A quicker post today from the ICAAC meeting because there’s lots of news coming down this afternoon. At a conference like this, where the focus is on new behavior of pathogens and new drug compounds to contain them, there is a natural focus on emerging antibiotic resistance. Out of the first two days of (hundreds of) papers and posters, here are just a few unnerving reports.
Infections with multi-drug resistant E. coli — known by the acronym ESBL for “extended spectrum beta-lactamase,” indicating resistance to penicillins and cephalosporins — have been assumed to be a hospital phenomenon. Hospitals are where people become sick and debilitated enough to be vulnerable to these organisms, and also where patients and health care workers are more likely to spread the organism around. But an analysis by Yohei Doi of the University of Pittsburgh and a multi-national team shows that is no longer the case. They surveyed records from five hospitals across the United States (in New York, Pennsylvania, Michigan, Texas and Iowa), and identified 291 cases of ESBL E. coli infection over 12 months — but also found that 107 of the patients, or 37 percent, had acquired their infections before they entered the hospital. In other words, multi-drug resistant E. coli is now spreading in the everyday world, in an undetected and untracked way.
More than half of the cases the Doi team found were due to a specific strain of E. coli known as ST131, which microbiologists have been keeping an eye on because it emerged only a few decades ago and quickly became a dominant strain. A project by researchers from Denmark’s Statens Serum Institute and the Minneapolis Veterans Affairs Medical Center demonstrates why that dominance is concerning. The groups examined a World Health Organization research center’s collection of E. coli isolates that stretched from 1968 to 2012. Of three isolates from 1968, soon after the clonal group was first spotted and close to when it presumably emerged, one was already multi-drug resistant. Over the decades, the organism has collected additional resistance factors. The group say: “Most of the … ‘recent’ isolates (2005-2011) were extensively multi-drug resistant, i.e., resistant to ampicillin, amoxicillin-clavulanate, ciprofloxacin, nalixidic acid, sulfamethoxazole and tetracycline.”
Finally, a team from the Netherlands examined the rapid emergence of ESBL E. coli in that country — a particular puzzle, because the Netherlands has strict regulations limiting which antibiotics can be used when, written in hopes of slowing down the emergence of resistance. As a result the Netherlands has one of the lowest rates of antibiotic use in humans in Europe. Nevertheless, when the researchers examined fecal samples that were volunteered by 1,713 Amsterdam residents living at home — that is, not hospital patients — they found that 8.5 percent were ESBL. That is, these community E. coli were resistant to penicillins and cephalosporins — and also in many cases to gentamicin, co-trimoxazole and Cipro.
Knowing that antibiotic use is kept to low levels — and therefore that there ought not to be selective pressure that would drive the emergence of resistance — the group looked for other ways that selective pressure might be being applied. They found two. I’ll quote from a statement they released to media attending ICAAC:
The 8.5 percent resistance… is approximately the same as we found a few years ago in the community in Spain and France, two countries where antibiotic use in general and resistance rates in hospitals are much higher than in Dutch hospitals. The prudent use of antimicrobials in the Netherlands contrasts with a very high use of antibiotics in food-producing animals. In the questionnaires, we have asked about antibiotic use, travel history and eating habits… The question remains whether the rise is due to travel to countries with higher resistance rates or to contamination through the food chain.
E. coli: PHIL, CDC
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