Haemolytic uraemic syndrome (HUS)

HUS is identified in the supplied sources as a haemolytic uraemic syndrome associated in several reports with STEC infection and, in one case, with E. coli sepsis ^[1][2][3]. The Danish surveillance-linked study notes an association between stx2a and stx2d subtypes and the risk of developing HUS ^[1]. Beyond this etiologic linkage, source-backed detail on formal diagnostic criteria or subtype classification is not yet available ^[4][5].

The case report describes vomiting, diarrhoea, fever, right upper quadrant pain, and altered mental status in an adult who subsequently met clinical features consistent with HUS ^[3]. Reported laboratory abnormalities included stage 3 acute kidney injury, anaemia, thrombocytopenia, deranged liver function, raised inflammatory markers, and peripheral blood film features of microangiopathic haemolysis ^[3]. The outcome in that case was gradual improvement with conservative management, but the supplied sources do not provide a broader severity spectrum or complication frequency ^[3]. The literature snippets also indicate that HUS has been associated with outbreaks of STEC and with mortality in some outbreak settings ^[2].

The supplied material places HUS in the context of STEC surveillance in Denmark and notes that improved molecular detection since 1997 has increased recognition of STEC cases, with similar increases recorded elsewhere in Europe ^[1]. One source states that outbreaks due to non-O157:H7 STEC resulting in HUS have attracted attention because of associated mortality and potential spread across large geographical regions ^[2]. Another case report shows HUS occurring after travel to Bali and Australia, but the source set does not support any broader travel-related pattern ^[3]. Source-backed detail on incidence, seasonality, endemicity, or age distribution is not yet available from the provided snippets ^[1][2][3].

The strongest source-supported transmission context is faecal-oral spread of STEC, which one source highlights as particularly relevant in developing-country settings ^[2]. The Danish study also indicates that nearly all diarrhoeal stool specimens are now examined for STEC, underscoring the diarrhoeal exposure pathway in surveillance practice ^[1]. The adult case report links HUS to E. coli sepsis, but the source set does not establish whether this represents a common transmission route or a distinct pathway ^[3].

The source set does not provide a stable, evidence-backed list of high-risk groups for HUS, so population-risk detail is not yet available ^[1][2][3]. The snippets do indicate risk considerations tied to STEC subtype, with stx2a and stx2d associated with HUS development ^[1]. One adult case shows that HUS can occur in a previously healthy adult after E. coli sepsis, but this is a case observation rather than a defined risk group ^[3].

The provided sources support prevention primarily through exposure control and surveillance-linked detection of STEC in diarrhoeal illness ^[1][2]. The Danish experience suggests that molecular testing and whole-genome sequencing improve characterisation of STEC and may aid recognition of strains associated with HUS ^[1]. The sources do not provide validated guidance on vaccines, post-exposure measures, or specific public-health interventions, so those details are not yet available from the evidence supplied ^[1][2].

In surveillance, HUS should be read as a severe syndrome that may signal STEC activity, including non-O157:H7 strains, and that may be more readily detected when diarrhoeal stool specimens are broadly tested for STEC ^[1][2]. The supplied literature also warns that expanding PCR panels and declining culture can complicate interpretation of mixed infections and outbreak linkage, increasing the need for careful curation of surveillance data ^[1]. Source-backed detail on formal case ascertainment rules for the NINDSS concept is not yet available from the snippets provided ^[4][5][6].

1. 1 Scheutz F et al. Shiga Toxin-Producing E. coli (STEC) from Danish Patients, 1997-2023: Diagnostic Trends and Bacteriological Findings. Microorganisms. 2025 Oct 12. PMID: 41156801. doi: 10.3390/microorganisms13102342. PubMed: https://pubmed.ncbi.nlm.nih.gov/41156801/
2. 2 Purwar S et al. Non-O157:H7 Shiga Toxin Producing Diarrhoeagenic Escherichia coli (STEC) in Southern India: A Tinderbox for Starting Epidemic. J Clin Diagn Res. 2016 Oct. PMID: 27891338. doi: 10.7860/JCDR/2016/21462.8714. PubMed: https://pubmed.ncbi.nlm.nih.gov/27891338/
3. 3 Yussuf U et al. Haemolytic Uraemic Syndrome in an Adult Following Escherichia coli Sepsis: A Case Report. Cureus. 2025 Sep. PMID: 41040750. doi: 10.7759/cureus.91417. PubMed: https://pubmed.ncbi.nlm.nih.gov/41040750/
4. 4 OUTCOME OF EPIDEMIC VERSUS ENDEMIC HAEMOLYTIC URAEMIC SYNDROME (HUS). Journal of Pediatric Gastroenterology &amp Nutrition. 1998. doi: 10.1097/00005176-199805000-00037. DOI: https://doi.org/10.1097/00005176-199805000-00037
5. 5 Haemolytic Uraemic Syndrome (HUS): Clinical Medicine Versus Clinical Anatomy. Austin Journal of Anatomy. 2017. doi: 10.26420/austinjanat.2017.1064. DOI: https://doi.org/10.26420/austinjanat.2017.1064
6. 6 Complement 3 glomerulopathy (C3G) and haemolytic uraemic syndrome (HUS). The Biomedical & Life Sciences Collection. 2021. doi: 10.69645/tjhc1878. DOI: https://doi.org/10.69645/tjhc1878

ICD-10

ICD-11

Total cases

380

Peak month

2005-12

Coverage

1 reporting countries · 2000-01-01 → 2026-06-01