Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postinfectious functional gastrointestinal disorders (FGIDs) may not be specific to gastroenteritis. This pilot study aimed to ascertain the 3- and 6-month incidence of functional gut disorders in people with non-gastrointestinal (GI) infection, gastroenteritis and healthy controls. This was a prospective study of three cohorts recruited from hospital (non-GI infections) and the community (others). FGIDs were diagnosed using self-completed Rome II modular questionnaires administered at baseline, 3 and 6 months. Thirty-six subjects with non-GI infection, 219 healthy subjects and 108 with bacterial gastroenteritis participated. No difference in incidence of FGID was detected between the GI and non-GI infection cohorts. Any FGID was more frequent in people who had a non-GI infection than in controls at both 3 [odds ratio: 4.34 (95% CI: 3.60-16.45)] and 6 months [4.76 (4.42-27.92)]. Irritable bowel syndrome (IBS) alone was more frequent in people with non-GI infections than in controls at 3 months (6.12 [1.30-29.12]) but did not quite reach statistical significance at 6 months (4.58 [0.79-26.46]). Our findings were unexpected. Postinfectious FGIDs may be related to non-GI and GI infection, although not all potential biases were controlled in study design. Further studies need to explore these preliminary findings and, if confirmed, the underlying mechanisms.
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PMID:Postinfectious irritable bowel syndrome may occur after non-gastrointestinal and intestinal infection. 1691 63

Noroviruses (NVs) cause human gastroenteritis through person-to-person transmission and via contaminated foods. In food poisoning, a major suspected cause is the consumption of raw oysters. We detected NVs from environmental water and oysters around a closed gulf where oysters are cultivated. We collected oyster and water samples once or twice a month for 30 months from October 2001 to March 2004. We then studied monthly changes in virus occurrence and in genetic relationships among 208 NVs isolated from water and oyster samples and from the feces of children suffering from acute gastroenteritis during the same period in the same region. In the analysis of untreated water flowing into farm sewage, NVs were detected year round. In other water samples -processed sewage, river water, and seawater-, oysters, and children's feces, NVs were detected mainly in winter. A comparison of NV nucleotide sequences showed genetic diversity, but some strains predominated in certain winter seasons. These predominant strains were detected across sample materials. In 2002/03, an identical strain was detected in sewage, river water, seawater, oysters, and feces. We also found that NV genetic types changed at the beginning of the season, in November or December, in both 2001/02 and 2002/03. This study showed a clear relationship between NVs detected in children's feces and those in environmental water and oysters. These results support the idea that NVs are transmitted from the feces of infected persons to oysters by the flow of water through farm sewage, rivers, and the sea, finally accumulating in the mid-gut gland of oysters.
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PMID:[Study on pollutant pathway of norovirus contamination in oysters]. 1692 83

Laribacter hongkongensis, a recently discovered bacterium associated with community-acquired gastroenteritis, has been found in the intestines of freshwater fish. To better understand the epidemiology and ecology of the bacterium, we carried out a surveillance study to investigate possible seasonal variation in the recovery of L. hongkongensis and its distribution in various organs in retail freshwater fish in Hong Kong. Forty whole freshwater fish of two species (20 grass carps and 20 bighead carps), and intestines from 120 grass carps were sampled during a one-year period. L. hongkongensis was isolated from 11 (55%) of the 20 grass carps and 6 (30%) of the 20 bighead carps; and the intestines of 49 (41%) of 120 grass carps. Seasonal variation in the recovery of L. hongkongensis from both whole fish and intestines was observed, with higher isolation rates in spring and summer than in fall and winter. There was also positive correlation between temperature and the isolation rates. When L. hongkongensis was cultured in vitro at different temperatures, shorter lag time and higher growth rate were observed at higher temperatures, with 37 degrees C being optimal among the tested temperatures. L. hongkongensis was commonly found in the gills, stomachs and intestines in both grass carps and bighead carps, and on the skin surface of one fish, but not in other organs. Proper handling of freshwater fish for cooking, especially the gills and gut, is recommended to prevent acquisition of L. hongkongensis, and other freshwater fish related infections.
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PMID:Seasonal and tissue distribution of Laribacter hongkongensis, a novel bacterium associated with gastroenteritis, in retail freshwater fish in Hong Kong. 1699 30

There are many viruses infecting the human gut: some are found to cause acute gastroenteritis regularly (although not always) like rotaviruses, enteric adenoviruses, small round structured viruses and astroviruses; others enter the host via the gut and most often cause systemic infection (entero-viruses, parvoviruses); and others are not regularly associated with human disease (reoviruses, viruses of the Coronaviridae family). The human gut can also be infected directly by HIV and, as a consequence of immuno-suppression, by viruses of the Herpesviridae family. Most remarkable during the last one to two years were the following results: increasing evidence that a tetravalent rhesus rotavirus-based vaccine can prevent severe disease after natural human rotavirus infection bringing this vaccine candidate close to approval by the Food and Drug Administration, USA; better, although not complete, understanding of correlates of protection from rotavirus infection; and fuller comprehension of the genomic and antigenic diversity of viruses of the Caliciviridae family infecting man. There is still no proficient tissue culture system for the human small round structured viruses, hindering the acquisition of basic knowledge of the replication of these viruses in the human gut. Except against rotaviruses, there are no vaccine candidates against human enteric viruses.
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PMID:Viral gastroenteritis. 1703 23

Campylobacter is the most common cause of bacterial gastroenteritis in the world. Poultry is the main reservoir of human infections. The widespread use of antibiotics in agriculture and veterinary medicine has resulted in the emergence of an increasing number of antibiotic-resistant Campylobacter strains that can be transmitted to humans through the food chain. Of particular concern to public health is the prevalence of resistance to macrolides and fluoroquinolones that are used in the treatment of life-threatening campylobacteriosis. The CmeABC efflux system has been shown to contribute to the intrinsic and acquired resistance to these antibiotics. In addition, by mediating resistance to bile, it is essential for colonization of the chicken gut in vivo. Inhibition of CmeABC may provide an effective means of reversing antibiotic resistance and decreasing the transmission of Campylobacter via the food chain. This would positively impact on public health by decreasing the morbidity, mortality and increased healthcare costs associated with the treatment of antibiotic-resistant Campylobacter.
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PMID:Antibiotic-resistant Campylobacter: could efflux pump inhibitors control infection? 1711 38

Both innate and adaptative immune responses contribute to the control of infectious diseases, including by limiting the spreading of zoonotic diseases from animal reservoirs to humans. Pigs represent an important animal reservoir for influenza virus infection of human populations and are also naturally infected by coronaviruses, an important group of viruses, which includes the recently emerged severe acute respiratory syndrome (SARS) virus. Studies on both innate and adaptative immune responses of pigs to influenza virus and coronaviruses contribute, therefore, to a better control of these infections in their natural hosts and will be briefly reviewed in this article. Pro-inflammatory cytokines, including type I interferon (IFN), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6), were found in lung secretions of influenza virus infected pigs, and correlated with the intensity of clinical signs, whereas prior vaccination against influenza strongly reduced the production of infectious virus and cytokines in the lungs upon challenge, which was associated with clinical protection. An early type I IFN production was also found in coronavirus infected pigs, including at mucosal sites. IFN induction by coronavirus is shown to involve interaction between a viral glycoprotein and a leukocyte subset, likely equivalent to plasmacytoid dendritic cells, present in the mucosae and associated lymphoid tissues. Given the IFN mediated antiviral and immunomodulatory effects, the use of IFN or IFN inducers may prove an efficient strategy for a better control of influenza virus and coronavirus infections in pigs. Because influenza and coronaviruses target mucosal surfaces, adaptative immune responses have to be characterized at mucosal sites. Thus, nasal and pulmonary antibody responses were analyzed in influenza virus infected or vaccinated pigs showing short-lived, but potentially protective local IgA and IgG antibody (Ab) responses. Interestingly, primary influenza virus infection induced long-lived increase of lung CD8(+) T cells and local lymphoproliferative responses. Pigs infected by a respiratory coronavirus (PRCV) showed virus-specific IgG Ab-secreting cells in the bronchial lymph nodes, whereas the transmissible gastroenteritis coronavirus (TGEV) induced more IgA Ab-secreting cells in gut tissues, which illustrates the importance of the route of antigen administration for inducing local immune effector mechanisms. Porcine viral infections provide, therefore, valuable models for evaluating the immune parameters that are important for controlling transmission of important viral zoonotic infections.
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PMID:Porcine innate and adaptative immune responses to influenza and coronavirus infections. 1713 2

The human enteropathogen, Yersinia enterocolitica, is a significant link in the range of Yersinia pathologies extending from mild gastroenteritis to bubonic plague. Comparison at the genomic level is a key step in our understanding of the genetic basis for this pathogenicity spectrum. Here we report the genome of Y. enterocolitica strain 8081 (serotype 0:8; biotype 1B) and extensive microarray data relating to the genetic diversity of the Y. enterocolitica species. Our analysis reveals that the genome of Y. enterocolitica strain 8081 is a patchwork of horizontally acquired genetic loci, including a plasticity zone of 199 kb containing an extraordinarily high density of virulence genes. Microarray analysis has provided insights into species-specific Y. enterocolitica gene functions and the intraspecies differences between the high, low, and nonpathogenic Y. enterocolitica biotypes. Through comparative genome sequence analysis we provide new information on the evolution of the Yersinia. We identify numerous loci that represent ancestral clusters of genes potentially important in enteric survival and pathogenesis, which have been lost or are in the process of being lost, in the other sequenced Yersinia lineages. Our analysis also highlights large metabolic operons in Y. enterocolitica that are absent in the related enteropathogen, Yersinia pseudotuberculosis, indicating major differences in niche and nutrients used within the mammalian gut. These include clusters directing, the production of hydrogenases, tetrathionate respiration, cobalamin synthesis, and propanediol utilisation. Along with ancestral gene clusters, the genome of Y. enterocolitica has revealed species-specific and enteropathogen-specific loci. This has provided important insights into the pathology of this bacterium and, more broadly, into the evolution of the genus. Moreover, wider investigations looking at the patterns of gene loss and gain in the Yersinia have highlighted common themes in the genome evolution of other human enteropathogens.
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PMID:The complete genome sequence and comparative genome analysis of the high pathogenicity Yersinia enterocolitica strain 8081. 1717 84

Infection by pathogenic organisms leads to mucosal damage and disruption of the gut's extensive commensal flora, factors which may lead to prolonged bowel dysfunction. Six to 17% of unselected irritable bowel syndrome (IBS) patients believe their symptoms began with an infection, which is supported by prospective studies showing a 4%-31% incidence of postinfectious IBS-(PI) following bacterial gastroenteritis. The wide range of incidence can be accounted for by differences in risk factors, which include in order of magnitude; severity of initial illness > bacterial toxigenicity > hypochondriasis, depression and neuroticism, and adverse life events in the previous 3 months. PI-IBS has been reported after Campylobacter, Salmonella, and Shigella infections. Serial biopsies after Campylobacter jejuni gastroenteritis show an initial inflammatory infiltrate, with an increase in enterochromaffin (EC) cells, which in most cases subsides over the next 6 months. Those who go on to develop IBS show increased numbers of EC and lymphocyte cell counts at 3 months compared with those who do not develop IBS. Interleukin-1beta mRNA levels are increased in the mucosa of those who develop PI-IBS, who also show increased gut permeability. Recover can be slow, with approximately 50% still having symptoms at 5 years. Recent studies suggest an increase in peripheral blood mononuclear cell cytokine production in unselected IBS, an abnormality that may be ameliorated by probiotic treatment. The role of small-bowel bacterial overgrowth in IBS is controversial, but broad-spectrum antibiotics do have a temporary benefit in some patients. More acceptable long-term treatments altering gut flora are awaited with interest.
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PMID:Role of infection in irritable bowel syndrome. 1723 25

Postinfectious irritable bowel syndrome (IBS) is a subgroup of IBS. Patients with an episode of bacterial gastroenteritis may have a 12-fold increased risk of developing IBS symptoms within the same year. The IBS can be manifested in each of its clinical types, but the diarrhea-predominant form occurs most commonly. The primary pathophysiologic factor in developing IBS after enteral infection may be defects in enteric nervous system which can produce abnormality in visceral hypersensitivity and intestinal motility. These patients also display exaggerated increases in mucosal immunocompetent T lymphocytes and an abnormally high pro- versus anti-inflammatory cytokine ratio, providing evidence to the contribution of the immune system in the development of postinfectious IBS. Via bi-directional brain-gut interactions both peripheral and central events can play a role in the development of clinical symptoms. Stress is associated with significant worsening of the complaints in IBS and may also result in a shift in the host-gut microbial relationship. IBS itself may predispose patients to acute bacterial gastroenteritis because of the altered intestinal motility. It needs further clarifying the relationship between IBS and small intestinal bacterial overgrowth syndrome. Upon the data so far the altered intestinal flora in IBS would merely reflect developments due to altered motility and not a causal relationship. The treatment of postinfectious IBS does not differ principally from that of the idiopathic IBS. Antibiotics or probiotics may lead to temporary symptomatic improvement, but, given the lack of evidence based data, they cannot be advised for routine use so far.
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PMID:[Postinfectious irritable bowel syndrome]. 1729 54

In addition to the severe invasive systemic disease of listeriosis, recent evidence suggests that the Gram-positive intracellular bacterial pathogen Listeria monocytogenes is also a causative agent of febrile gastroenteritis. We examined the listerial response to stresses normally encountered in the upper small intestine and demonstrate that osmotic stress appears to be at the top of the hierarchy of stress responses during gastrointestinal residence. Furthermore, we suggest that the increased osmolarity of the gastrointestinal lumen may be interpreted as an environmental cue signalling gut entry and that the underlying genetic element governing this response is the alternative stress sigma factor sigma(B).
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PMID:Gut osmolarity: a key environmental cue initiating the gastrointestinal phase of Listeria monocytogenes infection? 1743 59


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