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Diarrhea and Malnutrition
Published in Fima Lifshitz, Childhood Nutrition, 2020
Andrea Maggioni, Fima Lifshitz
Hemorrhagic colitis caused by E. Coli 0157:H7 was first recognized in 1982 during outbreaks in Oregon and Michigan.32 A very young age was a significant risk factor among the reported risk factors for diarrhea caused by this microorganism, other than ingesting contaminated food or water and person-to-person spread. In a recent survey, the risk of infection in day care settings was inversely related to the age of the children who attended.33 Similarly, the severity of symptoms and the risk of developing serious complication as hemolytic uremic syndrome was higher in children less than five years of age.34
The kidneys
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The haemolytic uraemic syndrome may be of the childhood or adult type. It may be sporadic or occur in an epidemic form, in which case it is particularly associated with diarrhoeal illness caused by verocytotoxin-producing Escherichia coli (E. coli 0157). In childhood the onset often follows an upper respiratory tract or diarrhoeal illness of ill-defined aetiology. The main features of the disease are acute renal failure, thrombocytopenia, confusion, and microangiopathic haemolytic anaemia. In adults the disease may also follow an episode of diarrhoea but other causes include HIV infection, malignancy, and drugs such as cyclosporin and cisplatin. Mutations in complement genes (e.g. factor H; see Chapter 4) have been shown to predispose to haemolytic uraemic syndrome in those cases that are familial. Haemolytic uraemic syndrome has a significant mortality in elderly people; however, most children and young and middle-aged adults survive although the recovery of renal function may be incomplete.
A Case Of Vero Cytotoxinproducing Escherichia Coli (VTEC)
Published in Meera Chand, John Holton, Case Studies in Infection Control, 2018
Taylor CM, Machin S, Wigmore S & Goodship THJ (2009). Clinical Practice Guidelines for the Management of Atypical Haemolytic Uraemic Syndrome in the United Kingdom, pp. 1–22. The Renal Association www.renal.org/guidelines/joint-guidelines#sthash.29lIW8fO.dpbs
Complement system network in cell physiology and in human diseases
Published in International Reviews of Immunology, 2021
Roberta Romano, Giuliana Giardino, Emilia Cirillo, Rosaria Prencipe, Claudio Pignata
The dysfunctional regulation of alternative complement pathway due to Factor H or I deficiency or C3 unresponsiveness to inhibition leads to the development of the atypical form of Hemolytic Uremic Syndrome. Usually caused, in its typical form, by Shiga-toxin producing Escherichia coli, atypical Hemolytic Uremic Syndrome is a thrombotic microangiopathy disease affecting mainly kidneys, in which deposits of C5b-C9 damage glomerular endothelium. Thereafter, intravascular hemolysis and platelets activation result in the formation of microthrombi [48]. Atypical forms account for 5 to 20% of cases of Hemolytic Uremic Syndrome and may be either due to mutations in one of more genes coding for regulatory or cascade proteins (loss of function mutations in CFH, CFI or gain of function mutations in CFB and C3) [49,50] or due to autoantibodies to factor H, detected in 5-13% of European atypical Hemolytic Uremic Syndrome patients. In such patients, genetic and autoantibodies testing are essential: the detection of anti-factor H autoantibodies may suggest the use of immunosuppressive drugs combined with plasma exchange, as therapeutic approach [51] as opposed to sero-negative atypical Hemolytic Uremic Syndrome forms in which the standard treatment choice is a humanized monoclonal antibody, Eculizumab, that binds the terminal complement component C5, as below described [51].
CFH and CFB mutations in Shiga toxin-associated haemolytic uraemic syndrome in a 6-year-old boy
Published in Paediatrics and International Child Health, 2020
Mehtap Ezel Çelakil, Burcu Bozkaya Yücel, Kenan Bek
Haemolytic uraemic syndrome (HUS) is characterised by thrombocytopenia, microangiopathic haemolytic anaemia and organ injury. The typical form of HUS is most commonly caused by Shiga toxin-producing Escherichia coli (STEC) O157: H7 through the ingestion of contaminated food or water and is generally preceded by a period of bloody diarrhoea. The pathophysiology of HUS is thought to be owing to the release of Shiga toxin which causes endothelial damage and activates the complement cascade, leading to thrombotic microangiopathy and renal damage [1]. Atypical HUS (aHUS) is secondary to defects in genes encoding the regulatory proteins of the complement system. Initial differentiation of the two entities is difficult because, in aHUS, a viral gastrointestinal infection and/or upper respiratory tract infection can precede the typical clinical picture as a triggering factor in 42–70% of patients [2,3].
Thrombotic thrombocytopenic purpura in a 2.5-year-old boy with dengue infection: a rare complication
Published in Paediatrics and International Child Health, 2020
Rajasekhar Reddy Gogireddy, Vasanth Kumar, Suchitra Ranjit, Rajeswari Natraj, Priyavarthini Venkatachalapathy, Indira Jayakumar, Saravanan Margabandhu
On Day 2, the urine output was low along with a serial drop in haematocrit from 0.32% to 0.27% and 0.22%. There is no evidence of significant haemorrhage-like gastrointestinal bleeding or continuous oozing from vascular access or epistaxis other than haematuria with stable haemodynamics. The oliguria did not respond to fluid and furosemide challenge and serum creatinine increased from 61.8 to 141.4 µmol/L (15.3–61.0) which is classified as class 3 AKI, as per the modified pRIFLE (paediatric risk, injury, failure, loss, end-stage renal disease) criteria. In view of the anaemia, thrombocytopenia, haematuria and AKI, intravascular haemolysis owing to haemolytic uraemic syndrome (HUS)/TTP was suspected. The peripheral blood smear demonstrated evidence of microangiopathy and lactate dehydrogenase (LDH) was 64.8 µkat/L (1.83–3.50). Direct Coomb’s test was negative, ruling out immune-mediated haemolysis. Other differential diagnoses for AKI such as acute tubular necrosis, sepsis and rhabdomyolysis were excluded. Laboratory data on admission and during hospitalisation are summarised in Table 1.