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Correspondence

Vancomycin-Resistant Enterococci in Turkeys and Farmers

N Engl J Med 1997; 337:1558-1559November 20, 1997

Article

To the Editor:

In enterococci vancomycin resistance of the VanA phenotype is usually due to the presence of seven genes organized in a cluster on a transposon (Tn1546).1,2 The recent emergence of vancomycin-resistant enterococci is believed to be due to the vertical clonal spread of resistant strains and the horizontal spread of the transposon itself among different strains of enterococci in a selective environment. Use of avoparcin — a glycopeptide, like vancomycin — as an antimicrobial growth promoter in animal feeds creates such a selective environment and causes the selection of vancomycin-resistant enterococci in the intestinal flora.

To determine whether vancomycin-resistant enterococci from animals can cause colonization in humans, we collected fecal samples from turkeys at 47 farms and from 47 turkey farmers. In addition, fecal samples from 48 turkey slaughterers and 188 healthy persons living in the same area were screened.3 Vancomycin-resistant enterococci were isolated from 50 percent of the samples from the turkeys, 39 percent of the samples from the turkey farmers, 20 percent of the samples from the turkey slaughterers, and 14 percent of the samples from area residents. The prevalence of vancomycin-resistant enterococci in 12 turkey flocks not receiving avoparcin was 8 percent, as compared with 60 percent in flocks fed avoparcin (P<0.001).

Almost all the vancomycin-resistant enterococci were Enterococcus faecium, and they were highly resistant to vancomycin (minimal inhibitory concentration, >64 mg per liter). The resistance to teicoplanin varied (minimal inhibitory concentration, 0.5 to 8 mg per liter).

Phenotypically identical strains were further analyzed by pulsed-field gel electrophoresis after digestion with SmaI. Most isolates showed variations in patterns. Only in samples from one farmer and his turkey flock were indistinguishable strains of vancomycin-resistant enterococci isolated with an identical pattern of the 17 bands. Moreover, genetic characterization of the vanA gene cluster by the polymerase chain reaction and hybridization showed that the two strains were identical in the tested areas containing a unique genetic element; this element proved to be different from the published vanA gene clusters in BM41471,2,4 in that there was an insertion in the intergenic area between the vanX and the vanY gene and a deletion in the right end of the gene cluster that removed the vanZ gene and created a larger positive band when a vanX probe was used, as shown in Table 1Table 1Phenotypic and Genetic Characteristics of Vancomycin-Resistant Enterococci in Fecal Isolates from Humans and Turkeys in the Netherlands and in Reference Strain BM4147..

Given the wide use and the selective pressure created by antibiotics and the differences in the prevalence of vancomycin-resistant enterococci in the populations studied, the most plausible explanation for these findings is the spread of vancomycin-resistant enterococci strain from the turkeys to the farmer. The absence of the vanZ gene may contribute to the observed low resistance to teicoplanin as compared with vancomycin.2 These findings confirm the high prevalence of vancomycin-resistant enterococci in healthy persons living in areas where avoparcin is used as an antimicrobial growth promoter. Our study also shows that humans and animals can carry the same clone of vancomycin-resistant enterococci.

Anthony E. van den Bogaard, D.V.M.
University of Maastricht, NL-6200 MD Maastricht, the Netherlands

Lars Bogø Jensen, Ph.D.
Danish Veterinary Laboratory, DK-1790 Copenhagen V, Denmark

Ellen E. Stobberingh, Ph.D.
University of Maastricht, NL-6200 MD Maastricht, the Netherlands

4 References
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