Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0740441 (acute diarrhea)
 2,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rotavirus infection is usually localized to the intestine but involvement of extra-intestinal sites, including the respiratory tract, liver, kidney, lymph nodes, and central nervous system, has been reported. The extra-intestinal spread of the virus may occur through blood since viraemia has been documented occasionally in animals and humans. Nevertheless, the questions of how common viraemia is in immunocompetent children and whether it is associated with extra-intestinal manifestations remain unsolved. Serum samples from 54 immunocompetent children hospitalized for acute diarrhea were evaluated prospectively for the presence of rotavirus RNA by nested reverse transcriptase-polymerase chain reaction (RT-PCR) to investigate this issue. Rotavirus antigens were detected in the stools of 14 children. A bacterial aetiology was documented in 14 cases, and in the remaining cases the aetiology remained unknown. Rotavirus RNA was detected in the blood of 9/14 (64.3%) rotavirus infected children but in no child with diarrhea of other origin. Positive RT-PCR was associated with high fever and/or evidence of extra-intestinal involvement. All positive samples were collected within 3 days of illness onset, suggesting that viraemia was detectable for only a few days. Children in whom rotavirus was detected only in stool samples had high fever but no other extra-intestinal feature. These data suggest that viraemia is common in children infected with rotavirus, which may be associated with extra-intestinal involvement.
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PMID:Viraemia is a common finding in immunocompetent children with rotavirus infection. 1583 82

Recently, rotavirus antigenemia and viremia have been identified in patients with acute gastroenteritis. This study examined rotavirus viremia in children hospitalized for acute gastroenteritis in order to establish its association with fecal shedding of rotavirus, infecting genotypes and antibody marker of acute infection. Thirty-one pairs of stool-serum specimens were collected from November 2004 to February 2005 together with clinical information. All paired specimens were screened for rotavirus RNA by RT-PCR using the VP6 gene primers. All stool and serum specimens were tested for rotavirus antigen and anti-rotavirus IgM respectively by ELISA. Sixteen of 31 stool-serum pairs showed the presence of rotavirus RNA. Nine stool and two serum specimens were positive only by RT-PCR. The total positivity in rotavirus RNA was significantly higher in both stools (80.6%) and sera (58.1%) than that of stool antigen (38.7%) and anti-rotavirus IgM (25.8%) (P < 0.01). All PCR positive paired specimens were typed for the VP7 (G) and VP4 (P) genes. Five of sixteen pairs could be typed for both genes. Three of the five pairs showed concordance (G2P[4]/G2P[4]) while two showed discordance (G12P[8]/G2P[4], G8P[4]/G2P[4]) in the genotypes detected in stool and serum specimens respectively. The study documents a high frequency of rotavirus viremia in patients with acute diarrhea. The discordance of rotavirus strains at the genotypic level in the serum and stool of individual patients with diarrhea suggests the susceptibility of extra-intestinal sites for rotavirus infection and the possibility of differential dissemination of rotavirus strains from the intestine.
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PMID:High frequency of rotavirus viremia in children with acute gastroenteritis: discordance of strains detected in stool and sera. 1904 Feb 95

Antigenemia is commonly detected in children with acute rotavirus diarrhea, but the prevalence of viremia has not been clearly defined. We examined antigenemia in plasma and RNAemia in peripheral blood mononuclear cells (PBMC) of children with acute diarrhea by EIA, RT-PCR, and Southern hybridization, using primers and a probe specific to rotavirus NSP4 gene. We detected the presence of rotavirus antigen in 33.3% and almost full-length NSP4 gene in 70.8% of the acute-phase plasma and PBMC, respectively. In contrast, antigenemia and RNAemia were detected in 0% and 4.2% of the convalescent-phase plasma and PBMC, respectively, which were similar to antigenemia (0%) and RNAemia (7.7%) in healthy controls. We demonstrated an increase in the proportions of activated myeloid dendritic cells (mDC) and activated plasmacytoid DC (pDC) in acute-phase PBMC of patients when compared to those in convalescent phase of patients and in PBMC of healthy controls. The activation of mDC peaked on days 2-4 after illness onset, and the activation of acute-phase pDC appeared to correlate with levels of antigenemia. High prevalence of NSP4 gene in acute-phase PBMC indicates possible rotavirus replication in white blood cells, and extraintestinal spread and the activation of DC may have implications for the prevention of rotavirus disease in children.
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PMID:Antigenemia, RNAemia, and innate immunity in children with acute rotavirus diarrhea. 2217 5

Porcine epidemic diarrhea virus (PEDV), a member of the genera Alphacoronavirus in the family Coronaviridae, causes acute diarrhea/vomiting, dehydration and high mortality in seronegative neonatal piglets. For the last three decades, PEDV infection has resulted in significant economic losses in the European and Asian pig industries, but in 2013-2014 the disease was also reported in the US, Canada and Mexico. The PED epidemic in the US, from April 2013 to the present, has led to the loss of more than 10% of the US pig population. The disappearance and re-emergence of epidemic PED indicates that the virus is able to escape from current vaccination protocols, biosecurity and control systems. Endemic PED is a significant problem, which is exacerbated by the emergence (or potential importation) of multiple PEDV variants. Epidemic PEDV strains spread rapidly and cause a high number of pig deaths. These strains are highly enteropathogenic and acutely infect villous epithelial cells of the entire small and large intestines although the jejunum and ileum are the primary sites. PEDV infections cause acute, severe atrophic enteritis accompanied by viremia that leads to profound diarrhea and vomiting, followed by extensive dehydration, which is the major cause of death in nursing piglets. A comprehensive understanding of the pathogenic characteristics of epidemic or endemic PEDV strains is needed to prevent and control the disease in affected regions and to develop an effective vaccine. This review focuses on the etiology, epidemiology, disease mechanisms and pathogenesis as well as immunoprophylaxis against PEDV infection.
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PMID:Porcine epidemic diarrhea virus infection: Etiology, epidemiology, pathogenesis and immunoprophylaxis. 2591 24

Porcine deltacoronavirus (PDCoV) (family Coronaviridae, genus Deltacoronavirus) is a novel swine enteropathogenic coronavirus that causes acute diarrhea/vomiting, dehydration and mortality in seronegative neonatal piglets. PDCoV diarrhea was first reported in the US in early 2014, concurrently with co-circulation of porcine epidemic diarrhea virus (PEDV) (family Coronaviridae, genus Alphacoronavirus). The origin of PDCoV in pigs and also its sudden emergence or route of introduction into the US still remains unclear. In the US, since 2013-2014, the newly emerged PDCoV and PEDV have spread nationwide, causing a high number of pig deaths and significant economic impacts. The current US PDCoV strains are enteropathogenic and infect villous epithelial cells of the entire small and large intestines although the jejunum and ileum are the primary sites of infection. Similar to PEDV infections, PDCoV infections also cause acute, severe atrophic enteritis accompanied by transient viremia (viral RNA) that leads to severe diarrhea and/or vomiting, followed by dehydration as the potential cause of death in nursing piglets. At present, differential diagnosis of PDCoV, PEDV, and transmissible gastroenteritis virus (TGEV) is essential to control viral diarrheas in US swine. Cell culture-adapted US PDCoV (TC-PDCoV) strains have been isolated and propagated by us and in several other laboratories. TC-PDCoV strains will be useful to develop serologic assays and to evaluate if serial cell-culture passage attenuates TC-PDCoV as a potential vaccine candidate strain. A comprehensive understanding of the pathogenesis and epidemiology of epidemic PDCoV strains is currently needed to prevent and control the disease in affected regions and to develop an effective vaccine. This review focuses on the etiology, cell culture isolation and propagation, molecular epidemiology, disease mechanisms and pathogenesis of PDCoV infection.
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PMID:Porcine deltacoronavirus infection: Etiology, cell culture for virus isolation and propagation, molecular epidemiology and pathogenesis. 2708 31

Porcine epidemic diarrhea virus (PEDV), a member of the genus Alphacoronavirus in the family Coronaviridae, causes acute diarrhea and/or vomiting, dehydration and high mortality in neonatal piglets. Two different genogroups of PEDV, S INDEL [PEDV variant containing multiple deletions and insertions in the S1 subunit of the spike (S) protein, G1b] and non-S INDEL (G2b) strains were detected during the diarrheal disease outbreak in US swine in 2013-2014. Similar viruses are also circulating globally. Continuous improvement and update of biosecurity and vaccine strains and protocols are still needed to control and prevent PEDV infections worldwide. Although the non-S INDEL PEDV was highly virulent and the S INDEL PEDV caused milder disease, the latter has the capacity to cause illness in a high number of piglets on farms with low biosecurity and herd immunity. The main PEDV transmission route is fecal-oral, but airborne transmission via the fecal-nasal route may play a role in pig-to-pig and farm-to-farm spread. PEDV infection of neonatal pigs causes fecal virus shedding (alongside frequent detection of PEDV RNA in the nasal cavity), acute viremia, severe atrophic enteritis (mainly jejunum and ileum), and increased pro-inflammatory and innate immune responses. PEDV-specific IgA effector and memory B cells in orally primed sows play a critical role in sow lactogenic immunity and passive protection of piglets. This review focuses on the etiology, transmission, pathogenesis, and prevention and control of PEDV infection.
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PMID:Porcine epidemic diarrhea virus (PEDV): An update on etiology, transmission, pathogenesis, and prevention and control. 3250 52