Predation, Parasites, and Pathogens

Gene loss, altered regulation, and reused biological machinery can help explain how harmless relationships become harmful. These mechanisms support parts of creationist corruption models, but do not establish an originally harmless world or explain every specialized apparatus for attacking a host.

By AI (GPT-6 Astra, high thinking) Draft:  September 2026

Summary

Creationist corruption models explain a real part of the evidence, but not the whole problem.  Biological relationships can become harmful through lost functions, altered regulation, or a change of host.  That makes an originally harmless relationship scientifically possible in particular cases.  It does not establish that every parasite began that way, or date the change to the Fall.

Three distinctions control the answer:

  • Working well is different from doing good. A structure can perform its biological function effectively while causing another organism severe harm. Improving its efficiency would make that problem worse.
  • Dependence is different from invasion. Losing the ability to make nutrients can explain why an organism needs a host. It does not by itself explain how the organism enters, exploits, or evades that host.
  • A possible history is different from a demonstrated history. A harmless relative or a useful medical application supplies a clue. Neither proves that the harmful organism had an originally harmless role.

The strongest evidence for corruption is the observed breakdown of beneficial symbiosis and the damaged genes preserved in dependent organisms.  The strongest difficulty is coordinated specialization for harming another organism, including parasitoid development and predatory venom.  Reuse of ordinary biological parts occurs on both sides.  The remaining question is whether their particular arrangement and history have been explained.

This article evaluates those empirical claims.  Whether Scripture teaches that animal death began with Adam is covered in Death Before the Fall.  Whether God has sufficient reasons to permit suffering is a further philosophical question.

What creationist accounts actually propose

The relevant creationist literature offers several mechanisms, not a single claim that parasites are organisms with missing genes.

In the 2008 Proceedings of the Microbe Forum, Joseph Francis distinguished genetic alteration from ecological displacement.  Disease could arise when an organism changed, or when it entered a setting where a previously useful activity became harmful.  His second category includes movement away from the place where a microbe performed a beneficial function.  The original goodness of these relationships is a theological starting point of his model.  Their subsequent alteration and displacement are biological proposals that can be investigated.1

Warren Shipton's 2019 paper on destructive parasites makes its breadth explicit:  "Parasitism arose through gene loss, the expression of front-loaded genes now facilitating pathological life cycles, or other scenarios."  His proposal includes changes in feeding, host relationships, and gene expression.  He also allows genetic material to come from other organisms.  He acknowledges that the available detail is insufficient for a conclusive account.2

Here, front-loaded means that an organism possessed genetic capacities before they became active in their present harmful role.  That is distinguishable from a damaged formerly useful system.  A capacity deliberately supplied for later host attack would create a different design question from an unintended breakdown of cooperation.  The proposed original function matters.

Shipton also suggests that some insects originally fed on plants or other invertebrates, and that some nematodes could originally have regulated insect populations.  His account therefore does not require the complete absence of consumption of living organisms.  Criticizing it as though it did would miss his actual position.  Whether that distinction solves the theological question is outside this article's scope.

These proposals have different evidential burdens.  A corruption account needs evidence of a previous useful activity and of the change that disrupted it.  A displacement account needs an appropriate former host or habitat.  A repurposing account needs evidence connecting an older function to the present one.  Invoking divine alteration without specifying biological consequences might be consistent with theology, but it supplies no distinct biological test.

Where corruption has substantial support

Beneficial partnerships can become harmful

The clearest example in the sources reviewed is Wolbachia, bacteria that live inside many insects.  Their effects depend on the bacterial lineage, the insect, and the surrounding conditions.  Some associations protect insects against viral disease, while others impose substantial costs.

Ewa Chrostek and Luís Teixeira's 2015 study connected a breakdown of the fruit-fly partnership to changed copy number in an existing region of the bacterial genome.  The result concerned the control of bacterial abundance inside the host.  Follow-up work by Elves Duarte and colleagues in 2021 showed that different alterations to the same region could also disrupt that control.  The relationship between genetic change and harm was investigated directly, rather than inferred solely from a comparison of distant species.34

This is strong evidence for a limited proposition:  an established partnership can become damaging when its regulation changes.  It supports the biological core of a corruption model.  It also corrects an overly narrow version of that model, since the original result involved additional copies of existing material, not simply missing genes.

The historical conclusion remains smaller than the theological one.  The experiment begins with bacteria already able to live inside an insect.  It does not explain the origin of that association, show that every related association was harmless, or identify an ancient date when cooperation first failed.

Leprosy preserves evidence of lost functions

The leprosy bacterium provides unusually clear evidence of genomic reduction.  In 2007, Laura Gómez-Valero and colleagues reconstructed ancestral gene content by comparing related mycobacteria.  Their analysis inferred that 1,537 of 2,977 reconstructed ancestral genes had lost their function in the leprosy lineage.  Many remained recognizable as damaged genetic remnants rather than having disappeared completely.5

Those numbers concern a reconstructed ancestral set.  They are not a claim that the investigators watched that many genes disappear, and they should not be confused with the number of intact genes in a modern bacterium.  The reconstruction uses shared sequences and gene order among relatives to infer which functions preceded the reduction.

The evidence is substantially stronger than the mere observation that a parasite has a small genome.  Recognizable damaged copies support actual loss.  Nevertheless, the study does not establish that the ancestor was harmless.  Its comparisons include other disease-causing mycobacteria.  Nor does loss of metabolic independence alone explain how leprosy bacteria came to occupy their particular host tissues.  Dependence and disease are related questions, but they are not interchangeable.

Plants show the same distinction

Field dodder, Cuscuta campestris, obtains resources from other plants.  Alexander Vogel and colleagues' 2018 genome study found missing functions associated with vigorous photosynthesis and nutrient acquisition from soil.  It also found evidence of genetic material acquired from hosts.  The resulting picture includes both losses and acquisitions.6

The losses fit an organism becoming dependent on resources supplied elsewhere.  Dodder also has specialized organs that connect it to a host.  Explaining reduced self-sufficiency does not automatically explain those connections.  Furthermore, once a parasitic relationship exists, functions made unnecessary by that relationship can decay.  The loss may therefore be a consequence of dependence, rather than the event that originally created it.

Parasitic Plants and Fungi measures this order across the broomrape family, dodder and Rafflesia, and shows the frog chytrid to be a case of displacement rather than alteration.

This is a recurring limit on the corruption argument.  Evidence of deterioration is real evidence, but its place in the causal sequence must be established.

Where the explanation remains incomplete

A more dangerous pathogen need not be merely a damaged one

Plague illustrates why the whole history matters.  Yi-Cheng Sun and colleagues' 2014 study of Yersinia connected the emergence of a different transmission ecology with changes that included both gains and losses of genetic functions.  Their comparison concerned related bacteria with different disease patterns.  It did not begin with a wholly harmless organism.7

Calling the result simply deterioration omits part of the evidence.  Calling it the invention of an entire pathogen from nothing would also be wrong.  Existing capacities were modified within an already complex biological system.  A creationist can reasonably argue that a harmful new relationship arose through alterations of pre-existing life.  That does not establish what the earlier organism was originally for, or explain every feature of its disease-causing descendants.

The relevant categories should therefore remain separate:  loss of a function, acquisition of a function, changed regulation, and changed ecological context.  The word corruption may cover several of them in ordinary language.  It cannot replace identifying which actually occurred.

Predatory equipment can reuse useful parts

Venom makes the distinction between function and benefit especially clear.  Helena Safavi-Hemami and colleagues reported in 2015 that certain fish-hunting cone snails use specialized insulin in their venom.  Insulin normally regulates energy metabolism.  Their study connected a venom form of this familiar hormone with effects on fish physiology and swimming behavior.8

This finding supports repurposing:  a harmful biological tool can have recognizable connections to an ordinary useful molecule.  A wholly new kind of chemistry need not be invented.  It also sharpens the problem, because the venom belongs to an effective prey-capture system.  Knowing the older molecular family does not establish the full history of its recruitment into that system.

The careful creationist conclusion is therefore that benign components can contribute to predation.  The stronger claim that these snails once used their entire present feeding apparatus harmlessly remains unestablished.  The experimental work did not reconstruct a plant-feeding ancestor or identify a recent historical transition from one.

Present ecological benefits are a separate matter.  A predator's contribution to an ecosystem could explain why its removal has consequences today.  It would not show how its hunting equipment originated, or whether the prey's suffering was absent earlier.  Predation, Venom, and Carnivory takes up these questions, measures each weapon, and finds an evidenced pre-Fall use only for claws and sharp teeth.

Parasitoid wasps are a problem of effective function

On 22 May 1860, Charles Darwin wrote to Asa Gray about the difficulty of reconciling beneficent design with parasitoid wasps.  He singled out "the Ichneumonidæ with the express intention of their feeding within the living bodies of caterpillars".  The same paragraph says he had not intended to write atheistically and was dissatisfied with his own attempted resolution.  His objection concerned the outcome of functioning biology, not an anatomical mistake.9

A parasitoid develops at a host's expense and normally kills it.  Some parasitoid wasps also use inherited virus-derived machinery in their relationship with the host.  Annie Bézier and colleagues' 2009 study found evidence that braconid wasps had incorporated an ancestral virus and retained parts of its machinery in a new biological role.  The evidence included relationships among sequences and proteins, not merely a superficial similarity of appearance.10

The process illustrates reuse, including losses and retained functions.  Its outcome is nevertheless a coordinated system supporting successful parasitism.  A description limited to broken genes would miss that arrangement.  The study supplies evidence for a particular evolutionary history; it does not observe every stage of that history.  A recent creationist chronology still needs independent evidence.

This example must not be generalized to all parasitoid wasps.  The paper concerns particular lineages and distinguishes different associated viral systems.  Neither the presence nor the absence of one virus-derived mechanism decides whether another parasitoid's life cycle has been explained.  The Parasitoid Wasps article examines the wider evidence.

Parasites that steer their host's behaviour pose the same problem more sharply;  Behaviour-Manipulating Parasites finds that the zombie-ant fungus and Sacculina meet that description and that no young-earth source names a harmless original role for either.

Brood parasites raise it in a third form, since their equipment is added and not lost;  Brood Parasites and Cheating Species finds measurable losses only in slave-making and inquiline ants, where they follow the parasitic habit.

Useful relationships do not settle original purpose

Viruses can benefit another organism

Viruses are not uniformly harmful to every organism they encounter.  Jeremy Barr and colleagues' 2013 study investigated bacteriophages, viruses that infect bacteria, at mucus-covered surfaces.  Experiments with cultured cells supported a protective effect against bacterial attack.  The researchers proposed that mucus-associated phages can contribute an additional layer of defense.11

That provides a concrete beneficial role, relevant to Francis's proposal that microbial relationships belong within the functioning living world.  It does not show that every virus began as a benefactor.  Nor is the relationship harmless from every perspective:  protection of the animal can involve destruction of bacteria.  Benefit must be stated relative to a particular organism and outcome.

Viruses and Phages tests these claims against cholera phages, the src gene and dated host jumps:  measured benefits are real, every pathogenic virus with a dated origin arrived by host jump or gene capture, and the phage-borne cholera toxin is where the design answer is weakest.

A proposed original role should therefore identify the beneficiary.  Useful for an ecosystem, useful for a host, and harmless to every living thing are different claims.  Moving between them silently makes a creationist explanation appear more complete than it is.

Flexible feeding is evidence of possibility

Shipton's discussion of mosquitoes has a real empirical starting point.  Justin George and colleagues documented malaria mosquitoes locating and feeding on caterpillars in a 2014 laboratory study.  The authors explicitly left the frequency of this behavior in the field unresolved.12

The finding shows that the observed feeding behavior is broader than a simple picture of an insect restricted to human blood.  It makes a change of food source less abstract.  It does not show which feeding habit came first.  Feeding on another insect also shifts the question of harm to a different host; it does not demonstrate universal harmlessness.

The same caution applies to a living harmless relative.  A relative supplies a comparison, not a photograph of an ancestor.  To infer direction, an account needs the wider distribution of traits, the relationships among organisms, and evidence for the intervening changes.

Ticks, Fleas, Lice, Mites, and Botflies sorts the ectoparasites by this test:  lice and vampire moths have living relatives on a harmless diet, fleas have only a proposal, and ticks and botflies have none.

A medical use is not an original function

Michael Behe states the design difficulty unusually plainly in The Edge of Evolution:  "Malaria was intentionally designed."  His discussion concerns the purposeful arrangement of the parasite's cellular machinery and the suffering associated with it.  This is an intelligent-design claim, not itself a young-earth chronology.13

A later medical discovery does not automatically resolve that difficulty.  In 2015, Ali Salanti and colleagues investigated whether a malaria protein's binding properties could help target cancer.  Their engineered research reagent bound 106 of 111 tested patient-derived cancer cell lines.  The study also included treatment experiments in preclinical models.14

The binding result was not a 95% cure rate.  Nor was it evidence that untreated malaria protects people against cancer.  The researchers deliberately adapted a biological property for a new purpose.  That demonstrates the usefulness of studying harmful organisms.  It does not establish that cancer treatment was the parasite's original natural role.

A convincing original-function account would require evidence that the proposed benefit occurred in the relevant organism and relationship before the harmful specialization.  Human ingenuity in finding a later application cannot supply that missing history.

Worms in the Human Body applies the harmless-relative test to six human worms:  hookworm and Ascaris pass, the filarial worms and Guinea worm do not, and pig-whipworm therapy failed its large trials.

Common objections and responses

Doesn't observed degeneration prove that creationists were right?

It confirms particular biological claims that creationists emphasize:  useful systems can deteriorate, and organisms can become more dependent.  Evolutionary explanations also allow adaptive loss and the deterioration of functions no longer maintained by selection.  The observation therefore does not uniquely distinguish creation from evolution.  The disputed questions concern the original state, the sequence of changes, and their timing.

If harmful machinery works well, does that disprove design?

It challenges a claim that each present structure was directly designed to benefit every affected creature.  It does not logically disprove an intelligence behind nature, because an inference of intelligence does not by itself identify intentions or moral character.  A Christian account must explain how the harmful outcome relates to its claim of original goodness.  Calling the machinery efficient does not answer that question.

Could every harmful system have had another use?

That is a possible proposal, not a result established for every system.  Repurposing becomes an explanation when the former role and the changes are supported.  The venom study shows that a familiar biological molecule can participate in predation.  It does not recover the entire ancestral feeding ecology.  Different levels of explanation should not be collapsed into one.

Does a complicated life cycle rule out gradual change?

Complexity alone cannot establish that.  The wasp evidence shows why inherited associations and reused machinery must be considered.  Conversely, naming natural selection does not reconstruct every historical step.  Both sides owe a specific account of the capacities under discussion, and neither can turn the other side's incomplete account into proof of its own.

Can harmless ancestors be inferred without observing them directly?

Yes, historical inference need not be direct observation.  But the inference must compare alternatives.  Damaged gene copies can support prior function.  Shared sequence relationships can support ancestry.  Neither fact alone determines whether the organism harmed its host.  Harmlessness requires additional ecological evidence or a reconstruction that actually bears on harm.

Why not settle the matter by saying that the Fall changed everything?

That can state a theological commitment.  It does not tell a biologist which changes occurred or provide an independent date for them.  The creationist proposals reviewed here become empirically useful where they specify alteration, displacement, or repurposing.  Their broader historical claim remains to be tested against evidence beyond those mechanisms.

Limits and unanswered questions

The evidence reviewed is deliberately selective.  It includes examples where corruption is well supported and examples where functional specialization makes the account harder.  It is not a survey establishing what fraction of all parasites can be explained by each mechanism.

Three questions remain especially important.  First, what evidence identifies an ancestor as harmless, rather than simply more metabolically independent?  Second, which changes explain entry into a host and exploitation of it, rather than dependence after the association already existed?  Third, what independent chronology places those events within a proposed creationist history?

These questions are not answered by counting damaged genes alone.  Nor are they answered by displaying a particularly distressing organism.  The first can establish real deterioration without establishing universal original goodness.  The second can expose a serious moral difficulty without reconstructing biological origins.

Bacterial Pathogens as Broken Bacteria examines the genome and regulatory evidence in detail.  Planned companion articles cover behavior-manipulating parasites, parasitic worms, ectoparasites, viruses and phages, parasitic plants and fungi, and brood parasites.  Each needs its own evidence.  Conclusions about a bacterium should not silently become conclusions about a cuckoo or a parasitic wasp.

Verdict

Corruption and repurposing are real biological possibilities, and some instances are directly supported.  Creationist explanations are strongest when they identify a specific lost function, altered partnership, or changed ecological relationship.  They are weakest when those findings are stretched into a complete history of all predation, parasitism, and disease.

The available evidence supports a mixed biological picture:  deterioration, dependence, acquired capacities, and effective specialization can occur together.  It establishes neither that every harmful organism was separately created in its present role nor that every one descended from an originally harmless form within a recent chronology.  The young-earth account has substantial mechanisms to work with, but important parts of its historical explanation remain unproved.

Sources


  1. 1.

    “Proceedings of the Microbe Forum, June 2007.”  Answers Research Journal 1:1–6.  Edited by Georgia Purdom and Joseph W. Francis.  2008.  Section Francis's Creation Microbiology and the Origin of Disease, page 3.  A conference proceedings volume from the Microbe Forum of June 2007, edited by Georgia Purdom and Joseph W. Francis.  Francis's contribution in it distinguishes genetic alteration from ecological displacement, and the article uses that distinction. ↩

  2. 2.

    Shipton, Warren A.  “Destructive parasites: expressions of God's creation?”  Journal of Creation 33(2):84–92.  2019.  Section Abstract, page 84.  Section Concluding remarks, pages 90–91.  A 2019 paper in the Journal of Creation that proposes an account of how destructive parasites came about.  The article uses it because the paper covers a wide range of mechanisms and admits that the available detail is not enough for a conclusive account. ↩

  3. 3.

    Chrostek, Ewa, and Luís Teixeira.  “Mutualism Breakdown by Amplification of Wolbachia Genes.”  PLOS Biology 13(2):e1002065.  2015.  Section Abstract and Author Summary, pages 1–2:  Page numbers are PDF pages.  Section Results.  A study of a symbiotic partnership with Wolbachia bacteria, which connected its breakdown to a change in the number of copies of a bacterial gene region.  The article uses it because it examines an established partnership directly, not how that partnership began. ↩

  4. 4.

    Duarte, Elves H. et al.  “Forward genetics in Wolbachia: Regulation of Wolbachia proliferation by the amplification and deletion of an addictive genomic island.”  PLOS Genetics 17(6):e1009612.  2021.  Section Abstract.  Section Results.  A study of Wolbachia bacteria that uses forward genetics, meaning it changes genes and then watches what the bacteria do, to find what controls how far they multiply in their host.  The article cites it for the general conclusion that regulation of an existing association can be disrupted, because different alterations to the same region could also disrupt that control. ↩

  5. 5.

    Gómez-Valero, Laura et al.  “Reconstructing the ancestor of Mycobacterium leprae: The dynamics of gene loss and genome reduction.”  Genome Research 17:1178–1185.  2007.  Section Abstract.  Section Results.  Section Reconstruction of the gene content and order of the M. leprae ancestor's genome.  A genome comparison that reconstructs the ancestor of Mycobacterium leprae, the leprosy bacterium, and traces the gene loss that followed in its lineage.  Its ancestral counts are inferred by comparative reconstruction.  The article uses it because the leprosy bacterium provides unusually clear evidence of genome reduction. ↩

  6. 6.

    Vogel, Alexander et al.  “Footprints of parasitism in the genome of the parasitic flowering plant Cuscuta campestris.”  Nature Communications 9:2515.  2018.  Section Abstract.  Section Introduction, figure 1.  Section Results.  A genome sequence of the parasitic field dodder, Cuscuta campestris, a plant that connects to its host and absorbs water and nutrients from it.  The draft genome is just under 477 million base pairs and has lost genes needed for high photosynthesis and for taking up nutrients from soil, and it contains evidence of genetic material from its hosts.  The article uses it as a plant case of both losses and acquisitions. ↩

  7. 7.

    Sun, Yi-Cheng et al.  “Retracing the Evolutionary Path that Led to Flea-borne Transmission of Yersinia pestis.”  Cell Host & Microbe 15:578–586.  2014.  Section Summary.  Section Discussion.  A study that retraces the evolutionary path by which Yersinia pestis, the bacterium that causes plague, came to spread through fleas.  The article cites it for the broad conclusion that both gains and losses of genetic functions contributed to that change. ↩

  8. 8.

    Safavi-Hemami, Helena et al.  “Specialized insulin is used for chemical warfare by fish-hunting cone snails.”  PNAS 112(6):1743–1748.  2015.  Section Abstract.  Section Results, figure 5.  Section Discussion.  A laboratory study of venom from two fish-hunting cone snails, Conus geographus and Conus tulipa, which found insulin in the venom.  Injected into fish, the venom insulin caused hypoglycemic shock, a dangerous drop in blood sugar, and the experiments support a predatory role without reconstructing every historical stage.  The article uses it because insulin, a hormone that regulates energy metabolism, here serves a predatory purpose. ↩

  9. 9.

    Darwin, Charles.  “Letter DCP-LETT-2814 to Asa Gray.”  Darwin Correspondence Project.  May 22, 1860.  Section Paragraph beginning With respect to the theological view of the question..  A letter from Darwin to Asa Gray, printed in the Darwin Correspondence Project edition of his letters.  The article uses it because the letter discusses the difficulty of reconciling beneficent design with parasitoid wasps. ↩

  10. 10.

    Bézier, Annie et al.  “Polydnaviruses of Braconid Wasps Derive from an Ancestral Nudivirus.”  Science 323:926–930.  2009.  Section Abstract and opening discussion, page 926:  Comparative evidence is in the following pages.  A 2009 paper in Science that traces the virus-derived material of braconid wasps to an ancestral nudivirus.  Its claim concerns specified wasp lineages.  The article uses it because it shows a parasitoid wasp reusing inherited virus machinery in its relationship with the host.  Mirror:  Rifters.com ↩

  11. 11.

    Barr, Jeremy J. et al.  “Bacteriophage adhering to mucus provide a non–host-derived immunity.”  PNAS 110(26):10771–10776.  2013.  Section Abstract.  Section Results.  Section Discussion.  A laboratory study of bacteriophages, which are viruses that infect bacteria, and how they stick to mucus, the coating on body surfaces.  It found that phage-to-bacteria ratios were higher on all mucosal surfaces sampled, from cnidarians to humans, than in the surrounding environment, and in cell cultures the extra phage on mucus protected the cells from bacterial infection.  The cell-culture evidence is kept separate from the broader ecological model, and the article uses the model for the proposal that mucus-bound phage can add a further layer of defense. ↩

  12. 12.

    George, Justin et al.  “Malaria Mosquitoes Host-Locate and Feed upon Caterpillars.”  PLOS ONE 9(11):e108894.  2014.  Section Abstract.  Section Discussion.  A laboratory study of the malaria mosquito Anopheles stephensi, whose females flew to caterpillars, landed on them and fed on their haemolymph, the body fluid of insects.  Females with access to caterpillars survived longer than females with no access to food.  The authors leave the field prevalence of this behavior unresolved, and the article uses the study as the empirical starting point for Shipton's discussion of mosquitoes. ↩

  13. 13.

    Behe, Michael J.  The Edge of Evolution: The Search for the Limits of Darwinism.  Free Press.  2007.  Chapter 10, All the World's a Stage, section When Bad Things Happen to Good People:  “Malaria was intentionally designed.”  A 2007 book by Michael Behe, who also wrote Darwin's Black Box, on the limits of Darwinian evolution.  The article uses it for his plain statement that malaria was intentionally designed. ↩

  14. 14.

    Salanti, Ali et al.  “Targeting Human Cancer by a Glycosaminoglycan Binding Malaria Protein.”  Cancer Cell 28(4):500–514.  2015.  Section Results, pl-CS Is Expressed on Most Human Cancer Cells, figure 2, table S1.  Section subsequent preclinical treatment sections.  A laboratory study that tested a laboratory-made form of a malaria protein on cancer cells, including treatment experiments in preclinical models.  The protein reacted with 95% (106/111) of patient-derived human cancer cell lines, a figure that describes binding to tested cell lines, not patients cured.  The article cites it as a later medical use of a malaria protein that does not by itself resolve the difficulty about design. ↩