Risk factors for the development of Escherichia coli O157:H7 associated with hemolytic uremic syndrome

Verotoxin-producing Escherichia coli (VTEC) O157:H7 is a major cause of hemorrhagic colitis that is often associated with the development of hemolytic uremic syndrome (HUS). In July, 1996, a severe mass outbreak of VTEC O157 infection occurred in Sakai city, Osaka. The present study investigates the risk factors which may contribute to the development of HUS in the early stages of the VTEC O157 infection. There was no significant difference between HUS-developed and non-HUS-developed groups with respect to sex, age, rates of clinical manifestations, such as fever, abdominal pain and bloody stool, use of anti-diarrheal agents, anti-motility agents, and/or antibiotic agents, and serum sodium concentrations at the early stage of VTEC O157 infection. Thus, these factors did not appear to be risk factors associated with the development of HUS. In contrast, leukocyte counts and C-reactive protein levels in the early stage of VTEC O157 infection were significantly higher in the HUS-developed group (P < 0.001), suggesting that these are risk factors associated with the development of HUS.     

Effect of early oral fluoroquinolones in hemorrhagic colitis due to Escherichia coli O157:H7

During the Sakai outbreak of Escherichia coli O157:H7 infection, which was linked to contaminated cafeteria school lunches, there were several treatment modalities with regard to antimicrobial drugs. Patient outcomes among three hospitals with different modalities were compared retrospectively. Hemolytic uremic syndrome did not develop in any of the 15 patients treated with oral fluoroquinolone therapy; however, HUS did develop in three of 15 patients treated with intravenous (i.v.) fosfomycin and in two of 12 patients treated with i.v. cefotaxime and oral fosfomycin. The results indicate that oral fluoroquinolone therapy administered within 3 days of illness is effective in preventing the development of HUS; however, prospective randomized double-blind studies on early antimicrobial therapy of O157 hemorrhagic colitis are necessary. Several antibiotics, including fluoroquinolones, were reported to induce the production or release of Shiga-like toxins (STX) from E. coli O157:H7 in vitro. Although patients were examined for fecal STX, no STX were detected in the stools of patients treated with oral fluoroquinolones. In fact, treatment with fluoroquinolones for 5 days eradicated E. coli O157 in all patients.     

Escherichia coli 0157: H7 infections associated with perforated appendicitis and chronic diarrhoea

Two unique associations of disease withEscherichia coli 0157H7 are presented. These cases broaden the spectrum of disease associated with this organism which currently includes bloody and non-bloody diarrhoea, haemolytic-uraemic syndrome, and thrombotic thrombocytopenic purpura.     

Neurological manifestations of hemorrhagic colitis in the outbreak of Escherichia coli O157:H7 infection in Japan

An outbreak of hemorrhagic colitis associated with Escherichia coli O157:H7 occurred in a kindergarten in Saitama, Japan from September to November, 1990. Seven patients admitted to our hospital showed neurological manifestations: generalized seizures, impaired consciousness, urinary incontinence, gaze nystagmus, phrenic nerve palsy, action tremor and vertigo. Two patients died. On the basis of the clinical courses and laboratory findings of the seven patients and postmortem findings of one case, these neurological symptoms were suspected to be induced by the verotoxin elaborated by Escherichia coli O157:H7.     

Clinical features and treatment of children with hemolytic uremic syndrome caused by enterohemorrhagic Escherichia coli O157:H7 infection: Experience of an outbreak in Sakai City, 1996

Presented is a study of 15 patients (seven males and eight females ranging between 5 and 10 years of age) with hemolytic uremic syndrome (HUS) associated with hemorrhagic colitis that was caused by enterohemorrhagic Escherichia coli (EHEC) O157:H7, encountered during the outbreak in Sakai City in July, 1996. The complete form of HUS, which includes the three characteristics hemolytic anemia, thrombocytopenia and acute renal dysfunction, was noted in eight patients, while an incomplete form of HUS, which did not include all three characteristics, was noted in seven patients. Regarding treatment, intravenous gamma-globulin was administered in nine patients and dialysis was performed in five patients (two males and three females) with the complete form of HUS. In three of these five patients, plasma exchange was also performed. Weaning from dialysis was accomplished by the 15th day of disease in all patients. Some patients developed pancreatitis, central nervous system symptoms, fundal hemorrhage and elevation of transaminase, although these abnormalities subsided uneventfully. Renal biopsy, which was performed in two patients who recovered from acute renal failure but still had mild proteinuria and a decrease in creatinine clearance, showed moderate changes in the glomeruli and tubulointerstitium. One year after onset of disease, hematological and urological findings were within normal limits in all patients except one with the complete form of HUS, who still had slightly decreased creatinine clearance.     

A severe outbreak of haemorrhagic colitis and haemolytic uraemic syndrome associated withEscherichia coli 0157: H7 in Japan

In 1990, an outbreak ofEscherichia coli 0157: H7 infection occurred in 174 children in a nursery school in Saitama, Japan. The organism was isolated from tap water supplied from the well in the school. Clinical manifestations varied from asymptomatic infection to non-bloody diarrhoea, haemorrhagic colitis, haemolytic uraemic syndrome (HUS) and death. Among culture-confirmed 42 cases ofE. coli 0157: H7, 7 children were asymptomatic, 21 children had only diarrhoea, and 14 children developed HUS. Bloody diarrhoea with abdominal pain following initial frequent diarrhoea appeared to be associated with subsequent HUS. In patients with HUS, both leucocyte count and lactate dehydrogenase activity continued to increase in the early phase of the disease, and on day 3 of illness attained markedly higher levels than in patients without HUS. These two parameters seemed to be important as predictors of the development of HUS.Committee for epidemiological and clinical study of epidemic diarrhoea due to pathogenicE. coli in a nursery school, Saitama, Japan     

Clinical experiences in Sakai City Hospital during the massive outbreak of enterohemorrhagic Escherichia coli O157 infections in Sakai City, 1996

In the middle of July, 1996, a massive outbreak of hemorrhagic colitis (HC) occurred among elementary schoolchildren in Sakai city. This is the most widespread outbreak of O157 infection ever experienced to our knowledge. Lunch foods supplied in the elementary schools in Sakai were contaminated by Escherichia coli (E. coli) O157. One hundred and twenty-one cases developed hemolytic uremic syndrome (HUS) from 12,680 symptomatic patients, including putative secondary infections, and three girls died during this outbreak. Sakai City Hospital is one of the core medical facilities in this community; hence, 425 children with HC were treated at the hospital. Antibiotics were used extensively on all patients. Among them, 12 children developed HUS. All 425 children, including the patients with HUS, recovered without significant sequelae. In the present paper, the clinical experiences during this massive outbreak of E. coli O157 infection in Sakai City Hospital are described.     

Bacterial genotype and neurological complications of Escherichia coli O157:H7-associated haemolytic uraemic syndrome

We examined the possibility of an association between the bacterial genotype of Escherichia coli O157:H7 and the likelihood of progression to neurological complications in childhood gastroenteritis-associated haemolytic uraemic syndrome (D+HUS). Bacterial stool isolates were available from 51 patients with HUS; 11 of these patients suffered a neurological complication. Bacteria were assessed for plasmid content, verotoxin (Shiga-like toxin) profile, verotoxin 2 subtype, and presence of the eaeA (effacement and attachment) marker. No association of bacterial genotype with central nervous system (CNS) manifestations was observed. Whilst the cause of CNS manifestions may be multifactorial, there is no evidence at present to implicate specific bacterial traits.     

Prevalence of verocytotoxigenic Escherichia coli serotype O157:H7 in children with diarrhoea attending a Sydney hospital

Abstract Verotoxin producing Escherichia coli, in particular serotype O157:H7, have been implicated as an important cause of acute gastroenteritis in children. This study was undertaken to determine if E. coli O157:H7 is an important cause of acute gastroenteritis in children in metropolitan Sydney. During the period from October 1990 to September 1991, stools from patients presenting with acute diarrhoea to The Children's Hospital, Camperdown, were examined for the presence of common bacterial pathogens. In addition, stools were grown on sorbitol McConkey agar and sorbitol non-fermenting organisms were serotyped with O157 antiserum by slide agglutination. The isolates were then tested with H7 antisera and investigated for the production of verocytotoxin and other pathogenic markers including plasmid-associated EHEC adhesin and chromosomally encoded attachment-effacement gene. Only two strains (isolated from two different patients, 0.1% of specimens tested) were agglutinated by O157 antiserum and both were non-motile (H^-). However, both strains produced verotoxin and expressed other virulence markers, suggesting that they were responsible for the diarrhoea. Both patients experienced mild, self limited gastroenteritis. We conclude that E. coli O157:H7 is an uncommon cause of acute gastroenteritis in Sydney children presenting to a children's hospital.     

Prolonged anemia by superinfection of parvovirus B19 in a boy with enterohemorrhagic <Emphasis Type="Italic">Escherichia coli</Emphasis> O157-associated hemolytic uremic syndrome

We report a 3-year-old boy with enterohemorrhagic Escherichia coli (EHEC) O157-associated hemolytic uremic syndrome (HUS). His anemia was associated with decreased reticulocyte count and persisted after the recovery from HUS. Superinfection of parvovirus B19 (PVB19) was proven by a transient febrile episode associated with IgM antibodies to the virus and the delayed appearance of IgG antibodies and typical rashes. We conclude that PVB19 infection could induce severe persistent anemia in EHEC-associated HUS. Reticulocytopenia is a clue to the diagnosis in such cases.