scholarly journals The Health Implication of Enterohaemorrhagic Escherichia coli (EHEC) 0157:H7: A Review on Haemolytic Uraemic Syndrome

2019 ◽  
pp. 1-10
Author(s):  
Onengiyeofori Ibama ◽  
Edna O. Ibegbulem ◽  
Donatus Onwuli ◽  
Adline Ben-Chioma
Keyword(s):  
Escherichia Coli ◽  
Haemolytic Anaemia ◽  
Bacterial Strain ◽  
Haemolytic Uraemic Syndrome ◽  
Clinical Manifestations ◽  
Specific Treatment ◽  
Kidney Injury ◽  
Electrolyte Imbalance ◽  
Health Concern ◽  
Enterohaemorrhagic Escherichia Coli

Consumption of foods, water, vegetables, fruits, undercooked/ground/raw meat, unpasteurized milk or milk products contaminated with the bacterium strain Escherichia coli 0157:H7 has become a serious public health concern. This strain naturally inhabits the digestive tract of healthy cattle, and is released into the environment through the faeces of the animal. This strain cause haemorrhagic enterocolitis or gastroenteritis, and then haemolytic uraemic syndrome (HUS). HUS is a disorder characterised by haemolytic anaemia, low platelet count and acute kidney failure, and this disorder is a consequence of the production and action of Shiga-like toxin produced mainly by this bacterial strain (accounting for 90 percent of all cases), and occurs mainly in children less than five (5) years of age, but also occurs in the elderly. After infection with this bacterial strain, the disorder begins with intestinal perforation and ulceration leading to bloody diarrhoea, and consequently acute kidney injury, thrombocytopenia and microangiopathic haemolytic anaemia. In conjunction with clinical manifestations, several laboratory investigations (haematological, biochemical and microbiological assays) are implicated in the diagnosis of HUS. There is currently no specific treatment for HUS; however, supportive care (such as treatment of hypertension, fluid and electrolyte imbalance, haemodialysis, blood transfusion, etc) happens to be the only ameliorative measure for this disorder.

Haemolytic uraemic syndrome

2020 ◽  
pp. 5027-5032
Author(s):  
Edwin K.S. Wong ◽  
David Kavanagh
Keyword(s):  
Escherichia Coli ◽  
Acute Kidney Injury ◽  
Complement System ◽  
Shiga Toxin ◽  
Thrombotic Microangiopathy ◽  
Initial Treatment ◽  
Haemolytic Uraemic Syndrome ◽  
Kidney Injury ◽  
Adamts13 Activity ◽  
Thrombocytopenic Purpura

Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy characterized by the triad of thrombocytopenia, microangiopathic haemolytic anaemia, and acute kidney injury. It is most often caused by Shiga toxin-producing Escherichia coli (STEC-HUS), and any HUS not caused by this is often termed atypical HUS (aHUS). aHUS may be caused by an underlying complement system abnormality (primary aHUS) or by a range of precipitating events, such as infections or drugs (secondary aHUS). Management of STEC-HUS is supportive. In aHUS, plasma exchange is the initial treatment of choice until ADAMTS13 activity is available to exclude thrombotic thrombocytopenic purpura as a diagnosis. Once this has been done, eculizumab should be instigated as soon as possible.

scholarly journals Rapidly progressive glomerulonephritis in children

2021 ◽  
Vol 38 (ICON-2022) ◽  
Author(s):  
Khemchand N Moorani ◽  
Madiha Aziz ◽  
Farhana Amanullah
Keyword(s):  
Immune Complex ◽  
Search Strategy ◽  
Rapid Development ◽  
Clinical Manifestations ◽  
Specific Treatment ◽  
Rapidly Progressive Glomerulonephritis ◽  
Kidney Injury ◽  
Antineutrophil Cytoplasmic Antibody ◽  
Good Prognosis ◽  
Cochrane Library

Rapidly progressive glomerulonephritis (RPGN), characterized by a rapid development of nephritis with loss of kidney function in days or weeks, is typically associated histologically, with crescents in most glomeruli; and is a challenging problem, particularly in low resource settings. RPGN is a diagnostic and therapeutic emergency requiring prompt evaluation and treatment to prevent poor outcomes. Histopathologically, RPGN consists of four major categories, anti-glomerular basement membrane (GBM) disease, immune complex mediated, pauci-immune disorders and idiopathic /overlap disorders. Clinical manifestations include gross hematuria, proteinuria, oliguria, hypertension and edema. Diagnostic evaluation, including renal function tests, electrolytes, urinalysis/microscopy and serology including (anti GBM antibody, antineutrophil cytoplasmic antibody (ANCA)) starts simultaneously with management. An urgent renal biopsy is required to allow specific pathologic diagnosis as well as to assess disease activity and chronicity to guide specific treatment. The current guidelines for management of pediatric RPGN are adopted from adult experience and consist of induction and maintenance therapy. Aggressive combination immunosuppression has markedly improved outcomes, however, nephrotic syndrome, severe acute kidney injury requiring dialysis, presence of fibrous crescents and chronicity are predictors of poor renal survival. RPGN associated post infectious glomerulonephritis (PIGN) usually has good prognosis in children without immunosuppression whereas immune-complex-mediated GN and lupus nephritis (LN) are associated with poor prognosis with  development of end stage kidney disease (ESKD) in more than 50% and 30% respectively. Given the need for prompt diagnosis and urgent treatment to avoid devastating outcomes, we conducted a review of the latest evidence in RPGN management to help formulate clinical practice guidance for children in our setting.Information sources and search strategy: The search strategy was performed in the digital databases of PubMed, Cochrane Library, google scholar, from their inception dates to December 2020. Three investigators independently performed a systematic search using the following search terms “Rapidly progressive glomerulonephritis” “children” “crescentic glomerulonephritis” “management” at the same time, backtracking search for references of related literature. doi: https://doi.org/10.12669/pjms.38.ICON-2022.5774 How to cite this:Moorani KN, Aziz M, Amanullah F. Rapidly progressive glomerulonephritis in children. Pak J Med Sci. 2022;38(2):417-425.   doi: https://doi.org/10.12669/pjms.38.ICON-2022.5774 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Treatment and management of children with haemolytic uraemic syndrome

2017 ◽  
Vol 103 (3) ◽  
pp. 285-291 ◽  
Author(s):  
Patrick R Walsh ◽  
Sally Johnson
Keyword(s):  
Escherichia Coli ◽  
Acute Kidney Injury ◽  
Shiga Toxin ◽  
Haemolytic Uraemic Syndrome ◽  
Pneumococcal Infection ◽  
Kidney Injury ◽  
Complement Cascade ◽  
Alternative Complement ◽  
Invasive Pneumococcal Infection

Haemolytic uraemic syndrome (HUS), comprising microangiopathic haemolytic anaemia, thrombocytopaenia and acute kidney injury, remains the leading cause of paediatric intrinsic acute kidney injury, with peak incidence in children aged under 5 years. HUS most commonly occurs following infection with Shiga toxin-producing Escherichia coli (STEC-HUS). Additionally, HUS can occur as a result of inherited or acquired dysregulation of the alternative complement cascade (atypical HUS or aHUS) and in the setting of invasive pneumococcal infection. The field of HUS has been transformed by the discovery of the central role of complement in aHUS and the dawn of therapeutic complement inhibition. Herein, we address these three major forms of HUS in children, review the latest evidence for their treatment and discuss the management of STEC infection from presentation with bloody diarrhoea, through to development of fulminant HUS.

Secondary, profound, sensorineural hearing loss after recovery from haemolytic uraemic syndrome due to enterohaemorrhagic Escherichia coli, and subsequent cochlear implantation, in two Japanese children

2013 ◽  
Vol 127 (3) ◽  
pp. 306-310
Author(s):  
S B Minami ◽  
H Takegoshi ◽  
Y Shinjo ◽  
K Kaga
Keyword(s):  
Escherichia Coli ◽  
Hearing Loss ◽  
Cochlear Implantation ◽  
Haemolytic Uraemic Syndrome ◽  
Disease Onset ◽  
Profound Hearing Loss ◽  
Enterohaemorrhagic Escherichia Coli ◽  
First Case ◽  
Hearing Function ◽  
One Year

AbstractObjectives:To describe two cases of profound hearing loss secondary to enterohaemorrhagic Escherichia coli infection, and to report the efficacy of subsequent cochlear implantation.Results:The first case was a four-year-old girl admitted to hospital with Escherichia coli O157 infection and haemolytic uraemic syndrome. Mild hearing loss was confirmed five months after discharge, progressing to profound loss three months later. At the age of seven years, she underwent cochlear implantation, with remarkable improvement in speech perception and production. The second case was a three-year-old boy admitted with haemolytic uraemic syndrome caused by Escherichia coli O111 infection. One year after disease onset, profound hearing loss was confirmed. Cochlear implantation at the age of five years produced significant recovery of auditory function.Conclusion:This study represents the first published report of secondary hearing loss after recovery from haemolytic uraemic syndrome caused by enterohaemorrhagic Escherichia coli. It indicates that cochlear implantation can restore hearing function in such patients.

scholarly journals SHORT PAPER The stimulating effect of fosfomycin, an antibiotic in common use in Japan, on the production/release of verotoxin-1 from enterohaemorrhagic Escherichia coli O157[ratio ]H7 in vitro

1997 ◽  
Vol 119 (1) ◽  
pp. 101-103 ◽  
Author(s):  
M. YOH ◽  
T. HONDA
Keyword(s):  
Escherichia Coli ◽  
Haemolytic Uraemic Syndrome ◽  
School Lunch ◽  
Short Paper ◽  
Escherichia Coli O157 ◽  
Haemorrhagic Colitis ◽  
Enterohaemorrhagic Escherichia Coli ◽  
Osaka Prefecture

In 1996 Japan had a big outbreak of enterohaemorrhagic Escherichia coli (EHEC) O157[ratio ]H7, especially in Osaka prefecture where about 6000 patients (mainly schoolchildren) suffered from diarrhoea, haemorrhagic colitis and haemolytic uraemic syndrome (HUS) due to EHEC infection via school lunch. Our survey of doctors who took care of those patients showed that most patients had received antibiotics, especially fosfomycin which comprised 84% of the prescribed treatment. Since the administration of antibiotics for EHEC infection is under discussion, we analysed the effect of fosfomycin on production/release of verotoxins (VTs). Addition of fosfomycin into EHEC culture in CAYE broth at 2 and 5 h after start of incubation caused marked increase of VT1 release. This observation warns of the possibility of fosfomycin treatment making the disease worse.

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