Atlanta
FARMERS are the prime suspects in the creation of a human 鈥渟uperbug鈥�,
according to genetic evidence linking a farmyard antibiotic to the emergence of
a drug-resistant human pathogen. The discovery will fuel calls for a ban on the
use of antibiotics to promote the growth of farm animals.
Bacteria called enterococci normally live harmlessly in the guts of people
and animals, but can kill people with impaired immune systems. Increasingly,
they are becoming resistant to drugs. And in 1986, a strain that was resistant
to vancomycin, an antibiotic used as a last resort, appeared in France. Similar
superbugs soon emerged elsewhere in Europe, and from 1989 they spread through
hospitals in the US.
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At first, experts blamed the emergence of vancomycin-resistant enterococci
(VRE) on the overuse of antibiotics in hospitals, but studies showing that pigs
and poultry harboured VRE raised suspicions that perhaps they were originally
foodborne pathogens.
Animals grow up to five per cent faster if they are given antibiotics in
their feed. One farmyard antibiotic, avoparcin, is structurally similar to
vancomycin鈥攚hich might explain why some enterococci from farm animals
resist vancomycin.
Evidence linking human VRE to farmyard antibiotics has been hard to find. But
at the emerging diseases meeting, Henrik Wegener of the Danish Veterinary
Laboratory in Copenhagen revealed the best data yet.
Wegener has sequenced the gene responsible for vancomycin resistance in
animal and human enterococci. Aside from the mutation that confers resistance,
genes from some of the bacteria also carry a second mutation, where one letter
of the genetic code, a G, is replaced with a T.
VRE samples from people contained both variants, bacteria from poultry in
several countries were all of the T variant, while bacteria from pigs were all
G. 鈥淭his supports the idea that animals are the source of VRE in humans, whereas
humans are an unlikely source of VRE for animals,鈥� says Wegener. 鈥淚f that was
the case, we would expect to see both in animals.鈥�
However, Tony Mudd of Roche Products, which makes avoparcin, remains
unconvinced: 鈥淭hese are interesting data, but I鈥檓 not sure you can categorically
state from them that it鈥檚 one-way traffic of resistance.鈥�
In 1997, the European Union banned avoparcin, but the general problem
remains. For many years in the US and Europe, farmers have fed animals a product
called virginiamycin. This resembles Synercid, a new drug to treat VRE. Studies
have already revealed Synercid-resistant Enterococcus faecium in farm
animals.
鈥淭he story about avoparcin and vancomycin is rewriting itself,鈥� says Wegener.
鈥淎nd the drug that was expected to be next in line after Synercid, a compound
called Ziracin, is practically identical to a growth promoter called avilamycin,
which has been primarily used for poultry.鈥� Again, animal VREs that are
resistant to avilamycin are also unaffected by Ziracin.
鈥淎ntimicrobial use in food production is a growing threat to human health,鈥�
agrees David Heymann of the WHO鈥檚 Division of Emerging and Other Communicable
Diseases in Geneva.
Wegener believes countries need to get rid of growth promoters entirely. He
says that Sweden did so in 1986 and still produces competitively priced food.
Wegener鈥檚 concerns are echoed by Britain鈥檚 National Consumer Council, which last
week released a report calling for a Europe-wide ban on the use of antibiotics
as growth promoters.