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)

Five Holstein Friesian calves varying in age from 7 to 9 weeks old, were suspected of suffering from an inherited granulocytopathy known as bovine leucocyte adhesion deficiency (BLAD). Four of them were examined clinically and at necropsy. The most significant clinical findings were fever, depression, weakness, emaciation, diarrhoea, pseudomembranous gingivitis, loose teeth, respiratory infection and occult blood in the faeces. Significant clinicopathological findings were marked leucocytosis, mainly due to a neutrophilia, hypoalbuminemia, hypogammaglobulinemia, increased alpha- and beta-globulins, elevated alkaline phosphatase enzyme activity, hypoglycaemia, and decreased blood urea concentrations. The necropsy revealed emaciated carcasses, granulomatous to necrotising gingivitis, pseudomembranous to necrotising enteritis with perforations, bronchopneumonia, splenic atrophy, and hypoplasia of the thymus. Histopathological examination supported the macroscopic findings.
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PMID:[Suspected inherited granulocytopathy in four Holstein Friesian calves]. 817 99

Anorexia and emaciation are symptoms which can be found in many diseases either singly or in combination with other unspecific clinical signs such as diarrhea and vomiting. Therefore accurately assessing the medical history, performing a thorough clinical examination and carrying out laboratory tests are all necessary steps in establishing a diagnosis. Further specific examinations such as radiography, ultrasonography or endoscopy may also have to be performed. Since anorexia and emaciation can result in severe consequences for the organism, establishing a definitive diagnosis is important to enable the appropriate therapy to be applied without delay.
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PMID:[Symptoms: anorexia and emaciation]. 834 27

Five specific pathogen free cats were inoculated with feline immunodeficiency virus (FIV) isolated in Japan to observe changes toward development of acquired immunodeficiency syndrome (AIDS)-like disease. All inoculated cats had lymphadenopathy and mild respiratory disease shortly after inoculation. Following the initial acute phase lasting for more than 40 weeks, the clinical signs gradually diminished in three animals, and the asymptomatic carrier (AC) stage was observed at 45 (1 cat) and 70 (2 cats) weeks postinoculation (p.i.). Two of the three cats developed respiratory signs and diarrhea at 105 or 106 weeks p.i. One cat died at 121 weeks p.i. with severe wasting, with necropsy findings consistent with AIDS-related complex (ARC). The others were surviving at 150 weeks p.i. with mild clinical signs or asymptomatic. Another group of two cats developed more severe illness without the AC phase. One died at 48 weeks p.i. with the ARC illness. The other cat developed marked emaciation with diarrhea at 75 weeks p.i., and died at 100 weeks p.i. with a histologic diagnosis suggestive of terminal immunodeficiency. Histologically, the lymph nodes showed serial changes toward the terminal illness, from follicular hyperplasia at the acute phase to the lymphoid depletion at the ARC and AIDS-like terminal stages. The FIV antigen was demonstrated in the lymph nodes. The virus was isolated from peripheral blood mononuclear cells of all the inoculated animals. These data demonstrated possible etiologic association of FIV with development of AIDS-like disorders in the cat.
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PMID:Pathologic features of acquired immunodeficiency-like syndrome in cats experimentally infected with feline immunodeficiency virus. 839 25

A single dose toxicity of calcipotriol (MC903), an anti-psoriasic agent, administered subcutaneously (s.c.) and percutaneously (p.c.) was studied in Slc:SD rats (s.c. and p.c.) and beagle dogs (s.c.). The LD50 values of MC903 were as follows: rats, 2.19 mg/kg in males and 2.51 mg/kg in females by s.c., and more than 15 mg/kg in both sexes by p.c.; dogs, more than 1.5 mg/kg in males by p.c. No sexual difference was noted in LD50 values of rats. Death of rats was observed from 1 to 3 days after administration by both routes. Dead animals showed decreases in body weight and locomotor activity, reddish tear, abnormal gait and dirty hair by both routes. Furthermore, dead animals administered by s.c. showed salivation, nasal discharge, piloerection, ptosis, diarrhea, urorrhea, nasal and vaginal bleeding, subnormal temperature, loose stool, cyanosis, irregular and deep respirations, clonic and tonic convulsions. Survival of rats showed similar signs to those of dead animals except for nasal discharge, nasal and vaginal bleeding, cyanosis, agonal respiration and convulsion. Discoloration of the kidney, white patch of the heart and a dilatation of the stomach wall were observed on macroscopic examinations. No mortalities were observed in dogs which showed vomiting, conjunctival congestion, circumoral and auricular reddenings, periblepharal purplish reddening, decreases in locomotor activity and defecation, emaciation, eye discharge, skin desquamation of treated area and an increase in respiration. On macroscopic examination, desquamation of the skin, reddening of the circumoral mucosa, pale gray yellow striations in renal tubules of the cortex and discoloration of the thyroid were observed. Histopathological findings revealed epidermal thickening with parakeratosis, fibrocytes, hypertrophy and hypersecretion of the sebaceous and sweat glands, formation of epitheloid glanulomas and infiltration of neutrophils in the subcutaneous tissues. Furthermore, moderate calcium deposits in the renal tubules, fatty cells and slight calcium deposits in interstitial tissues of the thyroid, and a cystic nest of an ectopic intestinal epithelium between muscle layers of the duodenum were observed at the highest dose. On the basis of results obtained in the present study, rats administered MC903 by s.c. or p.c. died probably due to the circulatory and renal disturbance resulted from effects of this drug on the heart and kidney.
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PMID:[Single dose toxicity studies of calcipotriol (MC903) in rats and dogs]. 874 15

The case of a 25-year-old male agricultural laborer with HIV infection and Pneumocystis carinii pneumonia (PCP) is described, whose radiological lesions simulated pulmonary tuberculosis. He presented with loss of weight and appetite of 6 months' duration, cough with expectoration and minimal hemoptysis for 2 months, chest pain, diarrhea with fever, and odonophasia for 1 month. He had received antitubercular treatment (rifampicin 450 mg and isoniazid 300 mg) 2 months prior to admission. He had been promiscuous, having had multiple sexual contacts with prostitutes. General examination demonstrated marked emaciation, pallor, dyspnea, and oral candidiasis. Auscultation indicated fine medium pitched crackles in both infraclavicular regions. Blood for ELISA and immunocomb test were positive for HIV-1 antibodies. Hemogram revealed Hb 6 gm%, and TLC with polymorphs 63%, lymphocytes 30%, eosinophils 5%, and basophils 2%. The total lymphocyte count was 2100/cu. mm. Chest roentgenography revealed bilateral diffuse homogenous infiltrative lesions involving both lungs, with evidence of multiple bilateral cavitation. Therapy included antitubercular treatment with ethambutol, isoniazid, rifampicin, and pyrazinamide, along with Gentian violet mouth paint and ketoconazole orally, 200 mg bid. The patient developed progressive respiratory distress and died on the 7th day after admission. Limited autopsy of both lungs showed foamy eosinophilic material filling the alveolar space, and Grocett's methenamine silver staining showed cyst walls of P. carinii as black. There was no evidence of pulmonary tuberculosis. In the present case, the diagnosis of PCP should have been kept in mind to increase median survival time (25.9 vs. 12.6 months without treatment) with the treatment of choice of trimethoprim plus sulphamethoxizole in doses of 20 and 100 mg/kg/day. Early diagnosis and treatment will improve the mean survival time in cases of PCP with HIV infection.
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PMID:Pneumocystis carinii pneumonia simulating as pulmonary tuberculosis in AIDS. 901 80

We report a 67 years old male that consulted due to bloody diarrhea of several months of evolution and emaciation. According to endoscopic and radiological findings, the diagnosis of severe ulcerative colitis was made. Fifteen days after admission, the patient was subjected to an emergency total colectomy due to a toxic megacolon. The pathological study showed an ischemic colitis with extensive longitudinal ulcers in the antimesenteric border, presence of granulation tissue with inflammation and transmural fibrosis. Intestinal transit was reconstituted six months later and after 12 months of follow up the patient is in good conditions.
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PMID:[Toxic megacolon secondary to ischemic colitis. Report of a case]. 903 12

Paratuberculosis, which is also known as Johne's disease, is a chronic, progressive enteric disease of ruminants caused by infection with Mycobacterium paratuberculosis. Cattle become infected with M. paratuberculosis as calves but often do not develop clinical signs until 2 to 5 yr of age. The clinical disease is characterized by chronic or intermittent diarrhea, emaciation, and death. Although animals with clinical disease are often culled from the herd, animals with subclinical paratuberculosis may cause economic losses because of reduced milk production and poor reproductive performance. Although the economic impact of paratuberculosis on the national cattle industry has not been determined, it is estimated to exceed $1.5 billion/yr. The diagnosis of subclinical paratuberculosis is difficult. Bacteriologic culture is the most definitive method of diagnosis, but culture is time consuming and labor intensive. Serological assays are not very useful because animals do not develop an antibody response until the clinical stages of disease. Development of assays to measure cell-mediated immunity is critical to accurate detection of paratuberculosis in subclinically infected animals. Although not considered a zoonotic agent, M. paratuberculosis has been identified in intestinal biopsy tissue from patients with Crohn's disease, an inflammatory enteritis in humans. Currently, the potential human health risk is being addressed by research evaluating pasteurization of dairy products in the US.
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PMID:Johne's disease: a hidden threat. 949 5

The moose (Alces alces L.) in an acid rain affected region in south-west Sweden has developed a complex disease with numerous clinical signs, most of which are consistent with those of secondary copper (Cu) deficiency and/or molybdenosis in cattle and sheep. The clinical signs of the moose disease reported to date include diarrhoea, anorexia, emaciation, achromotrichia, alopecia, sudden heart failure and osteoporosis. Findings at necropsy included mucosal oedema, atrophied lymphoid tissues of the mucous membranes of the alimentary tract, neuropathy, neuronal degeneration and uni- or bilateral corneal opacity. In a study of clinically healthy animals from the affected region in Sweden over a 12-year period (1982-1994), the hepatic Cu concentration decreased by 50% and the liver and kidney cadmium (Cd) concentration decreased by 25-35%, while the molybdenum (Mo) concentration increased by 20-40%. These changes are probably related to an increase in the pH of the soil and water in the moose environment and a consequent change in the uptake of these elements by the plants consumed by the moose. It is noteworthy that the occurrence of the disease in the mid 1980s coincided with increased liming undertaken to counteract the noxious effects of acid rain in this region. Clinical signs and lesions of the moose disease resemble those reported for Cu deficiency and/or molybdenosis in cattle and sheep. To elucidate the complex, multi-faceted clinical signs of the moose disease, the clinical signs and necropsy findings are discussed in relation to the biochemical functions of certain well-known Cu-dependent enzymes, e.g. depigmentation of hair due to depressed tyrosinase activity, osteoporosis by depressed lysyl oxidase activity, sudden heart failure due to decreased activity of lysyl oxidase, cytochrome c oxidase and Cu/Zn-superoxide dismutase; in addition, mucosal lesions and ulcerations due to loss of activity of diamine oxidase as well as of lysyl oxidase and cytochrome c oxidase. It is concluded from the present findings that the moose disease is most probably a Cu deficiency and/or a molybdenosis-type syndrome.
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PMID:'Mysterious' moose disease in Sweden. Similarities to copper deficiency and/or molybdenosis in cattle and sheep. Biochemical background of clinical signs and organ lesions. 949 61

A total of 1300 birds in flock of breeder Pharaoh quail (Coturinix coturnix) experienced a moderate rate of mortality (13%) during a 7-day period. Clinical signs included depression, ruffled feathers, prostration, lameness, inapetence, diarrhea, and periorbital sinus swelling with mucoid discharge and lameness. Gross lesions observed in dead quail were emaciation, carcass congestion, mild hepatomegaly with green discoloration, congested intestinal mucosa, caseous purulent arthritis-osteomyelitis, and thickened crop mucosal epithelium. Histopathologic examination revealed mild hepatic amyloidosis, proliferative parabronchitis, splenic reticular cell hyperplasia, thymic cortical atrophy, subacute bacterial osteomyelitis, periarthritis, and crop mycosis. Pasteurella multocida was isolated from the joints of these birds and the isolates were serotype 3 x 4. These findings suggest that Pharaoh quail are susceptible to P. multocida and are likely to develop subacute to chronic fowl cholera.
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PMID:Subacute to chronic fowl cholera in a flock of Pharaoh breeder quail. 953 3

A 2-year-old girl, who had prolonged thrush and spastic diplegia, was found to have a mother-to-child vertical transmission of human immunodeficiency virus type-1 (HIV). A brain computed tomography scan revealed a symmetrical calcification on the bilateral basal ganglia and periventricular white matter. She had an acquired immune deficiency syndrome (AIDS) encephalopathy of pure dominant pyramidal tract disorder without an intellectual deficit. Helper cell lymphocyte count (CD4) increased with the beginning of zidovudine (ZDV, also known as AZT) monotherapy but began to decrease after the 4th week to reach the baseline at 20th week. Zidovudine plus didanosine combination therapy was started at the 68th week, but because of intolerance, the combination was changed to ZDV plus lamivudine at the 98th week. By the 80th week, neither severe opportunistic infection nor deterioration of the neurological status was recognized, but chronic diarrhea appeared. The diarrhea advanced to the wasting syndrome at the age of 4 years and cytomegalovirus genome was confirmed in a biopsied specimen of the colon. Ganciclovir treatment was effective in stopping the diarrhea and increasing her bodyweight, but after the age of 5, resumption of diarrhea was followed by progressive emaciation and weakness. This work may provide some clues in treating children's AIDS.
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PMID:Encephalopathy and cytomegalovirus colitis in an AIDS child. 982 20


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