The world’s poultry industry has grown into a multibillion-dollar business, the success of which hinges on healthy intestinal tracts, which result in effective feed conversion. Enteric disease in poultry can have devastating economic effects on producers, due to high mortality rates and poor feed efficiency. Clostridia are considered to be among the most important agents of enteric disease in poultry. Diagnosis of enteric diseases produced by clostridia is usually challenging, mainly because many clostridial species can be normal inhabitants of the gut, making it difficult to determine their role in virulence. The most common clostridial enteric disease in poultry is necrotic enteritis, caused by Clostridium perfringens, which typically occurs in broiler chickens but has also been diagnosed in various avian species including turkeys, waterfowl, and ostriches. Diagnosis is based on clinical and pathological findings. Negative culture and toxin detection results may be used to rule out this disease, but isolation of C. perfringens and/or detection of its alpha toxin are of little value to confirm the disease because both are often found in the intestine of healthy birds. Ulcerative enteritis, caused by Clostridium colinum, is the other major clostridial enteric disease of poultry. Diagnosis of ulcerative enteritis is by documentation of typical pathological findings, coupled with isolation of C. colinum from the intestine of affected birds. Other clostridial enteric diseases include infections produced by Clostridium difficile, Clostridium fallax, and Clostridium baratii.

Background: Although serotype O157:H7 is the predominant enterohemorrhagic Escherichia coli (EHEC), outbreaks of non-O157 EHEC that cause severe foodborne illness, including hemolytic uremic syndrome have increased worldwide. In fact, non-O157 serotypes are now estimated to cause over half of all the Shiga toxin-producing Escherichia coli (STEC) cases, and outbreaks of non-O157 EHEC infections are frequently associated with serotypes O26, O45, O103, O111, O121, and O145. Currently, there are no complete genomes for O145 in public databases. Results: We determined the complete genome sequences of two O145 strains (EcO145), one linked to a US lettuce-associated outbreak (RM13514) and one to a Belgium ice-cream-associated outbreak (RM13516). Both strains contain one chromosome and two large plasmids, with genome sizes of 5,737,294 bp for RM13514 and 5,559,008 bp for RM13516. Comparative analysis of the two EcO145 genomes revealed a large core (5,173 genes) and a considerable amount of strain-specific genes. Additionally, the two EcO145 genomes display distinct chromosomal architecture, virulence gene profile, phylogenetic origin of Stx2a prophage, and methylation profile (methylome). Comparative analysis of EcO145 genomes to other completely sequenced STEC and other E. coli and Shigella genomes revealed that, unlike any other known non-O157 EHEC strain, EcO145 ascended from a common lineage with EcO157/EcO55. This evolutionary relationship was further supported by the pangenome analysis of the 10 EHEC str ains. Of the 4,192 EHEC core genes, EcO145 shares more genes with EcO157 than with the any other non-O157 EHEC strains. Conclusions: Our data provide evidence that EcO145 and EcO157 evolved from a common lineage, but ultimately each serotype evolves via a lineage-independent nature to EHEC by acquisition of the core set of EHEC virulence factors, including the genes encoding Shiga toxin and the large virulence plasmid. The large variation between the two EcO145 genomes suggests a distinctive evolutionary path between the two outbreak strains. The distinct methylome between the two EcO145 strains is likely due to the presence of a Bsu BI/Pst I methyltransferase gene cassette in the Stx2a prophage of the strain RM13514, suggesting a role of horizontal gene transfer-mediated epigenetic alteration in the evolution of individual EHEC strains.