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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #158804

Title: GENETIC RELATEDNESS OF ESCHERICHIA COLI O147 STRAINS CAUSING EDEMA DISEASE

Author
item HELGERSON, A - IOWA STATE UNIVERSITY
item SCHROEDER, R - IOWA STATE UNIVERSITY
item Sharma, Vijay
item POST, K - ROLLINS ANIM DIS DIAGN
item CORNICK, N - IOWA STATE UNIVERSITY

Submitted to: American Society for Microbiology
Publication Type: Abstract Only
Publication Acceptance Date: 2/27/2004
Publication Date: 5/23/2004
Citation: Helgerson, A.F., Schroeder, R., Sharma, V.K., Post, K., Cornick, N.A. 2004. Genetic relatedness of Escherichia coli O147 strains causing edema disease [abstract]. American Society for Microbiology. p. 671.

Interpretive Summary:

Technical Abstract: Edema disease is a systemic disease of weaned pigs caused by host adapted strains of E. coli that encode virulence genes for F18 fimbriae, shiga toxin 2e and heat stable entertoxin(s). Outbreaks of edema disease are most often caused by E. coli belonging to serogroups O138, O139 or O141. Conversely, enterotoxigenic E. coli (ETEC) O147 are primarily associated with post-weaning diarrhea. Recently, E. coli O147 strains have been recovered from outbreaks of edema disease across the U.S. We hypothesized that these isolates are clonal and have evolved from O147 ETEC by the acquisition of the stx2e gene. To test this hypothesis 53 strains of E. coli O147, recovered since 1996, were compared to 21 strains recovered between 1974-1995 using PFGE and multi-locus restriction typing (MLRT). Chromosomal DNA was digested with XbaI and resolved by PFGE. GelCompar II software was used for analyzing DNA banding patterns generated for each isolate and dendograms were constructed using the unweighted pair group cluster method with arithmetic averages (UPGMA) and applying the DICE coefficient. The majority of recent isolates (38/53) showed >80% similarity by PFGE and 37/38 contained the virulence genes f18, sta, stb and stx2e. The remaining recent isolates (15) grouped into 6 different clades (<70% similarity between clades). Isolates recovered prior to 1996 had <55% similarity to the new strains. Virulence genes typical of ETEC were present in 13/21 of these strains. Because housekeeping genes tend to be conserved in E. coli, MLRT analysis was used to determine whether the recently recovered edema disease isolates were distantly related to the older ETEC O147 strains. Seven highly conserved housekeeping genes (aspC, clpX, fadD, icdA, lysP, mdh, uidA) were selected for MLRT analysis, amplified by PCR and digested with either HhaI or HpaII and banding patterns were compared. Preliminary MLRT data for the clpX gene indicates that banding patterns of recent O147 isolates were similar to some of the older ETEC strains. Our data suggests that the majority of recent E. coli O147 isolates are closely related to one another and may have evolved from ETEC O147 strains.