impossible.

This is supposed to make creationists think Darwin must have been wrong because mutations can't improve fitness, being devolutionary, not evolutionary because of 'genetic entropy'. It ignores the fact that only an improvement in fitness in a given environment can produce more descendants than a deleterious mutation because fitness is defined as the ability to survive and reproduce. How increased fitness can be defined as a reduction in perfection is never explained because Behe 'forgot' to define 'perfection' leaving his marks to assume it means something made by their god.

And this daft notion is now cited by creationists to explain why an intelligent, omniscient and supposedly omnibenevolent god would design parasites. These are now explained as devolved from some initial perfection because of 'genetic entropy' made possible by Adam & Eve's 'sin' - Which is not religious superstition, because it was a historical fact! Got it!

So, we now have an explanation for bacteria, viruses and other parasites, that absolved creationism's god of any responsibility for them while blaming humans for their 'devolution'. However, the problem for this childish nonsense arises when we have parasites on those parasites, such as viruses that infect bacteria - how are bacteria responsible for Adam & Eve's sin and if they aren't why are they being punished for it?

Then it gets even more bizarre when we discover that many bacteria have mechanisms for protecting themselves from these viruses. How can 'devolution' produce an improvement in the organism's ability to survive and reproduce, and in what sense is an improvement a reduction in perfection?