Abstract
Escherichia coli are commensal bacteria in the gastrointestinal tract of mammals, but some strains have acquired Shiga-toxins and can cause enterohemorrhagic diarrhoea and kidney failure in humans. Shiga-toxigenic E. coli (STEC) strains such as E. coli O157:H7 and some non-O157 strains also contain other virulence traits, some of which contribute to their ability to form biofilms. This study characterized non-O157 E. coli from South African cattle faecal samples for their virulence potential, antimicrobial resistance (AMR), biofilm-forming ability, and genetic relatedness using culture-based methods, pulsed-field gel electrophoresis (PFGE), and whole genome sequencing (WGS). Of 80 isolates screened, 77.5% (62/80) possessed Shiga-toxins genes. Of 18 antimicrobials tested, phenotypic resistance was detected against seven antimicrobials. Resistance ranged from 1.3% (1/80) for ampicillin-sulbactam to 20% (16/80) for tetracycline. Antimicrobial resistance genes were infrequently detected except for tetA, which was found in 31.3% (25/80) and tetB detected in 11.3% (9/80) of isolates. Eight biofilm-forming associated genes were detected in STEC isolates (n = 62) and two non-STEC strains. Prevalence of biofilm genes ranged from 31.3% (20/64) for ehaAβ passenger to 100% for curli structural subunit (csgA) and curli regulators (csgA and crl). Of the 64 STEC and multi-drug resistant isolates, 70.3% (45/64) and 37.5% (24/64) formed strong biofilms on polystyrene at 22 and 37 °C, respectively. Of 59 isolates screened by PFGE, 37 showed unique patterns and the remaining isolates were grouped into five clusters with a ≥90% relatedness. In silico serotyping following WGS on a subset of 24 non-O157 STEC isolates predicted 20 serotypes comprising three novel serotypes, indicating their diversity as potential pathogens. These findings show that North West South African cattle harbour genetically diverse, virulent, antimicrobial-resistant and biofilm-forming non-O157 E. coli. Biofilm-forming ability may increase the likelihood of persistence of these pathogens in the environment and facilitate their dissemination, increasing the risk of cross contamination or establishment of infections in hosts.
Highlights
Shiga-toxigenic E. coli (STEC) strains such as E. coli O157 and non-O157 (e.g., O26, O45, O91, O103, O104, O111, O113, O121, O118, O128, O145, O148 and O174) have acquired genetic traits that make them pathogenic to humans
It was noted that PCR detection of Shiga toxins and virulence genes was not consistent after the second sub-culturing of the same bacterial glycerol stock (Figure S1 in the Supplemental Material)
Frequent detection of stx2 in South African non-O157 E. coli isolates with subtype stx2 could be cause for concern as stx2 has been reported to be more toxic in humans than stx1 [66]
Summary
Shiga-toxigenic E. coli (STEC) strains such as E. coli O157 and non-O157 (e.g., O26, O45, O91, O103, O104, O111, O113, O121, O118, O128, O145, O148 and O174) have acquired genetic traits that make them pathogenic to humans. These strains have caused both sporadic illness and outbreaks of food and water-borne infections worldwide [1,2,3]. The use of antibiotics for E. coli infections, especially STEC, remains a cause for concern as some strains exhibit resistance to a variety of antimicrobials, and antimicrobial therapy can heighten toxin production in STEC, increasing the risk of HUS [4,8]. Despite the fact that Shiga-toxins are the main virulence factors of STEC [10], additional accessory virulence factors such as adhesins, pili, intimin and hemolysin contribute to pathogenicity
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