Disease by coincidence – why we’re caught in the crossfire of a hidden war

By Ed Yong | August 16, 2010 9:00 am

Ecoli_dictyostelium

If you’re trapped in a building, it’s probably not the best time to start setting fire to things. But this is exactly what some bacteria do when they find themselves in a human; they cause diseases that are potentially fatal but not contagious. Without an escape, they risk going down with their host. This seems like a ludicrous strategy but we’re looking at it from the wrong perspective – our own. In truth, humans often have nothing to do with the diseases that plague us; we’re just collateral damage in an invisible war.

Like all living things, bacteria have to defend themselves against predators like amoebas. Some species do so using resistance genes that turn them from passive victims into aggressive fighters. And by coincidence, these same adaptations make them more virulent (good at causing disease) in human bodies. We’re just caught in the crossfire.

The idea that virulent bacteria have adapted to entirely different problems is called the “coincidental evolution hypothesis”. Sandrine Adiba from Pierre and Marie Curie University found evidence to support it by showing that the typically harmless gut bacterium Escherichia coli can cause disease in mice after it’s exposed to the threat of amoebas.

E.coli is mostly harmless, but some strains can cause severe food poisoning. When it’s not colonising the guts of mammals, it’s found in the soil; in both environments, it’s threatened by roving amoebas, which effectively engulf and digest it. Adiba found that one such predator – an amoeba called Dictyostelium discoideumwas very good at munching its way through harmless strains of E.coli, but a disease-causing strain known as 536 was too much to swallow.

Once engulfed, this hardy strain actually managed to reproduce inside the amoeba, weakening and eventually killing it. And if it can do that in a hungry amoeba, it can do that in a mammal cell; from its point of view, the two environments aren’t that different. Adiba confirmed that by pitting 31 different strains of E.coli against Dictyostelium. She found that those which tend to live in harmony with mammals also succumbed to amoebas, while resistant strains tend to cause disease.

The resistant strains had several genes that allowed them to avoid death by digestion. Some shield E.coli from enzymes called lysozymes that break down the outer walls of their cells. Others allow it to find food, by scavenging iron from within the amoeba’s body. These genes help to foil predators, but they’re also “virulence factors” that allow E.coli to successfully infect mammal cells. In fact, 76% of the resistant strains carry these weapons compared to just 16% of the vulnerable strains.

This was a single case study but it probably reflects a very common trend. Some scientists have suggested that for many bacteria, the ability to resist grazing amoebas came before the ability to cause disease in humans and other mammals. The former skill opened up the door to the latter.

There are many other examples that support this idea. Some E.coli strains wield poisons called Shiga toxins that are bad news for their hosts, but that also ward off a predator called Tetrahymena. When Salmonella enterica, another food poisoning germ, is threatened by amoebas, it ends up with more genetic variation at a part of its genome that affects how virulent it is.

Legionella pneumophila, which causes Legionnaires’ disease, might never even have been able to harm humans at all, were it not for amoebas. Legionella specialises in infecting our immune cells, including the macrophages that vacuum up foreign invaders. This ability to outsmart our defenders may again be coincidental; it’s more likely that the bacterium originally evolved to resist the digestive powers of amoebas, which also suck them up in the same way as macrophages.

And so far, we have just considered predators, which form one small part of the life of a bacterium. Competitors also shape their evolution. Earlier this year, I described how the normally harmless nose bacterium Streptococcus pneumonia becomes infectious when it battles against another species called Haemophilius influenzae. This competitor summons white blood cells to do away with Streptococcus, which can defend itself by producing a thicker coat. But this armour also allows Streptococcus to evade our own immune system, resulting in pneumonia, meningitis and other diseases. As I wrote back then, “many human diseases really have nothing to do with us at all.”

Reference: Adiba, S., Nizak, C., van Baalen, M., Denamur, E., & Depaulis, F. (2010). From Grazing Resistance to Pathogenesis: The Coincidental Evolution of Virulence Factors PLoS ONE, 5 (8) DOI: 10.1371/journal.pone.0011882

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CATEGORIZED UNDER: Bacteria, Evolution, Medicine & health

Comments (3)

  1. Wow, I find the hypothesis that virulent strains are pathogenic as a necessary consequence of other adaptations really intriguing. It makes sense, the more I think of it. With all the bacteria and other microscopic lifeforms out there, there’s bound to be some of them that ‘interact’ with us in unforeseen (and unintentional, from their perspective) ways.
    My only minor point of critique is that the team used a strain was known to be pathogenic to test their hypothesis. It would’ve been way more cool and convincing if they had artificially selected E. coli cells from a non-pathogenic strain that were able to resist the attacks of Dictyostelium, and show that this strain is more harmful for mice or capable to better resist macrophages.

  2. Apparently there is a suggestion that the S. aureus Vs. S epidermidis battle is also (that you have written about here earlier) may have induced virulence in S. aureus as it searches for a new niche to occupy.
    Also pneumo has another trick. Whilst producing a thicker coat it can also upregulate surface proteins that bind host factor H. Host factor H is one of the molecule the host uses to distinguish self from non-self. The bacteria essentially put on a host cell ‘suit’ and say “don’t look at me! You’re looking for that guy” and the Haemophilius’ trick can backfire.

  3. gillt

    Ed: “When Salmonella enterica, another food poisoning germ, is threatened by amoebas, it ends up with more genetic variation at a part of its genome that affects how virulent it is.”

    Do you mean to say “Salmonella in close proximity to amoebas have more genetic variation [...] than ones that aren’t threatened by amoebas”?

    Because it sounds like you’re saying amoebas give off some signal that directly affects the genome of nearby Salmonella, which would be weird.

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