However, the peptide group #1 from the main branch which is encoded by the largest number of alleles (N = 23), could be subdivided into two sets of sub-clusters: one set harboring strains isolated from domestic mammals (N = 9) and the other set being highly specific to environmental samples (N = 14). www.selleckchem.com/products/Trichostatin-A.html From this last set, five sequences (#19, 40, 74, 76 and 79) display a slightly higher GC

content (Figure 2B) as a potential “trace signature” of different ecological niches. In addition, within this same peptide group #1, the nucleotide alleles with the synonymous substitution G408A (#11, 39, 40, 41, 56, 66 and 79) were never recovered from poultry strains. This change is also present in alleles from peptide group #14 previously discussed and linked to small mammals [42]. The most obvious host signature established in our study is the non-synonymous substitution A64G corresponding to the change Ser22Gly in the amino acid sequence. This point mutation was previously observed by Ge et al. [43] in a study on antimicrobial resistance of strains isolated from poultry meat in which 76.2% ciprofloxacin-resistant C. jejuni harbored this particular substitution in their gyrA sequence (N = 42). Jesse et al. [44] also noticed this mutation in isolates from chicken and turkeys and suggested that it does not contribute to quinolone resistance but may be indicative of gyrA alleles predominantly found

in poultry. Our results confirm this finding: 11 isolates with the Ser22Gly but without the Thr86Ile substitution were classified as susceptible Selonsertib clinical trial to quinolones Interleukin-2 receptor according to the cut off values recommended by the European commission [45] (see Additional file 3). Also, peptide groups #3, 4, 5 and 8 with this particular change on codon 22, are significantly associated with poultry source (P = 0.001). This host signature could be used as a specific molecular marker of domestic birds. Our study also found that quinolone resistance was higher in isolates originating from poultry than from other sources. Recently, Han et al. [46] demonstrated that this particular mutation generates a fitness advantage for Campylobacter in chicken through

a reduced supercoiling activity of the GyrA enzyme. As DNA supercoiling is directly involved in gene expression, their findings suggested that the altered function of the enzyme modulates the fitness of resistant strains whose prevalence persists in poultry production even in the absence of fluoroquinolone use. The European report on antimicrobial resistance in zoonotic bacteria [12] reported very high fluoroquinolone resistance levels in Campylobacter isolated from broilers (76%) and broiler meat (58%). Our results concur with the report in that resistance levels vary substantially in different hosts. Conclusion The interest of the sequence-based method described herein targeting the gyrase subunit A lies not only in providing information on quinolone resistance but also on strain origin.