The bay at the Danish port of Aarhus is pretty enough, with the usual fare of beach-goers, holiday homes and yachts. But the bay’s most spectacular residents live in the mud beneath its water. Back in 2010, Lars Peter Nielsen found that this mud courses with electric currents that extend over centimetres. Nielsen suspected that the currents were carried by bacteria that behaved like electric grids. Two years on, it seems he was right. But what he found goes well beyond what even he had imagined.
Nielsen’s student Christian Pfeffer has discovered that the electric mud is teeming with a new type of bacteria, which align themselves into living electrical cables. Each cell is just a millionth of a metre long, but together, they can stretch for centimetres. They even look a bit like the cables in our electronics—long and thin, with an internal bundle of conducting fibres surrounded by an insulating sheath.
Nielsen thinks that each cable can be considered as a single individual, composed of many cells. “To me, it’s obvious that they are multicellular bacteria,” he says. “This was a real surprise. It wasn’t among any of our hypotheses. These distances are a couple of centimetres long—we didn’t imagine there would be one organism spanning the whole gap.”
The bacteria are members of a family called Desulfobulbaceae, but their genes are less than 92 percent identical to any of the group’s known members. “They’re so different that they should probably be considered a new genus,” says Nielsen. They’re only found in oxygen-starved mud, but where they exist, there’s a lot of them. On average, Pfeffer found 40 million cells in a cubic centimetre of sediment, enough to make around 117 metres of living cable.
There are bacteria in the soil that can resist our antibiotics. That’s predictable – these drugs are our versions of natural compounds that bacteria have been assaulted with for millions of years. Of course, they would have evolved resistance.
There are also disease-causing bacteria in our hospitals and clinics that can resist our antibiotics. That’s predictable too – we expose ourselves, often unnecessarily, to high doses of such drugs. Of course, bacteria would have evolved resistance.
Here’s something fascinating though: some of the genes that confer resistance to the harmless soil bacteria are exactly the same as the ones that confer resistance to the devastating clinical ones. Exactly the same, DNA letter for DNA letter.
This new discovery, by Gautam Dantas, suggests that environmental bacteria may be supplying genetic weapons to the ones that kill us (or the other way around). I’ve written about this secret arms trade for The Scientist. Check it out.
We aren’t single individuals, but colonies of trillions. Our bodies, and our guts in particular, are home to vast swarms of bacteria and other microbes. This “microbiota” helps us to harvest energy from our food by breaking down the complex molecules that our own cells cannot cope with. They build vitamins that we cannot manufacture. They ‘talk to’ our immune system to ensure that it develops correctly, and they prevent invasions from other more harmful microbes. They’re our partners in life.
What happens when we kill them?
Farmers have been doing that experiment in animals for more than 50 years. By feeding low doses of antibiotics to healthy farm animals, they’ve found that they could fatten up their livestock by as much as 15 percent. You can put the antibiotics in their feed or in their water. You can give the drugs to cows, sheep, pigs or chickens. You can try penicillins, or tetracyclines, or many other classes of antibiotics. The effect is the same: more weight.
Consistent though this effect is, no one really understands why it works. The safe bet is that the drugs are exerting their influence by killing off some of the microbiota. Now, Ilseung Cho from the New York University School of Medicine has confirmed that hypothesis. By feeding antibiotics to young mice, he has shown that the drugs drastically change the microscopic communities within their guts, and increase the amount of calories they harvest from food. The result: they became fatter.
On 13 June, 2011, a woman was transferred to the National Institutes of Health Clinical Center with an infection of Klebsiella pneumoniae. This opportunistic bacterium likes to infect people whose immune systems have been previously weakened, and it does well in hospitals. In recent years, it has also evolved resistance to carbapenems – the frontline antibiotics that are usually used to treat it. These resistant strains kill more than half of the people they infect, and the new patient at the NIH hospital was carrying just such a strain.
She was kept to herself, in her own room. Any doctors or visitors had to wear gowns and gloves. The only contacts she had with other patients were two brief stints in an intensive care unit.
The woman eventually recovered and was released on 15 July. But by then, she had already spread her infection to at least three other patients, despite the hospital’s strict precautions. None of them knew it at the time, for K.pneumoniae can silently colonise the guts of its host without causing symptoms for long spans of time.
The second patient was diagnosed with K.pneumoniae on 5 August, and every week after that, a new case popped up. The hospital took extreme measures. All the infected people were kept in a separate part of the hospital, and assigned a dedicated group of staff who didn’t work on any other patients. The outbreak was contained, but not before it had spread to 18 people in total, and killed 6 of them.
How did the bacteria manage to spread so effectively, despite everything that the hospital did to stem its flow? K.pneumoniae’s stealthy nature makes it nigh impossible to work out the path of transmission through normal means. Instead, Evan Snitkin from the National Human Genome Research Institute sequenced the entire genomes of bacteria taken from all the infected patients. His study is the latest in a growing number of efforts to use the power of modern genetic technology to understand the spread and evolution of diseases.
In Nicole King’s lab, a bacterium is making a group of tiny cells stick together. That might seem a little humdrum for a group whose members can build electric grids, create snow, and cripple nations. But King’s bacteria should not be overlooked, for they are recapping one of the most important events in the history of life: the move from one cell to many.
The cells in question are choanoflagellates – the closest living relatives of all animals. They’re not our direct ancestors, but they give us clues about what those ancestors were like when they were still swimming around as single cells. Choanoflagellates normally live in solitude, moving about with sperm-like tails and voraciously eating bacteria. But they can also form big colonies. If we can understand why this happens, we might get hints as to why our single-celled ancestors did the same.
King has now found the answer, and it’s a tantalising one. The solitary cells become sociable after being exposed a molecule called RIF-1 that’s produced by some of the bacteria that they eat. When they divide in two, the daughters normally go their separate ways; add a splash of RIF-1, and they stick together instead.
This raises an obvious question: did bacteria also help the single-celled ancestors of animals to band together? Did they contribute to the evolutionary foundation of every ant and elephant, every fish and finch? “That’s my favourite hypothesis,” says Rosie Alegado, the lead author on the new study. “Animals evolved in seas teaming with bacteria and have been passively exposed to bacterial chemical cues, intended and unintended.” But she cautions that this is still an open question.
A pregnant woman isn’t just eating for one, but for trillions. Aside from her baby, she’s also home to a multitude of bacteria and other microbes. They have been part of her life since she herself emerged from a womb, and they have influenced her health ever since. Now, as she enters her third trimester, her microbe community is radically changing.
The diversity of species is falling, while certain groups are rising to the fore. Oddly enough, the whole community starts to resemble the microbes of someone with metabolic syndrome – a collection of symptoms that increase the risk of diabetes and heart disease, such as obesity, high blood sugar levels, and inflammation. It’s a good reminder that context matters. These “unhealthy” changes in our gut microbes are actually normal in a different setting, and might even be necessary for a healthy pregnancy.
When bacteria start building cities, we’re in trouble. The normally free-floating cells can gather in large numbers and secrete a slimy matrix that they live within. These communities are called biofilms, and they grow wherever there is a surface to support them. Hospital catheters are prime real estate, but they’ll settle on everything from plumbing to oil refineries to ship hulls.
Within a biofilm, bacteria are extraordinarily durable. Antibacterial chemicals have a tough time reaching them within their slimy fortress. Even if they do, there’s always a batch of dormant cells that can persist through a chemical onslaught and restart the community. They’re involved in the majority of persistent hospital infections, and it’s easy to see why. You could bleach a biofilm for an hour and still fail to kill it. They’ve survived in pipes that are flushed with toxic chemicals for a week.
Since killing biofilms is a Sisyphean task, some scientists are trying to prevent them from forming at all. They’ve tried textured surfaces, chemical coats, and antibiotic-releasing layers. But Joanna Aizenberg has developed a new solution that goes well beyond what the competitors can do. Inspired by the flesh-eating pitcher plant, she created a material so slippery that biofilms simply cannot form upon it.
A malarial mosquito is a flying factory for Plasmodium – a parasite that fills its guts, and storms the blood of every person it bites. By hosting and spreading these parasites, mosquitoes kill 1.2 million people every year.
But Plasmodium isn’t the only thing living inside a mosquito’s guts. Just as our bowels are home to trillions of bacteria, mosquitoes also carry their own microscopic menageries. Now, Sibao Wang from Johns Hopkins Bloomberg School of Public Health has transformed one of these bacterial associates into the latest recruit in our war against malaria. By loading it with genes that destroy malarial parasites, Wang has turned the friend of our enemy into our friend.
Many groups of scientists have tried to beat malaria by genetically modifying the species of mosquito that carries it – Anopheles gambiae. Marcelo Jacobs-Lorena, who led Wang’s new study, has been at the forefront of these efforts. In 2002, his team loaded mosquitoes with a modified gene so that their guts produce a substance that kills off Plasmodium.
Insects have been around for almost 400 million years. That’s plenty of time for evolution to fashion countless horrific deaths for them. Case in point: some insects die because a little worm vomits glowing bacteria inside their bodies.
The worm is Heterorhabditis bacteriophora, a microscopic creature used by gardeners the world over to control insect pests. Its accomplice-in-insecticide is a shiny bacterium called Photorhabdus luminescens, which only lives in the worm’s guts.
When the worm infiltrates an insect, it vomits out the bacteria. These reproduce madly and produce toxins that kill the insect, converting its fallen cells into nutrients that nourish the worm. The bacteria also make amino acids that the worm needs to reproduce, and antibiotics that kill other bacteria trying to colonise the insect. (In the US Civil war, soldiers were sometimes contaminated with P.luminescens, which gave their wounds a mysterious blue shine and protected them from blood poisoning – they called it the “angel’s glow”.)
You’re barely human. For every one of your own cells in your body, there are many microbial ones. They not only outnumber you, but they affect your health and your mind. Bits and pieces of this microbial menagerie have been revealed over time, but a massive study – the Human Microbiome Project – has just unveiled the most thorough picture yet of the microscopic majority that colonises us.
I wrote about this for The Scientist, so head over there to guzzle the details.
The key point, however, is individuality. While some broad groups of microbes that everywhere, the study failed to find any species that are universally present in the same body part across all people. However, those incredibly diverse microbes do very similar things. Curtis Huttenhower, the lead author of this consortium of hundreds, compared the situation to the fact that every city has lawyers, bankers and salesmen, even though different individuals play those roles in different places.