Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duck plague (Duck virus enteritis) was disgnosed in a resident population of Muscovy ducks (Cairina moschata) on a small game farm in Alberta. This disease has not been reported previously in Canada. Clinical signs consisted of cyanosis, depression and acute death. Necropsy of two Muscovy ducks revealed lesions typical of the disease. There were ulcerations with pseudomembranes in the small intestine, ulcerations with caseous plaques in the esophagus and eosinophilic intranuclear inclusion bodies in the spleen. Clinical disease with mortality was reproduced in young ducklings injected with tissue homogenates from field cases. All surviving inoculated ducklings seroconverted to highly significant titres of neutralizing antibodies to duck virus enteritis (DVE) virus. All attempts to isolate the agent in embryonating duck eggs or primary tissues cultures of duck and chicken kidney were negative. Identification of the DVE virus was accomplished by serum neutralization with ducklings as the host system.
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PMID:An outbreak of duck virus enteritis (duck plague) in Alberta. 18 Mar 2

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

Structural and functional alterations in duodenal mucosa from 17 children with rotavirus enteritis were assessed. Structural changes were found in specimens from all patients. Patients with the most severe mucosal damage were more likely to require intravenous therapy to correct dehydration. Depression of one or more mucosal disaccharidases was found in 14 of 16 patients. Repeat duodenal biopsy three to eight weeks later in six patients showed marked improvement. The study clearly shows that rotavirus can cause a marked structural and functional lesion in the upper small intestine which is rapidly reversible.
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PMID:Structural and functional abnormalities of the small intestine in infants and young children with rotavirus enteritis. 21 31

42 horses were examined. The physical signs with relation to circulatory insufficiency and the abdominal disease were registered following a two-phased examination procedure. Great prognostic value was found in the degree of circulatory insufficiency judged by pulse rate and character, filling of the jugular vein, skin temperature, colour of mucous membranes, capillary refill time, sweating, depression, skin turgor and degree of enophthalmus. In making a causal diagnosis the abdomen was examined for shape, tenderness, peristaltic sounds, gastric dilation by siphoning, abnormal rectal findings and macroscopic changes in peritoneal fluid. Greatest diagnostic difficulties were encountered in cases of intestinal atonia, acute enteritis and torsion of the colon. In selected (severe) cases laboratory tests were obtained. Blood samples were examined for packed cell volume, hemoglobin, red and white blood cell counts, differential white blood cell count, blood gases and acid-base status, lactate, serum total protein and albumin, plasma sodium, potassium, chloride, calcium, magnesium, inorganic phosphorus, glucose, creatinine, BUN, total bilirubin, ASAT, CK, BASP and GGT. Peritoneal fluid was examined for red blood and white cell counts, total protein, specific gravity, pH and lactate, and enzymes as in blood. Laboratory results generally confirmed the clinical signs of shock, and packed cell volume and blood lactate were regarded to be of greatest prognostic interest. Although the performed laboratory information, macroscopic evaluation was thought to reveal sufficient information in most cases. It was concluded that supervening shock is of decisive importance in severe forms of colic, and that a careful and repeated evaluation of the circulatory insufficiency often provides one with a tentative prognosis although the final diagnosis is not obtained. In spite of therapy fatal outcome was found in all seriously shocked horses.
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PMID:Colic in the horse. A clinical and clinical chemical study of 42 cases. 52 9

Eastern equine encephalomyelitis (EEE) was the cause of heavy mortality in coturnix quail (Coturnix coturnix) reared commercially in South Carolina. The birds showed depression, tremor, and partial paralysis that advanced into complete paralysis, torticollis, and death within a few hours. The only consistent lesion on necropsy was a catarrhal enteritis in the duodenal area. The disease spread rapidly to all pens throughout the two houses on the farm in all birds over 2 weeks old, and mortality ranged from 40 to 90% in the various pens within the house. Total mortality exceeded 90,000 birds. Age groups on the farm ranged from 1 day to 8 weeks, at which time the birds went for slaughter. It appears that the initial infection was spread by cannibalism. EEE was diagnosed by isolating the virus in fertile eggs and suckling mice, with subsequent identification by complement-fixation. This is the first documented case of EEE in coturnix quail.
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PMID:Eastern equine encephalomyelitis outbreak in coturnix quail. 69 63

A mortality in muscovy ducklings caused by infection with the intestinal fluke, S. globulus, is described. The disease was characterised by depression, anorexia, wasting, diarrhoea and high mortality. The major pathological lesions were associated with the attachment sites of the flukes and consisted of severe enteritis with ulceration, principally affecting the jejunum, but also involving the duodenum and ileum. Experimental infections were produced in ducklings by oral administration of either G. austrialis infected with S. globulus metacercariae or S. globulus metacercariae or S. globulus metacercariae. The small, dextral, operculate snail G. australis was identified as the intermediate host and G. australis and an unidentified planorbid as transport hosts. L. tomentosa was also able to be a transport host. The epidemiology of the outbreak and aspects of acquired resistance are presented.
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PMID:The occurrence of the intestinal fluke Sphaeridiotrema globulus in domestic ducks in New South Wales. 84 14

A 5-week-old mixed-breed dog was examined because of emaciation and depression associated with chronic anorexia, diarrhea, and vomiting. Its rectal temperature was subnormal and it died on the day of admission. At necropsy, small focal lesions were distributed through the liver. Enteric alterations included catarrhal enteritis with fluid contents, excess production of mucus, and mucosal hyperemia. Microscopically, the hepatic lesions were disseminated foci of coagulative necrosis, with little or no associated inflammatory cell response. Numerous organisms morphologically consistent with Bacillus piliformis were demonstrated within viable hepatocytes at the periphery of the necrotic foci and in the intestinal mucosa. Numerous coccidial forms were found within the epithelial cells of the intestinal mucosa, which was focally necrotic.
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PMID:Tyzzer's disease in a dog. 127 Mar 43

Eastern equine encephalitis (EEE) was diagnosed in a flock of emus in southeastern Louisiana. The outbreak involved juvenile and adult breeders ranging in age from 20 to 36 months, with an attack rate of 76% and a case fatality rate of 87%. The diagnosis was confirmed by isolation and characterization of the viral agent, and by detection of EEE antibody in two recovered emus. High mortality was preceded by marked depression, hemorrhagic diarrhea, and emesis of blood-stained ingesta. On postmortem examination, hemorrhagic enteritis and multiple petechia of viscera were observed. Microscopic changes included severe necrosis of hepatocytes, intestinal mucosa, and necrotizing vasculitis of the spleen and lamina propria of the intestine. No nervous system lesions were observed. This outbreak occurred concurrently with EEE in horses and was attributed to unseasonably heavy rainfall with an abundance of arthropod vectors and proximity to free-living reservoir host species.
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PMID:Eastern equine encephalitis in a flock of emus (Dromaius novaehollandiae). 141 19

In the late 1970s, a new infectious disease in horses, involving acute enteritis, was recognised in the Potomac River area of Maryland, U.S.A. The causative agent was identified subsequently as a new species of rickettsial organism, later named Ehrlichia risticii. Since then, the disease has been reported in many other states, and in enzootic areas vaccination is common. Signs associated with the clinical disease included depression, fever, anorexia, decreased or absent intestinal sounds, profuse watery diarrhoea and laminitis. However, considerable variation in clinical manifestations has been reported in both the natural and experimental disease. Accurate diagnosis depends on serological testing; currently, the immunofluorescent antibody test (IFA) is used widely, although an enzyme-linked immunosorbent assay (ELISA) has been developed recently. Mortality in untreated cases is 15 to 35 per cent. Antibiotics of the tetracycline series have shown activity against the organism in vitro, in an in vivo murine model and appear to be useful in clinical cases.
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PMID:Equine monocytic ehrlichiosis (Potomac horse fever): a review. 177 55


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