Volume 18, Number 3—March 2012
Research
Pathogenic Potential to Humans of Bovine Escherichia coli O26, Scotland
Table 4
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.