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Scandinavia: Proof of vertical ESBL transmission through the broiler production pyramid Two independent papers contribute to the epidemiology of resistance to third and fourth generation cephalosporins in the European poultry industry. A team of Norwegian veterinary microbiologists investigated the steady and strong increase of the frequency of extended-spectrum beta-lactamase (ESBL)-resistant Enterobacteriaceae in their country’s broiler industry since 2006. Yet Norway has one of the lowest figures of antibiotic use in Europe and cephalosporins are banned from animal production. All isolates carry the same gene (blaCMY-2). As the authors suspected that these genes arrived with the animals at the top of the selection pyramid, and in 2011 they monitored the excretion of ESBL-carrying Enterobacteriaceae by “the only grandparent flock, imported from Scotland” during the entire study. From November 2011, this surveillance also included “64 out of 66 grandparent and parent flocks associated with the largest poultry cooperation in Norway (Nortura SA)”. To this they added samples from the national surveillance system (252 broiler flocks and 205 retail chicken meat samples), and all parent flocks (n=120) present in Norway in 2012. The grandparent flocks were monitored by eight samples during this period. The samples were cultured for E. coli and then tested for resistance to cefoxitin (and synergy to cloxacillin). All strains with the ESBL phenotype carried the ß-lactamase gene blaCMY-2 (plasmid), with the exception of 15 isolates (none from grandparent animals) which overexpressed the chromosomal gene AmpC. The farms were spread throughout Norway and without any obvious link with the local poultry density. Two of the 8 ESBL-carrying E. coli obtained from the grandparent animals were carriers of the blaCMY-2 gene, but all were also resistant to ciprofloxacin and nalidixic acid. A little over quarter (28%) of the 64 ESBLcarrying E. coli isolates carried the blaCMY-2 gene in 2011, but this percentage dropped to 8% of 120 in 2012 (p<0.05 compared to the previous year). The authors suggest that the gene was introduced “by import of breeding animals (hatching eggs) and, in some cases, grandparent animals”. Evidence came from Sweden (second study), where the selection pressure from antimicrobial use is low and the ESBL frequency high (around 50% in broilers), with a near-exclusive frequency of the blaCMY-2 gene. Here, too, the authors investigated the grandparent animals, imported into Sweden. They sampled the cages of the imported animals between July 2010 and August 2011 from 8 flocks: six were found positive (presence of ESBL-carrying E. coli). They also monitored a flock and its descendants until the production stage. The grandparent animals “imported from the UK” were sampled upon arrival in August 2011, then at 17, 21 and 28 weeks of age (February 2012). The parent animals issued from these grandparents were sampled at hatching, and then at 17, 21 and 28 weeks of age (October 2012). At each step (grandparent and parent flocks), presence of ESBL+ E. coli was detected. Broilers from this stock (5 farms) were sampled ad hatching and 5 days before slaughter (January 2013). Two samples taken at the hatchery and one taken from broilers were also found positive. All the isolates carried the blaCMY-2 gene. The isolates from grandparent animals were negative for all other ESBL-coding genes. Multi locus variable-number tandem-repeat analysis (MLVA) yielded five clonal clusters, one of which was present at all levels of the pyramid. This clonal cluster was present in the grandparent animals of the initial study, as well as in the flock previous to the one that arrived in 2011, but not in the same one at arrival. This “supports the hypothesis that the high proportion of Swedish broilers colonised with E. coli carrying blaCMY-2 can be explained, at least partly, by introduction through imported breeding stock and vertical transmission through the production pyramid”. Sources: J. Antimicrob. Chemother., 2014, AOP, 4 p. - doi:10.1093/jac/dku030) Vet. Microbiol., 2014, AOP, 18 p. - http://dx.doi.org/doi:10.1016/j.vetmic.2014.02.002