Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Naturally occurring bovine sarcocystosis caused death and illness in eight dairy heifers. Clinical disease was characterized by cachexia, peripheral lymph node enlargement, and anemia. Increased amounts of serum enzymes and anti-Sarcocystis antibody titers were present in affected animal. Macroscopic findings in two heifers at necropsy included emaciation and serous atrophy. Necropsied heifers (No. 1 and 2) contained different developmental stages of Sarcocystis cruzi; each stage was characterized by specific histopathologic findings. Heifer 1 had vascular endothelial schizonts in various soft tissues, with mild mononuclear cell infiltration, alveolar capillary fibrinous thrombi, and multifocal splenic necrosis. Heifer 2 had developing young S cruzi cysts, in myofibrils of cardiac and skeletal muscles, with a concurrent multifocal degenerative myositis. Marked lymphoid hyperplasia occurred in both heifers.
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PMID:Bovine saccocystosis: patholgic features of naturally occurring infection with Sarcocystis cruzi. 11 89

Ovine progressive pneumonia, a chronic, insidious disease of adult sheep, has a relentless course leading to dyspnea, emaciation, and death. Clinical observations and serologic tests are adequate for making a tentative diagnosis. The agar gel immunodiffusion test seems to be the best serologic procedure for indicating infection with the virus but cannot be used to predict morphologic changes or clinical disease, inasmuch as many clinically unaffected animals carry the virus. A definitive diagnosis is based on finding lesions and isolating virus. Affected lungs are large and heavy as a result of interstitial accumulation of lymphoid cells and fibromuscular tissue. Frequently, interstitial lesions are accompanied by bronchopneumonia from secondary bacterial infection. The causal virus can be isolated from infected lungs by cocultivation with primary ovine or bovine cells.
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PMID:Diagnostic features of ovine progressive pneumonia. 21 18

Thirty-five 6-week-old guinea fowl keets, seronegative for maternal antibodies to Newcastle disease virus, were infected with Herts strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (IM) or intranasally (IN). Clinical signs were first noticed four days post infection (PI) in the group infected IM but five days PI in the group infected IN with Herts strain of Newcastle disease virus. These clinical signs were similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Herts strain. The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets. The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets. Neither gross or microscopic lesions were observed in keets that had received the Kumarov strain.
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PMID:Pathogenicity of two strains of Newcastle disease virus in the grey-breasted helmet guinea fowl. 150 75

Trimetrexate is a nonclassical folate antagonist that is active against a number of experimental murine and human tumor cell lines. To assess its toxicity, rats were administered single or repeated (daily x5) doses by either the oral or the intravenous route. Oral doses were 0, 90, 180, 295, and 375 mg/kg (single dose) and 0, 32, 65, and 80 mg/kg (daily x5). Intravenous doses were 0, 6, 20, and 60 mg/kg (single dose) and 0, 10, 20, and 30 mg/kg (daily x5). In the oral studies, signs of toxicity first appeared 2 to 3 days after initiation of dosing. Clinical signs included hypoactivity, diarrhea, urine scald, rhinorrhea, emaciation, and death. Significant pathologic findings were degenerative enteropathy in small and large intestines, bone marrow hypocellularity, decreased WBCs (neutrophils, lymphocytes), generalized lymphoid depletion, and testicular tubular degeneration. Except for the testicular changes, these effects were most severe in animals dosed at 65 and 80 mg/kg in the oral x5 study (65-70% mortality). Repeated oral doses at 32 mg/kg and single oral doses through 375 mg/kg caused only mild to moderate effects and less than 5% mortality. In contrast, single intravenous doses at 60 mg/kg resulted in immediate death (20% mortality) due to apparent CNS toxicity. Intravenous doses below 60 mg/kg were essentially asymptomatic. Toxicity in the intravenous studies was limited to decreased WBCs, splenic and thymic lymphoid depletion (repeated dosing), and testicular tubular degeneration and/or atrophy. Except for the testicular lesions, most of the effects in the oral and intravenous studies were reversible within 4 weeks. The results show that the acute toxicity of trimetrexate in rats is somewhat dependent on its route of administration, although the spectrum of effects is qualitatively similar to that observed in other species and with other folate antagonists. The dose-limiting toxicity of trimetrexate in rats common to both routes of administration is myelosuppression.
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PMID:Toxicity of the anticancer folate antagonist trimetrexate in rats. 153 75

To elucidate relationship between disease progress and immunologic alteration in feline immunodeficiency virus (FIV) infection, we classified naturally infected cats into clinical stage groups using the working criteria modified from those for human immunodeficiency virus (HIV) infection. Among the five distinct stages described for HIV infection, the three phases; asymptomatic carrier (AC), AIDS related complex (ARC), and acquired immunodeficiency syndrome (AIDS), were evaluated for concanavalin A (Con A)-induced lymphocyte blastogenic activities by using glucose consumption assay. There was a significant decrease of lymphocyte response in AC phase. The loss of response became marked as the disease progressed to ARC and AIDS, with an almost complete loss of mitogen response in AIDS phase. In addition to the loss of a lymphocyte function, AIDS in FIV infection was characterized by marked emaciation, anemia or pancytopenia, and postmortem evidences of opportunistic infections and lymphoid depletion.
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PMID:Altered mitogen response of peripheral blood lymphocytes in different stages of feline immunodeficiency virus infection. 216 50

Feed containing sublethal T-2 toxin concentrations (12.5 and 25 ppm) was fed to adult rabbits. The animals ate 60-70% less toxin-containing food. The dry matter content of their feces decreased significantly (on an average by 10%). The nutrient digestibility of the feed containing 12.5 ppm T-2 toxin, was increased by 2-6% and that of the 25 ppm T-2 toxin level decreased by 4-11% as compared to the control values. The rabbits showed emaciation, subacute catarrhal gastritis, necrosis of the lymphoid cells of the intestinal mucosa, depletion and necrosis in the lymphoid follicles of the ampulla ilei, spleen and lymph nodes. Necrosis of the cells of mononuclear phagocyte system and myeloid hemacytogenesis was characteristic. The toxin concentration of feces, cecotroph and urine was proportional to intake.
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PMID:Effect of T-2 toxin on feed intake, digestion and pathology of rabbits. 259 40

Rabbits were treated with a single oral dose (1, 2, 4, 6, 8, 10 or 15 mg/kg body mass) of T-2 fusariotoxin. Doses of 4 mg or higher killed the animals in 24 to 48 h. As opposed to the controls, in the treated rabbits gross pathological and histopathological examinations revealed acute catarrhal gastroenteritis, necrosis of lymphoid cells of the gastrointestinal mucosa, centrolobular dystrophy of the liver, necrosis of cells of the mononuclear phagocyte system (MPS) in the liver, tubulonephrosis, focal dystrophy of the adrenal cortex, lymphocyte depletion involving both T- and B-cell-dependent zones of the lymphoid organs (spleen, lymph, ampulla ilei), and depletion and necrosis of the myelopoietic cell colonies of the bone marrow. Similar but milder changes were observed in surviving rabbits exsanguinated 48 h after treatment. In addition to the direct damage done to the digestive tract mucosa and liver, the toxin severely damaged the cells participating in humoral and cell-mediated immunity and in the local defence of the intestinal mucosa, and markedly impaired phagocytosis and granulocytopoiesis. In another experiment rabbits were given oral doses of 2 mg/kg body mass T-2 toxin daily for several days. One rabbit was killed by bleeding every day. In rabbits killed beyond day 7 there was subacute catarrhal gastritis, emaciation, and hypertrophy of the adrenal cortex.
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PMID:Acute toxicological experiment of T-2 toxin in rabbits. 262 5

The histopathological changes and the course of graft-versus-host (GVH) disease were studied in the rat model of small-bowel transplantation using the Lewis----LBN-F1 strain combination. Allograft-induced GVH disease led to the recipients' death from enteritis, dermatitis and emaciation after 14.4 +/- 2.9 days (heterotopic grafts) and 14.0 +/- 0.7 days (orthotopic grafts). Histologic evidence of dermatitis (epidermal hyperkeratosis and cutaneous infiltration by mononuclear and polymorphonuclear cells) and enteritis (villous blunting and sloughing, inflammatory infiltrate of the recipient's own intestine) appeared on the 9th to 13th postoperative days, and these changes became fulminant within 2-3 days. The lymphatic tissues of the Lewis grafts and the LBN-F1 host underwent a course of progressive lymphoid depletion and loss of follicular architecture beginning on the 5th postoperative day. Throughout the postoperative course, the small-bowel graft remained intact. The relative spleen weight progressively increased until shortly before death, when a marked reduction was observed. The clinical triad of diarrhea, diffuse dermatitis, and hypertrophy of the lymphoid organs followed by their atrophy suggests a diagnosis of GVH disease rather than rejection of the small-bowel allograft. The diagnosis can be confirmed by biopsy of a recipient lymph node or the intestinal allograft (cave perforation) if it is accessible.
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PMID:Graft-versus-host disease induced by small bowel allografts. Clinical course and pathology. 395

Five isolates of Aspergillus ochraceus, obtained from peanuts, were grown separately on sterile, moist corn for 14 days and fed to 1-day-old Babcock B-300 cockerels to evaluate their toxic effects. Two isolates were highly toxic, causing death of all birds during the 1st week of the experiment. Two isolates were moderately toxic, causing severe growth suppression with some deaths occurring throughout the 3-week test period. One isolate had no apparent effect. When the two most toxic isolates (diets) were diluted, survival time increased but severe growth suppression was evident. Postmortem examinations revealed a few small hemorrhages in the proventriculi of birds which died between the 2nd and 5th days. Emaciation, dehydration, and dry, firm gizzard linings were observed throughout the experiment. Extensive hepatic injury consisting of either fatty changes or necrotic foci was the principal microscopic finding. Suppression of bone marrow activity and depletion of lymphoid elements in the spleen and bursa of Fabricius were also found. The severity of the histopathological changes was directly related to the concentration of ochratoxin A in the diets.
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PMID:Mycotoxicity of Aspergillus ochraceus to chicks. 541 41

Studies on acute toxicities of bestatin (NK421) were carried out in both sexes of mice and rats, and male dogs. NK421 was administered subcutaneously, intraperitoneally and orally in mice and rats, and orally in dogs respectively. Mice and rats were observed for 14 days after treatment and LD50 values were calculated by the probit method. NK421 showed very low toxicity and no death occurred in any species following the oral administration of the maximum dose capable of dosing such as 4 g/kg for mice, 2 g/kg for rats and 1.2 g/kg for dog. General toxic signs seen in mice and rats following subcutaneous and intraperitonial injections were as follows; depression, suppressed movement, piloerection, inhibition of spontaneous movement, anorexia and emaciation. Death occurred within 5 days after administration. The toxic target organs of NK421 were found to be kidney, lymphoid tissue and liver based on histopathological examination of dead animals.
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PMID:Toxicological studies on bestatin. I. Acute toxicity test in mice, rats and dogs. 667 28


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