faecium draft genomes and a new pilus encoding gene cluster in strain E1071; the LBH589 clinical trial latter consists of three genes one of which is a relatively distant homolog

of bee1 (35% aa identity) and two are identical or highly homologous to bee2 or bee3 (100% and 98%, respectively) of a plasmid-encoded bee pilus gene cluster found in a small percentage of E. faecalis isolates [58]. To identify possible virulence genes in the E. faecium genomes, the enterococcal virulence factors listed in the Virulence Factors Database (VFDB) [59] were aligned to the ORF protein sequences using BLASTP and filtered with 50% identity and 50% match length. The homologs of efaA, EF0954 (a homolog of BopD which is a transcriptional regulator involved in biofilm production of E. faecalis[42, 60] ), cpsA and cpsB genes are present in all E. faecium strains (see surface polysaccharides above for cpsA and cpsB), and esp Efm and hyl Efm are exclusively present in some HA clade strains while the homolog of EF0818 (a putative hyaluronidase and annotated as a Family 8 polysaccharide lyase, also similar to the LPXTG protein EF3023) is exclusively present in the CA-clade strains (except strain 1,141,733). Homologs of other E. faecalis virulence

factors listed in the VFDB were not found in TX16 genome. We also searched the 22 E. Vistusertib concentration faecium isolates for the presence and absence of 13 resistance genes. Our data correspond to previously published data for some of the isolates [32, 61]. We

observed that there is a clear distinction between the isolates of the genetically defined CA clade and those of the HA clade with none of the CA clade isolates having any of the antibiotic resistance determinants analyzed (Table 3). On the other hand, all of the HA-clade isolates have multiple resistance determinants, including the pbp5-R allele that Protirelin confers ampicillin resistance previously reported by Galloway-Pena et al. [57], except for strains 1,231,501 and E1039. 1,231,501, which is in the HA-clade but lacks all antibiotic resistances including pbp5-R, may have lost the allele via recombination and acquired Saracatinib chemical structure pbp5-S or may even represent a more ancestral isolate. Indeed, 1,231,501 was shown to be a hybrid of HA and CA genomes by Palmer, et al., with the replacement (hybrid) region including pbp5-S, which could explain the origin of pbp5-S in this strain [34]. E1039, which has the pbp5-R allele but none of the other resistance genes, is genetically defined as a HA-clade isolate, but came from a healthy volunteer, perhaps explaining its lack of other antibiotic resistances. Interestingly, neither of these strains has IS16. D344SRF is the only other HA-clade isolate that lacks the pbp5-R allele; however, this strain is known to have spontaneously lost pbp5 and the surrounding region and contains many other resistances [62].