When bacteria fight bacteria, we lose

By Ed Yong | June 17, 2010 3:00 pm

Haemophilius_Streptococcus

There’s a war going on that you’re completely oblivious to, even though it’s happening right under your nose. Well, actually, inside your nose. Rival species of bacteria compete for precious real estate within the damp linings of your nasal passages. In some cases, this microscopic combat works in our favour, when harmless species repress the growth of deadlier ones. But not always – sometimes a species can only gain the advantage over its competitors by becoming more virulent, and we suffer collateral damage.

Elena Lysenko from the University of Pennsylvania has discovered one such rivalry, at least within the noses of mice. She studied the conflict between two species of bacteria – Haemophilus influenzae and Streptococcus pneumoniae, both of which can cause pneumonia, meningitis and other human diseases.

S.pneumoniae spends much of its time in our noses without causing any harm. Only in a minority of carriers does it gain the potential to cause diseases, such as pneumonia and sepsis. But that doesn’t make any sense, because these conditions are potentially fatal but not contagious. The bacteria risk killing their host (and by extension themselves) without gaining the opportunity to colonise a new one. Why would they go down this dead end route? Lysenko thinks she has an answer – S.pneumoniae turns nasty as a side effect of its tussle with H.influenzae.

There’s not enough space in a nose for these two bacteria. H.influenzae plays dirty – it actually summons our own immune system into battle, setting white blood cells called neutrophils against S.pneumoniae. This call-to-arms is so effective that in most cases, H.influenzae can completely oust its rival from a nose.

But S.pneumoniae has a defence. The bacterium is surrounded by a sugary capsule and there are at least 90 different types of these coats. Some of them are particularly thick and they act as suits of armour that protect the bacterium against white blood cells that try to engulf it. Encased in these shields, S.pneumoniae can evade the host’s immune system. It neutralises H.influenzae’s secret weapon but it also gains the ability to invade other tissues and cause serious diseases.

Lysenko demonstrated the effects of this battle using both mathematical models and experimental evidence. When she incubated H.influenzae with different strains of S.pneumoniae, she found that only those with armoured shells could hold their ground against their competitor. Strains without these thicks shells were soon driven out. And just to show that this competitive edge wasn’t due to the genes carried by different strains, she managed to turn a weedy strain into a tough one by transplanting an armoured shell onto it.

But why doesn’t S.pneumoniae use its armoured shells all the time? To find out, Lysenko pitted the different strains against each other in the absence of any other competing species. This duel revealed that the armoured strains are actually inferior to non-armoured ones in terms of colonising the nose. Presumably, making a heavy shell takes up a lot of energy, which means that these well-defended strains can’t grow as quickly as other more vulnerable ones.

They only gain the upper hand when H.influenzae is around. At that point, the ability to resist death by white blood cell more than makes up for their natural disadvantages. And of course, the armoured strains, by shrugging off attacks from the immune system, are better at causing invasive infections than their mild-mannered cousins.

Of course, Lysenko has only demonstrated that this happens in mice but it is likely that similar competitions operate in human noses. And that’s fascinating – it means that many human diseases really have nothing to do with us at all. They’re the result of battles waged between different species of bacteria, and we just happen to be caught in the crossfire.

Reference: Current Biology http://dx.doi.org/10.1016/j.cub.2010.05.051

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CATEGORIZED UNDER: Bacteria, Medicine & health

Comments (9)

  1. Jumblepudding

    So my nose is basically the Gaza strip?

  2. The problem of the ‘armoured’ or encapsulated strains being less efficient colonisers is somewhat overcome by their ability to undergo a shift in ‘armour quantity’. This process, called ‘phase variation’, results in lower quantities of sugary capsule being expressed at the sites of colonisation but once inside the blood or other tissues capsule production goes up to protect the pneumococcus in those environments. It’s thought that less capsule is better when trying to attach to and colonise a surface as bacterial adhesions can interact better with host cells when there isn’t so much capsule in the way.

    Great article Ed, I couldn’t help myself though :)

  3. Szwagier

    I propose a two-nose solution.

  4. Geoff

    Thanks, Ed…I might have to use this article in my Microbiology class next year!

  5. Geeze next time I get the sniffles, I’m going to have to call the UN.

  6. I wonder how hayfever affects the battle going on in my nose. All that mucus must swing things in one bacterias favour.

  7. Jenny

    So does that mean that with Haemophilus influenzae B vaccinations, there is less strep pneumo turning into serious pneumonia? What part does non-typeable H. influenzae play in all this?

  8. This would be great to use when teaching about resource allocation, evolution, and competition. It really shows the complexity of the natural world around us. I wonder if this shows us a path or reason for why some pathogens are so virulent and others are not. It’s always been perplexing, to me, that organisms have evolved to destroy their host and in essence themselves. THANKS for sharing! – Justan Educator

  9. Chris

    Great story Ed. I am a colleague of Elena Lysenko and she was pleased to see her research has not gone unnoticed.

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