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Enteric Infections (enteric + infections)
Selected AbstractsSeasonal variation of enteric infections and inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 7 2008Amnon Sonnenberg MD Abstract Background: The time trends of inflammatory bowel disease are characterized by short-term variations that affect Crohn's disease and ulcerative colitis alike. The aim of the present study was to test whether these variations might be related to exacerbations of inflammatory bowel disease secondary to superimposed gastrointestinal infection. Methods: The Hospital Episode Statistics (HES) comprises a data set of all patients admitted to hospitals throughout England, which includes inpatients and day cases. This data set was used to analyze the monthly variations in all hospital admissions for Crohn's disease (ICD10 code K50), ulcerative colitis (K51), bacterial intestinal infections (A04), viral intestinal infections (A08), diarrhea and infectious gastroenteritis (A09), upper respiratory infections (J06), pneumonia secondary to unspecified organism (J18), and unspecified acute lower respiratory infection (J22). Results: The temporal analysis revealed similar monthly fluctuations of hospital admissions for Crohn's disease, ulcerative colitis, and bacterial intestinal infections. Viral intestinal infections and infectious gastroenteritis were characterized by different seasonal variations that showed no relationship with any of the fluctuations of inflammatory bowel disease or bacterial intestinal infections. Similarly, respiratory infections resulted in marked cyclical variations in hospital admissions unrelated to any changes in inflammatory bowel disease or enteric infections. Conclusions: The similarity in the time trends of Crohn's disease, ulcerative colitis, and bacterial intestinal infections suggests that superinfection by intestinal bacteria are responsible for the fluctuations in hospital admissions for inflammatory bowel disease. (Inflamm Bowel Dis 2008) [source] Environmental triggers of type 1 diabetesJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 3 2001JJ Couper Abstract: High risk HLA class II alleles account for 40% of the genetic susceptibility to type 1 diabetes in Caucasians, but the majority of the genetically predisposed do not develop the disease. This supports some environmental modification of the autoimmune destruction of , cells that precedes type 1 diabetes. Identical twin studies and geographical variation in incidence also argue for a critical role of environmental factors. Attention has been directed to the possible harmful effect of cow's milk protein (or protective effect of breast-feeding) and enteric infections in early life. Natural history studies that follow children at increased risk of type 1 diabetes provide the best opportunity to study environmental triggers. The Australian Baby Diab Study has followed approximately 500 babies from birth who have a first-degree relative with type 1 diabetes. No prospective association between duration of breast-feeding or introduction of cow's milk and the development of islet autoimmunity was found. The same Australian cohort demonstrated a relationship between rotavirus infection and the first appearance or increase in islet antibodies. Enteroviral infection is seen more frequently in prediabetic children and prior to the onset of islet autoimmunity in Finnish cohorts. Environmental factors may interact. Breast milk protects against enteric infections; enteric infections in turn could increase immunity to dietary antigens by increasing intestinal permeability. It is also possible that an alteration in gut mucosal immune function in genetically susceptible individuals underlies any effect of dietary or viral proteins on the development of islet autoimmunity in early life. [source] Factors Influencing Standard Pretravel Health Advice,A Study in BelgiumJOURNAL OF TRAVEL MEDICINE, Issue 5 2007Kristina Van De Winkel MD Background Travelers with risk factors, medical conditions such as immunosuppression, medication intake, pregnancy, or elderly age, need adaptation or reinforcement of pretravel health advice. The literature provides little data on the frequency of these risk groups in the travel population. This study intended to investigate whether risk factors influencing standard travel advice are common in the population attending our travel clinic. Methods A prospective survey was carried out over a 2-month period in 2004 at the travel clinic of the Institute for Tropical Medicine in Antwerp, Belgium. A list of risk factors focused on the following three important advice categories: malaria prophylaxis, yellow fever vaccination, and travelers' diarrhea or other enteric infections. We counted how frequently a risk factor was observed for each advice category (potential influence) and, after considering the travel characteristics, how often a real adaptation of advice was necessary (actual influence). Results Of 2,227 travelers, 276 were found to have a possible influencing factor (12.4%). The potential influence was 10.9% (243/2,227) for malaria prophylaxis advice, 6.1% (136/2,227) for yellow fever vaccination, and 1.9% (43/2,227) for travelers' diarrhea advice. The actual influence was lower 8% (184/2,227), 5% (109/2,227), and 1.2% (27/2,227), respectively. The main interfering factors were as follows: for influence on malaria advice, age ,60 years (44%) and neuropsychiatric disorders (15.6%); for yellow fever vaccination, age ,60 years (63.2%) and immunosuppression (10.3%); and for influence on travelers' diarrhea advice, decreased gastric acidity (44.2%) and immunosuppression (32.6%). Conclusion Travelers with risk factors are not infrequently seen at our travel clinic. Some groups are more prominently present and could be the focus of travel group,specific instructions. The study suggests that being informed about risk groups is essential for advising travelers. [source] Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitorsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2000Laine This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors. Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins. Prolonged proton pump inhibitor use may lead to enterochromaffin-like cell hyperplasia, but has not been demonstrated to increase the risk of carcinoid formation. Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions. At present, we do not recommend that patients be tested routinely for H. pylori infection when using proton pump inhibitors for prolonged periods. Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen. The risk of enteric infection may increase with acid suppression, although this does not seem to be a common clinical problem with prolonged proton pump inhibitor use. The absorption of fats and minerals does not appear to be significantly impaired with chronic acid suppression. However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g. Zolllinger,Ellison syndrome), and vitamin B12 levels should probably be assessed in patients taking high-dose proton pump inhibitors for many years. Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events. Nevertheless, continued follow-up of patients taking proton pump inhibitors for extended periods will provide greater experience regarding the potential gastrointestinal adverse effects of long-term acid suppression. [source] Genetic analysis of Escherichia coli K1 gastrointestinal colonizationMOLECULAR MICROBIOLOGY, Issue 6 2000J. Martindale Strains of Escherichia coli expressing the K1 polysaccharide capsule colonize the large intestine of newborn infants, and are the leading cause of Gram-negative septicaemia and meningitis in the neonatal period. We used signature-tagged mutagenesis (STM) to identify genes that E. coli K1 requires to colonize the gastrointestinal (GI) tract. A total of 2140 mTn5 mutants was screened for their capacity to colonize the GI tract of infant rats, and 16 colonization defective mutants were identified. The mutants have transposon insertions in genes affecting the synthesis of cell surface structures, membrane transporters, transcriptional regulators, enzymes in metabolic pathways, and in genes of unknown function, designated dgc (defective in GI colonization). Three dgcs are absent from the whole genome sequence of E. coli K-12, although related sequences are found in other pathogenic strains of E. coli and in Shigella flexneri. Additionally, immunohistochemistry was used to define the nature of the colonization defect in five mutants including all dgc mutants. STM was successfully applied to examine the factors involved in E. coli K1 colonization, and the findings are relevant to the pathogenesis of other enteric infections. [source] Special Article: Modulation of natural immunity in the gut by Escherichia coli strain Nissle 1917NUTRITION REVIEWS, Issue 8 2010Ilja Trebichavsky The beneficial effect of probiotic Escherichia coli strain Nissle 1917 (EcN) suggests the gut epithelium plays a basic role in immune interactions with bacteria. Contrary to other commensal strains of Escherichia coli, EcN profoundly modulates the gut barrier to elevate its resistance to microbial pathogens. The present review documents the properties of EcN that have led to the protection of gnotobiotic pigs against lethal enteric infections. This effect could be important in light of the growing number of acquired deficiencies that paralyze gut immunity in humans. [source] Malnutrition as an enteric infectious disease with long-term effects on child developmentNUTRITION REVIEWS, Issue 9 2008Richard L Guerrant Malnutrition is a major contributor to mortality and is increasingly recognized as a cause of potentially lifelong functional disability. Yet, a rate-limiting step in achieving normal nutrition may be impaired absorptive function due to multiple repeated enteric infections. This is especially problematic in children whose diets are marginal. In malnourished individuals, the infections are even more devastating. This review documents the evidence that intestinal infections lead to malnutrition and that malnutrition worsens intestinal infections. The clinical data presented here derive largely from long-term cohort studies that are supported by controlled animal studies. Also reviewed are the mechanisms by which enteric infections lead to undernutrition and by which malnutrition worsens enteric infections, with implications for potential novel interventions. Further intervention studies are needed to document the relevance of these mechanisms and, most importantly, to interrupt the vicious diarrhea-malnutrition cycle so children may develop their full potential. [source] | ||||||||||