[Intestinal amebiasis. III. Ascariasis in chronic intestinal amebiasis].
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Differential diagnosis of intestinal amebiasis (106 patients), acute Flexner's dysentery (105 patients) and nonspecific ulcerative colitis (31 patients) based on the clinical data and rectoromanoscopic findings is described. Rapidly and gradually progressing in the first 7 days intestinal amebiasis is characterized by a gradual onset, normal t0 with mounting general weakness, celiectasia, diarrhea with hyaloid mucus, focal catarrh-hemorrhagic changes and appearance of individual oval transversal ulcers on the colon mucosa.
Three cases of intestinal amebiasis with varying clinical pictures are presented. One patient developed an amebic liver abscess and also amebic colitis, which was mistaken for Crohn's disease. A second patient with amebic dysentery had no Entamoeba histolytica trophozoites in fecal material because of previous therapy with an antiprotozoal drug. The third patient, who had colitis and severe constitutional symptoms, had trophozoites in the stool but negative serological tests. The diagnostic value of radiology and endoscopy, of examinations of stool and exsudate, and of histopathology and serology is discussed.
Intestinal amebiasis is still an important health problem in developing regions of the world. In order to advance our knowledge on the pathogenesis and to test the relevance of recently obtained in vitro observations, suitable in vivo experimental models of intestinal amebiasis are needed. In the past a variety of laboratory animals have been used, but the mouse, whose genetics and immunology is well known, has been seldomly used. Therefore, Entamoeba histolytica strain HM1:IMSS was directly inoculated into the cecum of C3H/HeJ mice, which were sacrificed at 5, 10, 15, 20, 25 and 30 days for histopathologic analysis. An ulcerative inflammatory disease highly reminiscent of human amebiasis was observed. Early 5 day lesions consisted of tiny erosions of the surface epithelium which evolved to deeper and more extensive destructive lesions of the cecal wall. Indeed, flask-shaped ulcers, intestinal perforations and intramural abscess formation were observed at later times. It was noticeable that, despite the lack of obvious significant tissue invasion by amebae, ulcerative disease was extensive and found virtually in all mice. These observations support the view that tissue invasion by trophozoites is not necessarily required for ulcerative disease to occur, suggesting a role for toxic factors released by amebae.
Three surveys were carried out in Managua. Nicaragua. In the first one it was found that 71% of the intestinal amebiasis cases of obligatory notification had no comparable diagnostic foundations; in the second one, 11.7% of the laboratory diagnoses as Entamoeba histolytica referred by 4 health centers were correct; and in the third one, it was obvious that only 9.4% of the doctors knew well what intestinal amebiasis is. The results suggest that intestinal amebiasis is being diagnosed excessively in Managua.
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Ninety-one patients with intestinal amebiasis (IA) were studied. All had been long suffering from IA due to the fact that it had not been diagnosed in time. Indications for emergency surgery were profuse hemorrhage, perforation of amebic ulcers, gangrene, and toxic dilatation of the large intestine. Planned operations were made in pseudopolyposis, strictures of the large intestine. Surgical treatment was performed along with specific therapy. Seven patients died due to late diagnosis, ineffective therapy and profound systemic and regional changes caused by these factors. It is necessary to differentiate ulcerative colitis, polyposis, and tumors of the large intestine with IA.
Of 115 patients with symptomatic intestinal amebiasis, 56 were treated with Ro 7-0207 and 59 with metronidazole in a double blind study. Results of treatment were similar in the two groups and side effects were of low intensity except in one patient who received Ro 7-0207 and developed numbness of hands and tongue, difficulty in speaking, and headache. These symptoms disappeared after termination of treatment.
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The author present the results obtained in the treatment of 100 patients suffering chronic intestinal amebiasis, employing a new drug--Etophamide, in a dose of 1,0 g per day, for three consecutive days. The tolerance of a new antiamebic drug was excellent in all patients, and the parasitological cure rate obtained was 92%. The author concluded that the new derivate amebicide used in this research is very effective for treatment of intestinal amebiasis infections.
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37/38 patients with reciprocal titers > or = 512 against Entamoeba histolytica in Denmark over a 5-year period were evaluated retrospectively in order to establish the clinical profile of extra-intestinal amebiasis in a non-endemic area. 24 of these had extra-intestinal amebiasis, all presenting 1 or more amebic liver abscesses on ultrasonography. Fever was the most common finding, present in 91% of the cases. The most striking observation was the lack of both abdominal pain and tenderness in 22% of the patients with liver abscess. Pulmonary symptoms and abnormal chest X-rays were each recorded in 45% of the cases. Liver abscesses with or without pulmonary involvement were the only extra-intestinal manifestations recorded. The condition was initially misconceived in more than half the cases, but most of the patients responded well once treatment with metronidazole was started.
There is controversy regarding the presence of colonic mucosal abnormalities or mucosal invasion by Entamoeba histolytica in patients with "nondysenteric intestinal amebiasis." To determine the role of E. histolytica in causing symptoms and mucosal changes and to detect if mucosal invasion by E. histolytica is present in nondynsenteric intestinal amebiasis, we evaluated 24 E. histolytica-infected patients (stool microscopy positive for E. histolytica) and 12 noninfected controls who presented with chronic gastrointestinal symptoms, but without dysentery, to a clinic in Calcutta. The colonic mucosa was evaluated at colonoscopy, and mucosal biopsies obtained from the cecum, sigmoid colon, and rectum were evaluated by light microscopy, indirect immunofluorescence microscopy, and scanning electron microscopy. At colonoscopy mucosal ulcerations were absent in all the controls and all except one of the E. histolytica-infected patients. E. histolytica trophozoites or cysts were not seen in the lamina propria or on the luminal surface in any infected patient by light and immunofluorescence microscopy. On scanning electron microscopy, structures that resembled rounded E. histolytica trophozoites were seen on the luminal surface in two of 19 cecal specimens from the infected patients. Moderate or severe mucosal inflammation was frequent on light microscopy in both the E. histolytica-infected patients and the noninfected controls with the cecum involved in two thirds of both groups. Antibodies to E. histolytica were detected in serum of 25% of study patients and 58% of controls. Mucosal inflammation did not correlate with stool positivity for E. histolytica or seropositivity for ameba antibody.(ABSTRACT TRUNCATED AT 250 WORDS)