Cases Of Hemolytic Uremic Syndrome Research Articles

Combination of everolimus with calcineurin inhibitor medication resulted in post-transplant haemolytic uraemic syndrome in lung transplant recipients--a case series

Post-transplant haemolytic uraemic syndrome (HUS) is a rare but serious disease with a high mortality rate, when left untreated. Immunosuppressive drugs like calcineurin inhibitors as well as mammalian target of rapamycin inhibitors have been reported as causative agents for post-transplant HUS. A retrospective observational study was performed in lung transplant recipients, who took part in an interventional study, in two centres. Haemoglobin, platelets, creatinine and lactate dehydrogenase levels were monitored during routine follow-up and patients with deteriorating kidney function were screened for post-transplant HUS. All cases of post-transplant HUS were identified by clinical and laboratory findings. Outcome was recorded until 6 months after diagnosis. A total of 2188 visits in 512 lung transplant recipients (outpatients) were analysed. Out of those, 126 patients took part in an interventional study. In this study, 67 were switched to everolimus in combination with calcineurin inhibitors 4 weeks after transplantation, 59 patients remained on standard immunosuppression (calcineurin inhibitors, mycophenolate mofetil and prednisolone). Five cases of post-transplant HUS were identified in the everolimus group. None of the patients had evidence of gastrointestinal infection or preexisting renal disease. Post-transplant HUS was treated with therapeutic plasma exchange and methylprednisolone pulse therapy. Everolimus was discontinued in all five patients. This treatment regimen led to normalization of haemoglobin, platelets and improved renal function. Two patients developed end-stage renal failure and were maintained on haemodialysis. One patient died due to multiorgan failure. Improvement of renal function was seen in two patients. No further cases were recorded in patients without everolimus during the study period. Our data should raise the awareness of post-transplant HUS in lung transplant recipients. Post-transplant HUS is a rare disease, but it is a serious cause of acute renal failure in lung transplant recipients treated with a combination of everolimus and calcineurin inhibitors.

A case of atypical hemolytic uremic syndrome due to anti-factor H antibody in a patient presenting with a factor XII deficiency identified two novel mutations

A 9-year-old boy with pallor and macrohematuria showed hemolytic anemia, thrombocytopenia and renal failure. There was no history of diarrhea and the stool culture was negative. A diagnosis of atypical hemolytic uremic syndrome (HUS) was confirmed; however, the cause of the prolonged activated partial thromboplastin time (APTT) was unknown. Plasma exchange and hemodialysis were performed because of progressive hemolytic anemia and renal dysfunction. Fresh frozen plasma was administered frequently to correct the prolonged APTT after hemolysis was controlled and C3 levels had recovered. Factor H (FH) and factor I (IF) levels were normal and we did not detect mutations of FH, IF and membrane cofactor protein. Further investigation revealed the presence of anti-FH antibody in the patient's plasma and a deficiency of coagulation factor XII. Analysis of the patient's coagulation system displayed <3% functional activity of factor XII, whereas levels of other coagulation factors were within the normal range. Two novel mutations (W222G and R447S) were identified upon analysis of the factor XII gene in this patient. Moreover, further investigation revealed that compound heterozygous mutations were present in two of the patient's three siblings, while the third sibling only had a mutation at W222G. The patient was treated for atypical HUS; however, no treatment was required for factor XII deficiency as he did not display a hemorrhagic tendency. We report here a rare case of atypical HUS due to anti-FH antibody presenting with a coagulation factor XII deficiency.

Syndrome hémolytique et urémique au décours d’une infection materno-fœtale à Escherichia coli K1

Hemolytic uremic syndrome (HUS) is primarily a disease of infancy and early childhood. In its classic form, it is preceded by a prodrome of Escherichia coli-mediated bloody mucoid diarrhea. Typical HUS is commonly related to an infection by shiga-toxin producing E.coli. Stool cultures may detect this bacteria or its toxin, and PCRs can detect the shiga-toxin virulence genes. Atypical cases of HUS are mainly related to abnormalities of the alternative complement pathway and mutations of H, I, or B factors. Some atypical cases of HUS may also be related to von Willebrand factor or vitamin B12 metabolism abnormalities. A number of HUS cases related to invasive pneumococcal infections (pneumonia or meningitis) have been reported. We report a case of HUS associated with a bacterial E.coli K1 infection in a newborn baby, with a good clinical outcome: there was no need for dialysis and normal renal function was quickly regained. The workup did not favor a toxinic origin or an abnormality on the alternative complement pathway.

A case of hemolytic uremic syndrome preceded by intussusception

Hemolytic-uremic syndrome (HUS) is the most common cause of acute renal failure in young children. It is classically characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and uremia. Further, not only is intussusception one of the differential diagnoses of HUS but it may also become a complication during disease progression. We report a case of HUS preceded by intussusception in a previously healthy 17-month-old boy. The patient presented at the emergency department with bloody stools that developed the day after reduction of intussusception. HUS was diagnosed 4 days after the reduction of intussusception. The patient was provided only supportive care and his laboratory test findings were normal at discharge.

Hemolytic uremic syndrome associated with novel influenza A H1N1 infection

Sirs, During 2009, a pandemic influenza A H1N1 virus emerged end spread all over the world [1]. Renal involvement in influenza A virus infection is rare, but one case of hemolytic uremic syndrome (HUS) during season influenza has been reported [2]. We present a patient with novel A H1N1 virus complicated with HUS. A previously healthy 11-year-old boy was transferred to our Children’s Clinic with a history of fever, coughing, fatigue, jaundice, and oliguria. He had no diarrhea. On admission his temperature was over 38.5°C, and his blood pressure was 130/80 mmHg. He had no edema. Laboratory investigations revealed a sign of hemolysis (with declining hemoglobin to 6.5 g/l, and reticulocytosis) with thrombocytopenia (38,000 mm) and renal failure (serum creatinine 280 μmol/l, blood urea nitrogen 22 mmol/l). Blood smear showed fragmented and damaged erythrocytes. Serum chemistry showed a high level of total bilirubin (48 μmol/ l) and a very high level of lactate dehydrogenase (LDH 4,800 μ/l, normal range 250–480 μ/l). Alanine and aspartate transferases were slightly elevated. Urine analyses revealed 3+ proteinuria, 3+ hemoglobinuria, and erythrocyte casts. Prothrombin time and activated partial thromboplastin time were normal, D-dimer was elevated, and direct and indirect Coombs tests were negative. C3 and C4 were normal. A chest X-ray showed viral, interstitial pneumonia. Two other family members also started coughing and developed fever and fatigue. Based on the above findings the patient was diagnosed with HUS. On the day of admission he was treated with ceftriaxone 100 mg/kg per day and infusion of low doses of dopamine and furosemide. On his second day in hospital we decided to start plasma therapy, which may be recommended in nondiarrheal/nonpneumococcal HUS. However, a few hours after the first doses of fresh-frozen plasma he showed aggravated hemolytic anemia (hemoglobin level decreased to 5 g/l, LDH severely increased). We stopped plasma infusion, and continued with fluid and diuretics. In the meantime we received his respiratory spacemen test, which was positive for novel influenza A H1N1 by real-time reverse transcriptase PCR. Oseltamivir (75 mg every 12 h) was started, and continued for 6 days. Symptoms subsided in the next few days. He gradually recovered, lost the fever, his urine output increased with improving renal function, and his blood count too. He was discharged after 15 days with serum creatinine 77 μmol/l, normal levels of LDH, and hemoglobin 10 g/l. Usually, influenza A H1N1 turns out to be a benign disease. The association of pneumococcal infection with the current and previous influenza pandemics is well known. Pneumococcal HUS is an uncommon condition, with reports of this complication in patients with invasive infections, but also in one patient during influenza A and pneumococcal coinfection [3, 4]. We did not confirm bacterial super infection in throat swab, sputum and blood culture in our patient. It is E. Golubovic (*) : P. Miljkovic Department of Pediatric Nephrology, Children’s Clinic, University of Nis, Zorana Djindjica 48, 18000 Nis, Serbia e-mail: ema.golubovic@gmail.com

Hemolytic Uremic Syndrome After an Escherichia coli O111 Outbreak

In August 2008, the largest known US serotype 1 Escherichia coli O111 outbreak occurred in Oklahoma, causing 341 illnesses, including hemolytic uremic syndrome (HUS). HUS is not well described in non-O157 E coli outbreaks but occurs in 2% to 15% of O157 infections, predominantly among children. We examined outbreak-related hospitalizations to characterize E coli O111 illness, the HUS attack rate, and factors associated with subsequent HUS diagnosis among hospitalized patients. Medical records were reviewed for clinical presentation and evidence of HUS among hospitalized patients identified during the outbreak investigation. Characteristics of hospitalized patients with vs without HUS were compared. HUS was identified in 26 of 156 (16.7%) confirmed or probable E coli O111 infections; 65.4% of patients with HUS required dialysis, and 1 patient died. The median age of patients with HUS was 43.5 years (age range, 1-88 years); adults composed 57.7% of HUS cases. Characteristics at hospital admission associated with subsequent HUS diagnosis included white blood cell count of at least 20000/μL (adjusted odds ratio [aOR], 11.3; 95% confidence interval [CI], 1.7-75.3), elevated serum creatinine level for age (9.7; 1.4-69.2), and vomiting before hospital admission (6.8; 1.5-31.3). Administration of antimicrobial agents (risk ratio [RR], 1.0; 95% CI, 0.5-1.8) or medication with antimotility effects (1.4; 0.6-2.9) was not associated with subsequent HUS. The HUS attack rate in this E coli O111 outbreak was comparable to that for E coli O157-related illnesses, but most cases occurred among adults. On admission, factors associated with subsequent HUS can identify patients who require close monitoring and early aggressive supportive care to improve outcomes.

Dangerous drug interactions leading to hemolytic uremic syndrome following lung transplantation

BackgroundTo report our experience of a rather uncommon drug interaction, resulting in hemolytic uremic syndrome (HUS).MethodsTwo consecutive cases of hemolytic uremic syndrome were diagnosed in our service. In both patients the use of macrolides in patients taking Tacrolimus, resulted in high levels of Tacrolimus.ResultsThe first patient was a 48 years old female with Bilateral emphysema. She underwent Single Sequential Lung Transplantation. She developed reperfusion injury requiring prolonged stay. Tacrolimus introduced (Day 51). The patient remained well up till 5 months later; Erythromycin commenced for chest infection. High Tacrolimus levels and a clinical diagnosis of HUS were made. She was treated with plasmapheresis successfully.The second case was a 57 years old female with Emphysema & A1 Antithrypsin deficiency. She underwent Right Single Lung Transplantation. A2 rejection with mild Obliterative Bronchiolitis diagnosed 1 year later and she switched to Tacrolimus. She was admitted to her local Hospital two and a half years later with right middle lobe consolidation. The patient commenced on amoxicillin and clarithromycin. Worsening renal indices, high Tacrolimus levels, hemolytic anemia & low Platelets were detected. HUS diagnosed & treated with plasmapheresis.ConclusionsThere are 21 cases of HUS following lung transplantation in the literature that may have been induced by high tacrolimus levels. Macrolides in patients taking Cyclosporin or Tacrolimus lead to high levels. Mechanism of action could be glomeruloconstrictor effect with reduced GFR increased production of Endothelin-1 and increased Platelet aggregation.

Hemolytic Uremic Syndrome Caused by Shiga Toxin–Producing Escherichia coli 0111

Shiga toxin-producing Escherichia coli (STEC) was first discovered in 1977 and since has caused serious complications including the life-threatening condition of hemolytic uremic syndrome (HUS). While HUS is most common in children, adults and especially elderly patients experience a higher incidence of death and disability. Because the majority of HUS cases have been described in children, pediatric treatment options have been used to treat adult and elderly patients with HUS. More research regarding the treatment, risk factors, and prognosis of HUS in adults needs to be performed to ensure that optimal care is provided. The authors present a case series of 5 adults with HUS who were part of the largest outbreak of E coli 0111 reported in the United States. To date, there are no published cases of HUS secondary to E coli 0111 in adults. The authors also include a literature review of HUS secondary to STEC.

Genetics and Genetic Testing in Hemolytic Uremic Syndrome/Thrombotic Thrombocytopenic Purpura

The hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are rare diseases that manifest with thrombocytopenia and microangiopathic hemolytic anemia accompanied by renal and neurologic dysfunction. Most childhood cases of HUS are caused by Shiga-toxin-producing bacteria and have a good prognosis. The other form, atypical HUS (aHUS), accounts for 10% of cases. Prognosis of aHUS and TTP has changed over time from fatal disorders to 60% to 80% survival in the plasma therapy era. In the past 10 years the molecular bases of aHUS and TTP have been discovered that mostly lead to uncontrolled activation of the complement system in aHUS and to abnormal von Willebrand factor processing in TTP. Identification of the underlying abnormality in an individual patient can provide prognostically significant information in predicting long-term outcome, response to therapies, and transplant outcome. It also paves the way for the use of specific new therapies in the near future.

Sorbitol-fermentingEscherichia coliO157, Scotland

To the Editor: Verotoxin-producing Escherichia coli (VTEC) of serogroup O157 causes severe gastrointestinal and renal illness; clinical signs may be mild diarrhea, hemorrhagic colitis, or hemolytic uremic syndrome (HUS). Typically, 10%–15% of reported VTEC infections quickly progress to HUS (1). Sorbitol-fermenting (SF)–O157 strains have emerged in continental Europe (2,3). Some evidence suggests that SF-O157 is more frequently associated with HUS than are non-sorbitol–fermenting strains (3–6). SF-O157 shows increased adherence to colonic epithelial cells and may in turn cause a more potent inflammatory host response, resulting in a higher risk for HUS (4). The potentially greater virulence of SF-O157 requires urgent identification of its reservoir(s) and vehicle(s) of infection, as well as determination of genetic or other predisposing factors for infection with this strain. To understand whether the host pathophysiologic responses to SF-O157 and non–SF-O157 strains differ, we analyzed a cohort of children with HUS who were infected with E. coli O157. During April and May 2006, Health Protection Scotland (HPS) identified 18 cases of verotoxin-producing SF-O157 infection in Scotland, 13 of which were associated with a nursery. HUS developed in 8 of the 18 patients; those with thrombotic microangiopathy were admitted to the renal unit of a specialist pediatric hospital, which immediately reports cases of HUS to HPS as part of national surveillance (7). To test the hypothesis that SF-O157 was more virulent than non–SF-O157, we performed an age-matched, nested case–case study of HUS case-patients and analyzed host clinical markers, treatment, and outcomes from SF-O157 and non–SF-O157 cases in 2006. Clinical questionnaires, patient information sheets, and consent forms were completed by clinicians for each case-patient and returned to HPS; data were entered into a database in Epi Info version 6 (Centers for Disease Control and Prevention, Atlanta, GA, USA). Statistical analysis by t test showed that nadirs for serum albumin were significantly higher for children with SF-O157 HUS (p = 0.03; Table) than for children with non–SF-O157 HUS and that children with SF-O157 HUS had significantly more sessions of hemodialysis than did children with non–SF-O157 HUS (p = 0.01; Table). All case-patients were oligoanuric; the 2 groups did not differ with respect to this parameter. Initial signs and symptoms were similar for both sets of patients, i.e., classic VTEC symptoms of bloody diarrhea and abdominal pain. This finding is in acccordance with those of other studies of SF-O157 outbreaks, which also noted signs and symptoms compatible with VTEC-associated gastroenteritis (5,6). Table Characteristics of patients infected with non–SF-O157 versus SF-O157 Escherichia coli, Scotland, 2006* Our study highlights a number of lessons. Medical practitioners rarely have the opportunity to recognize patients at such an appreciable and predictable risk of progressing rapidly to anuric renal failure as they do when they see children with early O157 infection. Failure to appreciate the potential gravity of O157 infection and the possible development of HUS may result in avoidable illness and even death. Our investigation of the prehospital management of SF-O157 and non–SF-O157 in this cohort found no difference in pharmacologic intervention or duration of delay in admission to hospital. Our study has limitations. A number of patients in the cohort were prescribed antimicrobial drugs and/or antimotility drugs or were sent home from the local hospital without hospital admission or further monitoring; such actions potentially exacerbate clinical outcomes (1,8). We recognize that comparison of the SF-O157 outbreak strain with non–SF-O157 strains (some of which caused sporadic cases) may be a potential confounding factor in the analysis. However, recently published work has indicated no statistically significant differences in the verotoxin proteins encoded by SF-O157 or non–SF-O157 strains or in their level of toxicity (9). Other virulence factors may contribute to increased likelihood of HUS (4). Our data suggest that infection with SF-O157 results in less severe colitis than does the more common non–SF-O157 infection. Less severe colitis could result in a lower risk for renal disease because less verotoxin would be translocated into the bloodstream and bound to the kidneys. However, patients infected with SF-O157 had anuria for longer periods and consequently had longer sessions of peritoneal and hemodialysis. Although unknown bacterial or host inflammatory cytokines may contribute to enhanced disease progression, this observation is surprising and requires further investigation. Additional research is needed to learn more about the virulence of SF-O157 strains and establish other host factors that contribute to disease progression.

Increased adherence and expression of virulence genes in a lineage of Escherichia coli O157:H7 commonly associated with human infections.

BackgroundEnterohemorrhagic Escherichia coli (EHEC) O157:H7, a food and waterborne pathogen, can be classified into nine phylogenetically distinct lineages, as determined by single nucleotide polymorphism genotyping. One lineage (clade 8) was found to be associated with hemolytic uremic syndrome (HUS), which can lead to kidney failure and death in some cases, particularly young children. Another lineage (clade 2) differs considerably in gene content and is phylogenetically distinct from clade 8, but caused significantly fewer cases of HUS in a prior study. Little is known, however, about how these two lineages vary with regard to phenotypic traits important for disease pathogenesis and in the expression of shared virulence genes.Methodology/Principal FindingsHere, we quantified the level of adherence to and invasion of MAC-T bovine epithelial cells, and examined the transcriptomes of 24 EHEC O157:H7 strains with varying Shiga toxin profiles from two common lineages. Adherence to epithelial cells was >2-fold higher for EHEC O157:H7 strains belonging to clade 8 versus clade 2, while no difference in invasiveness was observed between the two lineages. Whole-genome 70-mer oligo microarrays, which probe for 6088 genes from O157:H7 Sakai, O157:H7 EDL 933, pO157, and K12 MG1655, detected significant differential expression between clades in 604 genes following co-incubation with epithelial cells for 30 min; 186 of the 604 genes had a >1.5 fold change difference. Relative to clade 2, clade 8 strains showed upregulation of major virulence genes, including 29 of the 41 locus of enterocyte effacement (LEE) pathogenicity island genes, which are critical for adherence, as well as Shiga toxin genes and pO157 plasmid-encoded virulence genes. Differences in expression of 16 genes that encode colonization factors, toxins, and regulators were confirmed by qRT-PCR, which revealed a greater magnitude of change than microarrays.Conclusions/SignificanceThese findings demonstrate that the EHEC O157:H7 lineage associated with HUS expresses higher levels of virulence genes and has an enhanced ability to attach to epithelial cells relative to another common lineage.

Shiga Toxin 2–Specific but Not Shiga Toxin 1–Specific Human Monoclonal Antibody Protects Piglets Challenged with EnterohemorrhagicEscherichia coliProducing Shiga Toxin 1 and Shiga Toxin 2

Escherichia coli strains that produce Shiga toxin 2 (Stx2) are isolated from hemolytic-uremic syndrome (HUS) cases more frequently than are strains that produce both Shiga toxin 1 (Stx1) and Stx2, whereas strains that produce only Stx1 are rarely isolated from HUS cases. Studies have implicated Stx2 as the sole contributor to acute kidney failure and other systemic complications in humans. The aim of the present study was to determine whether Stx2-specific antibody would be as effective against Shiga toxin-producing Escherichia coli (STEC) strains that produce both Stx1 and Stx2 as it is against strains that produce only Stx2, compared with Stx1-specific antibody. We found that Stx2-specific and Stx1-specific antibodies protected 100% and 0% of piglets, respectively, against oral challenge with a Stx1- and Stx2-producing STEC strain. We conclude that Stx2-specific antibody is sufficient to protect piglets, and possibly humans, against STEC strains that produce both toxins.

Prevalence, Characterization, and Genotypic Analysis of Escherichia coli O157:H7/NM fromSelected Beef Exporting Abattoirs of Argentina

In Argentina, Escherichia coli O157:H7/NM (STEC O157) is the prevalent serotype associated with hemolytic uremic syndrome (HUS), which is endemic in the country with more than 400 cases per year. In order to estimate the prevalence and characteristics of STEC O157 in beef cattle at slaughter, a survey of 1,622 fecal and carcass samples was conducted in nine beef exporting abattoirs from November 2006 to April 2008. A total of 54 samples were found positive for STEC O157, with an average prevalence of 4.1% in fecal content and 2.6% in carcasses. Calves and heifers presented higher percentages of prevalence in feces, 10.5 and 8.5%, respectively. All STEC O157 isolates harbored stx(2) (Shiga toxin 2), eae (intimin), ehxA (enterohemolysin), and fliC(H7) (H7 flagellin) genes, while stx(1) (Shiga toxin 1) was present in 16.7% of the strains. The prevalent (56%) stx genotype identified was stx(2) combined with variant stx(2c (vh-a)), the combination of which is also prevalent (>90%) in STEC O157 post-enteric HUS cases in Argentina. The clonal relatedness of STEC O157 strains was established by phage typing and pulsed-field gel electrophoresis (PFGE). The 54 STEC isolates were categorized into 12 different phage types and in 29 XbaI-PFGE patterns distributed in 27 different lots. STEC O157 strains isolated from 5 of 21 carcasses were identical by PFGE (100% similarity) to strains of the fecal content of the same or a contiguous bovine in the lot. Five phage type-PFGE-stx profiles of 10 strains isolated in this study matched with the profiles of the strains recovered from 18 of 122 HUS cases that occurred in the same period.

Síndrome hemolítico-urémico: afectación renal a largo plazo

Introduction Hemolytic uremic syndrome (HUS) is the most frequent cause of non-pre-renal acute renal failure in pediatrics and it is usually secondary to acute infectious diarrhea, generally due to Shiga-toxin producing E. coli. It is characterized by acute renal failure, hemolytic anemia and thrombocytopenia. It can lead to renal sequels in the long term and to end-stage renal disease. Methods The aim of this retrospective study is to describe and analyze renal sequels and their prognostic factors in pediatric patients suffering from HUS in a Spanish tertiary hospital during the last 28 years. Results 43 children with this condition were admitted, with 38 of them having presented with diarrhea previously. Among those with a follow-up longer than 3 months, 21.6% (8/37) had a reduction in glomerular filtration rate (GFR) in the last visit. Including proteinuria and hypertension, we found up to 35.1% (13/37) prevalence of chronic kidney disease, with 8.1% (3/37) of the patients with end-stage renal disease. We found the following to be prognostic factors for renal injury in the long term in a univariate logistic regression: hypertension, a longer stay in the hospital, more prolonged anuria, more severe leukocytosis and lower GFR at discharge. Multivariate logistic regression showed an association with time in anuria. Conclusions Approximately one third of our cases of hemolytic uremic syndrome developed some degree of chronic kidney disease in the long term. A deeper and longer initial renal disfunction is associated with a higher probability of subsequent renal problems.

Set of virulence genes and genetic relatedness of O113 : H21 Escherichia coli strains isolated from the animal reservoir and human infections in Brazil

Escherichia coli strains of serotype O113 : H21 are commonly described as belonging to a Shiga toxin (Stx)-producing E. coli (STEC) pathotype worldwide. Albeit this STEC serotype is frequently identified among cattle and other domestic animals, to the best of our knowledge no human infections associated with STEC O113:H21 have been registered in Brazil to date. Here, we report the virulence profile and genetic relatedness of a collection of O113:H21 E. coli strains mainly isolated from the animal reservoir aimed at determining their potential as human pathogens. The strains from the animal reservoir (n=34) were all classified as STEC, whereas the few isolates recovered so far from human diarrhoea (n=3) lacked stx genes. Among the STEC, the stx2d-activatable gene was identified in 85% of the strains that also carried lpfAO113, iha, saa, ehxA, subAB, astA, cdt-V, espP, espI and epeA; the human strains harboured only lpfAO113, iha and astA. All the strains except one, isolated from cattle, were genetically classified as phylogenetic group B1. High mass plasmids were observed in 25 isolates, but only in the STEC group were these plasmids confirmed as the STEC O113 megaplasmid (pO113). Many closely related subgroups (more than 80% similarity) were identified by PFGE, with human isolates clustering in a subgroup separate from most of the animal isolates. In conclusion, potentially pathogenic O113:H21 STEC isolates carrying virulence markers in common with O113:H21 clones associated with haemolytic uraemic syndrome cases in other regions were demonstrated to occur in the natural reservoir in our settings, and therefore the risk represented by them to public health should be carefully monitored.

A case of hemolytic uremic syndrome after adjuvant chemotherapy with gemcitabine in a patient with pancreatic cancer

A case of hemolytic uremic syndrome after adjuvant chemotherapy with gemcitabine in a patient with pancreatic cancer

Hemolytic Uremic Syndrome and Death in Persons withEscherichia coliO157:H7 Infection, Foodborne Diseases Active Surveillance Network Sites, 2000–2006

Hemolytic uremic syndrome (HUS) is a life-threatening illness usually caused by infection with Shiga toxin-producing Escherichia coli O157 (STEC O157). We evaluated the age-specific rate of HUS and death among persons with STEC O157 infection and the risk factors associated with developing HUS. STEC O157 infections and HUS cases were reported from 8 sites participating in the Foodborne Diseases Active Surveillance Network during 2000-2006. For each case of STEC O157 infection and HUS, demographic and clinical outcomes were reported. The proportion of STEC O157 infections resulting in HUS was determined. A total of 3464 STEC O157 infections were ascertained; 218 persons (6.3%) developed HUS. The highest proportion of HUS cases (15.3%) occurred among children aged <5 years. Death occurred in 0.6% of all patients with STEC O157 infection and in 4.6% of those with HUS. With or without HUS, persons aged 60 years had the highest rate of death due to STEC O157 infection. Twelve (3.1%) of 390 persons aged 60 years died, including 5 (33.3%) of 15 persons with HUS and 7 (1.9%) of 375 without. Among children aged <5 years, death occurred in 4 (3.0%) of those with HUS and 2 (0.3%) of those without. Young children and females had an increased risk of HUS after STEC O157 infection. With or without HUS, elderly persons had the highest proportion of deaths associated with STEC O157 infection. These data support recommendations for aggressive supportive care of young children and the elderly early during illness due to STEC O157.

Genetic diversity of O157:H7 and non-O157 verocytotoxigenic Escherichia coli from Argentina inferred from multiple-locus variable-number tandem repeat analysis (MLVA)

Although serotype O157:H7 has been implicated in most cases of haemolytic-uraemic syndrome (HUS), there is growing concern about non-O157 serotypes of verocytotoxigenic Escherichia coli (VTEC). Multiple-locus variable-number tandem repeat analysis (MLVA) has been focused on the specific typing of O157:H7 isolates, but recently, a generic MLVA assay for E. coli and Shigella has been developed. We performed a study of the polymorphism in 7 generic VNTR loci both in VTEC O157:H7 and non-O157 isolates from Argentina, in order to asses the ability of the method to type this group of isolates and to get insight into their genetic diversity. Sixty-four isolates from cattle, patients with diarrhoea, and contaminated food belonging to 8 different serotypes were studied. All of them could be typed by this method and revealed 41 different MLVA genotypes. The MLVA dendrogram showed 2 main clusters which corresponded to O157:H7 and non-O157, respectively. Our results confirm the suitability of this MLVA method for analyzing VTEC isolates belonging to several serotypes, both O157:H7 as well as non-O157, highlight the genetic variability of the O157:H7 serotype and the need of additonal research in order to find more VNTR loci that could allow a higher discrimination among non-O157 VTEC.

Hemolytic uremic syndrome (HUS)—incidence and etiologies at a regional Children’s Hospital in 2001–2006

Hemolytic uremic syndrome (HUS) is a serious health concern in children. HUS has primarily been linked to Escherichia coli O157:H7 infections, but non-O157 strains are gaining attention. Hemolytic anemia, thrombocytopenia, and acute renal failure are the characteristics of the syndrome. This study investigated the incidence of HUS at a regional Children's Hospital between 2001 and 2006 by retrospective review. Cases of HUS were investigated for outcomes based on stool culture and an association of acute pancreatitis. A total of 44 cases were identified, of which 57% were female and 43% were male, with an age distribution of 13 months to 17 years and a median age of 3.44 years. Data revealed 13 cases in 2006 compared to two cases in 2001, with 84% of all illnesses occurring in the summer and fall seasons. The median duration of thrombocytopenia was eight days and 50% of all cases required dialysis. E. coli O157:H7 was the predominant pathogen; however, 53% of the cases had unknown etiology. This data may suggest a growing number of cases from 2001 to 2006 and a role for agents other than E. coli O157:H7. E. coli O157:H7 caused longer intensive care unit (ICU) stay. No association between HUS and acute pancreatitis was found.

Pneumococcal empyema and haemolytic uraemic syndrome in children: experience from a UK tertiary respiratory centre

The incidence of childhood empyema and pneumococcus-associated haemolytic uraemic syndrome (P-HUS) is increasing. Streptococcus pneumoniae is the most common pathogen causing childhood empyema and the association with invasive streptococcal infections...