Unlike previously identified superbugs that are usually from multiple strains, these E. coli bacteria belong to just one closely related clone, says Evgeni V. Sokurenko. "We now know that we are dealing with a single enemy, and that by focusing on this super-clone we can have a substantial impact on this worldwide epidemic." Above: This antibiogram compares the resistance of the H30-Rx strain to another strain of E.coli that also infects the urinary tract. (Credit: Mariya Billig)

‘Super-clone’ E. coli could be worse than hospital superbug

Virulent, drug-resistant forms of E. coli that have recently spread around the world emerged from a single strain of the bacteria, not many different strains, as has been widely believed.

The strain—which causes millions of urinary, kidney and bloodstream infections a year—could have a far greater clinical and economic impact than any other strain of bacteria, including the so-called MRSA superbug.

“We now know that we are dealing with a single enemy, and that by focusing on this super-clone we can have a substantial impact on this worldwide epidemic,” says Evgeni V. Sokurenko, professor of microbiology at the University of Washington.

Over the past decade, public health officials noted that E. coli belonging to the ST131 strains family emerged as a major cause of urinary tract and kidney infections.

These are the most common bacterial infection in women and the elderly. The ST131 bacteria were notable because they had acquired resistance to a class of relatively new antibiotics called fluoroquinolones, which were commonly used to treat urinary tract infections.

More recently, theses pathogens also acquired genes for extended-spectrum beta-lactamase. This change rendered a broad spectrum of antibiotics, including highly-potent penicillin derivatives and cephalosporins, ineffective against these strains of bacteria. As a result, the infections are increasingly difficult to treat.

Many strains, one clone

These various resistant strains were assumed to have emerged independently around the world in response to their exposure to antibiotics. The current research proves that to be incorrect.

For the new study, published in mBio, researchers sequenced the genomes of scores of ST131 bacterial samples collected from patients and animals around the world. Then, using a technique called whole-genome-sequence-based phylogenomic analysis, they constructed a family tree that revealed the bacteria’s evolutionary history.

Their analysis indicates that almost all ST131 strains responsible for the notoriously resistant infections are very closely related to each other. They arise from a single clone that is termed H30-Rx for its resistance to treatment.

“Astoundingly, we found that all of the resistance could be traced back to a single ancestor,” says Lance Price, professor of environmental and occupational health at the George Washington University School of Public Health and Health Services and an associate professor in the Pathogen Genomics Division of the Translational Genomics Research Institute in Arizona. “This superbug then took off, and now causes lots of drug-resistant infections.”

In addition, the H30-Rx strain is fast-growing and can spread from person to person. It infects both the healthy and infirm, young and old, and is adept at invading the bloodstream.

“In some hospitals it is responsible for up to half of E. coli infections. It is the most common single strain causing sepsis, a deadly form of blood infection that kills 20 percent to 40 percent of patients who develop it,” Sokurenko says.

“Due to its wide-spread resistance and virulence, the social and economic impact of H30-Rx clone could exceed that of any other bacterial strain known.”

The study’s findings may make it possible to develop “better tools to identify, stop or prevent its spread by finding better ways to block the transmission of the superbug, or by finding a diagnostic test that would help doctors identify such an infection early on, before it might have the chance to turn lethal,” says James R. Johnson, professor of medicine at the Veterans Affairs Medical Center and the University of Minnesota.

In addition to the United States team, researchers from the Universitatsklinikum Munster in Muenster, Germany and the Statens Serum Institute in Copenhagen, Denmark participated in the study, which was supported by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs, the TGen Foundation, the National Institutes of Health, and the US Army Medical Research and Materiel Command.

Source: University of Washington

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