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)

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteritis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were inoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities. Also we noted comparable diminution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: a study in gnotobiotic piglets. 392 24

We studied 3-wk-old piglets 40 h after experimental infection with transmissible gastroenteritis (TGE) virus to identify the mechanisms of diarrhea in this disease and to better understand infectious diarrhea in humans. Using continuous segmental marker perfusion in four regions along the gut, we found significant increases in net intraluminal accumulation of water and electrolytes only in the proximal jejunum, the region infected by the virus. In this jejunal segment studied in vivo, unidirectional sodium flux, extracellular fluid (ECF) to lumen, significantly increased, lumen to ECF significantly decreased, compared with matchfed littermates. The standard perfusate rendered hypertonic by adding mannitol (450 mosmol/kg), in the same segment of normal pigs, caused only an increase in ECF to lumen flux of sodium. TGE did not alter gross villous structure or intraluminal bacteria, bile salts, lactate, pH, or osmolality. Epithelial cell migration was accelerated in the jejunum of infected pigs. Isolated in suspension, these cells from TGE pigs exhibited increased active and passive sodium efflux, cells from mannitol-perfused pigs exhibited only increased active sodium efflux. In this viral enteritis, altered sodium transport occurring in the jejunum, the region of the intestine infected appears to be associated with defective epithelial cell function. The precise nature of the abnormalities in sodium transport, their relationship to disturbances of transport of other solutes, and to virus epithelial cell interaction remain to be defined.
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PMID:Transmissible gastroenteritis. Mechanisms responsible for diarrhea in an acute viral enteritis in piglets. 482 28

We looked for the presence of interferon in the digestive tract of newborn piglets infected with a virulent strain of transmissible gastroenteritis virus (Coronaviridae). High levels of type 1 interferon activity were found early in the disease in jejunal and ileal parts of the intestine as well as in the serum. Enterocytes appeared to be involved in the interferon synthesis. These findings raise the question of the role of interferon in the pathogenesis of viral enteritis.
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PMID:High interferon titer in newborn pig intestine during experimentally induced viral enteritis. 616 24

The interferon (IFN) response was studied in two different models of viral enteritis of the neonate. In rotavirus infected calves, IFN synthesis could be detected in the intestine and in the blood at the time of the diarrheic symptoms. A kinetic study on canulated calves suggested that systemic IFN is of intestinal origin. During TGEV infection (Transmissible gastroenteritis virus) of the newborn piglet, an acute disease which leads to 100% mortality, IFN was found at very high titres (1 000-20 000 u/ml) in the intestine, blood, urine and other organs. Intestinal IFN synthesis started some hours after the onset of diarrhea and was very transient, i.e. no more detectable two days p.i. Unlike the calf situation, IFN response in the serum lasted much longer suggesting an extra-intestinal origin. As a confirmation, piglets infected with cell-adapted strains had high levels of circulating IFN before the onset of intestinal IFN and of diarrhea. Virus and IFN were found in the lungs, due to a so far unrecognized tropism of TGEV for the macrophages. These findings indicate that the pathogenesis of TGEV is more complex than previously claimed.
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PMID:Interferon induction in rotavirus and coronavirus infections: a review of recent results. 620 63

Fecal specimens were obtained from 1,160 infants and young children with acute nonbacterial gastroenteritis over a period of 2 years. A total of 100 specimens were obtained from age-matched asymptomatic controls. The specimens were examined for the presence of viruses by electron microscopy. Viruses or virus-like particles frequently associated with enteritis were detected in 27% (314 of 1,160) of the symptomatic patients. No viruses or virus-like particles were detected in the 100 control subjects. Rotavirus was detected in 73% (230 of 314) of the virus-positive samples. The mean age of rotavirus-positive patients was 11.5 months, although the patients ranged in age from 2 weeks to 5 years. Of the symptomatic patients, 45 (14%) exhibited small virus-like particles (15 to 40 nm) in the feces in the absence of any other detectable pathogen. Some of the virus-like particles observed in these patients appeared to be similar to astrovirus, and some appeared to be similar to the Otofuke agent or possibly minireovirus. Significantly, however, the mean age of infants with enteritis from whom these small virus-like particles were recovered was 4.5 months (range, 10 days to 19 months). Our findings confirmed the already-known fact that rotaviruses constitute the most important cause of viral enteritis in young children. In addition, small viruses may be an important cause of gastroenteritis in infants under 5 months of age.
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PMID:Potential spectrum of etiological agents of viral enteritis in hospitalized infants. 640 78

1. We studied intestinal glucose transport in pigs during the acute and convalescent phases of an invasive viral enteritis, transmissible gastroenteritis. 2. When diarhoea was severe 40 h after experimental infection, net absorption of glucose, Na+ and water, measured by marker perfusion in the jejunum, was reduced; the enhancement of Na+ and water absorption in response to increasing perfusate glucose concentrations up to 120 mmol/l was diminished compared with the response observed in control and convalescent pigs. 3. Measured in vitro, 40 h after infection, unidirectional fluxes of 3-O-methyl-D-glucose across the jejunal epithelium were reduced and net absorption of the sugar was obliterated. Phlorizin (0.05 mmol/l), which completely inhibited net 3-O-methyl-D-glucose absorption in control tissue, had no significant effect on transmissible gastroenteritis jejunum. 4. Our data suggest that in this invasive viral enteritis, which closely resembles human rotavirus enteritis, glucose absorption is impaired as a result of defects in both active and passive glucose flux. 5. Differences between the mechanisms of viral diarrhoea, demonstrated by our study and those of the enterotoxigenic diarrhoeas, should be taken into consideration in formulating active therapeutic measures for children with acute viral diarrhoea.
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PMID:Intestinal glucose transport in acute viral enteritis in piglets. 724 53

Rotaviruses (RV) are the most common etiological agents in acute gastroenteritis (GE) in children in the first years of life. Data from the national scientific literature show that RV is responsible of 26% of all cases of hospitalisation for diarrea in children, resulting the most frequently identified agent. The Italian database of hospital discharge, freely available from the web site of the national Ministry of Health, was searched to investigate the epidemiology of RV gastroenteritis. The mean number of hospitalisation for RV enteritis in children in the first 4 years of live was 4.758 in the years 2001, 2002 and 2003, representing 84% of viral enteritis. RV was identified as agent in 17% of all intestinal infectious diseases in this age group. This percentage shows the important role of RV in severe gastrointestinal infections; it is however much lower than the value expected from specifically performed surveys. This underestimation may be attributed to the high number of undefined gastroenteritis found in the database (54%), to the scarce sensitivity of the hospital discharge code, and to the fact that the analysis was performed using only the principal diagnosis. A specific immunisation strategy, safe, effective, cost-effective and easy to perform, could have a great impact on the incidence of the disease and on the associated costs.
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PMID:[Hospitalisation associated with Rotavirus gastroenteritis in Italy, 2001-2003, evaluated by means of ICD9-CM diagnostic codes]. 1720 91

Noroviruses were detected in 48.4% of 192 children (<3 years of age) hospitalized for gastroenteritis in Palermo, Italy, during 2004; predominant genotypes were GGIIb/Hilversum and GGII.4 Hunter. Of children with viral enteritis, 19.6% had a mixed norovirus-rotavirus infection. The severity of infection was lower for norovirus than for rotavirus but increased in co-infection.
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PMID:Norovirus and gastroenteritis in hospitalized children, Italy. 1825 18

Transmissible gastroenteritis virus (TGEV), the etiological agent of transmissible gastroenteritis (TGE), is the major cause of viral enteritis and fetal diarrhea in swine neonates, resulting in significant economic losses to the swine industry. The Chinese vaccine strain H165 of TGEV was derived from a virulent field strain H16 by serial passage in vitro. Strain H165 has been proven to be safe in piglets and pregnant sows and displays efficacy against TGEV infection. In this study, we report the complete genome sequences of strains H165 and H16, obtained by sequencing several overlapping fragments amplified from viral RNA and our findings from sequence and phylogenetic analyses. The genomes were 28,569 nucleotides in length, including the poly (A) tail. No deletions or insertions were detected in the H16 genome sequence after continuous passage in vitro; however, we found 27 nucleotide mutations in strain H165 compared with strain H16, resulting in 16 amino acid changes distributed among the genes 1, S, 3, and sM. An A to G nucleotide mutation was found in the intergenic region between the 3a and 3b genes. Furthermore, six unique nucleotides identified in the genome sequence of H165 could be used as makers to differentiate the H165 vaccine strain from wild-type TGEV strains. Our findings from phylogenetic analysis may enhance our understanding of the evolution of TGEV, as well as the other coronaviruses.
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PMID:Molecular characterization of a Chinese vaccine strain of transmissible gastroenteritis virus: mutations that may contribute to attenuation. 2022 83

The primary causes of mortality were identified in postmortem examination of 339 (90.9%) of 373 farmed mink (Neovison vison; syn. Mustela vison) from January 2009 through June 2014 at the Utah Veterinary Diagnostic Laboratory (Logan, Utah). Mink were raised under farm conditions in the Intermountain West in North America, except for 1 submission of mink from Wisconsin. In the 339 mink where cause(s) of death were established, 311 (91.7%) died from a single disease or condition, whereas 28 (8.3%) had 2 diseases or conditions contributing to death. Where cause(s) of death were evident, 11 diseases accounted for 321 (94.7%) of the diagnoses: bacterial pneumonia (67, 18.8%), Aleutian mink disease (61, 17.7%), mink viral enteritis (56, 16.2%), hepatic lipidosis (28, 8.1%), nutritional myopathy (24, 7%), bacterial enterocolitis (17, 4.9%), bacterial septicemia (16, 4.6%), starvation (15, 4.3%), epizootic catarrhal gastroenteritis of mink (14, 4.1%), pancreatitis (13, 3.8%), and bacterial metritis (10, 2.9%). In 34 (9.1%) animals, a cause of death was not evident. In an additional 16 (4.3%) of the mink, botulism was suspected from clinical history but could not be confirmed by laboratory testing. Control measures for the most common causes of death in farmed mink include testing and removal of positive animals (Aleutian mink disease), vaccination (Pseudomonas aeruginosa pneumonia, mink viral enteritis), avoidance of obesity in mink (hepatic lipidosis), and environmental management, including maintaining clean water cups, floors, feed troughs, cages, feed silos, feed truck tires, workers' shoes, dining areas for farm personnel, leather mink handling gloves, street clothes, and coveralls.
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PMID:Causes of mortality in farmed mink in the Intermountain West, North America. 2607 44


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