Two distinct groups of porcine enteropathogenic Escherichia coli strains of serogroup O45 are revealed by comparative genomic hybridization and virulence gene microarray.
BACKGROUND
Porcine enteropathogenic Escherichia coli (PEPEC) strains of serogroup O45 cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors required for production of A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC pathogenicity. In this study, nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions in vivo, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments.


RESULTS
Based on their virulence gene profiles, the 10 strains were considered to be atypical EPEC. The differences in their genomes pointed to the identification of two distinct evolutionary groups of O45 PEPEC, Groups I and II, and provided evidence for a contribution of these genetic differences to their virulence in pigs. Group I included the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of the five other O45 PEPEC strains, which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found with respect to the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253).


CONCLUSIONS
We have genetically characterized a collection of O45 PEPEC strains and classified them into two distinct groups. The differences in their virulence gene and genomic island content may influence the pathogenicity of O45 PEPEC strains, and explain why Group I O45 PEPEC strains induced more severe A/E lesions in explants and challenged pigs than Group II strains.
Bruant
Guillaume
G
Groupe de Recherche sur les Maladies Infectieuses du Porc, Faculté de médecine vétérinaire, Université de Montréal, 3200 rue Sicotte, Saint-Hyacinthe, Québec J2S 7C6, Canada. guillaume.bruant@nrc-cnrc.gc.ca
Zhang
Yongxiang
Y
Garneau
Philippe
P
Wong
Justin
J
Laing
Chad
C
Fairbrother
John M
JM
Gannon
Victor P J
VP
Harel
Josée
J
D000818:Animals; D055028:Comparative Genomic Hybridization / Q000379:methods*; D004269:DNA, Bacterial / Q000235:genetics; D054308:Enteropathogenic Escherichia coli / Q000145:classification / Q000235:genetics* / Q000472:pathogenicity; D004927:Escherichia coli Infections / Q000382:microbiology; D005798:Genes, Bacterial; D016680:Genome, Bacterial; D044404:Genomic Islands; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods*; D013552:Swine / Q000382:microbiology; D013553:Swine Diseases / Q000382:microbiology; D037521:Virulence Factors / Q000235:genetics*
D004269:DNA, Bacterial; D037521:Virulence Factors