Fluoxetine and depersonalization syndrome.
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Biomedical subjects
Publications and source records attributed to M Islam.
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Hafnia alvei, a member of the family Enterobacteriaceae, was the only species of bacteria cultured from the stool of a 9-month-old child who was admitted with a 3-day history of watery diarrhea. The isolated strain of H. alvei failed to produce heat-labile or heat-stable enterotoxins or Shiga-like toxin I or II and did not invade HeLa cells, nor did it cause keratoconjunctivitis (determined by the Sereny test) in a guinea pig's eye. The strain, however, induced diarrhea in 8 of 12 adult rabbits with removable intestinal ties (removable intestinal tie-adult rabbit diarrhea [RITARD] assay) and in 1 of 2 orally fed animals. No diarrhea could be induced with Escherichia coli K-12 in eight RITARD assay rabbits and three orally fed rabbits, respectively. Microscopic examination of affected animals revealed moderate inflammatory cellular infiltration of the intestinal mucosa, in which bacterial attachment to the surface epithelium and loss of the microvillus border were evident in the ileum and colon. Electron microscopy demonstrated cellular modifications of the apical surface, with cupping or pedestal formation and increased terminal web density at sites of bacterial "attachment-effacement," a well-known characteristic and mechanism of diarrhea of enteropathogenic E. coli. Identical lesions were also induced by H. alvei in rabbit ileal loops, which ruled out naturally occurring rabbit enteropathogenic E. coli strains, which are known to produce similar lesions. It is concluded that at least some strains of H. alvei have the potential to cause diarrhea and that attachment-effacement is a virulence characteristic shared by bacteria other than E. coli.
Traditional enteropathogenic Escherichia coli serotypes demonstrate a plasmid-mediated localized adherence in cultured HeLa or HEp-2 cells and induce an attaching-effacing intestinal lesion, both of which are considered pathognomonic and causes of diarrhea. This study describes three E. coli strains from infantile diarrhea which share these properties but belong to serotypes (O2:H2, O2:H25 and O15:H2) not considered enteropathogenic.
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Thirty-seven children (median age, 2 years) with shigellosis in Bangladesh were subjected to postmortem examination to determine causes of death and the spectrum of intestinal histopathology. Infecting species were: Shigella dysenteriae 1, 7 cases; S. dysenteriae 2, 2 cases; Shigella flexneri, 23 cases; Shigella boydii, 4 cases; and mixed infection with Shigella boydii and Shigella sonnei, 1 case. Complicating conditions detected before death included malnutrition in 25 cases, pneumonia in 11 cases and septicemia in 8 cases. In all 37 cases the colon showed gross colitis, consisting of mucosal erythema and edema; superficial ulcerations were visible in 15 cases. Microscopically in the colon the lamina propria showed inflammatory cellular infiltration in 27 cases and crypt abscesses were present in 22 cases. In 9 cases each there were colonic glands in the submucosa and branching of colonic crypts, indicating increased regenerative activity of crypt cells. Severe lesions were mucosal denudation and deep ulceration in 15 cases with a pseudomembrane in 7 and pseudopolyposis in 2 of these patients. The most common underlying cause of death was colitis, whereas the most common immediate and associated causes were, respectively, septicemia and pneumonia. These results indicated that fatal childhood shigellosis results from severe colitis, often complicated by septicemia and concomitant malnutrition and pneumonia.
By enzyme-linked immunosorbent assay with group A-, subgroup-, and serotype-specific monoclonal antibodies (MAbs), we tested 414 stool specimens collected from pediatric and adult patients hospitalized with acute gastroenteritis between January and June 1988. Of 414 specimens tested, 124 (30%) were positive for group A rotavirus. The subgroup was determined in 110 specimens (88.7%); 16.1% were subgroup I, and 72.6% were subgroup II. Two specimens reacted with both subgroup I- and subgroup II-specific MAbs. Serotype determinations showed that serotype 1 (38.4%) was predominant over serotypes 2 (28.2%), 3 (2.5%), and 4 (23%). Three specimens reacted with more than one serotype-specific MAb. While the frequency of serotype 1 was highest in the two hospitals in Mymensingh, serotype 2 was most prevalent in one hospital in Dhaka. All human rotavirus strains with subgroup I and serotype 2 specificities showed a short electropherotype, and all but one strain with subgroup II and serotype 1, 3, or 4 specificities exhibited a long electropherotype.
The causes and pathogenesis of severe childhood pneumonia in a developing country were studied in lungs removed at autopsy from 119 Bangladeshi children who presented with pneumonia and/or diarrhea. Pneumonia was observed in 93 patients. Morphologic features included acute alveolar exudate in 51% (of the 93 patients), necrotizing pneumonia in 31%, interstitial pneumonia in 22%, and caseating granulomas in 4%, while a mixed pattern occurred in 16% of patients. Causes of pneumonia were Gram-negative bacteria in 27%, pneumococcus in 8%, cytomegalovirus (CMV) in 8%, Pneumocystis carinii (PC) in 4%, mycobacteria in 3%, aspergillus in 3%, mixed anaerobes in 3%, viral (not CMV) in 2%, Staphylococcus aureus in 1% and ascaris in 1%. Two causative agents were identified in 7% of patients. In 46% of the cases, no etiologic agent was identified. Our data suggest that most pneumonias had a bacterial etiology; however, viruses, including CMV, and other opportunistic organisms such as PC, were also important pathogens. Gram-negative pneumonia was partially attributed to concomitant intestinal infections. Opportunistic infections resulted from malnutrition and debilitated host defenses during prolonged fatal illnesses.
The clinical, biochemical, histopathological and immunological features of 30 cases of clometacin-induced hepatitis are described. The age range of the patients was 32-84 years with a notable female predominance of 29:1. The hepatitis was highly cytolytic with high values of transaminases but with little or no cholestasis. Gammaglobulins were higher than 18 g/l in 73% of the cases. 25 liver biopsies were performed and showed acute hepatitis with a predominant centrilobular necrosis in 17; chronic aggressive hepatitis was noted in 8 cases but 1 showed concomitant cirrhotic changes. Anti-tissue antibodies were looked for in all cases. Anti-smooth muscle antibodies of anti-actin cable type (titre 1/80 to 1/2, 560) were detected in 19 cases, anti-nucleus antibodies in 16 cases which were associated to the former in 14 cases. The above findings show that clometacin produces a hepatitis syndrome quite akin to autoimmune chronic active hepatitis (lupoid hepatitis) and to the hepatopathy induced by oxyphenisatin.
To describe the epidemiologic and clinical features associated with invasive amebiasis in Bangladesh, 85 hospitalized diarrheal patients with hematophagous trophozoites of Entamoeba histolytica in their stools were compared to a control group of 84 hospitalized diarrheal patients without amebiasis. Postmortem examinations were carried out in 22 deaths due to amebiasis. For the patients with amebiasis, there was a bimodal age distribution with peaks at 2-3 years and greater than 40 years, whereas the control patients had a unimodal distribution with the peak at 0-1 year. The sex distribution was equal in childhood but young adults were predominantly female and older adults predominantly male. The clinical features significantly associated with amebiasis were prolonged dysentery, prior measles rash, malnutrition, hyponatremia, hypokalemia, and hypoproteinemia (all P less than 0.05). The case fatality rate in amebiasis was 29%, which was significantly higher than 11% for the controls (P less than 0.05). Postmortem findings included extensive colitis with deep ulcers and complications, including colonic perforation in 2 cases, peritonitis in 4 cases, pneumonia in 9 cases, and septicemia in 5 cases. These results indicate that invasive amebiasis in this population differs from other diarrheal diseases, affecting mainly children greater than 2 years and adults and causing severe and fatal illness characterized by extensive colitis with diverse systemic consequences.
To describe the pathology and clinical features of segmental necrotising enterocolitis (SNE) in children and adults, 22 diarrhoeal patients (median age two years, range two months to 50 years) in Bangladesh with this lesion detected at autopsy were examined and compared with two groups of diarrhoeal control patients. Gross pathology consisted of purplish or black mucosal or transmural discoloration with erosions or ulcerations in segments of the jejunum or ileum of 18 cases and of the colon alone in four cases. Two patients had intestinal perforations. Microscopically all specimens showed coagulation necrosis or haemorrhagic necrosis indicative of mucosal ischaemia. In 20 cases there was submucosal oedema and nine showed pneumatosis of the bowel. From 11, one or more of the invasive diarrhoeal pathogens Shigella, Campylobacter and Entamoeba histolytica were detected. From the comparison with controls significant associations were found for a long duration of diarrhoea, blood and mucus in stool, abdominal distension or tenderness, shock not attributable to hypovolaemia, septicaemia, and low concentration of serum protein (p less than 0.05). These findings indicated that segmental necrotising enterocolitis develops sometimes as a fatal complication of prolonged diarrhoeal illnesses associated with shock and hypoproteinaemia and is caused by ischaemic injury to the intestinal mucosa.
The cause of death (besides dehydration) for 140 diarrhoeal patients who died in hospital following rehydration was determined by autopsy examination. Children under 5 years comprised 74% of the patients. Diarrhoeal pathogens were identified as Shigella spp. in 27%, enterotoxigenic Escherichia coli in 17%, Entamoeba histolytica in 16%, Campylobacter jejuni in 12%, Salmonella spp. in 4%, Vibrio cholerae in 4%, and Giardia lambliain 4% of cases. The most frequent underlying causes of death were colitis in 44% and pneumonia in 38%. The most frequent immediate causes of death were septicaemia in 27%, hypoglycaemia in 9%, and hypokalaemia in 9%; multiple causes of death were present in 89% of cases. Kwashiorkor or marasmus was present in 59% and fatty degeneration of the liver was detected in 61% of cases. It is concluded that, in susceptible children, diarrhoeal pathogens produce destructive inflammation in the intestine and cause death or contribute to it by provoking disease in other tissues, especially septicaemia and fatty liver, or by combining these effects with antecedent or concomitant conditions, especially pneumonia and malnutrition.
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To develop an animal model of the haemolytic-uraemic syndrome during shigellosis, rabbits were injected with lipopolysaccharides (LPS) extracted by the hot phenol-water method from Shigella dysenteriae I and from S. flexneri. Two intravenous injections of LPS spaced by 24 h elicited renal cortical necrosis in a generalized Shwartzman reaction characterized by fibrin deposition in glomerular capillaries and by elevated plasma creatinine concentration. Rabbits rendered leucopenic by busulphan treatment were protected against renal cortical necrosis after injection with LPS derived from S. dysenteriae I. Both LPS preparations derived from Shigella species were also active in producing fever in rabbits, death in rabbits, and gelation of limulus lysate with approximately the same potency as a standard LPS of E. coli 055:B5. These results demonstrated that the LPS of Shigella species given intravenously to rabbits produces renal cortical necrosis, which is caused by leucocyte-mediated intravascular fibrin deposition in renal blood vessels and which resembles histologically the renal lesion in the haemolytic-uraemic during shigellosis in humans.
From three fatal cases of diarrhoeal illness in Bangladesh, Yersinia species were isolated from tissues at post-mortem examination. One patient was infected with Y. enterocolitica serotype 0:7, 8 and two patients were infected with Y. intermedia. These patients were infected also with other enteric pathogens. These findings suggest that Yersinia may be important as pathogens in tropical diarrhoea and as co-pathogens in serious disease.