ANTIBIOTIC RESISTANCE:
Livestock Feed Ban Preserves Drugs' Power
Dan Ferber 

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Comments:
This article is in the January 4, 2002, issue of Science. Development
of antibiotic resistance is often cited as evidence for Darwinian evolution.
Yet we know that resistance to antibiotics is not through formation of a
new species. This article provides confirmation for a point that Lee Spetner
among others has made, that those members of a population that are
resistant to an antibiotic may in fact be less fit when the antibiotic is not
present than the members of the population that do not have the resistance to
the antibiotic. As he puts it in Not by Chance!, the bacteria really may
have lost sensitivity to the antibiotic, rather than gained resistance to it.
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ANTIBIOTIC RESISTANCE:

Livestock Feed Ban Preserves Drugs' Power
Dan Ferber 
CHICAGO--It's no secret that livestock fed antibiotics breed
drug-resistant bacteria that can cause dangerous infections in people. But a new study
suggests that the process is reversible. Banning a drug called avoparcin
from animal feed dramatically reduced the chances that potentially
dangerous gut microbes in hospital patients would be resistant to an important,
related drug, Belgian researchers reported last month at a meeting*
sponsored by the American Society for Microbiology. 
The results are the first to show that cutting antibiotic use on the
farm leads to reduced resistance in hospital patients--those who need
antibiotics the most, says microbiologist Stuart Levy of Tufts University School of
Medicine in Boston. "This says there's a strong connection between
what's done in animals and what you see in people," he says.
Farmers mix low doses of antibiotics into animal feed to keep infections
from spreading through a flock or herd. The antibiotics also help fatten
animals on less feed, although researchers aren't sure why. But
antibiotics almost inevitably spur some bacteria to develop resistance to the drugs,
and researchers have long warned that the bugs, or the resistance genes they
harbor, can make their way through the food chain to the human gut.
That, in turn, could make it harder to treat dangerous infections with
antibiotics akin to the drugs used on the farm (Science, 5 May 2000, p. 792). 
This concern prompted the European Union to ban avoparcin from livestock
feed in 1997 after more than 2 decades of use. Avoparcin and a human
antibiotic called vancomycin kill bacteria by preventing them from
building cell walls. Earlier studies showed that avoparcin-resistant gut microbes
in chickens and hogs also resist vancomycin. That could be bad news for
hospital patients, who receive vancomycin to fight enterococci that
cause life-threatening infections when they escape from the gut during
surgery.
Researchers suspected that the avoparcin ban would help prevent the
spread of vancomycin-resistant enterococci (VRE) in humans.
In monitoring the ban's effects, researchers have found a dramatic drop
in VRE among pigs, chickens, and supermarket chicken meat. Fewer VRE were
also found in the human population. But it wasn't clear whether this trend
extended to patients in hospitals, where most opportunistic enterococci
infections occur. 
To find out, microbiologist Greet Ieven of the University of Antwerp and
her colleagues cultured enterococci from stool samples of 353 patients in
May and June 2001 and tested how many microbes survived high levels of
vancomycin. Just three of the enterococci cultures, or 0.6%, stood up to
vancomycin--a big drop from the 5.7% resistance rate in 1996, when
avoparcin was still widely fed to livestock. Molecular genetic analysis confirmed
that the prevalence of a key vancomycin resistance gene plummeted from 5.7%
to 0.8%. Because the use of vancomycin in Belgian hospitals hasn't changed
in recent years, Ieven says, the results "confirm the hypothesis that VRE
in Europe originates [on farms]."

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