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)

We determined the presence or absence of rotavirus antigen by the enzyme-immunoassay in 126 fecal specimens obtained from infants with acute gastroenteritis, and also measured IgA antibody titers against rotavirus in stool samples. Rotavirus-positive specimens amounted to 72. Thirty-five specimens in 126 stool samples were found to contain the IgA antibody against rotavirus. The IgA antibody against rotavirus was detected in 21% and 44% of fecal specimens obtained from age groups of less than 3 years and 3 years or more, respectively, showing a significant difference between these 2 groups. The geometric mean titer of specific IgA antibody was also higher in the latter group than in the former. This specific IgA antibody was detected in 32% and 22% of boys and girls, respectively, showing a tendency of high incidence among boys. The detection rate of specific IgA antibody was significantly higher in rotavirus-negative fecal specimens (41%) than in rotavirus-positive fecal specimens (18%). As for infants having the rotavirus antigen in their feces, their symptoms were severe in many of the infants at the age of less than 3 years, while many of the infants at the age of 3 years or more only had mild symptoms. There was a significant difference between the 2 age groups. When these infants were analyzed according to the presence or absence of specific IgA antibody in their feces, no difference in scores of severity of clinical symptoms was seen between the 2 groups. However, IgA antibody-negative infants more frequently had fever, over 39 degrees C and significantly more developed whitish and watery stool in comparison with IgA antibody-positive infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fecal IgA antibody against rotavirus and clinical manifestations of acute viral gastroenteritis in children]. 217 May 43

In order to facilitate measurement of antirotaviral IgA in large collections of faeces and secretions, adaptations of enzyme immunoassay methods for estimating antirotaviral IgA and IgM in duodenal fluid, saliva, faeces and serum were studied. To quantitate specific IgA, a single dilution of each sample was assayed. Results were expressed as antirotaviral IgA units derived from a standard curve. Units were calculated by log-logit analysis on computer. There was strong correlation between antirotaviral IgA units and end-point titres in 257 faecal samples (correlation coefficient r = 0.92) and in 182 duodenal fluids and salivary samples (correlation coefficient r = 0.74). The assay was validated using acute and convalescent faeces from children with or without rotavirus infection. Immune conversions in IgA were detected in 33 (75%) of the children by units and 34 (77%) by titres. None of nine children with gastroenteritis due to other infectious agents showed immune conversions to rotavirus. A monoclonal capture IgM assay showed similar end-point titres and numbers of immune conversions when compared with a direct assay for antirotaviral IgM in serum and secretions. Use of the capture method eliminated false-positive reactions with the cell control. The assay for antirotaviral IgA units in secretions is simple, rapid, reproducible and reliable, and has proven of value in longitudinal epidemiological studies of rotavirus coproIgA profiles. Both the capture IgM technique and the single dilution IgA method permit analysis of large numbers of specimens and are appropriate for examination of immune responses to natural rotavirus infection or during vaccine trials.
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PMID:Evaluation of end-point titration, single dilution and capture enzyme immunoassays for measurement of antirotaviral IgA and IgM in infantile secretions and serum. 255 25

Serum anti-gliadin antibody (AGA) titres were estimated by diffusion in a gel enzyme-linked immunosorbent assay in children with coeliac disease (n = 11), protracted diarrhoea of non-coeliac causes (n = 110), acute gastroenteritis (n = 20), protein energy malnutrition (n = 20), and asymptomatic, well-nourished children (n = 66). The mean IgG and IgA AGA titres were significantly higher (p less than 0.001) in children with coeliac disease than in any other groups. There was no significant difference (p greater than 0.01) in AGA titres in relation to age, nutritional status, or severity of villous injury. In patients with coeliac disease AGA titres showed a good correlation with disease activity. The specificity and sensitivity of the assay are discussed.
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PMID:Serum anti-gliadin antibody profile in childhood protracted diarrhoea due to coeliac disease and other causes in a developing country. 260 3

Virus-specific serum IgM, IgA, and IgG were detected by ELISA in sera obtained from children with rotavirus gastroenteritis and fractionated by gel filtration. Specific IgM and IgG could be easily demonstrated, whereas IgA were very low. Moreover, polymeric IgA (p-IgA) were not present, whereas in the immune response against viruses causing systemic infections, they are synthetised in large amounts.
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PMID:Specific serum IgA in rotavirus gastroenteritis. 282 76

The development of mucosal immunity is presumed to be the most important marker of rotavirus infection. The practical difficulties of obtaining small-bowel secretions stimulated this study of the antibody response to acute rotavirus infection at other sites. Forty-four infants admitted to the hospital with rotavirus gastroenteritis had serum, saliva, and feces collected at the acute phase (median, 5.5 days), during convalescence (median, 33.5 days), and 4 months later (median, 12.2 weeks). A subgroup of 19 children also had duodenal juice collected in parallel. Rotavirus-specific immunoglobulin G (IgG), IgA, secretory immunoglobulin, and IgM were measured and compared in all samples. The results showed that the estimation of antirotavirus serum IgM, serum IgG, duodenal juice IgA, and duodenal juice IgM by an enzyme immunoassay indicated an immune response to severe primary rotavirus infection in all children. Four months later, the levels of serum IgG and IgA served as the most sensitive markers of the preceding rotavirus infection. The predictive accuracies of immune responses at different sites in relation to a positive IgA immune response in the duodenum were calculated. Fecal IgA predicted duodenal IgA rotavirus antibodies with accuracies of 86% at 1 month and 92% at 4 months. The high sensitivity of serum IgM and IgG in detecting rotavirus infection and the high predictive accuracy of fecal IgA as an indicator of duodenal IgA abrogates the need for duodenal intubation to detect (or monitor) an immune response to rotavirus infection. This finding has important practical implications for epidemiological studies of acute diarrhea in children and in rotavirus vaccine trials.
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PMID:Comparison of serum and mucosal antibody responses following severe acute rotavirus gastroenteritis in young children. 283 91

We studied rotavirus-specific antibodies in paired sera from 71 hospitalized infants with acute rotavirus gastroenteritis. Most of the infants were less than six months old. Infants with serological evidence of a secondary rotavirus infection were excluded. With an enzyme-linked immunosorbent assay, 46% of the 71 infants studied showed specific IgM in convalescent sera. Titers of specific IgG and IgA increased in 7% and 2% of the infants, respectively. The presence of specific IgM correlated positively with age and severity of clinical symptoms. With a neutralization test, 59% of the infants showed a seroconversion: 20% to a single serotype (7% to serotype 1, 7% to serotype 3, and 6% to serotype 4), 21% seroconverted to two serotypes (nearly exclusively to serotypes 1 and 3), and 18% seroconverted to three serotypes (exclusively to serotypes 1, 3, and 4). No infant seroconverted to serotype 2 or to the heterologous (bovine) serotype 6.
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PMID:Seroconversion patterns to four human rotavirus serotypes in hospitalized infants with acute rotavirus gastroenteritis. 284 6

Seventeen children (mean age: 2.0 years, range: 36 days-8 years) hospitalized with acute gastroenteritis were investigated. Thirteen children had a rotavirus infection while four did not. Rotavirus serum IgA as well as ScIg, i.e., antirotavirus immunoglobulin containing secretory component, increased rapidly after rotavirus infection. While rotavirus IgA persisted in serum for at least 6 months, rotavirus ScIg disappeared from serum in less than 4 months. Rotavirus IgG could be detected in serum during the early stage of the infection and was still high after 6 months. The patients with nonrotavirus acute gastroenteritis did not show any of the above-mentioned serological hallmarks of those with rotavirus infection. The amounts of rotavirus ScIg found in serum about 1 week after the infection correlated to the amounts of rotavirus ScIg in duodenal fluid. Six months after the infection, rotavirus IgA was found in the feces of the majority of the patients while rotavirus ScIg could be detected only in one patient. The amounts of rotavirus IgA in sera and intestinal secretions showed identical patterns in the acute phase of the disease as well as after recovery. The same applied to rotavirus ScIg. These findings could be useful in future evaluations of vaccines and immunity against rotavirus infections.
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PMID:Intestinal and serum immune response to a naturally acquired rotavirus gastroenteritis in children. 298 2

Secretory IgA (sIgA) and IgG from porcine milk and serum, respectively, [3H]uridine-labelled virus, swine testis and pig kidney cell lines were used to examine the neutralized virus-cell interaction. Transmissible gastroenteritis virus (TGEV), 99.99% neutralized by immunoglobulin, was able to attach to the cells. Moreover, sIgA enhanced virus attachment. However, the neutralized virus was unable to enter cells, as demonstrated by the action of proteinase K which removed it from the cell surface. It was also found that pre-attached virus was still neutralizable and that IgG and sIgA had similar TGEV-neutralizing capacities.
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PMID:Neutralizing secretory IgA and IgG do not inhibit attachment of transmissible gastroenteritis virus. 300 92

The preexisting levels of rotavirus IgA and IgG were measured in 225 children aged 6 months to 7 years in November, ie, before the "rotavirus season" from January to April. During the following 6 months, all episodes of acute gastroenteritis (GE) were evaluated clinically according to a score system and feces was examined for rotavirus, pathogenic bacteria, and parasites. Furthermore, rotavirus GE (n = 45) as well as asymptomatic rotavirus infections (n = 29) were diagnosed serologically. The preexisting concentrations of rotavirus IgA and IgG measured by ELISA were similar in these two groups. However, preexisting rotavirus IgA in the group of children who developed rotavirus GE correlated with less severe symptoms. Thus vomiting was found in 24% and 63% of the children with detectable and undetectable rotavirus IgA, respectively (P less than 0.025). Moreover, according to the total symptom score of rotavirus GE, 52% of the children with detectable preexisting rotavirus IgA had mild symptoms compared with only 13% of those with undetectable concentrations (P less than 0.025). Rotavirus IgG did not have any protective effect. Age per se had a protective effect; older age (greater than 1.5 years) was related to mild symptoms. According to previous studies of local and intestinal antibody response to a rotavirus GE, it is suggested that rotavirus IgA in serum reflects the immunological status of the intestine concerning rotavirus. It is recommended that studies of rotavirus vaccines include rotavirus IgA response and its protective effect.
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PMID:Protective effect of preexisting rotavirus-specific immunoglobulin A against naturally acquired rotavirus infection in children. 302 56

A prospective study to assess whether milk IgA antibodies against Escherichia coli heat labile-toxin protect breast-fed children against labile toxin-induced gastroenteritis was carried out among infants of a marginal urban area in Guatemala. One hundred and thirty children were kept under surveillance for diarrhea by periodic home visits. Stool specimens were collected from each child routinely every 2-3 weeks and during diarrheal episodes, to study the excretion of labile toxin-producing Escherichia coli. Milk samples from the children's mothers were obtained concomitantly with the fecal specimens of the infants to be analyzed for anti-labile toxin antibodies. Twenty infections by heat-labile toxin-producing Escherichia coli as a sole agent were documented among breast-fed infants. Nine of these infections resulted in gastroenteritis, while the remaining 11 were asymptomatic. At the time of infection children who became sick were ingesting breast milk with significantly (p = 0.028) lower titers of antilabile toxin IgA than those who remained healthy. Only one of the 8 infected children receiving breast milk with high titers (greater than or equal to 256) of anti labile toxin IgA developed diarrhea, compared to 8 of the 12 subjects being fed milk with low titers (less than or equal to 64) (p = 0.025). This is the first report documenting protection by IgA antibodies in milk against labile toxin-induced gastroenteritis in infected breast-fed infants.
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PMID:Breast milk anti-Escherichia coli heat-labile toxin IgA antibodies protect against toxin-induced infantile diarrhea. 305 53


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