Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1291077 (bloating)
 1,674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven sheep were assigned to three groups in order to study acute urea toxicity. Groups I, II and III were dosed with 0.5, 0.6 annd 0.75 g/kg of urea, respectively. The mean survival times were 165, 109 and 60 minutes, respectively. The following clinical signs such as pronounced muscle fasciculation, trembling, grinding teeth, ataxia, lateral recumbency, bloating, regurgitation, hyperesthesia, mydriasis and convulsions were observed. Anuria and lack of salivation were also present. The primary cause of death in this study was due to respiratory arrest and not cardiovascular collapse. Plasma examinations showed a marked increase in glucose, ammonia and urea levels but no change in ketone body concentration.
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PMID:Acute urea toxicity in sheep. 64 59

Cattle in two herds developed signs of bloating, increased salivation and lacrimation, depression, respiratory distress, ataxia, and death after ingestion of hay that contained large amounts of poison hemlock (Conium maculatum). Twenty of 30 Angus cows and calves were affected in the first herd (2 died). In the second herd, 5 of 30 Holstein heifers were affected (1 died). The Conium alkaloids, coniine and gamma-coniceine, were quantified in the hay, the plants from the responsible hayfield, and the urine of affected animals.
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PMID:Toxicosis in dairy cattle exposed to poison hemlock (Conium maculatum) in hay: isolation of Conium alkaloids in plants, hay, and urine. 155 71

Two clinically different episodes of nitrate toxicosis in heifers at the same dairy were evaluated to determine whether dietary supplements could have contributed to the confounding signs of illness. The first episode followed a 24-hour period of feeding mismanagement and resultant overconsumption of both a protein/nonprotein nitrogen supplement and a monensin supplement. This episode was characterized by ataxia, bloating, and death, without the classic clinical signs of dyspnea, salivation, cyanosis, and dark-colored blood, or the cardinal histologic changes of cyanosis, tissue staining, petechiations, or congestion. Approximately 5 weeks later, another episode developed, without the feeding mismanagement or the presence of supplements, and was characterized by classic signs of nitrate toxicosis along with response to methylene blue treatment. In both episodes, the feed source was the same, with high concentrations of nitrate. Heifers of both episodes had high ocular nitrate values, confirming the toxicoses. The difference was the availability of supplements. Calculation of exposure makes it unlikely that either the nonprotein moiety or the monensin moiety could have reached toxic values. However, the cell-level effects of monensin may have caused the animals to not display classic signs of nitrate toxicosis, confusing the diagnosis and treatment. This report demonstrates how field toxicosis can differ from reports of toxicoses caused by single etiologic agents. Practitioners must be aware of the potential for interactions between (and confounding by) commercially used feed components.
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PMID:Forage-related nitrate toxicoses possibly confounded by nonprotein nitrogen and monensin in the diet used at a commercial dairy heifer replacement operation. 202 41

Cresol poisoning was suspected in agroup of cattle presented for slaughter at a federaly inspected plant in Illinois. Four cattle died shortly after being unloaded at the slaughter facility, while another animal died after being returned to the feedlot of origin in Iowa. The clinical signs in the affected cattle were lethargy, depression, ataxia, leg weakness, sternal recumbency, dehydration, and severe bloating. Metacresol (3-methyl phenol), commonly found in disinfectants used to clean and sanitize farm equipment and barns, was detected in rumen content from 4 necropsied animals ranging from 25.3 to 52.6 ppm. The exact source of exposure was not identified, but was probably accidental on the farm of origin or on the trailers used for animal transit to the slaughter plant.
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PMID:Suspected cresol poisoning in cattle presented for slaughter. 1182 64

Celiac disease develops from an autoimmune response to specific dietary grains that contain gluten. Diagnosis can be made based on the classical presentation of diarrhea, fatty stools, and abdominal bloating and cramping, as well as the presence of specific serum antibodies. In addition, gluten ingestion has increasingly been found to be associated with other conditions not usually correlated with gluten intolerance. The subsequent diversity of the clinical presentation in these cases can complicate decision-making and delay treatment initiation in conditions such as ataxia, headaches, arthritis, neuropathy, type 1 diabetes mellitus, and others. This review explores the etiology and pathology of celiac disease, presents support for the relationship between gluten and other diseases, and provides effective screening and treatment protocols.
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PMID:Celiac disease and gluten-associated diseases. 1616 73

Non-celiac gluten sensitivity (NCGS) is a syndrome characterized by intestinal and extraintestinal symptoms related to the ingestion of gluten-containing food in subjects who are not affected by either celiac disease (CD) or wheat allergy (WA). The prevalence of NCGS is not clearly defined yet. Indirect evidence suggests that NCGS is slightly more common than CD, the latter affecting around 1% of the general population. NCGS has been mostly described in adults, particularly in females in the age group of 30-50 years; however, pediatric case series have also been reported. Since NCGS may be transient, gluten tolerance needs to be reassessed over time in patients with NCGS. NCGS is characterized by symptoms that usually occur soon after gluten ingestion, disappear with gluten withdrawal, and relapse following gluten challenge within hours/days. The 'classical' presentation of NCGS is a combination of irritable bowel syndrome-like symptoms, including abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation), and systemic manifestations such as 'foggy mind', headache, fatigue, joint and muscle pain, leg or arm numbness, dermatitis (eczema or skin rash), depression, and anemia. In recent years, several studies explored the relationship between the ingestion of gluten-containing food and the appearance of neurological and psychiatric disorders/symptoms like ataxia, peripheral neuropathy, schizophrenia, autism, depression, anxiety, and hallucinations (so-called gluten psychosis). The diagnosis of NCGS should be considered in patients with persistent intestinal and/or extraintestinal complaints showing a normal result of the CD and WA serological markers on a gluten-containing diet, usually reporting worsening of symptoms after eating gluten-rich food. NCGS should not be an exclusion diagnosis only. Unfortunately, no biomarker is sensitive and specific enough for diagnostic purposes; therefore, the diagnosis of NCGS is currently based on establishing a clear-cut cause-effect relationship between the ingestion of gluten and the appearance of symptoms by a standardized double-blind, placebo-controlled gluten challenge.
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PMID:Gluten Sensitivity. 2660 37

A young female Aldabra giant tortoise (Adabrachelys gigantea) was presented with anorexia, ataxia, severe constipation and bloating. Analysis revealed liver disease and collected biopsy diagnosed Candida krusei infection. Despite Itraconazole treatment, the tortoise got worse and died. Full necropsy was performed; microbiology showed Candida krusei presence in liver, but histopathology didn't confirm fungal presence with special stains, so scanning electron microscopy was essential to prove a detailed diagnosis of extensive mycosis.
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PMID:Multiple Organ Dysfunction Syndrome (MODS) induced by Candida krusei in an Aldabra giant tortoise (Aldabrachelys gigantea) and confirmed by electron microscopy analysis. 3002 65