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.

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