September 13, 2021 | David F. Coppedge

Evolution of Pathogens Is Mostly Questions, Not Answers

Do evolutionists understand the origin of pathogens? Short answer: no.
But there are non-Darwinian mechanisms at work.


The American Phytopathological Society considers the origin of new pathogenic activity one of the “Top 10 Questions in Molecular Plant-Microbe Interactions (MPMI).” This question is of vital interest to farmers and to anyone who likes to eat food from plants.

Their review paper 23 July 2021, “How Do Pathogens Evolve Novel Virulence Activities?” is notable for the number of times they say they “don’t know” how pathogens evolve.

  • In this review, we consider how far we have come in answering this question, some compelling open unknowns, and directions for future research.
  • the precise function of effectors and their host targets are still unknown in many cases
  • Also, there is little known about the molecular mechanisms that hold back pathogen virulence
  • We have some knowledge about the mechanisms for overcoming the defenses and exploiting host resources by pathogens, but we still do not know the key mechanisms that lead to the adaptation to a new host and, thus, determine pathogen host range.
  • In most cases, we do not know why some genomes have many more TEs [transposable elements] than others.
  • While there are now numerous examples of hybrid plant pathogens, the specific genetic mechanisms that increase virulence or host range of hybrids are largely unknown.
  • We may think that we know quite a lot about how pathogens evolve virulence but there are many unexplored areas and questions (Box 1).

It appears that Darwinian theory has not benefited farmers trying to grow their crops. The press release echoed by sums up the problem:

“How do pathogens evolve novel virulence activities?” is a large question that includes many smaller questions—and the answers discovered often bring even more questions.

Information Flow as a Different Approach

Progress might come from dropping Darwinian assumptions, or from dropping the notion that function arises through chance events. One oft-mentioned process is called “gene duplication and neofunctionalization.” This is the notion that if a gene duplicates through an accident in cell division, the copy is free to evolve a new function.

Duplication and neofunctionalization play important roles in shaping plant-pathogen genomes, in general, and effector repertoires, in particular. The effector repertoires of plant pathogens can number in the hundreds or thousands, yet their evolutionary origins are often unclear….

In general, we have well-characterized examples of genetic transfer events that give rise to virulence activities but it is not clear how often these phenomena occur in the field and whether novel virulence more often evolves de novo or via the transfer of existing virulence factors from some other system.

Should phytopathologists change their approach? Instead of looking at plant pathogens as products of genetic accidents, maybe they should consider it a matter of information flow. The authors admit that genetic transfer events are documented. Horizontal gene transfer (HGT) can be tested by genetic comparisons. “Stuff happens” is not a testable theory.

Anastomosis is the most likely mechanism behind the transfer of accessory chromosomes and HGT between different fungal lineages or species (Soanes and Richards 2014). Presence or absence of accessory or dispensable chromosomes have been associated with host specialization (Mirocha et al. 1992; Temporini and VanEtten 2004). Indeed, the transfer of accessory chromosomes to nonpathogenic isolates can be sufficient to generate a virulent pathogen (Li et al. 2020b). The acquisition of novel virulence activities through HGT has been documented in several cases (Soanes and Richards 2014).

There are even documented cases of transfer of genetic information between kingdoms:

Fungi and oomycetes are similarly recipients of horizontally transferred genes from other kingdoms that are involved in virulence activities, such as a subtilisin serine protease–encoding gene from a plant donor to an ancestor of Colletotrichum fungi (Armijos Jaramillo et al. 2013), a glucan glucosyltransferase–encoding gene from bacteria that probably allows vascular fungi to survive in the high osmotic conditions of plant xylem (Klosterman et al. 2011). and the necrosis- and ethylene-inducing peptide 1 (NEP1)-like proteins that oomycetes have probably acquired from ascomycetes (Richards et al. 2011).

In summary, the writers of this review silently admit that Darwinian theory has not helped them. The “chance” explanations (point mutations, gene duplication, chromosome duplication) don’t explain the emergence of pathogenic properties. The authors pay lip service to “gain of function” effectors through neofunctionalization, but find such answers unsatisfying.

While there are now numerous examples of hybrid plant pathogens (Depotter et al. 2016), the specific genetic mechanisms that increase virulence or host range of hybrids are largely unknown. Gain of effector function or, at least, gain of genetic capital for neofunctionalization (as discussed above) is plausible but by no means a satisfactory explanation for some of the more dramatic increases in host range.

This seems to imply that “gain of function” is a misnomer. It should be called “gain of genetic capital for” neofunctionalization, with the Darwinian assumption that if a copy of a gene exists, evolution can find a way to use it. (There’s been much talk about “gain of function” research on coronaviruses, but that involves intelligent design, not evolution.)

What they do find is loss-of-function pathogenesis. This fits with the thesis in Michael Behe’s 3rd book, Darwin Devolves. Either the pathogen becomes pathogenic by losing a response to the host plant, or the host plant loses the ability to fight it off (e.g., through a premature stop codon in a protective enzyme).

Loss-of-function mutations such as premature stop codons or deletions impair recognition by host surveillance systems of effector functions (Möller and Stukenbrock 2017). Avoiding recognition may also allow pathogens to overcome nonhost resistance (Thines 2019) and acquire the ability to infect new hosts (e.g., loss of PWT3 Avr enabled the emergence of the rice blast fungus as a novel pathogen of wheat [Inoue et al. 2017]).

As an analogy, a man losing his hands becomes resistant to handcuffs, but can still kick and cause harm. This is not the kind of “evolution” Darwin pictured. One cannot lose money on every sale but make up for it in volume.

In an ecological system, multiple species interact in complex ways. Some species set limits on other species. What appears to be happening in many cases is breakage of sophisticated systems, causing interactions to go awry. Broken genes allow some microbes to jump to nonhost species, causing damage unless those new hosts can hybridize and gain the genes that resist the pathogen. Some pathogens are beneficial organisms that find themselves in the wrong host. Dr Joe Francis of The Master’s University, for instance, suggests that the cholera pathogen serves a good function in its normal estuary habitat, but causes great harm if let loose in the human gut. The microbe obviously doesn’t know any better. It’s like a machine doing what it was designed to do. The emergence of a pathogen that seems novel may be analogous to invasive species: pre-existing information that finds itself in an environment without the normal checks and balances.

What about animal pathogens?

The origin of pathogens and toxins in animals is a huge subject, but some recent findings show non-Darwinian processes at work. At Live Science, JoAnna Wendel asked the question, “Why don’t poisonous animals die from their own toxins?” One of the most toxic animals on earth is the poison dart frog that lives in South America. One frog carries enough poison to kill 10 people.

Scientists have puzzled over why the frogs don’t die of their own poison. The poison attacks the sodium channels on which our brains, muscles and nerves depend; if the poison gets into a human, death usually is rapid. Interestingly, the frog is not born with the poison but acquires it through its insect prey.

Wendel asked scientists a the toxin doesn’t kill the frog. There are three “strategies” for avoiding autointoxication, she learned:

  1. The sodium channel changes shape so that the toxin cannot bind to it.
  2. The animal is able to rid its body of the toxin.
  3. The animal sequesters the toxin where it is harmless, for instance, by having proteins that bind to it like a sponge.

The Darwinian idea that these frogs “evolved adaptations” that create this situation is not gain of function. A frog did not set out to think of a “strategy” for surviving, thinking, “I will create a toxin that can block my enemy’s sodium channel.” In each case, something broke or was reprogrammed: the sodium channel, the input, or the protein sponge. These elements are each composed of complex specified information that would never arise by chance. Instead, the information for designed machinery was altered and found a repurposed application in a specific habitat.


Since Darwinism has left more questions than answers, it’s time for design science to offer explanations based on information flow. Scientists can observe information flow, and have already documented transfer of information between organisms that are thought to be distant on the Darwinian phylogenetic tree. Searching for the sources of information, and how it moved between organisms in an ecological system, appears to be a more productive way to do research. The world is waiting for answers to these serious issues that cause death and famine—better answers than, “stuff happens; tough luck.” This is an opportunity for design scientists and bio-engineers to apply their expertise and gain the respect of their peers by providing sound explanations and practical solutions.





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