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Volume 18, Number 3—March 2012

Research

Pathogenic Potential to Humans of Bovine Escherichia coli O26, Scotland

Margo E. Chase-ToppingComments to Author , Tracy Rosser, Lesley J. Allison, Emily Courcier, Judith Evans, Iain J. McKendrick, Michael C. Pearce, Ian Handel, Alfredo Caprioli, Helge Karch, Mary F. Hanson, Kevin G.J. Pollock, Mary E. Locking, Mark E.J. Woolhouse, Louise Matthews, J. Chris Low, and David L. Gally
Author affiliations: University of Edinburgh, Edinburgh, UK (M.E. Chase-Topping, E. Courcier, M.C. Pearce, M.E.J. Woolhouse); The Roslin Institute and Royal (Dick) School of Veterinary Studies, Edinburgh (T. Rosser, I. Handel, D.L. Gally); Scottish E. coli O157/VTEC Reference Laboratory, Edinburgh (L.J. Allison, M.F. Hanson); Scottish Agricultural College, Edinburgh (J. Evans, M.C. Pearce, J.C. Low); Biomathematics and Statistics Scotland, Edinburgh (I.J. McKendrick); Istituto Superiore di Sanità, Rome, Italy (A. Caprioli); University of Münster, Münster, Germany (H. Karch); Health Protection Scotland, Glasgow, UK (K.G.J. Pollock, M.E. Locking); University of Glasgow Veterinary School, Glasgow (L. Matthews)

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Table 4

Results of genotypic characterization by MLST and the presence of virulence genes for Escherichia coli O26 isolates, Scotland*

Genotypic characterization No. (%) Isolates from humans, n = 30
No. (%) isolates from cattle, Scotland, n = 33
Scotland Germany/Italy
MLST
ST
21 4 (36.4) 14 (73.7) 22 (66.6)
29 4 (36.4) 5 (26.3) 9 (27.3)
Other 3 (27.2) 0 2 (6.1)
ST complex†
29 10 (90.9) 19 (100.0) 31 (93.9)
10 1 (9.1) 0 2 (6.1)
espA
Allele 1 9 (81.8) 19 (100.0) 31 (100.0)
Other 1 (9.1) 0 0
ND 1 (9.1) 0 0
Upstream of LEE1§
Allele1 2 (18.2) 14 (73.7) 7 (21.2)
Allele2 5 (45.4) 5 (26.3) 20 (60.6)
allele3 0 0 1 (3.0)
allele4 1 (9.1) 0 3 (9.1)
allele5 1 (9.1) 0 0
allele6 1 (9.1) 0 0
ND 1 (9.1) 0 2 (6.1)
Presence of virulence genes
stx
stx 6 (54.5) 4 (21.1) 7 (21.2)
stx1 + 3 (27.3) 5 (26.3) 16 (48.5)
stx2+ 2 (18.2) 10 (52.6) 10 (30.3)
Eae
Absent 1 (9.1) 0 2 (6.1)
Present 10 (90.9) 19 (100.0) 31 (93.9)
sepL#
Absent 1 (9.1) 0 2 (6.1)
Present 10 (90.9) 19 (100.0) 31 (93.9)
hlyA**
Absent 3 (27.3) 7 (36.8) 6 (18.2)
Present 8 (72.7) 12 (63.2) 27 (81.8)
tccP††
Absent 11 (100.0) 19 (100.0) 33 (100.0)
Present 0 0 0
tccP2††
Absent 6 (54.5) 2 (10.5) 16 (48.5)
Present 5 (45.5) 17 (89.5) 17 (51.5)

*MLST, multilocus sequence typing; ST, sequence type; ND, not determined; stx, Shiga toxin; +, stx gene present; –, stx gene absent. LEE1 encodes the first operon of the locus of enterocyte effacement (LEE) and the 644-bp region sequenced includes the promoter for this operon amplified using the defined LEE primer pair in Table 2.
†The ST and ST complex were assigned in accordance with the E. coli MLST database (http://mlst.ucc.ie/mlst/dbs/Ecoli).
espA encodes for the surface-associated protein, espA. The allele numbers at each loci were assigned in the order in which they were discovered.
§Six different sequences were discovered for the region upstream of LEE1 in the E. coli O26 isolates. Approximately 644 bp of sequence data were determined, and all sequence variation between the E. coli O26 alleles occurs within a 91-bp region upstream of LEE1 in the region where regulators act in E. coli O157:H7. The allele numbers at each locus were assigned in the order in which they were discovered.
eae, gene that encodes intimin.
#sepL, gene confirming the presence of LEE pathogenicity island.
**hlyA, enterohemolysin.
††tccP/tccP2, genes encoding Tir-cytoskeleton coupling protein and Tir-cytoskeleton coupling protein 2, which are used in actin polymerization and subsequent attaching and effacing lesion formation.

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