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[Neurologic presentation in haemolytic-uraemic

syndrome]

[Article in Spanish]

Roche-Martnez A,Po P, Maristany-Cucurella M, Jimnez-Llort A,Camacho JA,Campistol J.

Servicio de Neurologa, Hospital Sant Joan de Deu, 08950 Esplugues de

Llobregat, Espaa. [email protected]

INTRODUCTION: Haemolytic-uraemic syndrome (HUS) is characterized bymicroangiopathic hemolytic anaemia, thrombopenia and multiorganic aggression,specially renal, gastrointestinal and central nervous system disturbances. Sporadic

in Spain (2/1,500,000 inhabitants), its clinical onset includes acute renal failure,

hypertension and central nervous system symptoms (irritability, drowsiness,convulsions, cortical blindness, hemiparesia or coma), due to metabolic distress,

hypertension or central nervous system microangiopathy. Few long-term outcome

studies have been published. PATIENTS AND METHODS: A retrospective

analysis of a series of 58 patients with HUS between 1981 and 2006, is reported. Clinical onset,laboratory, electrophysiology, neuroimaging tests, and prognosis factors are reviewed, together with long-term clinical

outcome. RESULTS: 22 children presented neurologic symptoms, seven had some

neurological test; one patient died; in five some neurological sequelae persisted

(hemiparesia, cognitive deficit, visual-perception deficit), the other 16 remainingasymptomatic. CONCLUSIONS: Neurological morbility is high in HUS (27% of

the children with neurological symptoms), with a 1.7% mortality. Seizure at onset

was not a poor prognosis factor in our group. No positive correlation can beestablished between neuroimaging and long-term outcome.

.

Kathmandu Univ Med J (KUMJ).2007 Oct-Dec;5(4):468-74. Links

Clinico-laboratory profile of haemolytic uremicsyndrome.

Jha DK, Singh R, Raja S, Kumari N,Das BK.

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Department of Pediatrics and Adolescent Medicine, B P Koirala Institute of

Health Sciences, Dharan, Nepal.

Objective: To study the clinical profile, the spectrum of functional abnormalities, prognostic factors and outcome of

children with haemolytic uremic syndrome (HUS). Materials and methods: This is a prospective, descriptive, single centre,

cohort study, conducted on 42 children during the period of January 2004 to January 2005. Results: The maximumnumbers of cases were below 24 months of age with mean age of 26.6 months and male: female ratio of 2.8:1. Most of the

cases (79%) occurred in the warmer months (April-September).The common clinical presentationswere bloody diarrhoea, pallor, oliguria & anuria, fever, vomiting, abdominaldistension and pain, involvement of central nervous system, chest andcardiovascular system and bleeding manifestations. The commonhaematological abnormalities were leucocytosis, thrombocytopenia, anaemiaand features of haemolysis in the peripheral blood. Electrolyte abnormalitiesobserved were in the form of hyponatremia, hypokalemia and hyperkalemia.Arterial blood gas analysis showed metabolic acidosis in 64% cases, wherethe estimations were done. The mean blood urea and serum creatinine levelswere 113.7 mg/dL and 2.5 mg/dL, respectively. Stool examination showedblood in all cases. Urine examination showed microscopic haematuria and

significant proteinuria in 74% and 38% cases, respectively. E. coli andShigella were isolated in stool in three cases each and one case showed mixedgrowth of E. coli and Salmonella. The mortality rate was 21%. Significantlyhigher mortality was observed in females, patients presenting with completeanuria, leucocytosis, hyperkalemia and systemic involvement like centralnervous system, cardio vascular system and chest. Conclusions: Female sex,complete anuria, leucocytosis, extra renal involvement and hyperkalemiawere associated with poor outcome. Key words: Haemolytic UremicSyndrome, Clinical Features, Outcome, Prognostic Factors.

77: Kathmandu Univ Med J (KUMJ).2004 Oct-Dec;2(4):291-6. Links

Prognostic indicators in haemolytic uraemicsyndrome.

Malla K,Malla T,Hanif M.

Kathmandu Medical College, Sinamangal. [email protected]

OBJECTIVE: This study aims to review the clinical presentations of Haemolytic Uraemic Syndrome (HUS) and to

compare the poor prognostic indicators with mortality. METHODS AND MATERIALS: Prospective study carried out inRenal Dialysis ward of Dhaka Shishu Hospital, Bangladesh from September 2001 November 2003 for a period of 26

months. All children admitted to renal dialysis ward with oliguria or anuria with pallor was included in this study. HUS was

confirmed after laboratory investigations showing features of hemolytic anaemia, thrombocytopenia and renalinsufficiency. Various clinical presentations were reviewed. Then bad prognostic factors were compared with mortality.

RESULTS: There were total 25 cases of HUS in 26 months.17 (68%) were males and 8(32%) females.21 (84%) children

were < 5 years. Only 4(16%) were > 5 years. Before onset of HUS 40% children had bloody diarrhoea, 36% had acute

watery diarrhoea and 24% had others symptoms. The other presentations noted were fever 88%, respiratory distress and

convulsion 52% and oliguria 40%, anuria 60%, reluctant to feed 40% and cough 28%. The main physical findings notedwere irritability 40%, pallor 100%, dehydration 28%, puffy face with oedema 32%, high blood pressure 16%,

hepatomegaly 28%, jaundice, sclerema and petechial rashes 8%, lethargic 16%, acidotic breathing 48% and rectal prolapse

12%. 44% children died after HUS and 56% recovered from the illness. Mortality was 66% when duration of illness before

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onset of HUS was > 14 days. With duration of anuria < 3 days there was no mortality but it was 91% and 100% with anuria

> 3 to 8 days and >8 days respectively. Mortality was 78% when age was < 18 months and it was 75% when age was > 5

years. Diarrhoea associated HUS had 27% and non diarrhoea associated HUS had 85% mortality. Mortality was 77% and

100% respectively when HUS was associated with convulsion and hypertension. WBC > 30,000 had mortality 100% and

decreased platelet count < 30,000 had mortality 80%. With creatinine level > 700 micromol/L mortality was 80% and with

Serum potassium level 5.6 to 7.5 mmol/L mortality was 67%. CONCLUSION: HUS comprised of

varieties of presentations. Diarrhoea was the commonest preceding illness before

onset of HUS. The bad prognostic indicators carrying high mortality was durationof illness before onset of HUS >14 days, anuria > 3 days, age < 18 months and >5

years, Non diarrhoea associated HUS, HUS associated with convulsion and

hypertension, WBC > 30,000/cumm, platelets < 30,000/cumm, creatinine level >700 micromol/L and serum potassium level 5.6 to 7.5 mmol/L. Since bad

prognostic factors may progress rapidly to mortality, consultation with

paediatrician and transfer to a tertiary care centre should be done when HUS isdiagnosed so that it can be managed appropriately in time.

AETIOLOGY

Pathogenesis

28: Annu Rev Pathol. 2008;3:249-77. Links

Pathogenesis of thrombotic microangiopathies.

Zheng XL,Sadler JE.

Department of Pathology and Laboratory Medicine, The Children's Hospital of Philadelphia and The University ofPennsylvania School of Medicine, Philadelphia, PA 19104, USA. [email protected]

Profound thrombocytopenia and microangiopathic hemolytic anemiacharacterize thrombotic microangiopathy, which includes two majordisorders: thrombotic thrombocytopenic purpura (TTP) and hemolyticuremic syndrome (HUS). TTP has at least three types: congenital or familial,idiopathic, and nonidiopathic. The congenital and idiopathic TTP syndromesare caused primarily by deficiency of ADAMTS13, owing to mutations in theADAMTS13 gene or autoantibodies that inhibit ADAMTS13 activity. HUS issimilar to TTP, but is associated with acute renal failure. Diarrhea-associatedHUS accounts for more than 90% of cases and is usually caused by infectionwith Shiga-toxin-producing Escherichia coli (O157:H7). Diarrhea-negativeHUS is associated with complement dysregulation in up to 50% of cases,caused by mutations in complement factor H, membrane cofactor protein,factor I or factor B, or by autoantibodies against factor H. The incompletepenetrance of mutations in either ADAMTS13 or complement regulatory

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genes suggests that precipitating events or triggers may be required to causethrombotic microangiopathy in many patients.

93: Thromb Haemost.2005 Aug;94(2):312-8. Links

Consequences of enterohaemorrhagic Escherichiacoli infection for the vascular endothelium.

Bielaszewska M, Karch H.

Institute for Hygiene and National Consulting Laboratory on Haemolytic UraemicSyndrome, University Hospital Mnster, Germany.

Microvascular endothelial damage underlies the pathological changes inhaemorrhagic colitis and the haemolytic uraemic syndrome (HUS) caused by

enterohaemorrhagic Escherichia coli (EHEC). Shiga toxins (Stxs) are presentlythe best characterised EHEC virulence factors that can cause the microvascular

endothelium injury. Stxs are released by EHEC in the intestine, absorbed across

the gut epithelium into the circulation, and transported to small vessel endothelialcells. Then, they presumably injure the host cell by inhibiting protein synthesis,

stimulating prothrombotic messages, or inducing apoptosis. The net result is a

multi-organ thrombotic process. Moreover, Stxs stimulate a variety of non-endothelial cells to produce and secrete inflammatory mediators (cytokines,

chemokines, adhesion molecules) which could potentiate the effects of Stxs on

endothelial cells. The association of HUS with Stx-negative E. coli strainsstimulated intensive research on putative non-Stx virulence factors, which mightalso contribute to the pathogenesis of HUS and haemorrhagic colitis. Based on

current data, cytolethal distending toxin, EHEC haemolysin, and subtilase

cytotoxin might be such candidates.

111: J Thromb Haemost. 2005 Apr;3(4):752-62. Links

Shiga toxin enhances functional tissue factor on

human glomerular endothelial cells: implicationsfor the pathophysiology of hemolytic uremicsyndrome.

Nestoridi E,Tsukurov O,Kushak RI, Ingelfinger JR, Grabowski EF.

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Cardiovascular Thrombosis Laboratory, MassGeneral Hospital for Children,

Harvard Medical School, Boston, MA, USA.

BACKGROUND: The pathogenesis of Shiga toxin (Stx)-mediated childhoodhemolytic uremic syndrome (HUS) is not fully delineated, although current

evidence implicates a prothrombotic state. We hypothesized that the tissuefactor (TF) pathway plays a major role in the pathophysiology of HUS.MATERIALS AND METHODS: We measured cell surface TF activity in response to tumor necrosis factor-alpha (TNF-

alpha) (20 ng mL(-1), 2-144 h), Stx-1 (10(-11) mol L(-1), 4-144 h), or their combination (TNF-alpha 22 h and Stx-1 for thelast 0.5-4 h of TNF-alpha incubation) on human glomerular (microvascular) endothelial cells (HGECs) and human

umbilical vein (macrovascular) endothelial cells (HUVECs). RESULTS AND CONCLUSIONS: Weobserved that while TNF-alpha caused an increase in cell surface TF activityon both cell types, the combination of TNF-alpha and Stx-1 differentiallyaffected HGECs. On these cells, TF activity was increased further by 2.67 +/-0.38-fold (n = 38, P < 0.001), consistent with our parallel observation that Stx-1 binds to HGECs but not to HUVECs. Anti-TF antibody abolishedfunctional TF while anti-tissue factor pathway inhibitor antibody enhanced

TF activity. Stx-1 alone did not induce TF activity on either cell type.Measurement of TF antigen levels and quantitative real-time polymerasechain reaction demonstrated that exposure to TNF-alpha markedly increasedTF protein and TF mRNA for HGECs, but the exposure to the combinationof TNF-alpha and Stx-1 did not increase further the amount of either TFprotein or TF mRNA. We conclude that cytokine-activated HGECs, but notHUVECs, undergo a significant augmentation of cell surface TF activityfollowing exposure to Stx, suggesting an important role for TF in thecoagulopathy observed in HUS.

213: Semin Thromb Hemost. 2002 Apr;28(2):167-72. Links

Assays of von Willebrand factor-cleaving protease:a test for diagnosis of familial and acquiredthrombotic thrombocytopenic purpura.

Furlan M, Lmmle B.

Central Hematology Laboratory, University Hospital, Inselspital, Bern,

Switzerland.

Endothelial cells secrete von Willebrand factor (vWF) multimers that arelarger than those found in the circulating plasma. These very largemultimeric forms of vWF, capable of spontaneously binding to andagglutinating the blood platelets under conditions of high fluid shear rate,are degraded by a specific metalloprotease cleaving the peptide bond 842Tyr-843Met of the vWF subunit. The vWF-cleaving protease was found to be

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deficient in patients with familial thrombotic thrombocytopenic purpura(TTP). The acute events in these patients can be successfully treated and prophylactically prevented by repletion of themissing protease using fresh frozen plasma (FFP). In another, apparently more common, form of TTP, the protease

deficiency is due to inhibiting circulating antibodies directed against the vWF-cleaving protease. Therapy of these patients

should include immunosuppressive treatment in addition to plasma exchange and replacement with FFP.Normalactivity of vWF-cleaving protease was established in patients witha clinically similar disorder: hemolytic-uremic syndrome (HUS).The level of vWF-cleaving protease activity is thus a laboratory parameterthat provides important information for the differential diagnosis andtreatment of patients with TTP/HUS. Several assays of vWF-cleavingprotease have been described and are summarized here.

GOOOOOD

7: Eur J Pediatr. 2008 Sep;167(9):965-71. Epub 2008 Jun 25.Links

What's new in haemolytic uraemic syndrome?

Johnson S,Taylor CM.

Department of Paediatric Nephrology, Birmingham Children's Hospital,Birmingham, B4 6NH, UK, [email protected].

Recent advances in understanding the aetiology of the disorders that makeup the haemolytic uraemic syndrome (HUS) permit a revised classification ofthe syndrome. With appropriate laboratory support, an aetiologically-basedsubgroup diagnosis can be made in all but a few cases. HUS caused byenterohaemorrhagic Escherichia coli remains by far the most prevalentsubgroup, and new insights into this zoonosis are discussed. The most rapidlyexpanding area of interest is the subgroup of inherited and acquiredabnormalities of complement regulation. Details of the pathogenesis areincomplete but it is reasonable to conclude that local activation of thealternative pathway of complement in the glomerulus is a central event.There is no evidence-based treatment for this diagnostic subgroup. However,

in circumstances where there is a mutated plasma factor such as complementfactor H, strategies to replace the abnormal protein by plasmapheresis ormore radically by liver transplantation are logical, and anecdotal successesare reported. In summary, the clinical presentation of HUS gives a strongindication as to the underlying cause. Patients without evidence of EHECinfection should be fully investigated to determine the aetiology. Wherecomplement abnormalities are suspected there is a strong argument for

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empirical and early plasma exchange, although rapid advances in this fieldmay provide more specific treatments in the near future.

GOOD

88: Br J Haematol.2005 Oct;131(2):247-52. Links

Haemolytic uraemic syndrome is an immune-mediated disease: role of anti-CD36 antibodies.

Rock G, Clark W, Sternbach M, Kolajova M, McLaine P.

Division of Hematology and Transfusion Medicine, Department of Pathology and

Laboratory Medicine, Ottawa Hospital, Ottawa, ON, [email protected]

Haemolytic uraemic syndrome (HUS) is a disorder in which plateletmicrothrombi are formed that have a particular propensity to deposit in thekidney microvasculature, resulting in impaired renal function andthrombocytopenia. The mechanism of formation of these microthrombi is notknown. In this study, we showed that plasma from five adult and sixpaediatric cases of HUS caused aggregation and release of adenosinetriphosphate from normal platelets. The plasma reacted against plateletlysate in a protein blot and all samples showed reactivity against a band at 88kDa, corresponding to the membrane antigen CD36. This was confirmed byprobing with Mo91, a monoclonal antibody to CD36. CD36 was also

identified in the immune complex formed by incubation of patient plasmaswith normal platelet lysate. In other studies, bands of 32 and 7.7 kDa wereobtained when purified verotoxin was protein blotted and probed with eitherpatient plasma or with anti-CD36 antibody Mo91 suggesting structuralhomologies between CD36 and verotoxin. While a direct cause-effectrelationship is not yet established, the data support the concept of animmunological pathogenesis for HUS and suggest that molecular mimicryinvolving one or both of the homologous domains in membrane-bound CD36and verotoxin lead to the development of antibodies capable of inducing thepathophysiological events characteristic of HUS.

CAUSES

CHILDREN

87: Int J Med Microbiol. 2005 Oct;295(6-7):405-18. Links

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Enterohaemorrhagic Escherichia coli in humanmedicine.

Karch H, Tarr PI, Bielaszewska M.

Institute for Hygiene, and National Consulting Laboratory on Haemolytic

Uraemic Syndrome, University Hospital Mnster, Robert Koch Str. 41, D-48149

Mnster, Germany. [email protected]

Enterohaemorrhagic Escherichia coli (EHEC) are the pathogenic subgroup ofShiga toxin (Stx)-producing E. coli. EHEC can cause non-bloody and bloody

diarrhoea, and the haemolytic uraemic syndrome (HUS). HUS is a major cause of

acute renal failure in children. E. coli O57:H7 is the predominant, but far frombeing the only, serotype that can cause HUS. The cascade leading from

gastrointestinal infection to renal impairment is complex, with the microvascular

endothelium being the major histopathological target. EHEC also produce non-Stx molecules, such as cytolethal distending toxin, which can contribute to the

endothelial or vascular injury. Because there are no specific therapies for EHEC

infections, efficient reservoir and human preventive strategies are important areas

of ongoing investigations. This review will focus on the microbiology,epidemiology, and pathophysiology of EHEC-associated diseases, and illustrate

future challenges and opportunities for their control.

10: Pediatr Infect Dis J.2008 Jul;27(7):595-601. Links

Surveillance of hemolytic uremic syndrome inchildren less than 15 years of age, a system tomonitor O157 and non-O157 Shiga toxin-producing Escherichia coli infections in France,1996-2006.

Espi E, Grimont F, Mariani-Kurkdjian P, Bouvet P,Haeghebaert S, FilliolI, Loirat C, Decludt B, Minh NN,Vaillant V, de Valk H.

Institut de Veille Sanitaire, Saint-Maurice, France. [email protected]

BACKGROUND: Since the 1980s, Shiga toxin-producing Escherichia coli(STEC), especially E. coli O157:H7, has been an important cause of foodborne disease in industrial countries. In France, as there was no routine screening for STEC inclinical laboratories, enhanced surveillance of hemolytic uremic syndrome (HUS) in children less than 15 years of age wasestablished in 1996 to monitor trends in the incidence of STEC infections. METHODS: The surveillance system was based

on a voluntary national network of pediatricians of 31 pediatric nephrology units in public hospitals. RESULTS: From

1996 to 2006, the mean annual incidence of HUS was 0.71 cases per 100,000 children less than 15 years of age and 1.87

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cases per 100,000 children less than 5 years of age. STEC infections were confirmed in 66% ofpatients; STEC O157 was the most common serogroup identified in STEC-related HUS (83%). In this 11-year period, 96% of HUS cases were sporadicand only 2 outbreaks caused by STEC O157 and by a dual infection of STECO26 and O80 were detected. CONCLUSIONS: An evaluation of the surveillance of pediatric HUSshowed that it is a simple and useful system for monitoring trends in STEC infections in France. It provides the

information needed to measure the impact of new and changing vehicles of STEC transmission, and evaluate theeffectiveness of prevention measures

12: Pediatr Nephrol.2008 Sep;23(9):1425-31. Epub 2008 May 21.

Links

Enterohaemorrhagic Escherichia coli and Shigelladysenteriae type 1-induced haemolytic uraemic

syndrome.Mark Taylor C.

Department of Nephrology, Birmingham Children's Hospital, Birmingham, B4

6NH, UK. [email protected]

Haemolytic uraemic syndrome (HUS) can be classified according to theaetiology of the different disorders from which it is composed. The mostprevalent form is that induced by shigatoxin producing Escherichia coli(STEC) and, in some tropical regions, by Shigella dysenteriae type 1. STEC

cause a zoonosis, are widely distributed in nature, enter the food chain indifferent ways, and show regional differences. Not all STEC are humanpathogens. Enterohaemorrhagic E. coli usually cause attachment andeffacing lesions in the intestine. This is not essential, but production of ashigatoxin (Stx) is. Because Stx are encoded by a bacteriophage, this propertyis transferable to nave strains. Laboratory methods have improved byidentifying STEC either via the toxin or its bacteriophage. Shigelladysenteriae type 1 produces shigatoxin, identical to Stx-1, but also hasentero-invasive properties that enterohaemorrhagic Escherichia coli (EHEC)do not. Shigella patients risk bacteremia and benefit from early antibiotictreatment, unlike those with EHEC.

PMID: 18493800 [PubMed - in process]

Euro Surveill. 2008 Feb 14;13(7). pii: 8041. Links

Comment in:Euro Surveill. 2008 Feb 28;13(9). pii: 8053; author reply pii/8054.

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Outbreak of verocytotoxin-producing E. coli O145and O26 infections associated with theconsumption of ice cream produced at a farm,

Belgium, 2007.De Schrijver K, Buvens G, Poss B, Van den Branden D, Oosterlynck O, DeZutter L, Eilers K,Pirard D,Dierick K, Van Damme-Lombaerts R,Lauwers C,Jacobs R.

Department of Control of Infectious Diseases, Antwerp, Belgium.

[email protected]

In October 2007, an outbreak of verocytotoxin-producing Escherichia coli

(VTEC) O145 and E. coli O26 occurred among consumers of ice cream produced

and sold in September 2007 at a farm in the province of Antwerp (Belgium). Theice cream was consumed at two birthday parties and also eaten at the farm. Five

children, aged between two and 11 years, developed haemolytic uraemic

syndrome (HUS), and seven other co-exposed persons contracted severe

diarrhoea. In three of the five HUS cases VTEC O145 infections were laboratoryconfirmed, one in association with VTEC O26. Identical isolates of E. coli O145

and O26 were detected with PCR and PFGE in faecal samples of patients and in

ice cream leftovers, in faecal samples taken from calves, and in samples of soiledstraw from the farm at which the ice cream was produced. Ice cream was made

from pasteurised milk and most likely contaminated by one of food handlers.

78: Epidemiol Infect. 2006 Aug;134(4):724-8. Epub 2005 Dec 22. Links

Haemolytic uraemic syndrome associated withinterfamilial spread of E. coli O26:H11.

Sayers G,McCarthy T,O'Connell M,O'Leary M, O'Brien D, Cafferkey M,McNamara E.

Department of Public Health, Health Service Executive Eastern Region, Dublin. [email protected]

In September 2000, haemolytic uraemic syndrome (HUS) was diagnosed in a 10-month-old child with a prodromal history

of vomiting and diarrhoea (non-bloody). Investigation revealed that a self-limiting gastrointestinal illness (mean duration

48 h) had occurred among immediate and extended family in the 2 weeks prior to the child's admission. Theepidemiology of the illness suggested person-to-person spread.

10
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79: Epidemiol Infect. 2006 Aug;134(4):719-23. Epub 2005 Dec 22.

Links

Sorbitol-fermenting Shiga toxin-producingEscherichia coli O157: indications for an animalreservoir.

Orth D, Grif K,Dierich MP, Wrzner R.

Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical

University and Austrian Reference Laboratory for EHEC/STEC/VTEC,

Innsbruck, Austria.

This study investigates a sorbitol-fermenting enterohaemorrhagic Escherichia coli

(SF EHEC) O157 infection in a farmer's family in the Austrian province ofSalzburg. 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 environmentalsurvey, 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-. Allfour 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, increasedsurveillance 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 mayrepresent a considerable health threat asthey can spread from farm animalsto humans and between humans.

87: Int J Med Microbiol. 2005 Oct;295(6-7):405-18. Links

Enterohaemorrhagic Escherichia coli in humanmedicine.

Karch H, Tarr PI, Bielaszewska M.

Institute for Hygiene, and National Consulting Laboratory on HaemolyticUraemic Syndrome, University Hospital Mnster, Robert Koch Str. 41, D-48149Mnster, Germany. [email protected]

Enterohaemorrhagic Escherichia coli (EHEC) are the pathogenic subgroup of

Shiga toxin (Stx)-producing E. coli. EHEC can cause non-bloody and bloody

diarrhoea, and the haemolytic uraemic syndrome (HUS). HUS is a major cause ofacute renal failure in children. E. coli O57:H7 is the predominant, but far from

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being the only, serotype that can cause HUS. The cascade leading from

gastrointestinal infection to renal impairment is complex, with the microvascular

endothelium being the major histopathological target. EHEC also produce non-Stx molecules, such as cytolethal distending toxin, which can contribute to the

endothelial or vascular injury. Because there are no specific therapies for EHEC

infections, efficient reservoir and human preventive strategies are important areasof ongoing investigations. This review will focus on the microbiology,

epidemiology, and pathophysiology of EHEC-associated diseases, and illustrate

future challenges and opportunities for their control.

30: J Appl Microbiol. 2008 Jan;104(1):14-25. Links

Escherichia coli serogroup O26--a new look at anold adversary.

Jenkins C, Evans J,Chart H,Willshaw GA,Frankel G.

Department of Medical Microbiology, Royal Free Hospital, NW3 2QG,London, UK. [email protected]

Escherichia coli serogroup O26 played an important part in the early work

on Verocytotoxin and is an established diarrhoeal pathogen. Recently,Verocytotoxigenic E. coli (VTEC) O26 has been increasingly associated withdiarrhoeal disease and frequently linked to outbreaks and cases ofhaemolytic uraemic syndrome (HUS). This review investigates the pathogenicity, geographicaldistribution, changing epidemiology, routes of transmission and improved detection of VTEC O26. Laboratory data on

VTEC O26 isolates and clinical data on HUS suggest a true difference in the incidence of VTEC O26 in different

geographic locations. However, few diagnostic laboratories use molecular methods to detect VTEC and so it is difficult to

assess the role of VTEC O26 in causing diarrhoeal disease. VTEC O26 is frequently found in thecattle population but rarely in food. However, the small number of outbreaks analysed to date arethought to be food-borne rather than associated with direct or indirect contact with livestock or their faeces. Theincrease in awareness of VTEC O26 in the clinical and veterinary setting has coincided with the development ofnovel techniques that have improved our ability to detect and characterize this pathogen.

153: Mol Biotechnol. 2004 Feb;26(2):117-22. Links

Infection by Shiga toxin-producing Escherichiacoli: an overview.

Karmali MA.

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Laboratory for Foodborne Zoonoses, Health Canada, 110 Stone Road West,

Guelph, Ontario, Canada, N1G 3W4. [email protected]

Shiga toxin-producing Escherichia coli (STEC), especially of serotype O157:H7,cause a zoonotic food or waterborne enteric illness that is often associated with

large epidemic outbreaks as well as the hemolytic uremic syndrome (HUS), theleading cause of acute renal failure in children. After ingestion, STEC colonize

enterocytes of the large bowel with a characteristic attaching and effacingpathology, which is mediated by components of a type III secretion apparatus

encoded by the LEE pathogenicity island. Shiga toxins are translocated from the

bowel to the circularoty system and transported by leukocytes to capillaryendothelial cells in renal glomeruli and other organs. After binding to the receptor

globotriaosylceramide on target cells, the toxin is internalized by receptor-

mediated endocytosis and interacts with the subcellular machinery to inhibitprotein synthesis. This leads to pathophysiological changes that result in HUS.

Specific therapeutic or preventive strategies are presently not available. The

recent sequencing of genomes of two epidemic E. coli O157 strains has revealednovel pathogenicity islands which will likely provide new insights into thevirulence of these bacteria.

PMID: 14764937 [PubMed - indexed for MEDLINE]

32: Pediatr Nephrol.2008 Feb;23(2):221-31. Epub 2007 Nov 30.Links

Role of the renin angiotensin system in TNF-alphaand Shiga-toxin-induced tissue factor expression.

Nestoridi E,Kushak RI, Tsukurov O, Grabowski EF, Ingelfinger JR.

Pediatric Nephrology Laboratory, MassGeneral Hospital for Children atMassachusetts General Hospital, Harvard Medical School, Boston, MA,USA.

Current evidence implicates a prothrombotic state in the development of

Shiga-toxin (Stx)-mediated hemolytic uremic syndrome (HUS). We recentlyreported that Stx modulates procoagulant activity by enhancing functionaltissue factor (TF) activity on cytokine-activated human glomerularendothelial cells (HGECs). Since angiotensin II (Ang II), the key effector ofthe renin angiotensin system (RAS), has been shown to increase TFexpression in vascular tissue, we examined the possible involvement of Ang IIin TF expression in HGECs. HGECs were exposed to tumor necrosis factor (TNF)-alpha +/- Stx-1 +/- AngII. Exogenous Ang II significantly increased TF activity and TF mRNA in TNF-alpha- +/- Stx-1-activated HGECs. This

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increase was mediated via Ang II type I receptor (AT(1)R), as losartan, an AT(1)R inhibitor, attenuated Ang-II-induced TF

activity. To study the effect of endogenous Ang II in TF expression by TNF-alpha +/- Stx-1, HGECs were incubated with

losartan or an AT(2)R inhibitor (PD 123319) or an angiotensin-converting enzyme inhibitor (enalapril). Losartan but not

PD 123319 decreased TF activity induced by TNF-alpha +/- Stx-1 (P < 0.05). Enalapril, also, dose dependently,

downregulated TF expression in HGECs exposed to TNF-alpha +/- Stx-1 (P < 0.05). AT(1)R mRNA was upregulated in

TNF-alpha- +/- Stx-1-activated HGECs (P < 0.05). These data indicate that TF expression inTNF-alpha- and Stx-1-activated HGECs is enhanced by exogenous Ang II

and that endogenous Ang II production may be upregulated by TNF-alpha+/- Stx-1. Hence, local RAS activation may be important in the developmentof the thrombotic microangiopathy observed in HUS.


Shiga toxin-mediated hemolytic uremic syndrome:time to change the diagnostic paradigm?

Bielaszewska M, Kck R, Friedrich AW, von Eiff C, Zimmerhackl LB, Karch

H,Mellmann A.

Institute of Hygiene and the National Consulting Laboratory on HemolyticUremic Syndrome, University of Mnster, Mnster, Germany. mbiela@uni-

muenster.de

BACKGROUND: Hemolytic uremic syndrome (HUS) is caused byenterohemorrhagic Escherichia coli (EHEC) which possess genes encodingShiga toxin (stx), the major virulence factor, and adhesin intimin (eae).However, the frequency of stx-negative/eae-positive E. coli in stools of HUSpatients and the clinical significance of such strains are unknown.

METHODOLOGY/PRINCIPAL FINDINGS: Between 1996 and 2006, we sought stx-negative/eae-positive E. coli instools of HUS patients using colony blot hybridization with the eae probe and compared the isolates to EHEC causing

HUS. stx-negative/eae-positive E. coli were isolated as the only pathogens from stools of 43 (5.5%) of 787 HUS patients;

additional 440 (55.9%) patients excreted EHEC. The majority (90.7%) of the stx-negative/eae-positive isolates belonged to serotypes O26:H11/NM (nonmotile), O103:H2/NM,

O145:H28/NM, and O157:H7/NM, which were also the most frequent serotypes

identified among EHEC. The stx-negative isolates shared non-stx virulence andfitness genes with EHEC of the corresponding serotypes and clustered with them

into the same clonal complexes in multilocus sequence typing, demonstrating

their close relatedness to EHEC. CONCLUSIONS/SIGNIFICANCE: At thetime of microbiological analysis, approximately 5% of HUS patients shed nolonger the causative EHEC, but do excrete stx-negative derivatives of EHEC

that lost stx during infection. In such patients, the EHEC etiology of HUS ismissed using current methods detecting solely stx or Shiga toxin; this canhamper epidemiological investigations and lead to inappropriate clinicalmanagement. While maintaining the paradigm that HUS is triggered byShiga toxin, our data demonstrate the necessity of considering geneticchanges of the pathogen during infection to adapt appropriately diagnosticstrategies.

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PMCID: PMC1995754

37: Berl Munch Tierarztl Wochenschr. 2007 Jul-Aug;120(7-8):279-87. Links

Enterohaemorrhagic Escherichia coli O26:H11/H-:a human pathogen in emergence.

Bielaszewska M, Zhang W, Mellmann A,Karch H.

Institut fr Hygiene, und Nationales Konsiliarlaboratorium fr Hmolytisch-Urmisches Syndrom, Universitt Mnster, Robert Koch Str. 41, 48149 Mnster,

Germany. [email protected]

Enterohaemorrhagic Escherichia coli (EHEC) O26:H11 have emerged as themost important non-O157:H7 EHEC, with respect to their ability to causediarrhoea and the haemolytic uraemic syndrome (HUS). HUS is a leadingcause of acute renal failure in children, and is mainly caused by EHECexpressing Shiga toxins (Stx) 1 and/or 2. Since 1996, EHEC O26, whichproduce Stx2 only and appear to have enhanced virulence, have beenincreasingly isolated from HUS patients in Germany. In contrast, EHEC O26found in cattle predominantly produce Stx1 as the sole Stx. Additionalpotential virulence factors of EHEC O26 include cytolysins (EHEChemolysin), serine proteases (EspP), lymphotoxins (Efal) and adhesins(intimin). The genes encoding the virulence factors are located within

pathogenicity islands (eae, efa1), bacteriophages (stx) or plasmids (EHEC-hlyA, espP). In addition, EHEC O26 possess, in contrast to other EHEC, the"high pathogenicity island" (HPI), which is also present in pathogenicYersiniae.This island contains genes involved in the biosynthesis, regulationand transport of the siderophore yersiniabactin. Comparative genomicanalyses between EHEC O26 and non-pathogenic E. coli, as well asinvestigations of mechanisms involved in the transfer of virulence genes,provide a deeper insight into the evolution of EHEC O26.These studiesdemonstrate how horizontal transfer of virulence genes, even from distantlyrelated organisms, can lead in brief intervals to the rise of a highly virulentclone within a particular E. coli serotype.The classical bacteriological

methods are no longer sufficient to determine the risk posed by EHEC O26.However, knowledge of the complete virulence profiles of these pathogensand understanding their stepwise evolution form a foundation for developingnew strategies to prevent human infections and new methods for theirlaboratory diagnosis.

PMID: 17715820 [PubMed - indexed for MEDLINE

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40: Clin Infect Dis.2007 Jul 1;45(1):39-45. Epub 2007 May 21. Links

Prevalence, virulence profiles, and clinicalsignificance of Shiga toxin-negative variants ofenterohemorrhagic Escherichia coli O157 infectionin humans.

Friedrich AW,Zhang W,Bielaszewska M, Mellmann A, Kck R, Fruth A,Tschpe H, Karch H.

National Consulting Laboratory on Hemolytic Uremic Syndrome, Institute for

Hygiene, University of Mnster, Mnster, Germany.

BACKGROUND: Escherichia coli O157, of the H7 clone, exists in humans

and in the environment as Shiga toxin (Stx)-positive and Stx-negativevariants. Stx production by infecting organisms is considered to be a criticalrequirement for the development of hemolytic uremic syndrome (HUS),which occurs in approximately 15% of E. coli O157-infected patients. It isunknown if loss of the stx gene during the early stage of anenterohemorrhagic E. coli infection prevents HUS, or if absence of the stxgene from E. coli O157 reduces or ablates virulence. METHODS: We determined thefrequency of stx-positive and stx-negative E. coli O157 isolates in stool samples obtained from patients who experienced

sporadic cases of diarrhea or HUS, as well as the frequency in samples obtained during outbreaks, and investigated the

clinical course of the disease.RESULTS: Among E. coli O157 isolates obtained from samples related to sporadic cases ofdiarrhea, stx-negative strains accounted for 4%. The proportion of stx-negative strains was significantly higher among

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