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Murder by “Blob”—the Miniature Version

It’s all so sudden.

The victim is on the left side of the screen—a single-celled little pulse of life, floating about in pond water somewhere. It’s got these little hairs called cilia. You don’t see them at first. They can turn into oars. Oars for escaping.

But it doesn’t know.

The killer comes in from the right, turning lazy circles in the water, like nothing’s going on. But that’s an act. As we’ll learn later, it is getting into position, moving close, finding an angle so it can point its … its what? I see no weapon. Does it have a weapon?

“I don’t know about this exact type of ciliate,” microbiologist Patrick Keeling wrote me, “but I know about other similar predators,” and at the very end of its snout-like appendage, it’s probably packing a bunch of “poisoned harpoons.” At nine seconds into the video, you can see it aim straight at the victim …

… There’s a shudder. The victim, which has been paddling along, suddenly gets smaller—much smaller—and stops moving. I saw no harpoon, but the water is muddy. If there is a needle, it would be very hard to see. “The poison,” Keeling figures, “causes paralysis where it hits.” But only for a beat.


Very quickly, the victim bounces back, gets larger, sticks out its cilia and begins paddling furiously, trying to get away. It’s beating so fast, its oars become a blur on its exposed side—but then comes the second blow.

This happens 15 seconds in; when I looked close, there’s a second snout, inside the killer’s body that grabs onto the victim, pulls, and fires. Is there a second dart? A bite? (It has no teeth, so it can’t bite.) But the victim now goes all quiet. The cilia disappear. This is a big catch. It would be like you or me eating an entire goat. “They eat by phagocytosis,” Keeling says. These small bits of pond life have cell walls, but those walls (if you’ve seen the 1956 horror pic The Blob, you know how this goes) can suck in and extend at the same time. The killer slowly surrounds, then pulls in its victim, like this:

GIF by Robert Krulwich
Phagocyte surface receptors lock and pull their prey in. GIF by Robert Krulwich

Can it stuff everything in? Won’t it gag? No, biologist David Caron wrote me. “Our (human) perception is that food particles have to be a small fraction of our own size. Not necessarily true to many single-celled organisms which can expand their membranes quite a bit to accommodate large prey items.” (Really large. This victim is roughly half the size of its killer.)

Well, at least it’s still. I wouldn’t want one of those things jiggling inside me. But here’s the thing: The victim, now stitched into a sack of its own, called a vacuole, may not be dead. That other yellowish package, already floating in there, both biologists say, is a previous victim, now awaiting “further breakdown.”

Still Alive?

“The prey is indeed alive when it gets eaten,” Keeling wrote. Does it stay alive?

“When a cell ‘dies’ is a hard question,” he says, “Some cells stay alive inside others for a long time, even after partially being digested.” There are single-celled creatures that feed on algae but leave the parts that turn sunshine into food—the chloroplast—alive and working for long periods.

So at the end of the video, neither Keeling nor Caron could say if the victim is dead. “Every food vacuole has its own processes … and its own timing,” Caron writes. It will die eventually, dissolved by acids, the unused bits flushed out. “Yes, essentially, they defecate,” Caron says, but how long that takes, we don’t know.

The victim, of course, has no questions. One moment it’s free, paddling about, then, in a flash, it’s shot, grabbed, swallowed, walled-in, and stuck. “What just happened?” it should wonder. But it can’t. Single celled creatures don’t wonder. At least I presume they don’t.

We do. Being three trillion cells bigger, we have the machinery to call experts, email videos, figure out motive, cause, possible weapon—and even, if you’re me, feel bad for the victim. This takes a lot of cells.

Not to brag, but when it comes to murders, this is an advantage we humans have over pond scum. It’s just better to be multicellular. (Unless you’re the victim. Dead humans and dead protozoa are pretty much the same—dead.) But alive, it’s people, not protozoa, who can enjoy a good murder mystery. That’s why my audience, small as it is, is (like you, I presume) entirely multicellular.

Thanks to the University of British Columbia’s Professor Patrick Keeling, who argued with me about my headline. He doesn’t think “murder” is the right word for what happened here. “I don’t think of it as murder,” he wrote me; it’s “more like hunting. I see it as being like the Serengeti on a small stage, where the lions and zebras all have their roles to play and there is no moral message in any of it.” I suppose that’s fair, but when I saw Wim van Egmond’s gorgeous video, what got me fascinated was how the killer killed. I couldn’t figure out how it did it. Having a very Agatha Christie reaction, I chose very Agatha Christie language. That, alas, is my excuse.

Thanks also to Professor David Caron at the University of Southern California, who on Christmas Eve watched the video and answered my questions so promptly, and to Elio Schaechter of the Small Things Considered blog, who told me who to call. And most of all, a pop of flashbulbs to Wim van Egmond, one of the world’s great microbiology photographers, who won first prize in 2015’s Nikon Small World video competition for this video of a single-celled Campanella ciliate being swallowed by a Trachelius predator. Apparently, he had scooped some pond water from a local pond, thinking he would show someone how to look through a microscope. When he leaned in and saw one protist swirling suspiciously close to its neighbor, he thought, “Eh, something’s up. I’m going to shoot this.” And he did. And he was so right.

Oh, and one last thing. Sometimes ciliates get inside their food AND GET OUT! This is Win van Egmond’s true-life video of two ciliates feasting on a baby copepod, and they both wiggle out—through a tiny hole …

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You’re Surrounded by Bacteria That Are Waiting for You to Die

Antibiotic-resistant Staphylococcus aureus bacteria (yellow) killing and escaping from a human white blood cell.
Antibiotic-resistant Staphylococcus aureus bacteria (yellow) killing and escaping from a human white blood cell.
Photograph by NIAID

You are filled with bacteria, and you are covered in them. And a whole lot of them are just waiting for you to drop dead.

As soon as you die, they’ll swoop in. This week, we learned exactly how microbes chow down on us. A brave and strong-stomached team of scientists spent months watching dead bodies decompose, tracking all the bacteria, fungi, and worms, day by day. Forensic scientists can use this timeline, published in Science, to help determine time—and even place—of death. (More on that in a previous Gory Details.)

The microbes in your intestines get first dibs, the scientists found. As soon as you die, they’ll start decomposing you from the inside out. Meanwhile, other bacteria on your skin or in the soil beneath you start mounting an attack from the outside in. As Michael Byrne at Motherboard so nicely summed it up, “Earth is just waiting for you to drop dead.”

That’s a little unsettling, if you think about it. And it begs the question: What keeps all those bacteria from decomposing you alive?

That’s silly, you say. I’m alive. Only dead things decompose.

Yes, but why?

What keeps all those bacteria from decomposing you alive?

As the new study points out, two of our most crucial defenses against being decomposed are toppled as soon as we die. Our immune system shuts down, and our bodies cool off. Bacteria like this; they don’t have an easy time growing in a hot body. (Think about it: When we have an infection our bodies develop a fever to ward it off.)

Basically, a big part of life involves your cells waging a battle to the death with bacterial cells. As long as you’re alive and healthy, your cells are winning. Decomposition is when your cells lose. 

One of the clearest descriptions I’ve read comes from Moheb Costandi’s “This is what happens after you die“:

Most internal organs are devoid of microbes when we are alive. Soon after death, however, the immune system stops working, leaving them to spread throughout the body freely. This usually begins in the gut, at the junction between the small and large intestines. Left unchecked, our gut bacteria begin to digest the intestines—and then the surrounding tissues—from the inside out, using the chemical cocktail that leaks out of damaged cells as a food source. Then they invade the capillaries of the digestive system and lymph nodes, spreading first to the liver and spleen, then into the heart and brain.

As soon as you die, your body essentially gets its first break from a war that it has been fighting every moment of your life.

When the bacteria start to win that war in a living person, we call it an infection, and we try to flush the invaders out of a wound. Or we go in with antibiotics to poison them.

Let’s pause for just a moment to appreciate those antibiotics. We thought we had outwitted bacteria. But now we’ve overused and misused antibiotics, giving the bacteria a chance to figure out our defenses. They’re adapting, becoming resistant to our weapons, and we’re already seeing the failure of some of our last lines of defense, leading to more infections, illness, and death.

Ultimately, we lose our battle with bacteria when we die. But until then, it’s pretty amazing to think of the fine line between life and becoming bacteria food. Imagine the evolutionary arms race that has led to an immune system so vigilant that it can fend off constant attack for decades. 

I’m just grateful not to be decomposing right now.

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A Floating Autobiography of a Cancer

I’ve written a feature for Nature News about a new way of monitoring and studying cancer, by tracking fragments of DNA that are released by tumours and travel around in the blood. This “circulating tumour DNA” can give away the presence and progress of a tumour. It also allows clinicians to study a cancer patient’s mutations, and potentially better tailor their treatments, without having to perform invasive (and often uninformative) biopsies.
Here’s a teaser; head over to Nature for the full story.

When cancer cells rupture and die, they release their contents, including circulating tumour DNA (ctDNA): genome fragments that float freely through the bloodstream. Debris from normal cells is normally mopped up and destroyed by ‘cleaning cells’ such as macrophages, but tumours are so large and their cells multiply so quickly that the cleaners cannot cope completely.

By developing and refining techniques for measuring and sequencing tumour DNA in the bloodstream, scientists are turning vials of blood into ‘liquid biopsies’ — portraits of a cancer that are much more comprehensive than the keyhole peeps that conventional biopsies provide. Taken over time, such blood samples would show clinicians whether treatments are working and whether tumours are evolving resistance.

As ever, there are caveats. Levels of ctDNA vary a lot from person to person and can be hard to detect, especially for small tumours in their early stages. And most studies so far have dealt with only handfuls or dozens of patients, with just a few types of cancer. Although the results are promising, they must be validated in larger studies before it will be clear whether ctDNA truly offers an accurate view — and, more importantly, whether it can save or improve lives. “Just monitoring your tumour isn’t good enough,” says Luis Diaz, an oncologist at Johns Hopkins University in Baltimore, Maryland. “The challenge that we face is finding true utility.”

If researchers can clear those hurdles, liquid biopsies could help clinicians to make better choices for treatment and to adjust those decisions as conditions change, says Victor Velculescu, a genetic oncologist at Johns Hopkins. Moreover, the work might provide new therapeutic targets. “It will help bring personalized medicine to reality,” says Velculescu. “It’s a game-changer.”

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We Are All Mosaics

Here’s something you probably learned once in a biology class, more or less. There’s this molecule called DNA. It contains a long code that created you and is unique to you. And faithful copies of the code live inside the nucleus of every one of the trillions of cells in your body.

In a later class you may have learned a few exceptions to that “faithful copies” bit. Sometimes, especially during development, when cells are dividing into more cells, a mutation pops up in the DNA of a daughter cell. This makes the daughter cell and all of its progeny genetically distinct. The phenomenon is called ‘somatic mosaicism’, and it tends to happen in sperm cells, egg cells, immune cells, and cancer cells. But it’s pretty infrequent and, for most healthy people, inconsequential.

That’s what the textbooks say, anyway, and it’s also a common assumption in medical research. For instance, genetic studies of living people almost always collect DNA from blood draws or cheek swabs, even if investigating the tangled roots of, say, heart disease or diabetes or autism. The assumption is that whatever genetic blips show up in blood or saliva will recapitulate what’s in the (far less accessible) cells of the heart, pancreas, or brain.

Two recent reports suggest that somatic mosaicism is far more common than anybody ever realized — and that might be a good thing.