Five of the six strains that hybridised with the BfpA probe were non-adherent after three hours, whereas five of the six BfpB-positive strains showed aggregative adherence

and one showed localised-like adherence. Adherence to HEp-2 cells was not associated with a positive PCR for either Lpf or Efa. Association of specific virulence determinants with clinical presentation The 67 aEPEC strains we investigated by PCR, DNA hybridisation and for adherence to HEp-2 cells originated from individuals with different clinical presentations (Table 2). Fifty-seven isolates were obtained from patients with diarrhoea, and ten were from asymptomatic individuals. Eleven isolates were from children with persistent diarrhoea (i.e., diarrhoea lasting #www.selleckchem.com/products/Thiazovivin.html randurls[1|1|,|CHEM1|]# more than 14 days), and 12 were from children with diarrhoea less than 14 days in duration. www.selleckchem.com/products/mek162.html Thirty-four strains were from patients in whom the duration of diarrhoea was not known. To determine if any of the putative accessory virulence determinants

of aEPEC that were sought in this study were associated with a particular clinical presentation, we compared the frequency of these determinants in isolates from patients with and without diarrhoea, and those known to have acute or persistent diarrhoea. The results showed that the frequency of the factors investigated did not differ significantly between the groups under comparison (P > 0.1, Fisher’s exact test, two-tailed). Table 2 Frequency of putative BCKDHB virulence-associated determinants of atypical EPEC strains in study subjects with different clinical presentations.   No. of strains positive for:a Clinical presentation BfpA BfpB Cdt Efa1 LpfO113 NleB1 All diarrhoea (n = 57) 5 6 7 7 13 18 No diarrhoea (n = 10) 1 0 0 1 0 2 Acute diarrhoea (n = 12) 1 4 4 2 3 3 Persistent

diarrhoea (n = 11) 2 0 1 0 1 4 a Only determinants that were present in more than three isolates overall were included in this analysis. Discussion The classification of diarrhoeagenic strains of E. coli into pathotypes has led to considerable improvement in our understanding of the epidemiology, pathogenesis and clinical presentation of infections with these bacteria, and has spawned novel strategies to diagnose and prevent these infections [29, 30]. Each pathotype of diarrhoeagenic E. coli carries a distinctive suite of virulence determinants, almost all of which show evidence of having been acquired on mobile genetic elements, such as plasmids, transposons, bacteriophages and pathogeniCity islands. Interestingly, apart from their shared virulence determinants, strains of each pathotype often differ from each other in terms of serotype, biotype, phage type, and even with regard to the nature of the specific virulence determinants they carry, e.g.