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2011

Rise of the Superbacteria
Newsweek, June 5, 2011
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When Philip Tarr heard the first reports of a massive outbreak of E. coli in Europe recently, they had a sickeningly familiar ring. Tarr, a microbiologist at Washington University, is an expert on the strains of E. coli that have periodically wreaked havoc in the United States. In 2006, for example, E. coli on contaminated spinach infected 199 people in the United States, causing kidney failure in a number of cases. The European outbreak seemed to fit the pattern: people were infected with E. coli apparently after eating contaminated vegetables.

But then Tarr got a rude shock. German hospitals sent samples of the E. coli to the Beijing Genome Center to have their DNA sequenced. On June 2, the Chinese researchers reported that the strain was not the same E. coli that contaminated the spinach, known as O157:H7. In fact, it was an entirely different strain, called O104:H4, that had never been associated with epidemics before. Tarr searched the medical literature for reports of the European strain. He could find only a handful of people who had carried it, and none of them got sick. But somehow this obscure microbe had turned vicious, triggering one of the biggest--if not the biggest--E. coli epidemics in history, with at least 1,730 infections and 18 deaths (at time of writing).
“We didn’t know this bug was out there,” says Tarr. “This outbreak is taking us all by surprise.”

The fact that someone like Tarr has been taken by surprise should be of concern to everyone. The new epidemic raises grave questions about how prepared the United States and other countries are for a similar outbreak.
What makes these outbreaks particularly confusing is that E. coli is, for the most part, a harmless creature. We are each home to billions of harmless E. coli that dwell in our gut. They live peacefully in every other mammal, too. E. coli is so harmless, in fact, that microbiologists began to rear E. coli in laboratory flasks a century ago, and it became the best-studied species on earth.

But in the mid-1900s, scientists began uncovering strains of E. coli that could cause life-threatening diarrhea. Unlike ordinary E. coli, they carried genes for a poison known as Shiga toxin, named for Japanese bacteriologist Kiyoshi Shiga. Over time, microbiologists identified a number of strains of disease-causing bacteria, classifying them by the proteins on their surface. In 1982, E. coli O157:H7 burst on the scene with particularly grisly flair. It struck 25 people in Medford, Ore., and then three months later the same strain caused an outbreak in Traverse City, Mich. Scientists were able to trace the bacteria back to undercooked hamburgers.

Since then, scientists have found a half dozen other strains that cause similar illnesses, but E. coli O157:H7 has been responsible for the lion’s share of E. coli food poisoning. It struck again in 1993 in contaminated hamburgers in Washington state, for example, sickening 732 people and killing four of them. But it has not used just hamburger to infect its victims. Along with the spinach outbreak of 2006, E. coli O157:H7 has turned up in lettuce, bean sprouts, and even cookie dough.

Researchers have found that E. coli O157:H7 and many other disease-causing strains live in cows and other livestock, in which they seem to be harmless. People can acquire the bacteria in contaminated beef. The microbes can get into vegetables through manure-laced irrigation water. Once the bacteria get into a human host, they turn vicious. In the large intestine, they insert molecular needles into gut cells and inject molecules that cause the cells to dump out nutrients for the bacteria to feed on.

This microbial feast causes painful diarrhea, but most people infected with E. coli O157:H7 can recover within a few days. For every 20 people who get infected, however, one or two have much worse in store. Their E. coli releases Shiga toxins, which move from the intestines into the surrounding blood vessels and spread to the rest of the body. They trigger blood clots, seizures, and kidney failure.

The sudden debut of E. coli O157:H7 in the 1980s made many people wonder how it had come to be. Was it the monstrous product of the modern food industry? Tarr and his colleagues analyzed the genome of the bacteria to estimate its time of origin. “These organisms have been around for 7,000 years,” says Tarr. It’s possible that E. coli O157:H7 and other pathogenic strains caused outbreaks for centuries before microbiologists could identify them as the cause.

Yet the great age of E. coli O157:H7 is no cause for complacency. Modern food production can spread the bacteria far faster than ever before. The 2006 spinach outbreak swept across the continental United States before public-health workers became aware of it.

A look at the genetic makeup of E. coli O157:H7 is cause for even more concern. It evolved into a deadly pathogen by picking up genes from other bacteria through a process called recombination. Viruses, for example, can move from one E. coli to another and insert genes from their old host into a new one. “E. coli are a cauldron of recombination,” says Tarr.

Public-health workers have learned to stay alert for outbreaks of E. coli O157:H7 and a half dozen other disease strains. But the European strain did not belong to any of these well-known suspects. Initially, it appeared that the bacteria were coming from cucumbers and other vegetables from organic farms in Spain, but O104:H4 has not turned up in tests at those places. Researchers are now left to wonder where exactly it came from.

The O104:H4 genome sequence suggests that it’s yet another concoction from evolution’s cauldron. The bacteria contain many segments of DNA not seen in other E. coli strains. This new DNA may be responsible for its high level of virulence--more than a quarter of victims went on to develop the dangerous form of the disease. The O104:H4 strain has even acquired new genes that make them resistant to antibiotics. As a result, doctors have few options to treat the bacteria. In Germany, physicians are resorting to an experimental antibody treatment to see if it can help.

The new epidemic adds to a growing concern about food safety in the United States. In May, the University of Florida’s Emerging Pathogens Institute released a report that estimates that food pathogens cause $14 billion in medical costs and lost wages yearly. Poultry tainted with the bacteria Campylobacter cause an estimated 600,000 cases of illness annually, for example, and put nearly 7,000 people in the hospital.

The European outbreak of E. coli O104:H4 will not cause much trouble in the United States. Only two Americans, both of whom had recently returned from Germany, have come down with the bacteria. But it is possible that the new strain could make its way to the United States and cause an epidemic at some point in the future. “There’s nothing European about this,” says Tarr. “I hope we can learn something from it.”

One frightening lesson is that O104:H4 is not going to be the last new deadly E. coli strain. Other ones will be evolving, and when they strike, ordinary tests will not detect them. Tarr believes this uncertainty may demand a new way to make fruits and vegetables safe from strains of E. coli we haven’t yet encountered.

“We’re going to have to rethink food safety,” Tarr says. It may even be necessary to take a drastic step, such as irradiating fresh produce. “I can tell you how to cook a hamburger to make it safe,” he says. “But I can’t tell you how to prepare a head of lettuce to make it safe.”

Copyright 2011 Carl Zimmer
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