Virulence Characteristics and Antimicrobial Resistance Profiles of Shiga Toxin-Producing Escherichia coli Isolates from Humans in South Africa: 2006–2013

Abstract

Shiga toxin-producing Escherichia coli (STEC) isolates (N = 38) that were incriminated in human disease from 2006 to 2013 in South Africa were characterized by serotype, virulence-associated genes, antimicrobial resistance and pulsed-field gel electrophoresis (PFGE). The isolates belonged to 11 O:H serotypes. STEC O26:H11 (24%) was the most frequent serotype associated with human disease, followed by O111:H8 (16%), O157:H7 (13%) and O117:H7 (13%). The majority of isolates were positive for key virulence-associated genes including stx1 (84%), eaeA (61%), ehxA (68.4%) and espP (55%), but lacked stx2 (29%), katP (42%), etpD (16%), saa (16%) and subA (3%). stx2 positive isolates carried stx2c (26%) and/or stx2d (26%) subtypes. All pathogenicity island encoded virulence marker genes were detected in all (100%) isolates except nleA (47%), nleC (84%) and nleD (76%). Multidrug resistance was observed in 89% of isolates. PFGE revealed 34 profiles with eight distinct clusters that shared ≥80% intra-serotype similarity, regardless of the year of isolation. In conclusion, STEC isolates that were implicated in human disease between 2006 and 2013 in South Africa were mainly non-O157 strains which possessed virulence genes and markers commonly associated with STEC strains that have been incriminated in mild to severe human disease worldwide. Improved STEC monitoring and surveillance programs are needed in South Africa to control and prevent STEC disease in humans.

Virulence Characteristics and Antibiotic Resistance Profiles of Shiga Toxin-Producing Escherichia coli Isolates from Diverse Sources

“…Thus, in this study, we investigated the presence of VFs in E. coli strains to broaden the knowledge of the properties of E. coli strains isolated from diverse sources. Recent epidemiological studies have revealed that the STEC serotypes O26, O103, O111, O145, and O157 are highly related to human infections (they may account for up to 80% of human STEC infections) [8] and our results are in agreement with reports from other countries describing the high pathogenic potential of strains associated with these serogroups [2]. The presence of non-LEE effector genes encoded by O-island O1-71 is highly attributed to strains that were often involved in outbreaks and serious disease in humans [41][42][43].…”

“…From these findings, it seems that STEC strains carrying the stx1 gene are more often confronted than those carrying stx2. Possession of OI-43/48, OI-71, and non-LEE effectors genes together with stx2, eae and a whole plasmid is the hallmark of highly virulent STEC strains that are frequently associated with outbreaks and serious diseases such as hemorrhagic colitis (HC) and HUS [8]. Since the carriage of combinations of stx genes has been correlated with severity of the disease, the stx gene profile provides us an overview of the pathogenic potential of these STEC strains from diverse sources.…”

“…Among the DEC, STEC includes the most dangerous strains and more than 400 serotypes that produce stxs have been identified, and this term was created since E. coli species possess the toxin, which is more or less identical to that produced by Shigella dysentery type I [6]. STEC possesses a broad range of virulence factors (VFs), which are encoded by chromosomal genes, and they are often located in pathogenicity islands (PAIs) or plasmids, with the production of stxs being the most crucial resulting in endothelial cell damage and possible hemolytic uremic syndrome (HUS) [7,8]. In addition, STEC is responsible for 2.8 million illnesses, and 3890 cases per year of enteric disease in humans, globally [8].…”

“…Resistance in commensal E. coli from healthy patients was first demonstrated over 50 years ago, and several recent studies have demonstrated the high or increased incidence of MDR in commensal E. coli from healthy children and adults from various countries [23][24][25]. Currently, the use of antibiotics to treat STEC infection in humans is controversial and not recommended in many countries according to the current clinical guidelines, as some antibiotics can induce the production of Shiga toxin [8,26,27]. However, antibiotic resistance is a matter of growing concern due to the wide spread of E. coli resistance to all antibiotics used in human therapy, and the dispersion of resistance via mobile genetic elements.…”

“…However, antibiotic resistance is a matter of growing concern due to the wide spread of E. coli resistance to all antibiotics used in human therapy, and the dispersion of resistance via mobile genetic elements. Additionally, STEC bacteriophages may carry antibiotic resistance-encoding genes that can be transferred to naïve E. coli which are then transformed into antibiotic-resistant strains [8,21].…”