Shiga toxin-producing Escherichia coli infection

Shiga toxin-producing Escherichia coli infection refers to infection with E. coli strains that produce Shiga toxin, also described as verotoxin-producing E. coli in the surveillance description [disease]. The literature provided identifies STEC as the primary cause of typical HUS and links it to a syndrome of microvascular injury and hemolysis ^[3][1]. The entity is also coded in the supplied metadata as ICD-10 A04.3 and ICD-11 1A03 [disease].

The main clinical manifestation described in the sources is diarrhoea, which may be bloody in about 60% of patients, and the reported median incubation period is three days ^[1]. STEC can also cause haemorrhagic colitis and the diarrhoea-associated form of HUS ^[2]. HUS is defined in the provided material as a triad of mechanical hemolytic anemia, thrombocytopenia, and acute renal injury, and one report notes nephrological and neurological thrombotic microangiopathy in a STEC-positive child ^[1][3]. HUS is reported in 5-15% of STEC infections, and in the literature review 73% of HUS cases required kidney replacement therapy ^[1][3].

STEC infection has major outbreak potential and is described as a leading cause of HUS in children ^[1]. The sources note a shift in epidemiology since the early 2010s, with decline of the historically predominant O157 serogroup and emergence of non-O157 STEC, especially O26 and O80 in France ^[1]. The 2010 reference states that STEC infections occur worldwide and are a major public-health concern because some non-O157 strains can cause illness comparable in severity to O157-associated disease ^[2]. The literature also indicates that STEC is zoonotic and distributed among domestic and wildlife animal species, with human infection linked to contaminated food, water, and animal or human contact ^[2][1].

Transmission occurs through ingestion of contaminated food or water, person-to-person spread, and contact with ruminants or their contaminated environment ^[1]. Another source also describes transmission through contact with infected animals or people and emphasizes a zoonotic character ^[2]. No source-backed detail on dose, environmental persistence, or seasonality is available in the supplied material.

Children are the group most clearly highlighted in the provided sources, both because STEC is described as the leading cause of HUS in children and because one review found 73% of reported atypical HUS cases initially classified as typical were pediatric ^[1][3]. The material also suggests heightened relevance for persons with exposure to contaminated food or water, ruminants, or their contaminated environments, as well as those with contact with infected animals or people ^[1][2]. Source-backed detail on other specific high-risk groups is not yet available.

The supplied sources do not provide a formal prevention schedule or vaccine-related guidance, but they do support prevention through exposure control focused on contaminated food, water, animals, and contaminated environments ^[1][2]. Because person-to-person spread is documented, hygiene and interruption of direct transmission are relevant public-health measures ^[1]. Source-backed detail on additional preventive interventions is not yet available.

In surveillance, STEC should be read as a syndrome-capable pathogen with both gastroenteric and post-infectious renal outcomes, not solely as a diarrhoeal infection ^[1][3]. The sources support continued clinical and bacteriological surveillance, including stool testing for Shiga toxins and STEC, because outbreaks are important and HUS may follow infection ^[1]. STEC positivity does not exclude atypical HUS when the presentation is atypical, so surveillance interpretation may need to distinguish microbiological detection from the full clinical syndrome ^[3].

1. 1 Bruyand M et al. Hemolytic uremic syndrome due to Shiga toxin-producing Escherichia coli infection. Med Mal Infect. 2018 May. PMID: 29054297. doi: 10.1016/j.medmal.2017.09.012. PubMed: https://pubmed.ncbi.nlm.nih.gov/29054297/
2. 2 Shiga Toxin-Producing Escherichia coli. Pathogenic Escherichia coli in Latin America. 2010. doi: 10.2174/978160805192211001010065. DOI: https://doi.org/10.2174/978160805192211001010065
3. 3 Mortari G et al. Shiga toxin-producing Escherichia coli infection as a precipitating factor for atypical hemolytic-uremic syndrome. Pediatr Nephrol. 2025 Feb. PMID: 39347991. doi: 10.1007/s00467-024-06480-9. PubMed: https://pubmed.ncbi.nlm.nih.gov/39347991/
4. 4 Freedman SB et al. Shiga Toxin-Producing Escherichia coli Infection, Antibiotics, and Risk of Developing Hemolytic Uremic Syndrome: A Meta-analysis. Clin Infect Dis. 2016 May 15. PMID: 26917812. doi: 10.1093/cid/ciw099. PubMed: https://pubmed.ncbi.nlm.nih.gov/26917812/
5. 5 Shiga Toxin--Producing Escherichia coli Infection. Clinical Infectious Diseases. 2004. doi: 10.1086/383473. DOI: https://doi.org/10.1086/383473
6. 6 Shiga toxin-producing Escherichia coli. Clinical Microbiology Newsletter. 1999. doi: 10.1016/s0196-4399(00)90001-1. DOI: https://doi.org/10.1016/s0196-4399(00)90001-1

ICD-10

A04.3

ICD-11

1A03

Total cases

132K

Peak month

2025-08

Coverage

7 reporting countries · 2000-01-01 → 2026-06-20