Imagine a friend of a friend brings his family to stay with you — his family of tiny survivalists. For weeks or months you all live quietly side by side with no problems. You share meals. Your kids play together.
Then one day you get sick — maybe felled by a bad cold or the flu. Suddenly certain the end is near, your jittery houseguest breaks out an armory's worth of chemical weapons. He abandons his community to save himself and hunt for a new home, wreaking havoc on the way out the door.
That's essentially the story line microbiologists in Buffalo, N.Y., have now worked out for why colonies of Streptococcus pneumoniae bacteria (aka pneumococcus) can camp out happily and harmlessly for months at a time in the nose and throats of humans, then abruptly turn on their hosts. The germs sometimes trigger painful earaches or even meningitis in kids, and often pneumonia in the elderly and others with weak immune systems.
It's no small problem. The World Health Organization calls diseases triggered by the microbe "a major global public health problem." In 2000 alone pneumococcus provoked an estimated 14.5 million bouts of serious illness worldwide, according to the WHO, and killed perhaps 826,000 children under the age of 5.
"We were interested in getting at the mechanism — why these bacteria would suddenly migrate from the throat to the middle ear, lungs, or bloodstream which are normally sterile," Anders Hakansson, a microbiologist at the State University of New York at Buffalo, tells Shots. "We wanted to know why people get sick." He thinks he and his colleagues may have figured it out.
In a cool bit of science they recently published in the journal mBio, the researchers describe how they created a microbial community in a lab dish that mimics what happens in the lining of the human nose and upper throat.
Normally S. pneumoniae bacteria organize themselves there into a stable and highly structured slick, or biofilm, with other microbes, Hakansson says. "You'll see towers growing up," he says, "with channels coming down for water and nutrients," all layered atop the human cells.
But when the scientists added a pinch of flu virus to the mix – or in several other ways tweaked the little ecosystem to mimic what happens to the body when we catch the flu – the bacteria changed dramatically.
Increasing the colony's temperature (mimicking the fever of flu), for example, or adding the stress-linked hormone norepinephrine prompted some of the microbes to abruptly break off from the community.
And as they dispersed, the bacteria switched on a set of genes that made each one far more virulent when the scientists squirted them into mice. (In contrast, squirts of bacteria taken from the stable colonies of S. pneumoniae migrated to the animals' throats and harmlessly set up shop there, just as they usually do in people.)
Hakansson says he suspects, though can't say for certain, that the lungs and middle ears are just cul-de-sacs where the activated, pioneering bacteria get stuck during their hunt for a new home in a healthier host. The fact that their human host gets very sick or even dies from such infections isn't good for the bacteria either.
At any given time, between 25 and 40 percent of children under age 5 are colonized with the bacteria, Hakansson says, and between 8 and 15 percent of adults. Typically, these bacterial campsites persist for a few days, weeks or months, and don't produce symptoms. "They don't mean to make us sick," Hakansson says.
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