scholarly journals Extra-corporeal membrane oxygenation and Eculizumab: Atypical treatments for typical haemolytic uraemic syndrome

2019 ◽  
Vol 21 (2) ◽  
pp. 191-193
Author(s):  
Matthew D Kelham ◽  
Liam Gleeson ◽  
Inma Alcalde ◽  
Rosalba Spiritoso ◽  
Alastair G Proudfoot ◽  
...  

A 19-year-old female with no medical history presented with bloody diarrhoea. Investigations revealed an acute kidney injury, thrombocytopenia and microangiopathic haemolysis. A diagnosis of haemolytic uraemic syndrome secondary to Shiga toxin-producing Escherichia coli 055 was confirmed and supportive therapy commenced in the intensive therapy unit. On day 11 of her admission, she rapidly deteriorated with evidence of refractory cardiogenic shock and neurological involvement, both features associated with a poor prognosis. Cross-specialty collaboration prompted a trial of veno-arterial extra-corporeal membrane oxygenation and Eculizumab, a complement inhibitor normally reserved for atypical haemolytic uraemic syndrome, as a bridge to organ recovery. To our knowledge, herein we present the first adult patient with haemolytic uraemic syndrome induced cardiogenic shock successfully supported to cardiac recovery with extra-corporeal membrane oxygenation. The potential role for Eculizumab in Shiga toxin-producing Escherichia coli/typical haemolytic uraemic syndrome is also discussed.

2016 ◽  
Vol 144 (15) ◽  
pp. 3305-3315 ◽  
Author(s):  
A. KUEHNE ◽  
M. BOUWKNEGT ◽  
A. HAVELAAR ◽  
A. GILSDORF ◽  
P. HOYER ◽  
...  

SUMMARYShiga toxin-producingEscherichia coli(STEC) is an important cause of gastroenteritis (GE) and haemolytic uraemic syndrome (HUS). Incidence of STEC illness is largely underestimated in notification data, particularly of serogroups other than O157 (‘non-O157’). Using HUS national notification data (2008–2012, excluding 2011), we modelled true annual incidence of STEC illness in Germany separately for O157 and non-O157 STEC, taking into account the groups’ different probabilities of causing bloody diarrhoea and HUS, and the resulting difference in their under-ascertainment. Uncertainty of input parameters was evaluated by stochastic Monte Carlo simulations. Median annual incidence (per 100 000 population) of STEC-associated HUS and STEC-GE was estimated at 0·11 [95% credible interval (CrI) 0·08-0·20], and 35 (95% CrI 12-145), respectively. German notification data underestimated STEC-associated HUS and STEC-GE incidences by factors of 1·8 and 32·3, respectively. Non-O157 STEC accounted for 81% of all STEC-GE, 51% of all bloody STEC-GE and 32% of all STEC-associated HUS cases. Non-O157 serogroups dominate incidence of STEC-GE and contribute significantly to STEC-associated HUS in Germany. This might apply to many other countries considering European surveillance data on HUS. Non-O157 STEC should be considered in parallel with STEC O157 when searching aetiology in patients with GE or HUS, and accounted for in modern surveillance systems.


2018 ◽  
Vol 138 (5) ◽  
pp. 279-281 ◽  
Author(s):  
MTR Pereboom ◽  
D Todkill ◽  
E Knapper ◽  
C Jenkins ◽  
J Hawker ◽  
...  

In June 2017, an outbreak of Shiga toxin–producing Escherichia coli (STEC) O157 infection with phage type 21/28 and identical genotypic profiles involving three children from Staffordshire was reported. Two cases developed haemolytic uraemic syndrome (HUS). Person-to-person transmission via a shared inflatable home paddling pool was the most likely route of infection, following contamination by the first case. The source of infection in the first case was not identified. We recommend that individuals experiencing gastroenteritis should not bathe in paddling pools and that water should be changed at frequent intervals throughout the day to minimise the spread of infection.


2020 ◽  
pp. 5027-5032
Author(s):  
Edwin K.S. Wong ◽  
David Kavanagh

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.


2019 ◽  
Vol 29 (5) ◽  
pp. 861-868 ◽  
Author(s):  
Douglas Hamilton ◽  
John Cullinan

Abstract Background Haemolytic Uraemic Syndrome (HUS) is a serious complication of Shiga toxin-producing Escherichia coli (STEC) infection and the key reason why intensive health protection against STEC is required. However, although many potential risk factors have been identified, accurate estimation of risk of HUS from STEC remains challenging. Therefore, we aimed to develop a practical composite score to promptly estimate the risk of developing HUS from STEC. Methods This was a retrospective cohort study where data for all confirmed STEC infections in Ireland during 2013–15 were subjected to statistical analysis with respect to predicting HUS. Multivariable logistic regression was used to develop a composite risk score, segregating risk of HUS into ‘very low risk’ (0–0.4%), ‘low risk’ (0.5–0.9%), ‘medium risk’ (1.0–4.4%), ‘high risk’ (4.5–9.9%) and ‘very high risk’ (10.0% and over). Results There were 1397 STEC notifications with complete information regarding HUS, of whom 5.1% developed HUS. Young age, vomiting, bloody diarrhoea, Shiga toxin 2, infection during April to November, and infection in Eastern and North-Eastern regions of Ireland, were all statistically significant independent predictors of HUS. Demonstration of a risk gradient provided internal validity to the risk score: 0.2% in the cohort with ‘very low risk’ (1/430), 1.1% with ‘low risk’ (2/182), 2.3% with ‘medium risk’ (8/345), 3.1% with ‘high risk’ (3/98) and 22.2% with ‘very high risk’ (43/194) scores, respectively, developed HUS. Conclusion We have developed a composite risk score which may be of practical value, once externally validated, in prompt estimation of risk of HUS from STEC infection.


2000 ◽  
Vol 124 (2) ◽  
pp. 215-220 ◽  
Author(s):  
B. DECLUDT ◽  
P. BOUVET ◽  
P. MARIANI-KURKDJIAN ◽  
F. GRIMONT ◽  
P. A. D. GRIMONT ◽  
...  

We conducted a study to determine the incidence of haemolytic uraemic syndrome (HUS) in children in France and to assess the role of Shiga-toxin-producing Escherichia coli (STEC) infection in the aetiology of HUS. In collaboration with the Société de Néphrologie Pédiatrique we undertook a retrospective review of all cases of HUS hospitalized from January 1993 to March 1995 and a 1-year prospective study (April 1995–March 1996) of epidemiological and microbiological features of cases of HUS. The polymerase chain reaction (PCR) procedure was used to detect stx, eae, e-hlyA genes directly from case stool samples. Serum samples from cases were examined for antibodies to lipopolysaccharide (LPS) of 26 major STEC serogroups. Two hundred and eighty-six cases were reported. The average incidence per year was 0·7/105 children < 15 years and 1·8/105 children < 5 years. During the prospective study, 122/130 cases were examined for evidence of STEC infection using PCR and/or serological assays and 105 (86%) had evidence of STEC infection. Serum antibodies to E. coli O157 LPS were detected in 79 (67%) cases tested. In conclusion, this study showed that STEC infection is an important cause of HUS in children in France, with a high proportion related to the O157 serogroup.


2012 ◽  
Vol 78 (12) ◽  
pp. 4065-4073 ◽  
Author(s):  
Maite Muniesa ◽  
Jens A. Hammerl ◽  
Stefan Hertwig ◽  
Bernd Appel ◽  
Harald Brüssow

ABSTRACTIn 2011, Germany experienced the largest outbreak with a Shiga toxin-producingEscherichia coli(STEC) strain ever recorded. A series of environmental and trace-back and trace-forward investigations linked sprout consumption with the disease, but fecal-oral transmission was also documented. The genome sequences of the pathogen revealed a clonal outbreak with enteroaggregativeE. coli(EAEC). Some EAEC virulence factors are carried on the virulence plasmid pAA. From an unknown source, the epidemic strains acquired a lambdoid prophage carrying the gene for the Shiga toxin. The resulting strains therefore possess two different mobile elements, a phage and a plasmid, contributing essential virulence genes. Shiga toxin is released by decaying bacteria in the gut, migrates through the intestinal barrier, and is transported via the blood to target organs, like the kidney. In a mouse model, probiotic bifidobacteria interfered with transport of the toxin through the gut mucosa. Researchers explored bacteriophages, bacteriocins, and low-molecular-weight inhibitors against STEC. Randomized controlled clinical trials of enterohemorrhagicE. coli(EHEC)-associated hemolytic uremic syndrome (HUS) patients found none of the interventions superior to supportive therapy alone. Antibodies against one subtype of Shiga toxin protected pigs against fatal neurological infection, while treatment with a toxin receptor decoy showed no effect in a clinical trial. Likewise, a monoclonal antibody directed against a complement protein led to mixed results. Plasma exchange and IgG immunoadsoprtion ameliorated the condition in small uncontrolled trials. The epidemic O104:H4 strains were resistant to all penicillins and cephalosporins but susceptible to carbapenems, which were recommended for treatment.


2005 ◽  
Vol 134 (4) ◽  
pp. 719-723 ◽  
Author(s):  
D. ORTH ◽  
K. GRIF ◽  
M. P. DIERICH ◽  
R. WÜRZNER

This study investigates a sorbitol-fermenting enterohaemorrhagic Escherichia coli (SF EHEC) O157 infection in a farmer's family in the Austrian province of Salzburg. The investigation commenced after a 10-month-old boy was admitted to hospital with the clinical diagnosis of a haemolytic–uraemic syndrome (HUS) and his stool specimen grew SF EHEC O157:H−. In a subsequent environmental survey, a stool specimen of the 2-year-old brother and faecal samples of two cattle from the family's farm were also found to be positive for SF EHEC O157:H−. All four isolates had indistinguishable phenotypic and molecular characteristics and were identical to the first strain detected in Bavaria in 1988. Despite identical isolates being demonstrated in Bavaria after 1988, and until this report, increased surveillance in neighbouring Austria had not found this organism. We propose that the strain may have recently spread from Bavaria to Austria. Although SF EHEC O157:H− strains are still rare, they may represent a considerable health threat as they can spread from farm animals to humans and between humans.


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