Shiga Toxin-ProducingEscherichia coliin Diarrheal Stool of Swedish Children: Evaluation of Polymerase Chain Reaction Screening and Duration of Shiga Toxin Shedding

Abstract

BackgroundShiga toxin (Stx)-producing Escherichia coli (STECs) are the most common cause of acute renal failure in children. The present study evaluated a 10-year STEC polymerase chain reaction screening regimen in children.MethodsAll routine stool culture specimens from patients below 10 years of age (n = 10 342) from May 2003 through April 2013 in the County of Jönköping, Sweden, were included. Patients were divided in 1 group where analyses of STEC were requested by the clinician (n = 2366) and 1 screening group (n = 7976). Patients who were positive for STEC were tested weekly until they were negative. Clinical data were collected through a questionnaire and by reviewing medical records.ResultsIn specimens from 191 patients, stx was found (162 index cases). The prevalence was 1.8% in the requested group and 1.5% in the screening group (P = .5). Diarrhea was the most frequent symptom reported in 156 cases and of these 29 (19%) had hemorrhagic colitis (HC) and 7 children developed hemolytic uremic syndrome (HUS). No difference regarding severity of symptoms between the groups was found. Stx2 predominated in cases with HC (P < .0001) and HUS (P = .04). Median stx shedding duration was 20 days (1–256 days), and no difference in duration was seen between stx types (P = .106–1.00) and presence of eaeA (P = .72).ConclusionsMost STEC cases were found in the screening group with comparable prevalence and disease severity as in patients where analysis was requested. Furthermore, non-O157 serotypes caused severe disease when carrying stx2, and prolonged shedding of STEC may be a risk for transmission.

Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review

“…This nomenclature reflects both the phylogeny and origin of the toxin as well as its pathogenicity. For example, the presence of Stx2 is strongly associated with hemorrhagic colitis and HUS compared to Stx1 or to the presence of both genes [22,23,62,63]. Within the Stx2 type, Stx2a (formerly named Stx2), Stx2c, and Stx2d activable [64] are associated with a higher risk for human disease [22,65].…”

“…The propensity to develop the disease varies according to microbiological and individual characteristics, although the determinants of the disease are not fully elucidated. First, the risk of HUS is greater for O157:H7 E. coli (≈10%) and Stx2v-harboring strains than for non-O157 serotypes and Stx1-harboring strains (≈1%) [22,23,41,43,50,62,63]. Since the first documented outbreaks in the 1980s, the O157:H7 strain has genetically diversified and concurrently acquired enhanced virulence due to bacteriophage-related insertions, deletions, and duplications [106].…”

“…A sequential two-step strategy with a non-culture assay, followed by culture for STEC in the event of positive Shiga toxin, represent an unacceptable delay for the isolation of STEC strains. Selective testing on the basis of a patient's age or season of the year is also inappropriate, and it has been shown that the prevalence of Stx was identical whether routine screening is implemented or if the analysis is based on physician's request [63]. In 2000, 68% of US clinical laboratories reported routinely testing stool specimens for E. coli O157:H7 with stool culture, an immunoassay, or both [275].…”

“…Multiplex PCR [288] and real-time PCR [254] have been developed and allow an earlier diagnosis (less than 24 h) compared to traditional methods. PCR found Stx in the stools of infected patients during a median of 20 d (1-256 d) after onset of symptoms [63]. Early isolation and characterization of STEC strains enable epidemiological surveillance and cluster detection by performing molecular analyses such as whole-genome sequencing [289].…”

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“…Humans can become infected with STEC by ingesting contaminated food or water or by transmission from infected animals or humans [34]. Prevalence of STEC infection in human was 15% by Salmanzadeh-Ahrabi et al, [35], 2.3% by Rajendran et al, [36], 1.7% by van Duynhoven et al, [37], 7% was reported in patients with diarrhoea in Morogoro, Tanzania in 2006 by Raji et al, [38] and 56% by Matussek et al, [39]. The overall prevalence of virulence-associated gene VT1 only, VT2 only, VT1 and VT2 and eaeA were 10.7%, 20.8%, 68.5%, 3.9%, respectively as reported by Wang et al, [31].…”