Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A fecal filtrate of human origin containing the Norwalk agent of epidemic viral gastroenteritis was administered by stomach tube to chimpanzees in an attempt to induce diarrheal disease. Significant postchallenge serum antibody rises against Norwalk viral antigens were demonstrated in all animals using the techniques of immune electron microscopy and radioimmunoassay. In addition, viral antigens were detected in feces from five of nine animals using radioimmunoassay. Clinical illness characterized by diarrhea and/or vomiting did not occur. Infection was transmitted subsequently by feeding four additional chimpanzees a fecal filtrate prepared from one of the previously infected animals. Development of an antibody response in four animals and detection of viral antigen in two animals that received this passage filtrate indicated that viral replication had occurred in the absence of clinical illness. The availability of the chimpanzee as an experimental animal host susceptible to infection with the Norwalk agent should facilitate the study of epidemic viral gastroenteritis.
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PMID:Experimental infection of chimpanzees with the Norwalk agent of epidemic viral gastroenteritis. 9 64

Three healthy, young adults suddenly experienced the onset of slow gastric emptying. Their symptoms began in February, 1975 in association with a brief illness consistent with a viral gastroenteritis. They complained of early satiety, nausea, and vomiting when they ate solid food and they had lost 11-25 kg in body weight in 8-12 mo. On admission, their physical examinations and laboratory studies were within normal limits. Their stomachs emptied a barium mixture normally, and fiberoptic endoscopy did not detect any abnormalities. The slowed gastric emptying of food was documented with radioisotopic gastric emptying studies. The prolonged emptying rates of 2 patients were reduced 90% with metoclopramide. In association with metoclopramide therapy, the patients were able to eat more food, and they regained 8-10 kg of body weight in 4-6 mo. Their histories raise the possibility that their initial illness may have damaged the mechanisms which control the gastric emptying of food.
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PMID:Sudden onset of slow gastric emptying of food. 45 51

Infants and young children are particularly susceptible to a recently identified viral enteritis which is highly contagious and seems both common and universal. In this disease, virus invades the upper intestinal epithelium, causing acute diarrhoea with early fever and vomiting. We studied a similar disease in pigs, infecting three-week-old animals with transmissible gastroenteritis virus (TGE), which also invades the upper intestinal epithelium. In this model, diarrhoea is massive 16-40 hours after infection, when stools contain increased electrolytes but no excess of sugar. In the jejunum of intact pigs at the 40-hour stage we found altered Na+ and water flux, decreased mucosal activities of disaccharidases and Na+, K+-ATPase, but normal adenylate cyclase activity. At the same stage the response of Na+ flux to glucose was blunted in jejunal epithelium studied in Ussing short-circuit chambers and in suspensions of villous cells; Cl- flux responded normally to theophylline, and thymidine kinase and sucrase activities of cells isolated from jejunal villi were similar to those found in crypt cells. Probably by 40 hours after infection most virus has been shed from the mucosa. Viral diarrhoea clearly differs from enterotoxigenic diarrhoea. Consideration of its pathogenesis must take into account the dynamic nature of the mucosal epithelium and the factors governing differentiation of enterocytes as they migrate from crypt to villus. Sufficient information is available now to characterize one specific and apparently prevalent viral enteritis in man and to identify additional viral enteritides. There is hope that preventative therapy can be developed. Our understanding of the mechanisms of viral diarrhoea is limited, but the availability of an animal model and the promise of others makes us optimistic that these deficiencies can be remedied. Greater understanding of the pathogenesis of viral diarrhoea should better the active therapy of affected infants and children.
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PMID:Viral gastroenteritis: recent progress, remaining problems. 104 55

Children suffering from mild to moderate (3 to 6%) dehydration likely caused by viral gastroenteritis are often hospitalized because they are unable to tolerate oral fluids. We studied 17 such children, aged one to six years, who were otherwise healthy. All had isonatremic dehydration and were treated with 30 ml/kg of 3.3% dextrose and 0.3% saline over a period of three hours in the emergency department before being discharged. No patient required admission to the hospital. Only one patient required another course of rapid intravenous rehydration and subsequently improved without hospitalization. Although all our patients experienced vomiting before treatment, 65% had no vomiting after treatment. Rapid intravenous rehydration is an effective treatment, for children with mild to moderate dehydration secondary to presumed viral gastroenteritis, that obviates the need for hospitalization.
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PMID:Rapid intravenous rehydration in the pediatric emergency department. 204 10

During a 15-month period, 621 hospitalized children with acute gastroenteritis and 152 control children were investigated for etiologic agents of the disease. Putative enteropathogens were identified in 86% of the patients and 10% of the controls. Common viral agents associated with gastroenteritis among children included rotaviruses (45%) and enteric adenoviruses (4%). Bacterial pathogens infecting children were Salmonella serotypes (24%), enterotoxigenic Escherichia coli (9%), Campylobacter jejuni (7%), enteropathogenic E. coli (7%), Shigella (4%), and enterotoxigenic Aeromonas sp. (1%). The highest incidence of infections was observed in the 3-25 month age group. Mixed infections were observed in 12% of the patients. Viral gastroenteritis was clinically mild and of short duration. Upper respiratory tract infections, vomiting, and watery stools were common features. In contrast, bacterial gastroenteritis was more severe; stools were frequently bloody and abdominal pain, cramps, shock, convulsions, and milk intolerance were predominant clinical features. Comparative analysis revealed differential features of bacterial and viral gastroenteritis which should help clinicians to make a tentative diagnosis and to start treatment early.
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PMID:Microbial etiology of acute gastroenteritis in hospitalized children in Kuwait. 279 54

In recent years it has been demonstrated that a group of viruses, Rotavirus for the children and Norwalk agent for adults, are a highly significant cause of acute gastroenteritis during the months of winter ("winter vomiting disease"). The Rotavirus was identified by Bishop et al. as a double-stranded RNA virus that can be isolate from faeces of children with acute gastroenteritis. Viral gastroenteritis is an autolimitate disease, although under certain conditions it may even lead to severe disease and death by profound dehydration and electrolyte imbalance; it is characterized by nausea, vomiting, diarrhea and others minor symptoms. This entity only affects children between 3 months and 6 years of age, with a little prevalence for the males. Breast-fed babies are commonly thought to be less likely than artificial-fed babies to suffer from infective diarrhea. Rotavirus infection is also known to occur in parents of infected children, but in this situation the symptoms are generally mild or absent and they needn't medical attention. The Rotavirus invade mainly the epithelium of the proximal intestine where they make a cytopatic and physiologic alteration (deficience in Na and K-ATPsa activity) that determines a disturbances of water and electrolyte transport across the epithelium thus contribute to the diarrhea. The best methods for detecting this type of viral gastroenteritis are electron microscopy and, specialy, the complement fixation test. In this moment we have not specific therapy for this new disease but because its epidemiological importance it must be in all clinical minds.
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PMID:[Viruses and gastroenteritis (author's transl)]. 624 84

The essence of the problem, as previously reported, indicated that few complications of acute appendicitis occur as long as the infection is contained within the appendix, but once the invading bacteria have penetrated the peritoneal appendicular surface or have invaded the regional circulation, any one or more of a series of serious complications can develop. Thus, rightfully, emphasis has been placed upon early removal of the inflamed appendix before penetration has occurred as the best method of preventing complications. We have shown that early appendectomy is predicated on early diagnosis and that diagnostic delay is not limited to extremes of age. The diagnosis may be obscured by an accurate, although misleading, history of prior acute attacks, by precident acute disease, such as viral gastroenteritis and by unimpressive symptoms blunted by intercurrent chronic illness, such as diabetes mellitus. If the elements of periumbilical pain, anorexia, nausea or vomiting and the migration of pain to the right lower abdominal quadrant are contained within the clinical history, one must suspect transmural progression of acute appendicitis; frequent inpatient examinations will allow earliest diagnosis and, thereby, fewest perforations and their attendant serious complications. Misdiagnosis is common. Any patient observed for an ostensibly nonsurgical acute condition of the abdomen who fails to improve markedly during a brief course of appropriate specific or supportive therapy must be thoroughly re-evaluated as a potential surgical candidate. Despite the proliferation of accessible laboratory tests and imaging procedures, the early diagnosis of appendicitis rests upon the clinical skills of the physician. A high index of suspicion is crucial. As Doctor Warfield M. Firor, former senior surgeon commented: "Pain and tenderness at any point where the appendix can lie must raise the diagnostic possibility of appendicitis."
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PMID:Reasons for delay of the diagnosis of acute appendicitis. 670 39

Diarrheal diseases are a major cause of childhood morbidity and mortality worldwide. Viruses are the leading cause of diarrhea, and rotavirus is the major cause of severe dehydrating diarrhea in both developed and developing countries. Children with viral gastroenteritis generally present with watery non-bloody diarrhea, often with vomiting and low grade fever. Disease is self-limited and treatment is simple--fluid and electrolyte replacement, preferably via the oral route, with early refeeding. While various adjunctive therapies, such as bismuth subsalicylate and oral immunoglobulins, appear promising, they cannot be routinely recommended at this time. Prevention is the key: by good personal hygiene--particularly good handwashing, by maintaining safe water supplies, and in the future, by an effective rotavirus vaccine.
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PMID:Rotavirus and other viral causes of gastroenteritis. 783 2

Rotaviruses and adenoviruses are the main aetiologic pathogens of gastroenteritis in infants. Adults may also be concerned with usually mild clinical symptoms. An epidemic of viral gastroenteritis occurred in a long-term hospitalization ward from July 25 to August 21, 1991: 101 patients. This study involved 26 females and 6 males with a mean age of 86 years (range 70-101 years), presenting clinical symptoms of gastroenteritis. The clinical attack rate was 27.7%. Outcome was favourable for the majority of patients who recovered in 4-5 days. The main clinical signs were diarrhoea (90.6%), hyperthermia (18.8%) and vomiting (18.8%). Virology investigations gave the diagnosis of 8 rotavirus infections, 6 adenovirus infections and 2 rotavirus and adenovirus mixed infections. Among staff members, 3 rotavirus and one adenovirus infections were diagnosed. The precise origin of the epidemic could not be determined from rotavirus electropherotypes obtained from stools of elderly and paediatric patients hospitalized during the same period. This outbreak recalls the viral involvement in diarrhoeal episodes of elderly people. These episodes of viral gastroenteritis are responsible for high morbidity in the elderly and may upset a precarious physiological state.
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PMID:[Epidemic of viral gastroenteritis in an elderly community]. 789 6

An outbreak of diarrhoea and vomiting began at a hospital for the elderly on the 25 October 1991. The symptoms and pattern of spread suggested a viral aetiology from a point source. Electron microscopy confirmed the presence of Norwalk virus. The first wave of illness affected 37 patients and 28 staff. Secondary cases occurred on all wards. Analytical studies of food consumed at three lunchtime meetings by staff and visitors to the hospital demonstrated a clear association between eating sandwiches and subsequent illness. The source of the outbreak was probably a food handler involved in the preparation of sandwiches. Control measures were implemented and the outbreak was declared over on the 11 November 1991. At this time 95 patients and 69 staff (including six visitors) had been affected. The implications for the future investigation and prevention of outbreaks of viral gastroenteritis in closed communities are discussed. An audit of the action taken during the outbreak resulted in the development of standards for the investigation and control of local outbreaks.
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PMID:A hospital outbreak due to Norwalk virus. 791 86


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