Hemorrhagic Enterocolitis Research Articles

Hämolytisch-urämisches Syndrom bei Kleinkindern durch Verotoxin-produzierende Escherichia coli

Between September and November 1988, six children (aged 4-17 months) from a parish in Upper Bavaria fell ill with a haemolytic-uraemic syndrome. The illness had been preceded by a gastroenteritis with at times haemorrhagic stools. All patients needed peritoneal dialysis for acute renal failure. A 12-month-old girl was left with statomotoric developmental impairment due to cerebral involvement, but the other five children were cured. In the first four children to be admitted stool examinations for the common enteritis-causing microorganisms had been negative. But in the following two, specific gene probes demonstrated enterohaemorrhagic E. coli O157: H- with formation of verotoxin 2 (Shiga-like toxin II). This group of microorganisms must be taken into account in the diagnosis of haemorrhagic enterocolitis, because they can cause severe complications.

Fatal enterocolitis in harbour seals (Phoca vitulina) caused by infection with Eimeria phocae

Coccidiosis due to Eimeria phocae infection has been described in harbour seals (Phoca vitulina) from the western Atlantic population, but not in any detail in seals from the eastern Atlantic...

Bacterial Colitis

Bacterial colitis results in an inflammatory-type diarrhea that is characterized by bloody, purulent, and mucoid stool. These diseases have been designated as bacterial hemorrhagic enterocolitis. Associated symptoms include fever, tenesmus, and severe abdominal pain. The pathologic changes range from superficial exudative enterocolitis to a transmural enterocolitis with ulceration. Common pathologic bacteria causing bacterial colitis include Campylobacter, Salmonella, Shigella, Escherichia, and Yersinia species. The primary source of transmission is fecal-oral spread and ingestion of contaminated food and water. Although detailed history and identification of specific risk factors assist in the diagnosis, definitive diagnosis requires bacterial identification. Therefore, the physician must be familiar with the disease pathophysiology, epidemiology, and specific diagnostic modalities for clinical diagnosis and management. Specific tests are used to detect enteric pathogens and include stool and rectal swab culture, histology, and identification of specific bacterial toxins. Although many of these bacterial colitis infections are self-limiting, antibiotics should be used for high-risk patients and patients with complicated disease.

Increased Levels of Macrophage Migration Inhibitory Factor in Sera of Patients with Escherichia coli O157:H7-Induced Enterocolitis

Verotoxin-producing Escherichia coli O157:H7 is a pathogen that causes severe hemorrhagic enterocolitis and sometimes leads to serious conditions such as hemolytic-uremic syndrome. Various inflammatory parameters have been assessed for their efficacy in predicting the severity of E. coli O157:H7-induced colitis (9, 10), but no serological biomarker has been identified which can precisely determine the presence and severity of this colitis. Macrophage migration inhibitory factor (MIF) is a unique cytokine that has been shown to play a role in several inflammatory diseases (4, 7). We here report increased levels of MIF in sera of patients with verotoxin-producing E. coli O157:H7-induced enterocolitis. Serum samples were obtained from 24 patients with E. coli O157:H7-induced enterocolitis, 30 sex- and age-matched patients with bacterial enterocolitis induced by pathogens other than O157:H7 (Salmonella, Vibrio, and non-verotoxigenic E. coli) as disease controls, and 55 healthy individuals as normal controls. Serum MIF concentrations were measured with an enzyme-linked immunosorbent assay specific for MIF (IDLISA; Sapporo Immunodiagnostic Laboratory, Sapporo, Japan) as described previously (7). E. coli O157:H7 was diagnosed by stool culture, which is the gold standard diagnostic method for this pathogen. As shown in Fig. ​Fig.1,1, the serum MIF levels in patients with E. coli O157:H7-induced enterocolitis (23.67 ± 2.36 ng/ml; P < 0.001 versus normal controls and disease controls) were sixfold higher than those in normal controls and threefold higher than those in disease controls (3.99 ± 0.17 and 8.23 ± 0.60 ng/ml, respectively). Furthermore, serum MIF levels provided a level of differentiation of subjects with E. coli O157:H7-induced enterocolitis that was comparable to that afforded by detection of E. coli O157:H7 from stool culture (cutoff value, sensitivity, specificity, and positive predictive value by serum MIF: 12.5 ng/ml, 0.875, 0.950, and 0.840, respectively). On the other hand, leukocyte counts and levels of C-reactive protein in peripheral blood samples were increased in patients with E. coli O157:H7-induced enterocolitis and disease controls compared with normal controls, but there was no significant difference between patients with E. coli O157:H7-induced enterocolitis and disease controls (data not shown). FIG. 1. Serum MIF concentrations in infectious colitis induced by verotoxin-producing E. coli O157:H7. Values are means ± standard error. Serum MIF levels were measured in 55 normal controls (NC), 30 patients with bacterial colitis induced by pathogens ... We previously demonstrated that MIF is a pivotal cytokine in the pathogenesis of inflammatory bowel disease and other types of colitis (8). In addition, recent studies have shown that MIF is immediately released in large quantities from the pituitary and other tissues in response to lipopolysaccharide (LPS) (1, 3). In particular, increased MIF levels in serum have been reported in patients with endotoxemias such as sepsis (4, 6). In mice, targeted disruption of MIF diminishes the immune response to LPS (2). Thus, MIF is considered to be an important molecule in the development of endotoxemia and subsequent severe inflammation. It has been hypothesized that LPS is involved in the pathophysiology of verotoxigenic E. coli infection (5). In this study, we showed that serum MIF levels were markedly increased in patients with verotoxin-producing E. coli O157:H7-induced colitis compared with those in patients with nonspecific colitis and healthy individuals. These findings suggest that the acute-phase response of circulating MIF to the endotoxin induced by E. coli O157:H7 plays a role in the development of enterocolitis. Although further studies are needed to clarify the role of MIF in the pathophysiology of E. coli O157:H7-induced colitis, MIF may make a major contribution to the development of enterocolitis caused by verotoxigenic E. coli O157:H7.

Adenovirus enterocolitis in pediatric patients following bone marrow transplantation: report of 2 cases and review of the literature.

We report 2 cases of adenovirus enterocolitis in pediatric patients who underwent bone marrow transplantation. The first case involved a 17-year-old adolescent boy with combined immunodeficiency and non-Hodgkin lymphoma who developed chronic graft versus host disease and persistent adenovirus duodenitis. Case 2 involved a 3-year-old boy who received a mismatched unrelated bone marrow transplant for metachromatic leukodystrophy; the boy developed severe graft versus host disease and died of multiorgan failure. At autopsy, diffuse hemorrhagic enterocolitis with changes of severe graft versus host disease and extensive mucosal invasion by adenovirus was found. Awareness and early recognition of this uncommon complication of concomitant graft versus host disease and adenovirus infection could impact therapy and outcome of patients with bone marrow transplant.

Human pentastomiasis discovered postmortem

The autopsy of an 18-year-old girl who had died suddenly at home revealed generalised pentastomiasis. The location of this disease in the intestines was responsible for death by hemorrhagic enterocolitis. This discovery constituted an atypical case in our daily practice of forensic medicine.

Bacterial hemorrhagic enterocolitis.

Bacterial diarrhea can be classified into two clinical entities, noninflammatory diarrhea and inflammatory diarrhea syndromes. The latter type of diarrhea is characterized by bloody and puruloid mucus stool, and is often accompanied by fever, tenesmus, and severe abdominal pain. Pathogenic bacteria causing the inflammatory diarrhea syndrome include Salmonella, Vibrio, Shigella, enteroinvasive and enterohemorrhagic Escherichia coli, Campylobacter, Yersinia, Chlamydia, and Clostridium difficile. The pathologic changes in the inflammatory diarrhea syndrome range from a superficial exudative enterocolitis to a transmural enterocolitis with overt ulceration. This syndrome is also designated as bacterial hemorrhagic enterocolitis because of its usual manifestation by bloody diarrhea. The diagnostic approach needs information on the patient's age, travel history, epidemiological associations, sexual practice, and medical history, including usage of antibiotics. Bacterial information can be obtained by microscopic study, culture, and the identification of specific bacterial toxins. Flexible colonoscopy with biopsy is useful for the differentiation of bacterial hemorrhagic enterocolitis from idiopathic ulcerative colitis and ischemic colitis. Physicians should be familiar with the diagnostic modalities used to detect the specific pathogens causing hemorrhagic bacterial enterocolitis; namely, bacterial culture, serology, histology, and nucleic acid technologies.

The epidemiology, pathogenicity and microbiology of foodborne Escherichia coli O157:H7

Escherichia coli are generally considered to be members of the common, indigenous microbiota of the human and other animal intestinal tracts. In fact, they are generally beneficial in several ways. Several virotypes (particular virulent strains) within the species that have the capacity for causing gastrointestinal disease in humans were discovered within the last 50 years. The virotypes have been studied particularly for their epidemiology and the mechanisms by which they are able to cause disease. The virotypes of E. coli described in this review are enterotoxigenic, enteropathogenic, enteroaggregative, enteroinvasive, diffusely-adherent, and enterohemorrhagic (EHEC). Many of the virotypes are responsible for causing widespread outbreaks of diarrheal disease, most of which are self-limiting. The exceptions are the EHEC that are featured in this review. EHEC produce shiga-like toxins and are capable of causing hemorrhagic enterocolitis and hemolytic uremic syndrome, a potentially fatal disease. # 2002 Lippincott Williams & Wilkins

Bovine adenovirus type 10: properties of viruses isolated from cases of bovine haemorrhagic enterocolitis

The isolation, serological classification and growth properties of adenoviruses isolated from fatal cases of haemorrhagic enterocolitis in calves are described. Four viruses, from different submissions, were isolated in cultures of calf testis cells and were identified as adenoviruses by electron microscopy. The four isolates were serologically identical and were classified as bovine adenovirus type 10 in cross-neutralisation tests with other bovine, ovine and porcine adenovirus species. Their growth in the nucleus of infected cells was accompanied by the production of typical adenovirus-associated inclusions. A serological survey to determine the incidence of infection with the virus in cattle in Northern Ireland demonstrated the presence of low levels of neutralising antibodies in 55 per cent of cattle over two years old, although only 8 per cent were positive at a 1/500 dilution of serum.

147 O - Effect of preoperative hyperthermia with radio-chemo-therapy on resectability of locally advanced rectal cancer. A phase II clinical

In locally advanced rectal cancer pre-operative radio-chemotherapy can increase resectability and may provide local control in unresectable cases, but response rates are still unsatisfactory. In a phase II study we investigated whether regional hyperthemia in combination with preoperative radio-chemo-therapy (HRCT) is feasible and will result in downstaging as well as improve resectability. 18 patients (pts) with primary non resectable rectal cancer entered the trial. Initial tumor stage was assessed by endorectal ultrasound (EU) and computed tomography (CT). Pre-operative treatment consisted of 5-FU (300–500 mg/m 2 , dose escalation) and leucovorin (50mg) on days 1–5 and 22–28. Regional hyperthermia (RHT) was carried out using the SIGMA 60 applicaton BSD 2000 once a week prior to radiotherapy. Radiotherapy was applied in prone position using a belly board, three-field technique, standard blocks, 5×1,8 Gy up to 45 Gy. Re-staging was carried out using EU and CT. Four weeks after HRCT, surgery was performed. Treatment-related adverse events were observed in 3 pts with grade III gastrointestinal toxicity requiring a short hospitalisation because of dehydration and/or abdominal discomfort. One patient developed grad IV toxicity with haemorrhagic enterocolitis and treatment was stopped. After treatment 14/18 pts (78%) proved resectable (R0 n = 11/R2 n = 3; Abdomino-perineal resection n = 5 and sphincter saving surgery n = 9). Nonresectable disease after explorative laparotomy was found in 4/18pts in 5 of 18 pts (27%) postoperative complications were observed with anastomatic leakage (n = 2) and perineal abscess (n = 3). A complete histological remission (pCR) was confirmed in 2/18 pts (11%). In median follow up of 13 months (rang 3–21 months) all but one R0-resected pts (n = 11) had no evidence of tumor recurrence. The patients with non-resectable carcinomas (n = 4) had a progression free survival with the range of 5–28 months. Preoperative HRCT in fessible and effective in primary non resectable rectal cancer resulting in a resectability rate of 78% with pCR in 11% of the patients. Treatment related toxicity and postoperative complication-rate are acceptable. Our results suggest that RHT in addition to radio-chemotherapy can improve treatment results in rectal cancer. Therefore a randomized phase III- study has been initiated to validate the effects of HRCT in locally advanced non resectable rectal cancer.

Acute Hemorrhagic Enterocolitis in Ratites: Isolation of Eastern Equine Encephalomyelitis Virus and Reproduction of the Disease in Ostriches and Turkey Poults

Two emus died with acute hemorrhagic enterocolitis. Eastern equine encephalomyelitis (EEE) virus was isolated in Vero cells from non-pooled samples of brain and intestine. Enterocolitis with splenic and hepatic necrosis was reproduced by intramuscular or oral inoculation of this isolate in two ostriches and three turkey poults.

Biological activities and chemical composition of a cytotoxin of Klebsiella oxytoca.

A low-molecular-mass cytotoxin produced by Klebsiella oxytoca isolated previously from patients with antibiotic-associated haemorrhagic enterocolitis was purified, and its biological and chemical properties were elucidated. The toxin inhibited the syntheses of DNA and RNA by HEp-2 cells dose-dependently, whereas protein synthesis was only slightly inhibited, as measured by the incorporation of radioactive precursors. When synchronously cultured HEp-2 cells were examined in the presence of cytotoxin, inhibition of DNA synthesis occurred promptly within 5 h, but cell-rounding, the earliest visible morphological change, was not observed until 6 h after exposure. The intracellular levels of ATP decreased with an approximately similar time course. These results suggest that cytotoxicity toward HEp-2 cells is primarily due to the inhibitory effect of the cytotoxin on nucleic acid synthesis, possibly on DNA synthesis. Cell rounding and cell death were induced even in the absence of the cytotoxin after incubation with the cytotoxin for 6 h. The cytotoxin was heat-labile, cytotoxic activity decreasing to 50% of the initial level on heating at 70 degrees C for 20 min. Plasmids were extracted from three strains of K. oxytoca producing the cytotoxin and analysed by agarose gel electrophoresis. Two strains possessed plasmids of different sizes, but one strain possessed no plasmid, indicating that the cytotoxin is probably chromosomally encoded. Analysis by NMR and FAB-mass-spectrometry revealed that the molecular mass of the cytotoxin should be 217.1062 Da (exact mass), its molecular formula being C8H15O4N3.

Differences in signs and lesions in sheep and goats with enterotoxemia induced by intraduodenal infusion of Clostridium perfringens type D

Summary Enterotoxemia was induced in 4 lambs and 4 goat kids by continuous intraduodenal infusion of a whole culture of Clostridium perfringens type D. Clinical signs, hematologic values, biochemical alterations, and postmortem lesions in the lambs and goat kids were compared. The 4 lambs and 4 goat kids died within 25 hours of beginning the infusions. Lesions were not observed in the gastrointestinal tract of the 4 lambs; however, severe hemorrhagic enterocolitis was found in the 4 goat kids. This difference between the lambs and goat kids in the lesions caused by experimentally induced enterotoxemia may explain the discrepancies reported between sheep and goats in clinical signs, response to treatment, and efficacy of vaccination observed in naturally induced enterotoxemia in the 2 species.

Attaching and effacing Escherichia coli infection as a cause of diarrhea in young calves

Summary A form of enteric Escherichia coli infection was identified in 60 calves from 59 farming operations. The E coli responsible for these infections principally colonized the colon, inducing a distinctive lesion described as attaching and effacing. Hemorrhagic enterocolitis or blood in the feces was observed on 40% of the farms. Of affected calves, 86.6% were dairy calves (average age, 11.8 days). Forty-four calves were infected concurrently with other enteropathogens (cryptosporidia, rotavirus, coronavirus, enterotoxigenic E coli, bovine viral diarrhea virus, coccidia). Verotoxin-producing E coli was recovered from 31 calves; 8 were serotype 0 111:NM isolates, 3 were serotype 05:NM, and 1 was serotype 026:NM.

Production of a unique cytotoxin by Klebsiella oxytoca

Certain strains of Klebsiella oxytoca isolated from patients with hemorrhagic enterocolitis produced a unique cytotoxin. The cytotoxin induced rounding of tissue culture cells, such as HEp-2, Vero, CHO and HeLa cells. The induced morphologic changes were indistinguishable between cell types. Seventy to 80% of the rounded cells died in 48 h incubation. The cytotoxin was purified 1000-fold from culture supernatant by Sephadex G-25 and Bio-Gel P-2 gel filtration followed by reversed-phase high-performance liquid chromatography. The molecular weight of the purified cytotoxin was estimated to be ⩽651 by mass spectrometry. The minimum concentrations of the purified cytotoxin required to cause 50% of rounding of cells were 0.6 μg/ml for HEp-2, 0.8 μg/ml for Vero, 0.8 μg/ml for CHO and 1.4 μg/ml for HeLa cells. The type strain of K. oxytoca, ATCC 13182, did not produce the cytotoxin and only the clinically isolated strains did, suggesting that the cytotoxin may play a role in the pathogenesis of the organisms.

Cis-Dichlorodiammineplatinum(II) (NSC-119 875): Preclinical toxicologic evaluation of intravenous injection in dogs, monkeys and mice

cis-Dichlorodiammineplatinum(II), a compound with antineoplastic and antimitotic activity, which inhibited the synthesis of DNA and to a lesser extent of RNA and proteins, was submitted to a preclinical pharmacologic evaluation in 16 dogs, 10 monkeys, and 120 mice. The LD50 following a single dose iv in Swiss mice was 13.4 mg/kg for males and 12.32 mg/kg for females. The minimum lethal dose for the dog was a single iv injection of 2.5 mg/kg or 5 daily consecutive injections of 0.75 mg/kg and for the monkey, 5 daily doses of 2.5 mg/kg. The treatment elicited severe morbidity within 5–17 days and the time of onset was dose related. Toxic signs included severe hemorrhagic enterocolitis, severe hypocellularity of the bone marrow and lymphoid tissues and marked renal lesions (renal tubular necrosis in the dog and nephrosis in the monkey). Dogs also showed occasional pancreatitis and monkeys myocarditis and occasional degeneration of the spermatogenic cells. Renal lesions were the most severe toxic changes in survivors and were manifested by azotemia, hypochloremia, proteinuria, appearance of urinary erythrocytes, leukocytes and decreased 24-hr excretion of lactate dehydrogenase in dogs and by protracted polyuria in monkeys. Occasional hypocalcemia also occurred. In dogs and monkeys that survived the treatment, toxicity regressed entirely within 55–124 days. Treatment affected primarily tissues with a high rate of cell division (intestines, bone marrow, lymphoid tissues and occasionally testes) and tissues known for primary excretion of the compound (intestines and kidneys).

Chronic toxicity of adriamycin: A new antineoplastic antibiotic

Adriamycin, a new antitumor antibiotic, was administered for 3 mo to rabbits and dogs by iv injection of daily single doses of 0.125, 0.250 and 0.5 mg/kg body weight. The lowest dose caused neither mortality nor any sign of toxicity with reference to body weight, blood picture and function and morphology of the liver, kidneys, heart and skin and its appendages. The testis presented some inhibition of spermatogenesis. With the higher doses the following were observed: mortality, hemorrhagic enterocolitis, arrest or reduction of body growth, alopecia and melanosis (dog), total depression of hemopoiesis with particular damage to the platelets, blood coagulation changes, hypoproteinemia, hyperazotemia, morphologic renal damage (rabbit) and depression of spermatogenesis. From the toxicologic point of view, the product behaves as a typical inhibitor of cellular reproduction. Damage to the most actively proliferating tissues was more prevalent and occurred earlier with respect to parenchymal damage.

Pneumoportogram in idiopathic intestinal necrosis

A patient who was critically ill was found on radiographie examination to have gas in the bowel wall and eleven hours later in the portal vein. At operation and at postmortem examination, the mesenteric vessels were open. The cause of the extent and severity of the ulcerations and bowel necrosis was obscure. The diagnosis was idiopathic hemorrhagic enterocolitis necroticans.

Acute hemorrhagic necrosis of the gastrointestinal tract.

MASSIVE gastrointestinal bleeding has always been a serious diagnostic and therapeutic problem. The problem is even greater when the bleeding occurs in an old person who may simultaneously exhibit a multitude of serious organic disturbances interfering with proper investigation.In 1954 Wilson and Qualheim1 described a form of acute hemorrhagic enterocolitis in 20 chronically ill patients, many of whom presented massive gastrointestinal hemorrhage. Some underwent unnecessary surgical exploration because of an erroneous diagnosis. This condition has not been generally recognized, and not mentioned in the extensive review of the causes of the gastrointestinal hemorrhage by Brick and Jeghers.2 Kane et . . .

A Form of Acute Hemorrhagic Enterocolitis Afflicting Chronically Ill Individuals: A Description of Twenty Cases

A Form of Acute Hemorrhagic Enterocolitis Afflicting Chronically Ill Individuals: A Description of Twenty Cases