Genome Sequence of Avian Pathogenic Escherichia coli LPO2 Causing Peritonitis in Chicken

Open Access
Kurundu Hewage, Eranda
Graduate Program:
Master of Science
Document Type:
Master Thesis
Date of Defense:
Committee Members:
  • Subhashinie Kariyawasam, Thesis Advisor
  • Avian Pathogenic E. coli
  • Comparative Genomics
  • Chicken Layers
  • Peritonitis
  • Whole genome sequencing
  • Virulence genes
Layer peritonitis is considered a major cause of morbidity and mortality in laying hens which leads to significant economic losses to the egg industry worldwide. Among the bacterial pathogens, E. coli is the most common bacterial species associated with layer peritonitis. However, the pathogenesis of layer peritonitis has not been elucidated yet. The objectives of the current study are; 1) to identify potential virulence factors encoded in peritonitis causing E. coli LPO2 strain using whole genome sequencing and compare it with other genomes of avian pathogenic E. coli (APEC) and human extraintestinal pathogenic E. coli (ExPEC), and 2) to determine homology among the strains. Optical map of E. coli LPO2 revealed that the chromosome of E. coli LPO2 is approximately 4.91 Mb in size. Whole genome sequencing generated two large contigs which cover the whole chromosome except 18 Kbp gap region. A total of 5,318 coding sequences were identified which includes several virulence associated genes such as invasins, adhesins, iron acquisition systems, toxins and virulence regulatory protein providing insights into the genetic basis for the pathogenic potential of E. coli LPO2 strain. Furthermore, on comparison of the genomic contigs of E. coli LPO2 strain with other complete genomes of APEC and human ExPEC showed a close similarity of E. coli LPO2 to APEC O1 strain as compared to APEC O78 strain. In addition, 128 genes were found to be common to all APEC strains which included several virulence and/ or fitness associated genes. Similarly, comparison of these common genes in APEC with human ExPEC revealed high level of homlogy (more than 90%) between APEC and human ExPEC suggesting that the APEC may be a potential source for human ExPEC. We identified E. coli LPO2 specific genes that were not shared with APEC strains associated with colibacillosis suggesting that some of those genes may be involved in causing peritonitis in layers.