Hospital Systems

Evidence brief: Prevalence, virulence profiles and antibiotic susceptibility patterns of Shiga toxin producing Escherichia coli O157:H7 among children 6–59 months in Longido, Arusha-Tanzania

A sourced PLOS One study, published 2026-07-10. Read the researchers’ findings, methods and context, with links to connected African health evidence.

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Illustrative stock photograph from Unsplash. It does not depict the reported event, study participants or a confirmed Kenyan facility. Source: https://images.unsplash.com/photo-1582750433449-648ed127bb54

Published in PLOS One on 2026-07-10, this study is presented as an attributed evidence briefing. The excerpts below are the original researchers’ words, reproduced under their Creative Commons Attribution licence. HealthSignal has selected the abstract and, where needed, opening background paragraphs; the complete methods, results, limitations and references remain in the linked paper.

Original authors: Martin Michael Martin, Haikael David Martin, Beatus Modesty Lyimo

Source: PLOS One • DOI 10.1371/journal.pone.0353396

Read the complete primary study ↗ · Creative Commons Attribution licence

From the researchers

Abstract

Shiga toxin producing Escherichia coli (STEC) is a zoonotic pathogen associated with diarhoeal disease and severe complications in children, yet its epidemiology in pastoral settings of Tanzania remains insufficiently characterized. This study determined the prevalence, virulence gene profiles and antibiotic susceptibility patterns of STEC among children aged 6‍-59 months with diarhoea in Longido District, northern Tanzania. A hospital based cross-sectional‍ study was conducted between July and August 2025, enrolling 150 participants from four health facilities. Stool samples were collected and analyzed using culture, serological conformation and multiplex polymerase chain reaction targeting five genes; rfbE, stx1, stx2, eaeA and hlyA. STEC was operationally defined by detection of stx1 and/or stx2. Antibiotic susceptibility was assessed using the Kirby-Bauer disk diffusion method. The prevalence of STEC was‍ 13.3% (20/‍150). All stx2 positive isolates co-occurred with stx1. Virulence genes showed a heterogeneous but significantly clustered distribution, with rfbE (20.0%) and stx1 (13.3%) predominating. Significant co-occurrence was observed‍ between stx1 and eae and between stx1 and hlyA (p < .001). Animal contact, raw milk consumption and use of untreated water were significantly associated with STEC infection. Firth penalized logistic regression confirmed these exposures as independent predictors. Antibiotic susceptibility profiles were uniform, with complete susceptibility to ciprofloxacin,‍ gentamicin, cefotaxime and ceftazidime while ampicillin and trimethoprim showed complete resistance. These findings indicate that STEC transmission in pastoral communities is strongly driven by zoonotic and environmental exposures, characterized by clustered virulence determinants and consistent antibiotic profiles. Limitations include the cross-sectional design and short sampling period, which may not capture seasonal variation. Strengthened surveillance and integrated One Health interventions are needed to reduce disease burden.

Introduction

Shiga toxin producing Escherichia coli (STEC), particularly the O157:H7 serotype, is an important zoonotic pathogen responsible for food and water-borne diarrhoeal disease globally [1]. Transmission occurs primarily through contaminated food or water and direct or indirect contact with animal reservoirs, especially ruminants, which constitute the principal natural host [2]. In humans, STEC‍ infection ranges from mild, self-limiting diarrhoea to severe complications such as hemorrhagic colitis and hemolytic uremic syndrome (HUS) [3]. The HU‍S is a life threatening condition characterized by acute renal failure, hemolytic anaemia and thrombocytopenia, with the highest risk in young children and other vulnerable population [4]. Disease severity is largely mediated by Shiga toxins (Stx1 and Stx2), which damage endothelial cells and disrupt vascular integrity [5].

S‍TEC is a recognized cause of global foodborne outbreaks linked to contaminated meat, dairy products, fresh produce and water sources [6]. It is estimated to cause 2.8 million acute illness annually, resulting in considerable health care costs [7]. Despite this burden, the epidemiology of STEC remains insufficiently characterized in many low and middle-income countries [7]. Limited laboratory capacity and weak surveillance systems contribute to underdiagnosis and underreporting, obscuring the true disease burden [8]. In Sub Sahara Africa, diarrhoeal diseases remain a leading cause of morbidity and mortality among children under five years of age [9]. Diarrhoeagenic Escherichia coli‍ is a major cause of diarrhoeal disease, but data on specific pathotypes like STEC remain limited. Prevalence estimates vary widely due to differences in study design, diagnostic methods and limited molecular techniques, underscoring the need for standardized epidemiological studies.

Reading this evidence

Use the full paper to check the study design, participant selection, comparator and outcome definitions before drawing a practical conclusion. An association does not by itself show cause and effect. A reported performance measure needs its denominator and uncertainty. A finding from a particular facility, sample or time period should retain that scope when it is discussed elsewhere.

This briefing makes the source accessible within the wider hospital systems desk. It does not assess an individual patient or certify a product. When considering relevance to another health system, examine the original authors’ account of context and limitations, then seek local implementation evidence. The related reporting below provides other studies to read alongside this one; it is a topic connection, rather than a claim that their results are directly comparable.

© 2026 Martin Michael Martin, Haikael David Martin, Beatus Modesty Lyimo. Excerpts reproduced under CC BY. Selection, formatting and contextual notes by HealthSignal. The researchers are the authors of the source study, not members of HealthSignal’s staff.

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HealthSignal’s publication desk curates source-based health analysis and attributed research briefings. Study authors and originating institutions are credited within each article. Preparation used AI assistance; source and licence checks do not constitute independent replication or clinical endorsement.

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