Clostridium difficile

by Matt Shipman

Depending on who you ask, there are anywhere from 100 to almost 200 different species of Clostridium bacteria. And you do not want to attend their family reunion.

Clostridium species are responsible for all sorts of awful medical conditions. Botulism, which is rare but sometimes lethal, is usually caused by C. botulinum – though C. butyricum and C. baratii occasionally get in on the act. C. perfringens can cause food poisoning and gas gangrene – which kills muscle tissue and can be fatal (it’s thought to have killed hundreds of thousands of soldiers during World War I). And tetanus, which kills thousands of people around the world each year, is caused by C. tetani.

In short, Clostridium can be a nasty bunch.

One of the most interesting species of Clostridium is called C. difficile. It is interesting not because it causes health problems (though it does), but because of who it doesn’t make sick, because it appears to be getting more dangerous, and because of a new way doctors are starting to treat it.

C. difficile causes severe diarrhea and, in some cases, an inflammation of the colon (or large intestine) that can be fatal. Disgusting and scary, sure. But not any more interesting than its equally scary cousins C. botulinum or C. tetani.

One of the things that is particularly interesting about C. difficile is that lots of people carry it around in their guts all the time. Researchers think that about three percent of healthy adults have C. difficile living in their digestive systems. That’s more than a million people in the United States alone. And here’s the thing – the C. difficile is not making them sick.

That’s because there are lots of other bacteria that also live in our guts. These “good” bacteria keep the C. difficile bacteria from growing out of control and making you sick.

But people that don’t have a healthy population of good bacteria in their digestive systems can be in trouble, because the population of C. difficile bacteria can increase pretty quickly (and make those people sick). Older adults often have weak populations of good bacteria, but young people aren’t immune to the problem. For example, you might take antibiotics to kill a type of bacteria that is making you sick – but the antibiotics can also kill off some of the good bacteria living in your guts. That shortage of good bacteria might be all C. difficile needs to start a population boom that ends up giving you diarrhea or worse.

If you are part of the 97 percent of people who don’t already have C. difficile in your system, you may be wondering how C. difficile could find its way into you. In a word: poop.

People who have C. difficile in their guts also have C. difficile and C. difficile spores in their feces. So someone who doesn’t do a good job of washing his or her hands can spread those spores from their hand to, say, the kitchen table. Then the spores might hitch a ride on an apple or a sandwich into someone else’s mouth. Once the spores have found a nice place to grow (like someone’s intestines), they’ll “germinate,” or develop, into C. difficile bacteria and begin colonizing their new home. And these spores are tough. They can live in almost any environment for weeks.

That, of course, is bad news. But it’s not the really bad news.

All organisms evolve, changing over time to adapt to their environment. And, for some reason, C. difficile appears to be changing in ways that make it more dangerous for humans.

Since 2000, researchers have identified several new strains (or types) of C. difficile that are better at spreading from person to person and also make people sicker. But while the researchers can tell that C. difficile is evolving, they don’t really understand how it is evolving. For example, they know that lots of people are getting sick – but the traditional assumptions used to explain how the disease is spreading often don’t seem to apply.

Researchers are hoping that more research into the genetic make-up of these C. difficile strains will help them figure out exactly what is happening – how the bacteria are evolving, and how they are spreading. Ultimately, that should help us find better ways to limit the spread of C. difficile.

The good news is that researchers are making progress in finding ways to treat people who suffer from illness caused by C. difficile. And one of the most promising lines of research is fecal transplants. Yes, that means what you think it means.

Doctors take feces from someone with a healthy population of good gut bacteria and then implant it into the guts of a person who C. difficile is making sick. The idea is that the good gut bacteria effectively attack the C. difficile bacteria – or at least limit the size of the C. difficile population.

A study published in January 2013 found that 13 out of 16 patients suffering from C. difficile illness no longer had diarrhea after the first “infusion,” or fecal transplant. And another two patients got better after a second infusion. That’s a success rate of 15 out of 16 patients, which is much higher than the success rates for patients receiving other antibiotic-based treatments (the best of which had a success rate of four out of 13 patients). In short, feces that are teeming with a diverse collection of bacteria can actually save people’s lives.

Like I said, C. difficile is interesting.


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Michelle D. Cairns, Richard A. Stabler, Nandini Shetty, and Brendan W. Wren. The continually evolving Clostridium difficile species. Future Microbiol. 2012 August;7(8):945-957. (DOI:10.2217/fmb.12.73)

Gould C.V., McDonald L.C. Bench-to-bedside review: Clostridium difficile colitis. Crit. Care. 2008; 12(1), 203. (DOI: 10.1186/cc6207)

Els van Nood, M.D., Anne Vrieze, M.D., Max Nieuwdorp, M.D., Ph.D., Susana Fuentes, Ph.D., Erwin G. Zoetendal, Ph.D., Willem M. de Vos, Ph.D., Caroline E. Visser, M.D., Ph.D., Ed J. Kuijper, M.D., Ph.D., Joep F.W.M. Bartelsman, M.D., Jan G.P. Tijssen, Ph.D., Peter Speelman, M.D., Ph.D., Marcel G.W. Dijkgraaf, Ph.D., and Josbert J. Keller, M.D., Ph.D. Duodenal Infusion of Donor Feces for Recurrent Clostridium difficile. N Engl J Med. 2013 January; 368:407-415 (DOI: 10.1056/NEJMoa1205037)

About the Author

Matt Shipman is a science writer and public information officer at North Carolina State University. Before coming to NC State he covered the nexus of science, politics and policy as a reporter for Inside EPA, Water Policy Report and Risk Policy Report. His science communication blog, Communication Breakdown, is part of the SciLogs network presented by Spektrum der Wissenschaft in association with