Malevolent Design - The Sneak Tactics of Toxoplasma gondii

Toxoplasma gondii.

Image by Michael Holmes

Toxoplasma gondii parasite uses unconventional method to make proteins for evasion of drug treatment

Here we are with yet another example of an organism that, if there is a designer behind it, that designer can only be described as malevolent and determined to maximise the suffering and misery in the world.

It is, of course, another example of a nasty little parasite which, if you subscribe to the creationist view that complexity 'proves' design, has been designed to ensure we are as vulnerable to is as possible by helping it evade the immune system and other mechanisms, supposedly designed by the same designer god to protect us from the parasites it designs to harm us.

This example is the parasite Toxoplasma gondii, which is notorious for manipulating its natural victims, which are felines and their prey species. For example, mice infected with T. gondii lose their fear of cats so they get eten and the parasite gets into its primary host; infected chimpanzees develop a liking for the smell of leopard urine.

Humans are not the natural secondary host, but the parasite readily infects us as we catch it from cats. It is thought that about one third of humans are infected. Once infected it is impossible to get rid of from the body because, even if antibodies are produced by our immune system, the parasites go into a dormant state as cysts which can form in any organs of the body, including the brain.

Toxoplasma gondii, it's evolution and its pathology in humans. Toxoplasma gondii: Overview, Evolution, and Pathology in Humans

Toxoplasma gondii is a protozoan parasite that infects warm-blooded animals, including humans, but primarily completes its life cycle in felines. It is a member of the phylum Apicomplexa, which includes other parasitic organisms such as Plasmodium (responsible for malaria). The parasite is notorious for its widespread prevalence and potential to cause severe disease in immunocompromised individuals and during pregnancy.

---

Evolutionary History

Toxoplasma gondii evolved from a common ancestor shared with other apicomplexans. Its evolutionary journey highlights adaptations for survival in both definitive (cat) and intermediate (other animals) hosts.

1. Apicomplexan Origin:
   • The phylum likely evolved from free-living photosynthetic algae.
   • The apicoplast, a remnant plastid, is a key organelle in T. gondii, crucial for fatty acid synthesis and other metabolic functions.
2. Host Adaptations:
   • Unlike its relatives with narrow host ranges, T. gondii evolved to infect a vast array of intermediate hosts. This adaptability is attributed to its ability to form hardy oocysts that can survive in the environment and tissue cysts that persist in hosts.
3. Clonal Lineages:
   • Population studies show three predominant clonal lineages (Types I, II, III), which emerged around 10,000 years ago, likely through a genetic bottleneck. These lineages exhibit differences in virulence and geographic distribution.

---

Lifecycle

1. Sexual Stage:
   • Occurs only in the intestines of felines, the definitive host. Cats excrete oocysts in their faeces.
2. Oocysts:
   • Environmentally resilient and infectious after sporulation, oocysts can contaminate food, water, and soil.
3. Intermediate Hosts:
   • Oocysts are ingested by other animals (e.g., rodents, birds, and humans). The parasite then forms tachyzoites (rapidly dividing forms) and bradyzoites (slowly dividing cyst forms) in tissues like the brain and muscles.
4. Transmission to Cats:
   • Cats are infected when they eat intermediate hosts harbouring tissue cysts, perpetuating the lifecycle.

---

Pathology in Humans

Humans typically acquire T. gondii through undercooked meat, contaminated water, or contact with infected cat faeces. Most infections are asymptomatic, but in certain populations, the parasite can cause significant disease.

1. Acute Toxoplasmosis:
   • Symptoms: Flu-like symptoms (fever, swollen lymph nodes, fatigue).
   • Immune response usually controls the infection, leading to cyst formation.
2. Latent Infection:
   • Tissue cysts persist, primarily in the brain and muscles, remaining dormant unless the immune system is compromised.
3. Immunocompromised Individuals:
   • Reactivation of latent infection can cause life-threatening conditions, such as toxoplasmic encephalitis, especially in individuals with HIV/AIDS or undergoing chemotherapy.
4. Congenital Toxoplasmosis:
   • If a woman acquires the infection during pregnancy, the parasite can cross the placenta, causing miscarriage, stillbirth, or severe congenital abnormalities (e.g., hydrocephalus, blindness, mental impairment).
5. Neurological and Behavioural Effects:
   • Emerging research suggests T. gondii might influence behaviour and mental health. It has been associated with altered risk-taking, neuropsychiatric disorders like schizophrenia, and changes in personality traits, though causation remains under investigation.

---

Diagnosis and Treatment

1. Diagnosis:
   • Serological tests detect specific IgM and IgG antibodies.
   • PCR assays can identify parasite DNA, particularly in congenital infections.
2. Treatment:
   • Acute infections: Combination therapy with pyrimethamine and sulfadiazine, supplemented with folinic acid to prevent folate depletion.
   • Chronic latent infections usually do not require treatment unless reactivated.

---

Control and Prevention

• Hygiene: Proper handwashing after handling soil, cats, or raw meat.
• Cooking Practices: Ensure meat is thoroughly cooked to destroy tissue cysts.
• Cat Care: Regular cleaning of litter trays and preventing cats from hunting can reduce environmental contamination.

Toxoplasma gondii remains a fascinating and medically important organism due to its evolutionary ingenuity, widespread distribution, and complex interactions with hosts, including humans.

How they do this is the subject of a paper in the Journal of Biological Chemistry by researchers from Indian University School of Medicine and a news release by Indiana University.

Toxoplasma gondii parasite uses unconventional method to make proteins for evasion of drug treatment

---

A study by Indiana University School of Medicine researchers sheds new light on how Toxoplasma gondii parasites make the proteins they need to enter a dormant stage that allows them to escape drug treatment. It was recently published with special distinction in the Journal of Biological Chemistry.

---

Toxoplasma gondii is a single-celled parasite that people catch from cat faeces, unwashed produce or undercooked meat. The parasite has infected up to one-third of the world's population, and after causing mild illness, it persists by entering a dormant phase housed in cysts throughout the body, including the brain.

Toxoplasma cysts have been linked to behaviour changes and neurological disorders like schizophrenia. They can also reactivate when the immune system is weakened, causing life-threatening organ damage. While drugs are available to put toxoplasmosis into remission, there is no way to clear the infection. A better understanding of how the parasite develops into cysts would help scientists find a cure.

Through years of collaborative work, IU School of Medicine Showalter Professors Bill Sullivan, PhD, and Ronald C. Wek, PhD, have shown that Toxoplasma forms cysts by altering which proteins are made. Proteins govern the fate of cells and are encoded by mRNAs.

But mRNAs can be present in cells without being made into protein. We've shown that Toxoplasma switches which mRNAs are made into protein when converting into cysts.

Professor William J. Sullivan Jr., Corresponding author
Department of Pharmacology & Toxicology
Indiana University School of Medicine
Indianapolis, Indiana, USA.

Lead Author Vishakha Dey, PhD, a postdoctoral fellow at the IU School of Medicine and a member of the Sullivan lab, examined the so-called leader sequences of genes named BFD1 and BFD2, both of which are necessary for Toxoplasma to form cysts.

mRNAs not only encode for protein, but they begin with a leader sequence that contains information on when that mRNA should be made into protein.

Dr. Vishakha Dey, lead author.

Department of Pharmacology & Toxicology
Indiana University School of Medicine
Indianapolis, Indiana, USA.

All mRNAs have a structure called a cap at the beginning of their leader sequence. Ribosomes, which convert mRNA into protein, bind to the cap and scan the leader until it finds the right code to begin making the protein.

What we found was that, during cyst formation, BFD2 is made into protein after ribosomes bind the cap and scan the leader, as expected. But BFD1 does not follow that convention. Its production does not rely on the mRNA cap like most other mRNAs.

Dr. Vishakha Dey.

The team further showed that BFD1 is made into protein only after BFD2 binds specific sites in the BFD1 mRNA leader sequence. Sullivan said this is a phenomenon called cap-independent translation, which is more commonly seen in viruses.

Finding it in a microbe that has cellular anatomy like our own was surprising. It speaks to how old this system of protein production is in cellular evolution. We're also excited because the players involved do not exist in human cells, which makes them good potential drug targets.

Professor William J. Sullivan Jr.

The Journal of Biological Chemistry featured the new study as an "Editor's Pick" paper, which represent a select group of the journal’s publications judged to be of exceptionally high quality and broad general interest to their readership.

This paper describes a mechanism by which a parasite that causes toxoplasmosis in humans can respond to stress and allow the parasite to thrive. The discovery of this mechanism provides a basis for treating these infections. Moreover, a similar mechanism is important in cancer, suggesting that it may be a therapeutic target for multiple human diseases.

Professor George N. DeMartino, PhD, associate editor of the Journal of Biological Chemistry
University of Texas Southwestern Medical Center.

Additional co-authors on the study include IU School of Medicine's Michael Holmes, PhD, and Matheus S. Bastos, PhD. The work was funded by the National Institutes of Health and the Showalter Foundation.

Translational control mechanisms modulate the microbial latency of eukaryotic pathogens, enabling them to evade immunity and drug treatments. The protozoan parasite Toxoplasma gondii persists in hosts by differentiating from proliferative tachyzoites to latent bradyzoites, which are housed inside tissue cysts. Transcriptional changes facilitating bradyzoite conversion are mediated by a Myb domain transcription factor called BFD1, whose mRNA is present in tachyzoites but not translated into protein until stress is applied to induce differentiation. We addressed the mechanisms by which translational control drives BFD1 synthesis in response to stress-induced parasite differentiation. Using biochemical and molecular approaches, we show that the 5′-leader of BFD1 mRNA is sufficient for preferential translation upon stress. The translational control of BFD1 mRNA is maintained when ribosome assembly near its 5′-cap is impaired by insertion of a 5′-proximal stem-loop and upon knockdown of the Toxoplasma cap-binding protein, eIF4E1. Moreover, we determined that a trans-acting RNA-binding protein called BFD2/ROCY1 is necessary for the cap-independent translation of BFD1 through its binding to the 5′-leader. Translation of BFD2 mRNA is also suggested to be preferentially induced under stress but by a cap-dependent mechanism. These results show that translational control and differentiation in Toxoplasma proceed through cap-independent mechanisms in addition to canonical cap-dependent translation. Our identification of cap-independent translation in protozoa underscores the antiquity of this mode of gene regulation in cellular evolution and its central role in stress-induced life-cycle events.

Abbreviations

AP2apetala-2BFD1Bradyzoite Formation Deficient-1BRBinding RegionCDSprotein-coding sequenceFLucfirefly luciferaseNLucNano luciferaseRLURelative Luciferase UnitsuORFsupstream open reading frames

Cellular adaptation and differentiation processes in response to cellular stresses are initiated by reprogramming of gene expression. A central feature of this reprogramming is the rapid lowering of global protein synthesis in favor of selective translation of a subset of mRNAs that include transcription factors that activate genes for stress remediation or differentiation (1, 2, 3). We have shown that this paradigm governs life cycle stage transitions in protozoan parasites that underlie transmission and pathogenesis of infectious disease (3, 4, 5). The study of translational control in these early-branching eukaryotes not only promises to reveal potential novel drug targets but also sheds important mechanistic insights into the evolutionary origins of these regulatory processes (6, 7, 8).

Toxoplasma gondii is an obligate intracellular parasite of warm-blooded animals that causes opportunistic disease in humans. Upon ingestion, the parasites transform into a rapidly replicative stage (tachyzoite) that disseminates throughout the host body before converting into a quiescent stage (bradyzoite) housed in tissue cysts that can be sustained for the life of the host. Tissue cysts are a major route of transmission through the consumption of raw or undercooked meat (9). Reactivation of bradyzoites can occur when patients become immunocompromised, producing life-threatening damage to critical areas where tissue cysts typically reside, such as the brain, heart, and skeletal muscle (10). Current treatments of toxoplasmosis only target replicating tachyzoites and do not appear to exert appreciable activity against the formation or viability of tissue cysts (11). The formation of latent tissue cysts allows Toxoplasma to persist in its host and prevents a radical cure of this infection.

Given the importance of bradyzoites in driving parasite transmission and chronic disease, much research is aimed at understanding the molecular mechanisms orchestrating the conversion between tachyzoites and bradyzoites (12). Differentiation between life cycle stages requires the reprogramming of gene expression, while chromatin remodeling machinery and several apetala-2 (AP2) factors have been shown to contribute to the transcription of bradyzoite-inducing genes (13). Recently, Lourido and colleagues identified a “master regulator” transcription factor termed BFD1 (Bradyzoite Formation Deficient-1) that is necessary and sufficient for bradyzoite formation (14).

BFD1 is a SANT/Myb-like DNA-binding protein whose mRNA is present in tachyzoites but not translated until parasites are exposed to a bradyzoite-induction stress (14). We previously suggested with polysome profiling that BFD1 mRNA is preferentially translated when tachyzoites are subjected to a stress that induces bradyzoite differentiation (15). These studies indicate that expression of BFD1 protein is predominantly regulated by translational control and the elevated levels of BFD1 are sufficient to confer transcription events directing cyst formation. Consistent with this idea, the 5′-leader sequence of BFD1 mRNA is about 2.7 kb in length, harboring multiple predicted upstream open reading frames (uORFs), which are known in other model systems to regulate start codon selection and translation efficiency of the protein-coding sequence (CDS) (16). Moreover, a CCCH-type zinc finger mRNA-binding protein called BFD2 (also referred to as ROCY1) has recently been described that is suggested to direct the stress-dependent translation of BFD1 (17, 18).

Bulk cellular translation begins with eIF4F association with the 5′-cap of mRNAs through its eIF4E subunit, which then recruits the ribosomal preinitiation complex that proceeds to scan the 5′-leader for an optimal start codon (19). This cap-dependent translation can be modulated by uORFs that can be bypassed by scanning ribosomes or allow for re-initiation for efficient CDS translation (20). Cap-independent mechanisms have also been described, most commonly among viruses and less frequently for cellular mRNAs (21, 22, 23). Translation that can occur independent of eIF4E cap association and the subsequent ribosome scanning typically involves direct entry of ribosomes onto the 5′-leader sequence by secondary structures that interface with trans-acting proteins to recruit initiating ribosomes (22, 23).

In this study, we addressed the mechanisms of preferential translation of BFD1 during stress-induced bradyzoite differentiation. Utilizing luciferase reporter assays and genetically modified Toxoplasma parasites, we show that BFD1 translation can occur through a cap-independent mechanism that involves BFD2 binding to the 5′-leader sequence. By comparison, preferential translation of BFD2 during stress occurs by cap-dependent processes. Our results represent the first evidence of cap-independent translation in protozoa, suggesting that it is an ancient mechanism of gene regulation present in early-branching eukaryotes and is critical for directing differentiation in the Toxoplasma life cycle.

We can, of course, dismiss Michael J. Behe's biologically nonsensical excuse of 'devolution' from some presupposed initial perfection because any change which makes an organism better at producing descendants is classically evolutionary and it take mental gymnastics to a new hight of absurdity to believe that something better is less perfect than what preceded it.

So, as always, what creationists need to find the moral and intellectual courage to address is the question of evil and why their supposed creator creates these nasty little parasites that are responsible for so much suffering and misery in the world. Are they just the result of incompetent design or the malevolent design of an omnipotent, omniscient designer? Or are they the result of a mindless natural process?

Refuting Creationism - Another Gap Closed - No God Found

A mating pair of wild-type (left) and mir-193 mutant (right) Bicyclus anynana butterflies.

Photo credit: Shen TIAN

A mating pair of peppered moths, Biston betularia, showing the melanistic and pale forms.

A microRNA solves an evolutionary mystery of butterfly and moth wing colouration - NUS Faculty of Science | NUS Faculty of Science

A regularly-cited example of observed Darwinian evolution is that of the peppered moth which occurs in two forms, the white, speckled form and a melanistic, almost black form. During the industrial revolution, as English northern towns grew and became polluted by smoke from coal-burning factories, so the melanistic form became more common.

Experiments showed that the lighter form became easier for predators to see when the moths were roosting on tree trunks that had become coated in soot, while the melanistic form became harder for predators to see.

Following the decline of the northern towns, the light form again increased back to the former ratio, showing the importance of environmental change in evolution.

This tendency to have melanistic forms is common in the lepidoptera (moths and butterflies) and this tendency was believed to be under th control of as single genomic region surrounding the protein-coding gene “cortex“, common across many species, showing their descent from a common ancestor.

However, new research by international researchers from Singapore, Japan, and the United States of America, led by Professor Antónia MONTEIRO and Dr Shen TIAN from the Department of Biological Sciences at the National University of Singapore (NUS), has shown that 'cortex' is not directly involved in producing melanism, instead, this is controlled by a microRNA from within the 'cortex' genomic region, as another example of how microRNA's control many functions within cells, particular gene expression.

Refuting Creationism - Domesticated Dogs 2000 Years Before 'Creation Week'

A tibia, or lower-leg bone, of an adult canine from Swan Point, Alaska, radiocarbon dated to about 12,000 years old.

François Lanoë
School of Anthropology

Eurasian/North American Grey Wolf, Canis lupus.

By User:Mas3cf - This file was derived from: Eurasian wolf.JPG, CC BY-SA 4.0, Link

How did humans and dogs become friends? Connections in the Americas began 12,000 years ago | University of Arizona News

At least 2,000 years before Creationists' little god created a small flat planet with a dome over it in the Middle East, human in Alaska were feeding domesticated dogs on salmon, according to the findings of palaeontologists from the University of Arizona.

But of course, the parochial Bronze Age pastoralists from the infancy of our species who made up that myth, couldn't possibly have known anything about when dogs were domesticated, or Alaska for that matter because, as we can see from the tales they made up, they knew nothing of the world beyond a day or two's walk from their pastures and were completely ignorant of the geography, geology and history of the planet and life on it - which is why they made up such implausible origin myths in the first place.

That there were people feeding salmon to their domesticated dogs about 12,000 years ago is the subject of a paper published recently in Science Advances by the Arizona University team led by Assistant Professor François Lanoë, of the School of Anthropology in the College of Social and Behavioral Sciences. They explain their findings in an Arizona University News release

Refuting Creationism - How the 'Lizard' Part of Your Brain Influences Your Thinking

In a new Northwestern Medicine study, scientists sought to better understand how humans evolved to become so skilled at thinking about what’s happening in other peoples’ minds.

Amygdala is the organ in the limbic system (inner mind) —though a tiny little one is significantly responsible for our emotions which falls in the bracket of implicit memories.

Overthinking what you said? It’s your ‘lizard brain’ talking to newer, advanced parts of your brain: For Journalists - Northwestern University

Few things upset creationists more than evidence that they are not only apes and share a common ancestor with the other African apes, but that they also share a common ancestor even with non-mammals such as reptiles, and yet, as the American evolutionary biologist, Theodosius Dobzhansky reminds us, nothing in biology makes sense without the Theory of Evolution (TOE).

And one thing that does make sense is how the human brain is the result of an evolutionary process with ancestry in those common ancestors, including lizards.

A second thing that creationists who have deluded themselves into believing that mainstream biomedical scientists are giving up on the TOE and adopting the childish notion of intelligent design, will find distressing, is the news that the team who did this piece of research are firmly convinced that the structure of our brain and the way it works is the result of evolution, not magic.

The third thing is how this explains empathy, of which creationists often feign ignorance, claiming they get their sense of right and wrong from their invisible friend and have a handbook to tell them how to behave. The curious belief that even influenced supposed Christian intellectual 'giants' such as the smugly self-satisfied, C.S. Lewis, is despite the fact that one of the Golden Rules of human society, that even the founder of Christianity, Jesus, allegedly told his followers to apply - "Do unto others what you would they do unto you" or words to that effect, depend entirely on having the empathetic ability to know what someone else would want.

The research explains how this ability in humans comes from an ancestral ability to read social signals and form relationships, including an understanding of social hierarchies, possessed even by lizards.

Malevolent Design - How Malaria Is Being Redesigned to Keep On Killing Children

Photomicrograph of a blood smear contains a macro- and microgametocyte of the Plasmodium falciparum parasite

Photo Credit: CDC/Dr. Mae Melvin - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL) #2704, Public Domain, Link

Study uncovers first evidence of resistance to standard malaria treatment in African children with severe malaria

In another twist of the arms race with human medical science Plasmodium falciparum, the malevolently designed parasite that causes malaria and kills hundreds of thousands of children a year, mostly in Africa, has developed resistance to Artemisinin. Scientists were already aware that resistance had arisen in cases of uncomplicated malaria, but this is the first such incidence of resistance in the more severe form of the disease.

Indiana University School of Medicine researchers, in collaboration with colleagues at Makerere University in Uganda have discovered a case of complicated malaria in a child in Uganda.

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.
  

---

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.

---

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

---

(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.

---

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.

Transitional Form News - Precambrian Common Ancestor of Insects, Arachnids, and Nematode Worms

3D laser scans enable the researchers to study the fossils’ shape and curvature.

Droser Lab/UCR

Researchers Scott Evans (left) and Ian Hughes examine a fossil bed at Nilpena Ediacara National Park.

Droser Lab/UCR.

Tiny worm makes for big evolutionary discovery | UCR News | UC Riverside

The refutation of creationism continues today with news of another one of those 'non-existent' transitional species that turn up with monotonous regularity only to be dismissed by creationists as 'not transitional but fully formed' with now two gaps in the record where there was originally one, or by simply dismissing the dating method as unreliable and coincidentally wrong by an order of magnitude sufficient to make 6-10,000 years look like x-million years.
Another big disappointment for creationists is the fact that this one is from before the Cambrian when their traditional disinformation claims lots of species popped into existence without ancestors by magic in a single event called the 'Cambrian explosion'. The Cambrian 'explosion' was of course a period of some 6-10 million years during which many of the basic body plans of multicellular organisms evolved.

This fossil however was before then and was clearly the ancestral stem species from which a whole range of Cambrian organism, collectively known as Ecdysozoa evolved. These are a group of organisms with an outer cuticle which is shed periodically as the organism grows. The vast group includes nematode worms and arthropods such as insects, spiders, crustaceans like crabs, shrimps, lobsters, and the horseshow crab. So, this discovery, which the palaeontologists have named Uncus dzaugisi sits at the base of this branch of the evolutionary tree. It resembled a nematode worm.

Tell me all about the Ecdysozoa, please. Ecdysozoa is a major clade of animals within the larger group known as Protostomia, distinguished by their unique mode of growth, which involves periodic moulting of an external cuticle. The term "ecdysozoa" comes from the Greek word ecdysis, meaning "to strip off" or "to shed," referring to this moulting process.

Characteristics of Ecdysozoa

1. Moulting (Ecdysis):
   • The defining feature of Ecdysozoans is the shedding of their cuticle—a tough, non-living outer layer made of proteins, polysaccharides (like chitin), or collagen. This process allows them to grow, as the rigid cuticle limits continuous size increase.
   • After moulting, a new, larger cuticle is secreted, which hardens over time.
2. Body Structure:
   • Many have a hydrostatic skeleton, relying on fluid pressure in their body cavity for movement and structure.
   • Most lack cilia or flagella in their adult form, distinguishing them from other protostomes.
3. Diversity:
   • The group includes some of the most diverse and abundant organisms on Earth, ranging from microscopic species to large, visible ones.
4. Nervous System:
   • Typically, they have a ventral nerve cord and a dorsal brain, with varied sensory adaptations.

---

Major Groups Within Ecdysozoa
Ecdysozoa includes eight phyla, with two of the most well-known being Arthropoda and Nematoda:

1. Arthropoda
   • The largest and most diverse group of animals, including insects, arachnids, crustaceans, and myriapods.
   • They have segmented bodies, jointed appendages, and a hard exoskeleton.
   • Examples: Butterflies, crabs, spiders, centipedes.
2. Nematoda (Roundworms)
   • Microscopic to macroscopic worms with a cylindrical, unsegmented body.
   • Found in nearly every habitat on Earth, often as parasites in plants and animals.
   • Examples: Caenorhabditis elegans (a model organism), Ascaris (a human intestinal parasite).
3. Tardigrada (Water Bears)
   • Microscopic, water-dwelling animals known for their extreme resilience to harsh environments.
   • They can survive desiccation, radiation, and even the vacuum of space.
4. Onychophora (Velvet Worms)
   • Segmented, soft-bodied terrestrial animals with slime glands used for capturing prey.
5. Priapulida
   • Marine worms with a tubular body, often found burrowing in sediment.
6. Kinorhyncha
   • Tiny, segmented marine animals often referred to as "mud dragons."
7. Loricifera
   • Microscopic animals inhabiting marine sediment, with a complex, retractable body.
8. Nematomorpha (Horsehair Worms)
   • Parasites as larvae, often controlling the behaviour of their insect hosts.

---

Evolution and Phylogeny

• Ecdysozoa was proposed as a clade in 1997, based on molecular evidence (notably studies of ribosomal RNA).
• They share a common ancestor with other protostomes but diverged early to adopt their unique moulting strategy.
• Their evolutionary success is evident in their sheer numbers and adaptability, especially in arthropods.

---

Ecological and Economic Importance

1. Ecological Roles:
   • Many ecdysozoans are key components of ecosystems as decomposers, predators, prey, and parasites.
   • Insects, a subgroup of arthropods, are critical for pollination and nutrient cycling.
2. Economic Impact:
   • Beneficial: Insects (e.g., bees) aid in agriculture, while nematodes play a role in soil health.
   • Harmful: Some ecdysozoans are pests or parasites causing diseases in humans, animals, and crops.

---

Fun Facts

• Tardigrades can enter a state called cryptobiosis, surviving for decades without water or food.
• Arthropods are the most successful phylum, with over a million described species, and likely many more undiscovered.
• Nematodes may account for about 80% of individual animals on Earth.

The discovery was made by a team from University of California, Riverside (UCR), led by Professor Mary Droser a distinguished professor of geology. The have explained their findings in the journal, Current Biology, and in a UCR press release:

Tiny worm makes for big evolutionary discovery

---

UC Riverside scientists have described ‘Uncus,’ the oldest ecdysozoan and the first from the Precambrian period

---

Everyone has a past. That includes the millions of species of insects, arachnids, and nematode worms that make up a major animal group called the Ecdysozoa. Until recently, details about this group’s most distant past have been elusive. But a UC Riverside-led team has now identified the oldest known ecdysozoan in the fossil record and the only one from the Precambrian period. Their discovery of Uncus dzaugisi, a worm-like creature rarely over a few centimeters in length, is described in a paper published today in Current Biology.

Scientists have hypothesized for decades that this group must be older than the Cambrian, but until now its origins have remained enigmatic. This discovery reconciles a major gap between predictions based on molecular data and the lack of described ecdysozoans prior to the rich Cambrian fossils record and adds to our understanding of the evolution of animal life.

Mary L. Droser, co-author Earth and Planetary Sciences University of California, Riverside
Riverside, CA , USA.

The ecdysozoans are the largest and most species-rich animal group on Earth, encompassing more than half of all animals. Characterized by their cuticle — a tough external skeleton that is periodically shed — the group comprises three subgroups: nematodes, which are microscopic worms; arthropods, which include insects, spiders, and crustaceans; and scalidophora, an eclectic group of small, scaly marine creatures.

Like many modern-day animal groups, ecdysozoans were prevalent in the Cambrian fossil record and we can see evidence of all three subgroups right at the beginning of this period, about 540 million years ago. We know they didn’t just appear out of nowhere, and so the ancestors of all ecdysozoans must have been present during the preceding Ediacaran period.

Ian V. Hughes, first author
Organismic and Evolutionary Biology
Harvard University, Cambridge, MA, USA.

DNA-based analyses, used to predict the age of animal groups by comparing them with their closest living relatives, have corroborated this hypothesis. Yet ecdysozoan fossil animals have remained hidden among scores of animal fossils paleontologists have discovered from the Ediacaran Period.

Top: Uncus fossil from Nilpena Ediacara National Park. The numbers correspond to the coordinates of this fossil on the fossil bed surface. Bottom: 3D laser scans enable the researchers to study the fossils’ shape and curvature.

Droser Lab/UCR.

Ediacaran animals, which lived 635-538 million years ago, were ocean dwellers; their remains preserved as cast-like impressions on the seabed that later hardened to rock. Hughes said uncovering them is a labor-intensive, delicate process that involves peeling back rock layers, flipping them over, dusting them off, and piecing them back together to get “a really nice snapshot of the sea floor.”

This excavation process has only been done at Nilpena Ediacara National Park in South Australia, a site Droser and her team have been working at for 25 years that is known for its beautifully preserved Ediacaran fossils.

Nilpena is perhaps the best fossil site for understanding early animal evolution in the world because the fossils occur during a period of heightened diversity and we are able to excavate extensive layers of rock that preserve these snapshots. The layer where we found Uncus is particularly exciting because the sediment grains are so small that we really see all the details of the fossils preserved there.

Assistant Professor Scott Evans, co-author
Earth, Ocean, and Atmospheric Sciences
Florida State University, Tallahassee, FL, USA.

While the team didn’t set out to find an early ecdysozoan during their 2018 excavation, they were drawn to a mysterious worm-like impression that they dubbed “fishhook.”

Sometimes we make dramatic discoveries and sometimes we excavate an entire bed and say ‘hmmm, I’ve been looking at that thing, what do you think?’ That’s what happened here. We had all sort of noticed this fishhook squiggle on the rock. It was pretty prominent because it was really, really deep.

Because it was deep, we knew it wasn’t smooshed easily so it must have had a pretty rigid body. At this point we knew this was a new fossil animal and it belong to the Ecdysozoa.

Ian V. Hughes

After seeing more of the worm-like squiggles the team paid closer attention, taking note of fishhook’s characteristics. Other defining characteristics include its distinct curvature and the fact that it could move around — seen by trace fossils in the surrounding area. Paul De Ley, an associate professor of nematology at UCR, confirmed its fit as an early nematode and ruled out other worm types.

The team called the new animal Uncus, which means “hook” in Latin, noting in the paper its similarities to modern-day nematodes. Hughes said the team was excited to find evidence of what scientists had long predicted; that ecdysozoans existed in the Ediacaran Period.

It’s also really important for our understanding of what these early animal groups would have looked like and their lifestyle, especially as the ecdysozoans would really come to dominate the marine ecosystem in the Cambrian.

Ian V. Hughes

The paper is titled “An Ediacaran bilateran with an ecdysozoan affinity from South Australia.” Funding for the research came from NASA.

Highlights

• A new, motile bilaterian is described from the Ediacaran of South Australia
• Features including morphology and movement suggest an ecdysozoan affinity
• This discovery firmly places ecdysozoans in the Precambrian

Summary
Molecular clocks and Cambrian-derived metazoans strongly suggest a Neoproterozoic origin of many animal clades.^1,2,3,4 However, fossil bilaterians are rare in the Ediacaran, and no definitive ecdysozoan body fossils are known from the Precambrian. Notably, the base of the Cambrian is characterized by an abundance of trace fossils attributed to priapulid worms,^5,6 suggesting that major divisions among ecdysozoan groups occurred prior to this time. This is supported by ichnofossils from the latest Ediacaran or early Cambrian left by a plausible nematoid,^7,8,9 although definitively attributing this inferred behavior to crown-Nematoida remains contentious in the absence of body fossils.¹⁰ Given the high probability of the evolution of Ecdysozoa in the Proterozoic, the otherwise prolific fossil record of the Ecdysozoa, and the identification of more than 100 distinct Ediacaran genera, it is striking that no Ediacaran body fossils have been confidently assigned to this group. Here, we describe Uncus dzaugisi gen. et. sp. nov. from the Ediacara Member (South Australia), a smooth, vermiform organism with distinct curvature and anterior-posterior differentiation. The depth of relief of Uncus is unique among Ediacara fossils and consistent with a rigid outer cuticle. Ecological relationships and associated trace fossils demonstrate that Uncus was motile. Body morphology and the inferred style of movement are consistent with Nematoida, providing strong evidence for at least an ecdysozoan affinity. This validates the Precambrian origin of Ecdysozoa, reconciling a major gap between predicted patterns of animal evolution and the fossil record.⁴

Hughes, Ian V.; Evans, Scott D.; Droser, Mary L.
An Ediacaran bilaterian with an ecdysozoan affinity from South Australia
Current Biology, DOI: 10.1016/j.cub.2024.10.030

© 2024 Elsevier.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

I think my favourite quote from one of the scientists is "We know they didn’t just appear out of nowhere, and so the ancestors of all ecdysozoans must have been present during the preceding Ediacaran period", which just about describes the difference between someone who knows the Theory of Evolution is correct because he understands the evidence for it, and a creationists who believes in fully formed living organisms made from nothing, magically popping into existence from nowhere, with magic spells cast by an unproven supernatural deity their mummy and daddy told them about.

The ancestral form, the transitional species, was in exactly for rock formation of exactly the right age which the theory of evolutionary decent with modifiction from a common ancester predicted.

And in case a creationist is tempted to try the 'radiometric dating is flawed/wrong/faked fallacy. The Ediacaran rock formation these fossils were found in was independently dated several different ways that all converged on a 98-million-year span from 635 to 538 million years ago known as the Ediacaran. The Most important being the Uranium-Lead (U-Pb) dating of zircons found in the layers of volcanic ash sandwiched within the rocks. To compress 600 million years of radioactive decay into less than 6-10,000 years would have caused Earth's rocks to melt and the seas to boil away. And the weak nuclear force would have been so weak that atoms could not have formed, let alone life, and there would have been no planet and no universe to fine tune for it either.

---

Advertisement

Refuting Creationism: Why Creationism Fails In Both Its Science And Its Theology

A systematic refutation of creationism, exposing the childish parodies, fallacies and pseudo-science that underpins it. This book takes the reader through the major themes of creationism from the Big Bang, through abiogenesis and the origin of the genetic code, the evidence for evolution, falsifying the claims of creationism with scientific evidence. Also exposed is the deliberate disinformation to be found on creationist websites and publications and the absurdity of the belief that the Bible, particularly the origin myths in Genesis, is real science and genuine history, written or inspired by an omniscient, inerrant creator god

Available in Hardcover, Paperback, or ebook for Kindle

Advertisement

The Failure of Creationism: The Theory That Never Was

An exposé of the failure of creationism and especially the Discovery Institute's Wedge Strategy, showing that the Theory of Evolution is as central to biomedical science today as it was when the DI launched its disinformation campaign in 1991. Creationism is not a science; it is religious fundamentalism and, as was shown in the Kitzmiller case, Intelligent design is creationism dressed in a lab coat.

Available in paperback, hardcover, or ebook for Kindle

Advertisement

Thank you for sharing!

Tweet Link