Shiga Toxin–Producing
            <i>Escherichia coli</i>
            and the Hemolytic–Uremic Syndrome

Freedman, Stephen B.; van de Kar, Nicole C.A.J.; Tarr, Phillip I.

doi:10.1056/nejmra2108739

Cited by 12 publications

(3 citation statements)

References 92 publications

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“…Food-borne outbreaks of severe hemorrhagic enterocolitis complicated by life-threatening hemolytic uremic syndrom (HUS) are an utterly devastating incident and a major challenge for public health (1,2). The largest outbreak caused 3,816 documented infections in Northern Germany in 2011, including 845 cases of HUS (3).…”

Section: Introductionmentioning

confidence: 99%

Do asymptomatic STEC-long-term carriers need to be isolated or decolonized? New evidence from a community case study and concepts in favor of an individualized strategy

Sayk,

Hauswaldt,

Knobloch

et al. 2024

Front. Public Health

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Asymptomatic long-term carriers of Shigatoxin producing Escherichia coli (STEC) are regarded as potential source of STEC-transmission. The prevention of outbreaks via onward spread of STEC is a public health priority. Accordingly, health authorities are imposing far-reaching restrictions on asymptomatic STEC carriers in many countries. Various STEC strains may cause severe hemorrhagic colitis complicated by life-threatening hemolytic uremic syndrome (HUS), while many endemic strains have never been associated with HUS. Even though antibiotics are generally discouraged in acute diarrheal STEC infection, decolonization with short-course azithromycin appears effective and safe in long-term shedders of various pathogenic strains. However, most endemic STEC-strains have a low pathogenicity and would most likely neither warrant antibiotic decolonization therapy nor justify social exclusion policies. A risk-adapted individualized strategy might strongly attenuate the socio-economic burden and has recently been proposed by national health authorities in some European countries. This, however, mandates clarification of strain-specific pathogenicity, of the risk of human-to-human infection as well as scientific evidence of social restrictions. Moreover, placebo-controlled prospective interventions on efficacy and safety of, e.g., azithromycin for decolonization in asymptomatic long-term STEC-carriers are reasonable. In the present community case study, we report new observations in long-term shedding of various STEC strains and review the current evidence in favor of risk-adjusted concepts.

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Section: Introductionmentioning

confidence: 99%

Do asymptomatic STEC-long-term carriers need to be isolated or decolonized? New evidence from a community case study and concepts in favor of an individualized strategy

Sayk,

Hauswaldt,

Knobloch

et al. 2024

Front. Public Health

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“…Shiga toxin-producing Escherichia coli (STEC) can cause enterocolitis, and in about 15-20% of cases, the gastrointestinal phase is followed by hemolytic uremic syndrome (HUS) [1]. After STEC infection, Shiga toxin (Stx) crosses the intestinal barrier, enters the circulation, and induces multi-organ damage by activation of endothelial cells and induction of thrombo-inflammatory pathways [2].…”

Section: Introductionmentioning

confidence: 99%

“…The main target organs are the kidney and the central nervous system (CNS) leading to acute kidney injury (AKI) and severe neurological symptoms. STEC-HUS is clinically defined by non-immune hemolytic anemia, thrombocytopenia, and AKI [1]. Typically, children ≤ 5 years of age are affected by STEC-HUS.…”

Section: Introductionmentioning

confidence: 99%

Volume expansion mitigates Shiga toxin-producing E. coli-hemolytic uremic syndrome in children

Böckenhauer,

Schild,

Kemper

et al. 2024

Pediatr Nephrol

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Background Shiga toxin-producing E. coli-hemolytic uremic syndrome (STEC-HUS) is associated with high morbidity and relevant mortality. Previous small studies showed that volume expansion could improve the course and outcome of STEC-HUS. The aim of this single-center study was to evaluate the effect of volume expansion on the clinical course and outcome in STEC-HUS. Methods Data of pediatric patients with STEC-HUS were analyzed retrospectively. Course and outcome of patients treated with volume expansion (VE) from 2019 to 2022 (n = 38) were compared to historical controls (HC) from 2009 to 2018 (n = 111). Results Patients in the VE group had a significant relative median weight gain compared to HC (7.8% (3.4–11.3) vs. 1.2% (− 0.7–3.9), p < 0.0001) 48 h after admission. The need for dialysis was not reduced by VE (VE 21/38 (55.3%) vs. HC 64/111 (57.7%), p = 0.8). However, central nervous system involvement (impairment of consciousness, seizures, focal neurological deficits, and/or visual disturbances) was significantly reduced (VE 6/38 (15.8%) vs. HC 38/111 (34.2%), p = 0.039). None of the patients in the VE group died or developed chronic kidney disease (CKD) stage 5, whereas in the HC group, three patients died and three patients had CKD stage 5 at discharge. Conclusions This study suggests that volume expansion may be associated with the mitigation of the acute course of STEC-HUS, especially severe neurological involvement and the development of CKD. Prospective trials should lead to standardized protocols for volume expansion in children with STEC-HUS. Graphical abstract

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