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)

The life cycle of a species of murine Eimeria, isolated from a commercial source of mice is described using experimental infections. A pure strain was established starting from a single oocyst administered to Eimeria-free Swiss white mice. The prepatent period was 6 1/2 to 7 days, and the patent period lasted 6 to 10 days. Oocysts were subspherical or ovoid, with a smooth double-layered colourless membrane. Micropila was absent. The sporulated oocysts measured 15.7-25.1 x 14.1-22.0 microns (X780 = 21.3 x 16.9 microns). One to 4 polar granules were present. The oocyst residuum was absent. Sporocysts were ellipsoid, measured 11.5 x 6.3 microns (n = 780), with Stieda body and a compact subspherical sporocyst residuum. The sporozoites were elongated, 17.7 x 3.2 microns (n = 100), partially curled around each other. The endogenous stages were found only in the large intestine, with at least 4 generations of schizonts. Mature 1st generation schizonts, first seen 24 hr post-infection (HPI) measured 10.3 x 10.6 microns and had 8 to 25 merozoites 5.0-10.0 x 1.0-3.0 microns. Mature 2nd generation schizonts were first seen 48 HPI, measured 14.4 x 8.1 microns and had 8 to 20 merozoites 11.0-16.0 x 2.0-3.0 microns. Two forms of presumably 3rd generation schizonts appeared between 72 and 96 HPI: one measuring 13.9 x 8.5 microns, containing large merozoites (17.0-19.0 x 2.0-4.0 microns) and the other measuring 7.3 x 10.4 microns, where 6 to 10 merozoites (8.0-13.0 x 1.0-3.0 microns) were found. Fourth generation schizonts measuring 10.4 x 11.9 microns, with 26 a 48 or more merozoites (8.0-13.0 x 2.0-3.0 microns) were first seen at 132 HPI. Mature macro and microgamonts were first observed at 144 HPI. The sporulation of 72.0% of the oocysts in 2.0% (w/v) potassium dichromate at 23-24 degrees C occurred in 9 days. Usually the infected mice showed depression, anorexia, weight loss, diarrhea or dysentery, and dehydration. The clinical picture w as more pronounced at 6 to 10 days post-infection (DPI). Mortality was highest between the 8th and 13th DPI, with a peak at 9 DPI in groups which received 1.1 x 10(4) to 4.4 x 10(4) oocysts. Groups infected with 5.5 x 10(3), 8.8 x 10(4) or 1.76 x 10(5) oocysts showed different results. Epithelial destruction, edema, inflammation, necrotizing enteritis followed by glandular regeneration and realing were observed restricted to the large intestine. The isolated Eimeria was named E. falciformis var. pragensis based on its morphobiological characteristics.
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PMID:[Morphobiology and pathogenicity of Eimeria falciformis var. pragensis Cerna, Seraud, Mehlhorn & Scholtyseck, 1974 in mouse (Mus musculus)]. 184 3

425 drunken drivers were examined for their driving sentability. The amount of persons with known diseases of digestion (or gastro-enteritis) among the drivers were higher than the average among the normal population. The patients with ulcus and gastritis showed higher nervosity, depression and emotional instability during the medical examination. In addition they showed a higher degree of openness and a tendency to lower blood alcohol concentrations at previous drunken driving. While judging their sentability (for driving) no differences could be made among persons with and without gastro-enteritis.
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PMID:[Diseases of stomach mucosa in the history of alcoholic traffic violators in street traffic]. 224 89

An outbreak of diarrhoea occurred in a Jersey herd after the introduction of new stock. One of the cows was examined and treated unsuccessfully. Clinical findings included depression, fever, dehydration, congestion, signs of colic and a severe diarrhoea. The post mortem examination revealed emaciation, pseudomembranous enteritis, mesenteric lymphadenopathy and focal disseminated hepatic necrosis. Salmonella typhimurium was isolated from the faeces, mesenteric lymph nodes and liver.
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PMID:Salmonellosis in an adult dairy cow. 228 88

Abdominal eumycotic mycetoma caused by Pseudallescheria boydii was diagnosed in a 3-year-old male Siberian Husky. The dog was examined because of weight loss and signs of depression. Initially, pyrexia was the only clinical finding. Antibiotic and corticosteroid treatment was ineffective. Two weeks later, the dog's appetite had decreased, it had vomited a few times, and the caudal portion of the abdomen was sensitive to palpation. Hematologic and serum biochemical abnormalities consisted of anemia, leukocytosis, hypoglycemia, hypoalbuminemia, hyperglobulinemia, and high alkaline phosphatase activity. One week later, the dog's condition continued to worsen, and testicular swelling was observed. The dog was castrated. Microscopic examination of specimens obtained at surgery revealed pyogranulomatous periorchitis with mycetoma granules. Ketoconazole treatment was initiated and continued until the dog died one month later. Necropsy revealed multifocal duodenal ulcers, with transmural pyogranulomatous enteritis, pancreatitis, and peritonitis. This case is unique because the etiologic agent apparently entered via the intestinal tract rather than by contamination of an external wound.
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PMID:Eumycotic mycetoma caused by Pseudallescheria boydii in a dog. 246 20

A retrospective analysis of the medical records of 30 consecutive cases of diarrhea occurring in dogs that were hospitalized in a teaching hospital was performed. A prospective analysis of culture results for Clostridium perfringens of dogs with diarrhea were compared with those of a control nondiarrheal group. Hospital-acquired diarrhea in dogs was found to be associated with multiple serotypes of enterotoxigenic Clostridium perfringens. Other potential etiologic agents could not be isolated. Clinical signs were variable, and included mild depression, anorexia, and soft to watery diarrhea with or without frank blood, mucus, and tenesmus. Fever was not present. There were no hematologic or serum biochemical abnormalities, nor were there any consistent virologic or parasitologic findings. Salmonella spp or Campylobacter spp were not identified by fecal culture. No risk factors could be identified. A dog that was euthanatized on the day it developed diarrhea had intestinal histologic findings suggestive of clostridial enteritis. Dogs with diarrhea had significantly higher fecal clostridial counts than did dogs without diarrhea (mean log10 counts +/- SD = 6.34 +/- 1.79 vs 4.75 +/- 2.07). Enterotoxin was found in the feces of 41% of diarrheic dogs but in only 7% of dogs without diarrhea.
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PMID:Nosocomial diarrhea associated with enterotoxigenic Clostridium perfringens infection in dogs. 254 85

Five-day-old bobwhite quails were inoculated with reovirus and Cryptosporidium previously isolated from the intestinal contents of young, commercially raised bobwhite quails experiencing severe enteritis. Quails inoculated with reovirus alone did not develop clinically apparent disease, infection was localized principally in the intestinal tract, and no lesions were detected. Quails inoculated with Cryptosporidium, alone or with reovirus, developed severe enteritis with high mortality and marked growth depression. Cryptosporidia caused blunting of intestinal villi and provoked a mononuclear cell response in the lamina propria. The severity of intestinal lesions correlated with numbers of parasites. An apparent synergistic effect in dually infected quails was indicated by enhanced Cryptosporidium oocyst shedding, greater numbers of cryptosporidia in the intestinal tracts, and systemic reovirus infection. In addition, multifocal liver necrosis was detected in dually infected quails but was absent in quails infected with only reovirus or Cryptosporidium. The results suggest that Cryptosporidium promoted systemic spread of reovirus, and reovirus intensified Cryptosporidium infection, but no significant synergistic effect on mortality or weight gain was detected. The most important agent in the naturally occurring acute enteritis of bobwhite quails was Cryptosporidium.
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PMID:Experimental reproduction of enteritis in bobwhite quail (Colinus virginianus) with Cryptosporidium and reovirus. 283 66

Two foals aged 35 and 48 h from 2 Thoroughbred studs died several hours after developing clinical signs of depression, severe haemorrhagic diarrhoea and dehydration. Both foals had an acute haemorrhagic enteritis extending from the anterior jejunum to the terminal ileum which was characterised histologically by villus necrosis. Necrotic villi were surrounded by large numbers of rod-shaped Gram positive bacteria. Clostridium perfringens was recovered from the intestines of both foals and the isolates were considered to be C. perfringens type C. Other cases of diarrhoea were also observed in foals of the same age on these 2 studs, but the aetiology of these was not determined.
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PMID:Haemorrhagic necrotising enteritis in foals associated with Clostridium perfringens. 286 48

Sporulated oocysts of Eimeria acervulina were administered orally to cage-housed broilers at a dose of 3.5 X 10(5) resulted in mild subclinical coccidiosis. Clostridium perfringens incorporated in feed at a level of 2.5 X 10(8) organisms/g. produced lesions characteristic of necrotic enteritis. Mortality of 8% (7/80) occurred in birds fed a ration inoculated with Cl. perfringens alone. Mortality of 35% (28/80) was observed in birds which received an oral dose of E. acervulina and which were fed simultaneously with a ration containing Cl. perfringens. Birds which were fed an inoculated ration two days after an oral dose of E. acervulina showed 41% (33/80) mortality. Birds which received an inoculated ration for two days before administration of an oral dose of E. acervulina demonstrated 18% mortality (15/80). Birds which were fed an inoculated ration four days after an oral dose of E. acervulina showed 10% mortality. Infection with E. acervulina reduced the pH of intestinal contents with a simultaneous depression in serum protein. A 39% increase in intestinal passage time from 178 to 248 minutes occurred on the fifth day after infection with E. acervulina. These experiments suggest that necrotic enteritis, attributed to proliferation of a toxigenic strain of Cl. perfringens, followed intestinal stasis and minimal lesions induced by mild intestinal coccidiosis.
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PMID:Etiology and pathogenesis of necrotic enteritis. 286 8

One week after infection with a virulent strain of hemorrhagic enteritis virus (HEV), turkeys were vaccinated for Newcastle disease. The effect of a virulent strain of HEV on turkeys' immune response to Newcastle disease vaccine and the mitogenic response of their whole blood peripheral lymphocytes were examined. The results revealed a statistically significant difference (P less than .01) in the Newcastle disease hemagglutination inhibition (NDHI) antibody titers from turkeys infected with virulent HEV. The NDHI antibody titers were lower in turkeys exposed to virulent HEV before vaccination. There was an initial depression in phytohemagglutinin (PHA) response 1 week postinfection in turkeys infected with virulent HEV strain.
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PMID:Immunosuppressive effects of virulent strain of hemorrhagic enteritis virus in turkeys vaccinated against Newcastle disease. 298 88

Young female pastel mink and young female Sprague-Dawley rats were injected intraperitoneally on 3 sequential days with 50 mg/kg of either 2,4,2',4' tetrachlorobiphenyl (TCB) or 3,4,3',4'-TCB and sacrificed after 7 days. Two control groups were established for each species; one allowed free access to food, and one pair-fed to the 3,4,3',4'-TCB-treatment group. Heart blood was collected from each mink immediately after sacrifice. A complete set of tissues was collected from all animals and placed in buffered formalin. The rats displayed no clinical signs of illness following the administration of either congener, nor were there any significant gross or microscopic lesions created in this species. Mink in the 2,4,2',4'-TCB and control groups remained free of clinical signs and significant gross or microscopic lesions. Mink in the 3,4,3',4'-TCB group developed anorexia within 48 hr after the initial injection, and depression and melena by Day 4. Necropsy on Day 7 revealed a severe necrotizing enteritis with moderate to marked villus atrophy and fusion in the small intestines of all mink in this treatment group. The epithelial necrosis generally spared the basal one-third of the mucosa, and the deep crypt epithelium was often moderately hyperplastic. The mechanism by which 3,4,3',4'-TCB causes this unique lesion is unknown.
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PMID:Comparative toxicology of tetrachlorobiphenyls in mink and rats. II. Pathology. 303 Aug 68


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