A method of enhancing verocytotoxin production by Escherichia coli

Al-Jumaili, I J; Burke, Dave; Scotland, Sylvia M.; Al-Mardini, Hanan; Record, C. O.

doi:10.1016/0378-1097(92)90516-q

Cited by 21 publications

(15 citation statements)

References 16 publications

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“…We speculate that commercially available rapid antibody-based toxin detection kits could be used for the same purpose. Mitomycin C induction further increased the sensitivity of our antibody-based Stx2 detection kit, a strategy that has been suggested by others (1,6). Antibiotics such as ciprofloxacin that have been associated with increased toxin expression due to bacteriophage induction may also prove use-ful for amplifying toxin expression in clinical samples (14,15).…”

Section: Case Reportmentioning

confidence: 82%

Shiga Toxin-Producing Escherichia coli -Associated Kidney Failure in a 40-Year-Old Patient and Late Diagnosis by Novel Bacteriologic and Toxin Detection Methods

et al. 2003

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Infection with Shiga toxin-producing Escherichia coli (STEC) is the most common cause of kidney failure in children. High morbidity is also associated with infections in the elderly. We describe STEC-associated kidney failure in a 40-year-old patient, including the methods used to identify STEC a month after disease onset. CASE REPORTA 40-year-old African-American male with a 10-year history of hypertension presented at a community hospital with several days of abdominal cramps, vomiting, and loose stool with interspersed blood. Upon admission, he was found to be in acute renal failure with anemia and occult blood in the stool. He was afebrile, with an elevated blood pressure of 243 over 172 mm Hg and an otherwise normal physical examination that included neurologic, skin, and abdominal examinations. Admission laboratory results included an abnormal hematocrit of 27.4%, a platelet count of 69,000/mm 3 , a blood urea nitrogen level of 83 mg/dl, and a creatinine level of 6.6 mg/dl. Endoscopic procedures were done to investigate the source of his blood loss. A colonoscopic biopsy showed mild chronic colitis with benign lymphocytic hyperplasia. Esophagoduodenoscopy showed a bulbar ulcer with signs of recent hemorrhage.On hospitalization day 5, a microangiopathic hemolytic process was considered on the basis of a peripheral blood smear that showed occasional schistocytes, polychromasia, normal platelets, helmet cells, and no spherocytes. Three days later, bone marrow biopsy results indicated a left shift of erythroid precursors, increased megakaryocytes with enlargement and cytoplasmic vacuolization, and increased stainable iron. At that time, the patient's anemia persisted with a hematocrit of 24%, a platelet count of 111,000/mm 3 , a lactate dehydrogenase level of 588 (normal, 120 to 190) U/liter, a reticulocyte count of 5.6%, and a creatinine level of 9.5 mg/dl. Coagulation parameters were essentially normal, and haptoglobin was markedly diminished.On hospitalization day 9, the patient commenced hemodialysis and plasmapheresis, as well as high-dose prednisone for renal failure. The working diagnosis was thrombotic thrombocytopenic purpura (TTP). He was transferred to Walter Reed Army Medical Center for continued care on approximately day 20 of illness, after he had received three plasmapheresis treatments.A dietary history was taken from the patient upon his transfer to our hospital. He noted that he had eaten fast food restaurant hamburgers 4 and 6 days prior to the onset of his initial gastrointestinal symptoms. In addition, he reported that he had eaten a steak the evening before the onset of his illness. The steak had been marinated overnight, transported to the desert in an ice chest, and grilled many hours later. After several transfusions, the patient's laboratory findings were as follows: hematocrit, 35.7%; platelet count, 290,000/mm 3 ; creatinine level, 12.3 mg/dl; haptoglobin, less than 10 (normal, 30 to 200); lactate dehydrogenase level, 855 U/liter; reticulocyte count, 6.1%. The patient's peripheral b...

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Section: Case Reportmentioning

confidence: 82%

Shiga Toxin-Producing Escherichia coli -Associated Kidney Failure in a 40-Year-Old Patient and Late Diagnosis by Novel Bacteriologic and Toxin Detection Methods

et al. 2003

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“…MMC induces a decrease in white blood cells and platelets, which is similar to the results of cyclophosphamide treatment. In addition, streptomycin restrains the normal intestinal flora, which can result in EHEC O157:H7 being the dominant member of the flora [35], [36], thus, enhancing the EHEC O157:H7 susceptibility of mice. So, in this study, BALB/c mice were selected as the model and injected with MMC intraperitoneally and fed with nalidixic acid water during the period of infection with EHEC O157:H7.…”

Section: Discussionmentioning

confidence: 99%

The N-Terminal Domain of EspF Induces Host Cell Apoptosis after Infection with Enterohaemorrhagic Escherichia coli O157:H7

et al. 2013

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Enterohemorrhagic Escherichia coli (EHEC) employs a type III secretion system (TTSS) to export the translocator and effector proteins required for mucosal colonization. As an important bacterial effector protein in locus of enterocyte effacement four, the EspF protein causes F-actin filament aggregations to form attaching and effacing (A/E) lesions, and induces the destruction of brush-border microvilli and cytoskeletal rearrangements to form pedestals. However, the molecular pathogenesis of A/E lesions due to EHEC O157:H7 infection is unclear. In this study, we constructed an espF-deficient mutant (ΔespF) with a 162-bp deletion in the N-terminal domain by using overlap extension PCR. The results showed that EHEC EspF translocated into intestinal epithelial cells, targeted mitochondria and induced apoptosis. The ΔespF mutant, compared to EHEC prototype Guangzhou strain, had lower cell attachment and effacement abilities, lower caspase-9/3 and lactate dehydrogenase levels, lower bacterial adhesion, weaker mitochondria apoptosis, and a higher mouse survival rate. Our results demonstrate the probable function of the EspF N-terminal domain, which targets mitochondria and binds mitochondria heat shock protein 70 to induce cell apoptosis via A/E lesions. These findings may be invaluable in clarifying the molecular pathogenesis of EspF of EHEC O157:H7.

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“…Previous studies have documented how prophage-inducing stimuli (e.g., mitomycin C) and low-iron conditions can greatly augment Stx production (1,15,51,53). However, these studies analyzed a limited number of human STEC isolates, and until now, little information existed regarding how bovine-associated STEC isolates respond to these stimuli.…”

Section: Discussionmentioning

confidence: 99%

“…No HUS-associated STEC isolates producing Stx1 only were identified in the ongoing epidemiological study of STEC in the United States; consequently, Stx1-producing isolates from Germany were obtained. All these isolates contained stx 1 and not a recently identified variant, stx 1c ( Table 2). The six Stx1-producing HUS-associated STEC isolates all contained amplifiable eae and ehxA sequences.…”

Section: Characterization Of Stx2-producing Stec Isolatesmentioning

confidence: 99%

Comparison of Shiga Toxin Production by Hemolytic-Uremic Syndrome-Associated and Bovine-Associated Shiga Toxin-Producing Escherichia coli Isolates

Ritchie

Wagner

Acheson

et al. 2003

Appl Environ Microbiol

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There is considerable diversity among Shiga toxin (Stx)-producing Escherichia coli (STEC) bacteria, and only a subset of these organisms are thought to be human pathogens. The characteristics that distinguish STEC bacteria that give rise to human disease are not well understood. Stxs, the principal virulence determinants of STEC, are thought to account for hemolytic-uremic syndrome (HUS), a severe clinical consequence of STEC infection. Stxs are typically bacteriophage encoded, and their production has been shown to be enhanced by prophage-inducing agents such as mitomycin C in a limited number of clinical STEC isolates. Low iron concentrations also enhance Stx production by some clinical isolates; however, little is known regarding whether and to what extent these stimuli regulate Stx production by STEC associated with cattle, the principal environmental reservoir of STEC. In this study, we investigated whether toxin production differed between

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A method of enhancing verocytotoxin production by Escherichia coli

Cited by 21 publications

References 16 publications

Shiga Toxin-Producing Escherichia coli -Associated Kidney Failure in a 40-Year-Old Patient and Late Diagnosis by Novel Bacteriologic and Toxin Detection Methods

Shiga Toxin-Producing Escherichia coli -Associated Kidney Failure in a 40-Year-Old Patient and Late Diagnosis by Novel Bacteriologic and Toxin Detection Methods

The N-Terminal Domain of EspF Induces Host Cell Apoptosis after Infection with Enterohaemorrhagic Escherichia coli O157:H7

Comparison of Shiga Toxin Production by Hemolytic-Uremic Syndrome-Associated and Bovine-Associated Shiga Toxin-Producing Escherichia coli Isolates

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