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Query: UMLS:C0232605 (regurgitation)
 8,217 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1977, outbreaks of disease associated with serious losses occurred on twenty cattle farms. This disease was due to the fact that the animals had been fed brewers' grains. The clinical picture was marked by anorexia, profuse salivation, regurgitation and dehydration. The course of the disease varied with the severity of the attack. Toxicological tests were negative. Cl. botulinum type B as well as toxin type B were found to be present in the brewers' grains fairly often. As a rule, Cl. botulinum was also detected in the rumen contents and faeces. The treatment of the animals is described; this resulted in recovery in a number of cases. When experimental animals were fed brewers' grains from farms on which outbreaks had occurred, this induced similar clinical pictures. The results of studies on the aetiology and pathogenesis are discussed. It is concluded that the clinical picture was an atypical form of botulism caused by Cl. botulinum type B. Possible causes of this abnormal clinical picture are discussed in greater detail.
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PMID:[Food poisoning in cattle caused by ingestion of brewers' grains contaminated with Clostridium botulinum type B (author's transl)]. 34 20

Seven Florida sandhill cranes (Grus canadensis pratensis) and 6 greater sandhill cranes (Grus canadensis tabida) were exposed to lead-base paint containing 27% lead. One bird of each subspecies died enroute to the hospital, with a clinical history of anorexia, weakness, and open-mouth breathing of 36 hours' duration. There were no gross lesions, and microscopic lesions were limited to focal hepatic necrosis and hemosiderosis. Two of each subspecies of cranes developed clinical signs of lead poisoning, which included anorexia, weakness, green diarrhea, regurgitation, and open-mouth breathing. Diagnosis of lead poisoning was confirmed on the basis of blood lead concentrations ranging from 146 microgram/100 ml to 378 microgram/100 ml. These 4 cranes were treated successfully with calcium disodium edetate intramuscularly. Seven of the birds remained clinically normal despite high blood lead levels, especially in the greater sandhill cranes.
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PMID:Lead poisoning in sandhill cranes. 41 73

Ten captive-reared African black-footed penguins (Spheniscus demersus) from a large outdoor colony were monitored for avian malaria, using several diagnostic tests. One treatment regimen was evaluated. Thin smear blood evaluation enabled detection of seven parasitemias involving Plasmodium relictum and Plasmodium elongatum in the penguins. Leukocytosis (relative lymphocytosis) was characteristic of infected birds. Parasitemia was detected as early as 21 days prior to onset of clinical signs (depression, anorexia, regurgitation, pale mucous membranes, and respiratory distress). The single bird that died had clinical signs only a few hours prior to its death. Treatment consisted of 0.03 mg of primaquine phosphate base/kg body weight, administered orally once daily for 3 days. Oral chloroquine phosphate therapy, given simultaneously, was administered in an initial loading dose of 10 mg of chloroquine phosphate base/kg body weight, followed by doses of 5 mg/kg at 6, 18 and 24 hours after the initial chloroquine dose. This treatment regimen prevented mortality and cleared parasites from the blood. Recurrences of malaria occurred in two birds that had received this treatment.
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PMID:Avian malaria in African black-footed penguins. 52 78

The authors report about 3 cases of the congenital adreno-genital syndrome in first-born children with a high weight at birth (3900, 3600, and 4200 g) who perished in early infancy. One child, who was considered to be a boy, died of septic postoperative complications; during the operation the uterus, ovaries, tubes, phenomena of pseudofemale hemaphroditis were observed. The considerably enlarged adrenals were gyral, goffered and their cortex consisted of cells of the fetal zone. Two other boys, who perished at the age of 3 1/2 and 2 1/2 months, were sick from the birth. In the clinical picture there prevailed anorexia, dehydration, regurgitation, periodic vomiting, convulsions, clonic spasms, Hyponatrema, hyperkalemia, sudden arrest of the heart, rose no suspicion in pediatricians with respect to the salt-losing form of the adreno-genital syndrome. Post-mortem examination revealed congenital hyperplasia of the adrenals, whose cortex consisted of the fetal zone cells.
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PMID:[Congenital adrenocortical hyperplasia]. 127 80

We describe 17 full-term newborns presenting with vague symptoms related to the upper gastrointestinal tract (anorexia, poor feeding, retching, regurgitation, and incessant crying) during their stay in the maternity unit. After an esophagogastroduodenoscopy performed between days 2 and 5 of life, the babies could clearly be divided into two groups. Twelve babies (group 1) had an extremely severe esophagitis (circular ulcerations), without gastroduodenitis. In the remaining five babies (group 2), the upper gastrointestinal tract was unaffected. Allergic, infectious, metabolic, and toxic etiologies were excluded. Esophageal pH monitoring data were within normal ranges in all. All babies of group 1 were treated as follows: prone anti-Trendelenburg position, cisapride, and cimetidine syrup. Symptoms and lesions disappeared within 48-72 h. Reendoscopy after 72 h showed an almost normal esophagus with greatly improved histology. These observations highlight four points of interest: (a) the existence of an extremely severe ulcerative esophagitis in apparently healthy newborns, (b) the very rapid clinical and histological recovery, (c) the difficulties in predicting esophagitis on clinical grounds, and (d) the mysterious origin despite thorough assessment. The distribution of the lesions (more severe in the upper esophagus), the early onset (almost at birth), the very rapid healing, and the absence of gastric and duodenal lesions are in favor of a possible "traumatic" origin (pharyngeal, esophageal, and gastric suction at birth). Finally, because the condition described is transient, questions arise regarding the necessity of treatment, and we currently do not recommend overtreating newborns presenting with similar symptoms and/or endoscopic findings.
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PMID:Esophagitis of likely traumatic origin in newborns. 140 53

Four female fistulated camels (Camelus dromedarius), 4-5 years of age, were each given two grams of 10% monensin intraruminally daily for six days to study the effect of monensin on the rumen fermentation pattern. Signs of toxicity appeared on the sixth day, and included depression, anorexia, muscular weakness, inability to stand, salivation and regurgitation of ruminal contents. On the eighth day, two animals died. The ruminal contents were replaced in the survivors, but they died on the tenth and eleventh day from the start of the experiment.
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PMID:Monensin poisoning in dromedary camels. 145 38

In a double-blind, placebo-controlled, crossover trial, we investigated the effects of the prokinetic drug cisapride in patients with cystic fibrosis and chronic recurrent distal intestinal obstruction syndrome (DIOS). After a baseline period, 17 patients (12.9 to 34.9 years; 12 boys) received, in random order, cisapride (7.5 to 10 mg) and placebo three times daily by mouth, each for 6 months. Gastrointestinal symptoms (flatulence, abdominal pain, fullness, abdominal distension, nausea, anorexia, heartburn, diarrhea, vomiting and regurgitation) were scored three times monthly and physical examinations assessed. At baseline and at each 6-month period, assessment included food intake for 7 days, 3-day stool collection, pulmonary function tests, and abdominal radiographs. During cisapride therapy compared with placebo, there were significant reductions in flatulence (p less than 0.005), fullness, and nausea (p less than 0.05). Patients with the worst symptom scores benefited most from cisapride. With cisapride, 12 patients felt better and three worse (p less than 0.05); physicians judged 11 patients improved and two worse (p less than 0.05). No side effects were noted. There were no significant differences between cisapride and placebo periods in nutritional status, x-ray scores, pulmonary function, food intake (fat, protein, calories), stool size and consistency, and fecal losses of fat, bile acids, chymotrypsin, and calories. For acute episodes of DIOS, intestinal lavage was needed 6 times in 4 patients during treatment with cisapride, and 11 times in 6 patients receiving placebo. In comparison with unselected patients with cystic fibrosis and pancreatic insufficiency who were receiving enzyme supplements and who had no distal intestinal obstruction, fecal fat losses (percentage of intake) were almost twice as high in the study group with DIOS (31.2 +/- 20.6% vs 16.2 +/- 17.6%; p less than 0.01). We conclude that in the dosage used, long-term treatment with cisapride appears to improve chronic abdominal symptoms in patients with cystic fibrosis and DIOS, but fails to abolish the need for intestinal lavage. Cisapride treatment had no effect on digestion and nutritional status of cystic fibrosis patients with pancreatic insufficiency.
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PMID:Effects of cisapride in patients with cystic fibrosis and distal intestinal obstruction syndrome. 223 Dec 17

As far as the authors know this is the first case of Key-Gaskell-syndrome being described in Switzerland. The clinical signs of megaoesophagus, anorexia, constipation, dryness of all mucous membranes, reduced tear production, protrusion of the membrana nictitans, mydriasis, regurgitation and bradycardia are pathognomonic and can't be mistaken by any other disease. The subject of the Key-Gaskell-syndrome is a dysfunction of the autonomic nervous system. Histopathological changes are exclusively related to the autonomic nervous system and to neurons of some nuclei in the cranial nerves. Less severe changes can be found in the neurons of the spinal cord or in the dorsal root ganglia. The etiology remains still unclear. There is a relationship to the grass sickness syndrome in horses and to dysautonomia of man and dog.
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PMID:[Key-Gaskell syndrome in a cat in Switzerland]. 271 Nov 66

Myenteric ganglioneuritis and encephalomyelitis were diagnosed in an umbrella cockatoo. The cockatoo exhibited clinical signs that were milder than those associated with this syndrome, such as anorexia, muscle wasting, regurgitation, depression, and changes in fecal consistency. The gross lesions also differed from earlier reports in that only the duodenum and proximal jejunum were grossly dilated. Normally the proventriculus and ventriculus are dilated without visible intestinal changes. The histopathological lesions, however, such as perivascular cuffs in the brain stem and muscular mass of the ventriculus and proventriculus, were similar to earlier reports. A virus was suspected, although transmission and isolation of a virus has not occurred in other reports and was not attempted in this case.
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PMID:Encephalitis, proventricular and ventricular myositis, and myenteric ganglioneuritis in an umbrella cockatoo. 275 72

A ferret was examined because of anorexia, repeated episodes of regurgitation, and subsequent dehydration. Radiography had revealed a radiodense midesophageal foreign body. Results of endoscopy of the esophagus, however, could not confirm the diagnosis. Contrast radiography revealed esophageal perforation, with subsequent penetration of the foreign body into the right pleural space, causing pleural effusion. Surgical repair of the esophagus was performed, and a gastrostomy feeding tube was inserted to provide adequate nutrition during esophageal healing. Nine days after surgery, radiography revealed a severe stricture at the esophageal surgical site. Surgery was repeated; the esophagus was transected, the stricture was removed, and esophageal tissues were closed in 2 layers. Systemically administered antibiotics and gastrostomy tube feedings were continued throughout the post-operative healing period. The esophagus healed with a mild stricture that diminished over time in response to corticosteroid administration.
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PMID:Medical and surgical management of esophageal foreign body in a ferret. 279 82


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