Shiga toxin-producing (STEC) represents a major issue for public health because of the severity of the associated illnesses, including haemolytic uraemic syndrome (HUS). In 2015, investigation of a case of HUS revealed an outbreak of Shiga toxin-2-producing O26 : H11 infection in a nursery in Italy. The investigation showed that the infection was transmitted to cases' contacts via person to person. The case finding was performed by testing for STEC stool samples of the HUS case's contacts within the family and the nursery. STEC O26 isolates were characterized by whole genome sequencing. Confirmed cases were repeatedly tested to monitor the duration of STEC shedding. Eleven STEC O26 cases were identified, including adults and asymptomatic patients. Clinical illness was only observed in children. Strain characterization revealed that a single clone harbouring the a and genes and the complete array of STEC-associated virulence genes, belonging to ST(21), was implicated in the outbreak. To reduce bacterial shedding, patients were treated with cefixime following clinical recovery. This antibiotic was well tolerated and did not induce any apparent consequences on patients' health. This study confirms that Stx2-producing O26 represents an emerging public health problem. The occurrence of outbreaks of infection by Stx2-producing O26 in nurseries is of particular concern, given the high probability of infection progressing in severity and resulting in secondary cases.
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http://dx.doi.org/10.1099/jmm.0.000738 | DOI Listing |
Appl Environ Microbiol
January 2025
Division of Environmental Health Sciences, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA.
Cattle and other domestic ruminants are the primary reservoirs of O157 and non-O157 Shiga toxin-producing (STEC). Living in areas with high ruminant density has been associated with excess risk of infection, which could be due to both direct ruminant contact and residual environmental risk, but the role of each is unclear. We investigated whether there is any meaningful risk to individuals living in ruminant-dense areas if they do not have direct contact with ruminants.
View Article and Find Full Text PDFHum Gene Ther
January 2025
BridgeBio Gene Therapy, Palo Alto, California, USA.
Complement-mediated thrombotic microangiopathy (TMA) in the form of atypical hemolytic uremic syndrome (aHUS) has emerged as an immune complication of systemic adeno-associated virus (AAV) gene transfer that was unforeseen based on nonclinical studies. Understanding this phenomenon in the clinical setting has been limited by incomplete data and a lack of uniform diagnostic and reporting criteria. While apparently rare based on available information, AAV-associated TMA/aHUS can pose a substantial risk to patients including one published fatality.
View Article and Find Full Text PDFIntroduction: Thrombotic microangiopathies (TMA) represent distinct pathological and clinical entities with known chronicity and recurrence. Kidney biopsy is the gold standard to diagnose TMA in patients with renal manifestations but the prognostic significance of acute or chronic phase of the disease has not been well studied. We examined the clinical characteristics, management, and predictors of acute vs.
View Article and Find Full Text PDFCan J Kidney Health Dis
January 2025
Multiorgan Transplant Program, Division of Nephrology, Department of Medicine, McGill University Health Centre, Montreal, QC, Canada.
Background: Kidney failure is a prevalent condition with tendency for familial clustering in up to 27% of the affected individuals. Living kidney donor (LKD) transplantation is the optimal treatment option; however, in Canada, more than 45% of LKDs are biologically related to their recipients which subjects recipients to worse graft survival and donors to higher future risk of kidney failure. Although not fully understood, this observation could be partially explained by genetic predisposition to kidney diseases.
View Article and Find Full Text PDFJ Thromb Haemost
January 2025
Department of Pathology and Laboratory Medicine; Institute of Reproductive Medicine and Developmental Sciences, The University of Kansas Medical Center, Kansas City, KS 66160. Electronic address:
Background: A loss-of-functional mutation (W1183R) in human complement factor H (CFH) is associated with complement-associated hemolytic uremic syndrome; mice carrying a similar mutation (W1206R) in CFH also develop thrombotic microangiopathy but its plasma von Willebrand factor (VWF) multimer sizes were dramatically reduced. The mechanism underlying such a dramatic change in plasma VWF multimer distribution in these mice is not fully understood.
Objective And Methods: To determine the VWF and CFH interaction and how CFH proteins affect VWF multimer distribution, we employed recombinant protein expression, purification, and various biochemical and biophysical tools.
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