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.
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.
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.
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.
A child from the village of Chamba in rural Malawi has very little in common with one living in the city of Philadelphia in the USA. They eat different food, speak different languages, and enjoy different lifestyles. But they are both united by the fact that they are vessels for teeming hordes of bacteria.
These children, like all of us, are home to trillions of bacteria and other microbes. These passengers outnumber our own cells by ten to one, and their genes outnumber ours by a hundred to one. Collectively, they’re known as the microbiome, and they are as much a part of us as any one of our own organs. They break down our food, safeguard our health, and affect our minds. And they have become intensely fashionable.
Microbiome research is booming, fuelled by the realisation that these microbes might provide a deeper understanding of our bodies, and new ways of diagnosing or treating diseases. But, with some exceptions, most microbiome studies have focused on wealthy populations from Europe, North America and Japan. There’s a risk that the bacteria of people from the developing world will be ignored.
Tanya Yatsunenko has led one of the largest efforts yet to remedy that problem. Working with Rob Knight and Jeffrey Gordon, she amassed an international collection of faecal samples and studied the gut microbes of people three diverse populations: 100 Guahibo people from the Venezuelan Amazon; 115 people from four Malawian villages; and 316 people from three American cities. The recruits ranged from newborn babies to 70-year-old adults.
“The paper represents a heroic effort,” says David Relman, who studies the microbiome at Stanford University. “It’s the most definitive cross-culture and multi-age assessment of the human microbiome to date.”
Many insects eventually evolve to resist insecticides. This process typically takes many generations and involves tweaks to the insect’s genes. But there is a quicker route. Japanese scientists have found that a bean bug can become instantly resistant to a common insecticide by swallowing the right bacteria.
The bug forms an alliance with Burkholderia bacteria, and can harbour up to 100 million of these microbes in a special organ in its gut (see arrow above). Some strains of Burkholderia can break down the insecticide fenitrothion, detoxifying it into forms that are harmless to insects. In fields where the chemical is sprayed, these pesticide-breaking bacteria rise in number. And if bugs swallow them, they become immune to the otherwise deadly chemical.
I’ve written about this story for The Scientist, so head over there to read the details of the study.
I regularly write about the microbiome – the trillions of bacteria that share our bodies with us, and the genes that they carry. At the recent International Human Microbiome Congress in Paris, I was immediately struck by two things. First, the field is clearly growing. It’s full of scientists who are doing great work to understand our bacterial associates, and who are glad that the microbes are finally hitting the big time.
But I also felt a familiar twang. When one of the initial speakers described the quest to sequence our microbiome as the “biggest life sciences project of all time”, and when people spoke of new ways to diagnose and treat diseases, I was reminded about the hype that surrounded the Human Genome Project, back when our DNA had not yet been fully sequenced. When people showed communities of microbes that were associated with diseases, with no clear sense as to which caused which, I thought of the endless number of observational studies looking at risk factors for cancer, heart disease, autism, and other conditions.
And it worried me. While I’m fascinated by the microbiome, and was thrilled to be part of the conference, I also wondered if the current optimism would lead to a backlash down the line. There’s precedent for this. The Human Genome Project is currently experiencing just such a backlash, as are large studies that try to find genetic variants that underlie human diseases. The so-called War on Cancer is still being fought several decades later, and patients are getting impatient. And I found many other microbiome scientists who shared my concerns, at the conference and beyond.
This was the basis of a piece that I wrote for Nature News. It looks at the potential for hyping yet another ‘Big Science’ endeavour. But it also considers legitimate reasons why the microbiome may deliver on its promises more quickly than the genome has. In particular, diagnostic tests seem to be a rich area to focus on, with a good chance of providing short-term gains. Check out the full piece for more.
Last year, I wrote about an intriguing study which showed that our hordes of gut bacteria tend to cluster into one of three communities. Each individual has one of these three “enterotypes”. As I wrote at the time, “There seem to be just three preferred ways of building a community of gut bacteria.”
Or are there? I’ve just spent three days at the International Human Microbiome Congress in Paris, where several hundred scientists gathered to discuss the nature of the several trillion bacteria we carry. One of the most intriguing debates, which ran across the first days of the conference, revolved around whether the enterotypes are actually discrete meaningful entities, or just points along a continuum of gut bacteria.
This reflects an age-old debate in science between “lumpers and spliiters” but it matters if, as suggested, the enterotypes could one day be used to stratify patients according to their risk of disease or which treatments they should receive. I wrote about the debate for Nature News. Head over there for more details.
Disclosure: MetaHIT, the conference organisers and the scientists behind the enterotype paper, paid for my travel and accommodation to the conference, so that I could chair the final panel on the future of the microbiome.
A bout of Salmonella food poisoning isn’t a pretty affair. Your digestive tract churns, you can’t keep your food down, and you feel exhausted. But you aren’t the only one affected. Your gut contains trillions of bacteria, which outnumber your own cells by ten to one. They are your partners in life, and they are also transformed by the presence of the invading Salmonella.
Minority members of this intestinal community start to bloom, greatly increasing in number as the guts around them become inflamed. And these gut bacteria start to trade genes with Salmonella.
These swaps are a regular part of bacterial life. In their version of sex, two cells become united by a physical bridge, through which they shunt rings of DNA called plasmids. These rings can act like mobile weapons packages. Some give otherwise harmless bacteria the ability to cause disease. Others confer resistance to antibiotics. It’s a network of shady arms trading, and in your inflamed bowels, it happens at an unprecedented level.