The effect of banning avoparcin on VRE carriage in The Netherlands

Abstract

Sir, Acquired resistance against antibiotics is closely related to the amount of drug used, a fact observed ever since these agents were introduced into human and veterinary medicine. However, the rate of development of resistance appears to have accelerated in the past decade. In animals, antibiotics are not only used for therapy and prevention of bacterial infections, but are also added to animal feed to act as growth promoters. In some countries, antibiotic use for growth promotion is greater than veterinary usage.1 In countries using avoparcin, a glycopeptide antibiotic, as a growth promoter, vancomycin-resistant enterococci (VRE) are commonly found in the commensal flora of food animals, on meat from these animals and in the commensal flora of healthy humans despite very limited use of vancomycin in hospitals.1 In The Netherlands in 1996 and 1998, approximately 1500 and 1260 kg of vancomycin, respectively, was used for human therapy, whilst an estimated 80000 kg of avoparcin was used yearly in farming until 1997. By contrast, in those countries not allowing the use of avoparcin, no VRE have been detected in food animals, food of animal origin or healthy humans in the general population.1 Sweden banned the use of all antibiotics as growth promoters in 1986 and no VRE have been found in the faecal flora of animals, foods of animal origin or in healthy humans from the general population1 or in hospitalized patients. The only VRE isolated from a hospital patient contained the VanB gene cluster and was acquired abroad.2 The Swedish example strongly suggests that removal of the selective pressure in animals can remove VRE from the human population in time. Moreover, not only has clonal spread of VRE occurred from animals to humans, but it has also been shown that the VanA gene cluster can be disseminated from animal to human enterococcal strains.3