Sequencing and Functional Annotation of Avian Pathogenic Escherichia coli Serogroup O78 Strains Reveal the Evolution of E. coli Lineages Pathogenic for Poultry via Distinct Mechanisms

Abstract

f Avian pathogenic Escherichia coli (APEC) causes respiratory and systemic disease in poultry. Sequencing of a multilocus sequence type 95 (ST95) serogroup O1 strain previously indicated that APEC resembles E. coli causing extraintestinal human diseases. We sequenced the genomes of two strains of another dominant APEC lineage (ST23 serogroup O78 strains 7122 and IMT2125) and compared them to each other and to the reannotated APEC O1 sequence. For comparison, we also sequenced a human enterotoxigenic E. coli (ETEC) strain of the same ST23 serogroup O78 lineage. Phylogenetic analysis indicated that the APEC O78 strains were more closely related to human ST23 ETEC than to APEC O1, indicating that separation of pathotypes on the basis of their extraintestinal or diarrheagenic nature is not supported by their phylogeny. The accessory genome of APEC ST23 strains exhibited limited conservation of APEC O1 genomic islands and a distinct repertoire of virulence-associated loci. In light of this diversity, we surveyed the phenotype of 2,185 signature-tagged transposon mutants of 7122 following intra-air sac inoculation of turkeys. This procedure identified novel APEC ST23 genes that play strain-and tissue-specific roles during infection. For example, genes mediating group 4 capsule synthesis were required for the virulence of 7122 and were conserved in IMT2125 but absent from APEC O1. Our data reveal the genetic diversity of E. coli strains adapted to cause the same avian disease and indicate that the core genome of the ST23 lineage serves as a chassis for the evolution of E. coli strains adapted to cause avian or human disease via acquisition of distinct virulence genes. Avian pathogenic Escherichia coli (APEC) imposes substantial economic and welfare costs on poultry producers worldwide. Respiratory infections typically involve inflammation of the air sacs and lung and may spread to visceral organs, causing perihepatitis, pericarditis, peritonitis, salpingitis, and sepsis (1). A need exists for effective cross-protective vaccines to control APEC in poultry, since autologous bacterins confer limited serotype-specific protection, and control via antibiotics is hindered by resistance and restrictions on prophylaxis. Diverse serotypes are associated with disease, and the molecular mechanisms underlying mucosal colonization and systemic translocation are ill defined. Serogroup O1, O2, and O78 strains are frequently isolated from diseased poultry and mostly belong to multilocus sequence types 95 and 23 (ST95 and ST23) (http://mlst.ucc.ie/mlst/dbs/Ecoli), as evidenced by recent surveys in chickens (2) and turkeys (3). The genetic traits that define the APEC pathotype and the extent of inter-and intra-ST and serogroup diversity are incompletely understood.Sequencing of the complete genome of a ST95 strain of APEC serotype O1:K1:H7 (APEC O1) revealed that it is closely related to extraintestinal pathogenic E. coli (ExPEC) strains associated with human urinary tract infections (4). This is further evident from multilocus sequence ...

In silico phylogenetic and virulence gene profile analyses of avian pathogenic Escherichia coli genome sequences

“…These characteristics were corroborated by multilocus sequence typing (MLST) and genome comparison data (Johnson et al 2007, Moulin-Schouleur et al 2007) and led to a further hypothesis that APEC strains could act as UPEC or NMEC and, therefore, constitute a zoonotic risk. A recent work (Dziva et al 2013) demonstrated that an APEC strain was more closely related to a human ST23 ETEC (enterotoxigenic E. coli) than to strain APEC O1. This suggests that the core genome of ST23 strains has the potential to generate variants able to cause disease on avian or human, depending of the accessory genome.…”

Structure of the bacterial plant-ferredoxin receptor FusA

“…These species include E. coli and members of the genera Shigella , Yersinia and the family Pasteurellaceae617. Studies on FusA homologues in these species are limited, however upregulation in response to iron limitation and the presence of host factors has been demonstrated24. In a recent study, the E. coli homologues of both FusA and the predicted periplasmic protease FusC were shown to be important for the fitness of the UPEC strain CFT073 in systemic infection of mice.…”

YjjQ Represses Transcription of flhDC and Additional Loci in Escherichia coli

“…The gfc-encoded group 4 capsule is synthesized by various E. coli strains, as shown for enteropathogenic E. coli (EPEC) O127:H6, enterohemorrhagic E. coli (EHEC) O157:H7, and APEC O78:H9 (29,54,55). Furthermore, strains with mutation of the gfc locus in APEC O78:H9 strain X7122 are attenuated (54), while the group 4 capsule masks surface structures of EHEC O157:H7 and affects intestine colonization (55). The gfc locus is absent in UPEC strains (29).…”