Prevalence, Persistence, and Molecular Characterization of Glycopeptide-Resistant Enterococci in Norwegian Poultry and Poultry Farmers 3 to 8 Years after the Ban on Avoparcin

Abstract

Environmental reservoirs of glycopeptide-resistant enterococci (GRE) in Norway have been linked to former growth promoting use of the glycopeptide avoparcin in poultry production. We have examined the prevalence of fecal GRE in poultry and poultry farmers 3 to 8 years after the Norwegian avoparcin ban in 1995 and performed molecular analyses of the GRE population. Fecal samples from poultry farmers and their flocks on 29 previously avoparcin-exposed farms were collected on five occasions during the study period (1998 to 2003). All flocks (100%) were GRE positive in 1998. Throughout the study period, 78.5% of the poultry samples were GRE positive. Glycopeptide-resistant Enterococcus faecium (GREF) was isolated from 27.6% of the farmer samples in 1998 and from 27.8% of the samples collected between 1998 and 2003. The prevalence of fecal GRE in poultry declined significantly during the study period, but prevalence in samples from the farmers did not decline. PCR analysis revealed a specific Tn1546-plasmid junction fragment in 93.9% of E. faecium isolates. A putative postsegregation killing (PSK) system linked to Tn1546 was detected in 97.1% of the isolates examined. Multilocus sequence typing of glycopeptide-susceptible (n ‫؍‬ 10) and -resistant (n ‫؍‬ 10) E. faecium isolates from humans (n ‫؍‬ 10) and poultry (n ‫؍‬ 10) on two farms displayed 17 different sequence types. The study confirms the continuing persistence of a widespread common plasmid-mediated vanA-pRE25-PSK element within a heterogeneous GRE population on Norwegian poultry farms 8 years after the avoparcin ban. Moreover, it suggests an important role of PSK systems in the maintenance of antimicrobial resistance determinants in reservoirs without apparent antimicrobial selection.

The effects of subtherapeutic antibiotic use in farm animals on the proliferation and persistence of antibiotic resistance among soil bacteria

“…Antibiotic resistance in soil S Ghosh and TM LaPara biotics contains numerous resistant bacteria (Levy, 1978;Aarestrup et al, 2002;Sørum et al, 2006), but that resistance among soil bacteria returned to preapplication levels within 6 months of manure application (Sengelov et al, 2003). We hypothesize, however, that if an excessive quantity of these bacteria is applied to soil, then antibiotic resistance can spread among the indigenous soil bacteria because of lateral gene transfer of the resistance determinants (Andrews et al, 2004).…”

“…This problem has become more pertinent over the last few decades because of a gradual transition from small farms to concentrated animal feeding operations (CAFOs). Thus, there is an increased risk of adding persistent antibiotic residues and resistant fecal bacteria to soil, potentially leading to the proliferation of resistance among indigenous bacteria (CheeSanford et al, 2001;De Liguoro et al, 2003;Sørum et al, 2006).…”

Erratum: Can landscape ecology untangle the complexity of antibiotic resistance?

“…Changes in resistance patterns over time are also often detected, but these changes are not always reflective of obvious changes in antibiotic usage 5,7,22 . A major challenge in this sort of study is to correctly characterize exposure to antibiotics and any other factor that might select for changes in antibiotic resistance.…”

“…For example, as some countries have reduced the amount of antibiotic used in animal agriculture, specific resistance has persisted in the apparent absence of primary selection pressure 5,7,22 . A more thorough genetic analysis of these isolates reveals that linkages to other antibiotics 5,47 can partially explain this persistence.…”

“…The presence of resistance was thought to exert a fitness cost on the organism: when the antibiotic was removed, the organism was expected to lose its resistance or else be competitively replaced by a susceptible organism with higher fitness. This assumption has been questioned [19][20][21] , and recent evidence demonstrates that, in the absence of selection pressure due to antibiotic use, resistance levels in bacterial populations are often slow to decline, if at all 5,7,22 . In fact, some organisms with antibiotic-resistant phenotypes and genotypes seem to be fitter than their susceptible counterparts [23][24][25][26] , and compensatory mutations have been observed that allow the resistant organism to retain its fitness level 27 .…”