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

Type II ostertagiosis was found at necropsy in 9 American bison (Bison bison) from 3 farms in New York. Clinical signs included severe diarrhea, emaciation, unthrifty coats, anemia, and weakness. In severely affected animals, the macroscopic abomasal changes consisted of irregular thickening and edema of the mucosa, resulting in a pebbly or morocco-leather appearance. Microscopically, many gastric pits and glands were dilated, lined by hyperplastic epithelium, and contained nematode sections or debris. Parasites recovered included Ostertagia ostertagi, Trichostrongylus axei, Trichostrongylus lerouxi, Cooperia oncophora, Haemonchus contortus, Nematodirus helvetianus, Trichuris discolor, Setaria labiato-papillosa, Dictyocaulus viviparus, Hypoderma lineatum, and Sarcocystis sp. Nodules in the small and large intestine were attributed to Oesophagostomum sp. Trichostrongylus lerouxi, Trichuris discolor, and Nematodirus helvetianus are reported from bison for the first time.
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PMID:Ostertagiosis in captive bison in New York State: report of nine cases. 15 57

Twenty five cattle were infected with T. vivax, 25 with T. congolense, and 25 served as controls. Pathogenic clinical signs of trypanosomal infection were not observed. Secondary bacterial infections were common. Fever, increased heart and respiratory rates, anorexia, and emaciation developed. Elevations in parasitemai and body temperature were positively correlated in the T. vivax group. Infected groups were affected non-uniformly, with some animals in each group remaining asymptomatic and tending to have lower parasitemias. The T. vivax parasitemia was cyclic and the organisms had a genaration time of 7.9 SD 2.5 hours. The first peak of parasitemia in both infections was closely associated with the development of pancytopenia, i.e. anemia, leukopenia, and thrombocytopenia. The bone marrow erythroid response in the T. congolense group was significantly greater thn that in either the T. vivax or control groups. Leukopenia was due to concomitant neutropenia and lymphopenia.
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PMID:Experimental bovine trypanosomiasis (Trypanosoma vivax and T. congolense). I. Sumptomatology and clinical pathology. 54 98

Donkeys experimentally infected with Trypanosoma brucei showed dullness, weakness, fever, inappetence, conjunctivitis, tachycardia and polydyspnoea soon after detectable parasitaemia. The parasitaemia was generally low with transient high peaks except in the terminal stage when there was sustained high parasitaemia. A moderate anaemia was present as from the second week of infection but it was not progressive. There was a marked leucopoenia within 24 h of patent parasitaemia. Death occurred 2 to 2 1/2 months after infection and at necropsy there was severe emaciation as well as mild serous effusion. Histologically, there was a nonsuppurative encephalomyelitis, cranial neuritis, extensive haemosiderosis, hyperplasia of follicles in lymph nodes and spleen and giant cell reaction in lymph nodes. Trypanosomes were present in the cerebrospinal fluid, the eye and serous effusions. These observations are similar to those previously reported in other animals infected with T. brucei.
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PMID:Clinical, haematological and pathological studies in donkeys experimentally infected with Trypanosoma brucei. 90 95

Acute and chronic forms of disease can be distinguished in Trypanosoma vivax infection in the goat. The main difference between the acute and chronic form seems to be the presence of microthrombi in the acute stage of infection; these consist of platelets, trypanosomes, monocytoid cells and some fibrin. This thrombus formation seems directly related to the high parasitaemia in acute trypanosomiasis and may result in ischaemia which could also explain the haemorrhages, the oedema of the lungs and other tissues, and the necrotic changes found in several organs. The anaemia, associated with erythrophagocytosis, haemosiderosis, extramedullary haemopoiesis and hyperactivity of the bone marrow, seemed to be of haemolytic origin. The factors leading to emaciation seemed to be degenerative atrophy of muscular tissue and loss of protein in the urine caused by a possible immune complex glomerulonephritis.
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PMID:The pathology and pathogenesis of Trypanosoma vivax infection in the goat. 102 33

A spontaneous infection with Schistosoma mansoni was found in a chimpanzee (Pan troglodytes versus) recently imported from Sierra Leone, Africa. Clinical signs consisted of anemia, liver enlargement, bronchial rales, and emaciation. The primary gross pathologic lesions included a fibrotic firm nodular liver and pulmonary edema and consolidation. Histopathologic examination revealed changes similar to the experimental syndrome of Manson's schistosomiasis in the chimpanzee. The diagnosis was confirmed by the presence of the eggs and larvae of Schistosoma mansoni.
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PMID:A natural case of Schistosoma mansoni in the chimpanzee (Pan troglodytes versus). 120 45

Feline immunodeficiency virus (FIV) has morphological, physical and biochemical characteristics similar to human immunodeficiency virus (HIV), the cause of AIDS in man. However, it is antigenically and genetically distinct from HIV; an antigenic relatedness with equine infectious anaemia virus has been demonstrated. FIV has been molecularly cloned and sequenced. Diagnostic tests are commercially available and attempts at preparing inactivated, subunit and molecularly engineered vaccines are being made in different laboratories. During FIV infection a transient primary illness can be recognized, with fever, neutropenia and lymphadenopathy. After a long period of clinical normalcy a secondary stage is distinguished with signs of an immunodeficiency-like syndrome. The incubation period for this stage can be as long as 5 years, during which gradual impairment of immune function develops. Many FIV-infected cats are presented for the first time showing vague signs of illness: recurrent fevers, emaciation, lack of appetite, lymphadenopathy, anaemia, leucopenia and behavioural changes. Later, the predominant clinical signs observed are chronic stomatitis/gingivitis, enteritis, upper respiratory tract infections, and infections of the skin. Neoplasias, neurological, immunological and haematological disorder are seen in a smaller proportion. The immunodeficiency-like syndrome is progressive over a period of months to years. Concomitant infection with feline leukaemia virus has been shown to accelerate the progression of disease. In vitro, phenotypic mixing between FIV and an endogenous feline oncovirus (RD114) has been demonstrated which leads to a broadening of the cell spectrum of the lentivirus. Bovine immunodeficiency virus (BIV) has been isolated only once, and all attempts to obtain additional isolates have failed; it has been recovered from the leucocytes of cattle with persistent lymphocytosis, lymphadenopathy, lesions in the central nervous system, progressive weakness and emaciation. As with the feline representative, BIV also was found to possess a lentivirus morphology and to encode a reverse transcriptase with Mg++ preference; it replicates and induces syncytia in a variety of embryonic bovine tissues in vitro. Antigenic analyses have demonstrated a conservation of epitopes between the major core protein of BIV and HIV. The original isolate has been molecularly cloned and sequenced. Besides the three large open reading frames (ORFs) comprising the gag, pol, and env genes common to all replication-competent retroviruses, five additional small ORFs were found. Numerous point mutations and deletions were found, mostly in the env-encoding ORF. These data suggest that, within a single virus isolate, BIV displays extensive genomic variation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Animal immunodeficiency viruses. 133 43

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Severe losses of yaks (Bos grunniens) were investigated in the most eastern region of Bhutan. The most serious disease was a fatal chronic skin disease with emaciation and anaemia. Post mortem examinations revealed major lesions in the liver, consisting of hepatic megalocytosis, bile duct proliferation, fibrosis and remodelling of the hepatic structure. There was also renal megalocytosis, ascites and mild to moderate icterus. Pyrrolizidine alkaloid poisoning was diagnosed and confirmed by demonstrating sulphur-bound pyrrolic metabolites of the alkaloids in preserved liver tissue. Skin lesions with hyaline parakeratosis were an important feature. Similar lesions were found in the mucosa of the oral cavity. No records could be found of such skin lesions in any other species or disease. Pyrrolizidine alkaloid poisoning seriously affects the livelihood of the local population which depends almost entirely on the yak. Various control measures are discussed. The key to be found is the identification of the toxic plants.
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PMID:Pyrrolizidine alkaloid poisoning of yaks (Bos grunniens) and confirmation by recovery of pyrrolic metabolites from formalin-fixed liver tissue. 158 77

The acquired immunodeficiency syndrome (AIDS) was first diagnosed in burundi in 1983 when a large number of patients were registered with Kaposi's sarcoma, cryptococcal meningitis, and disseminated candidiasis. In the 1st phase of the disease the vi rus is dormant. In the 2nd phase seroconversion appears; and in the 3rd phase generalized adenopathy emerges. In the 4th phase the full-blown disease appears as a result of cellular immunity deficit with emaciation, fever, sweating, chronic diarrhea, asthenia, blood parameter changes (lymphopenia, thrombocytopenia, leukopenia, anemia, and specific immune disorders). The early phases can be diagnosed by serological tests. During 1989 a group of 155 patients with 1st signs of seropositivity were studied in the central hospital of Bugumbura. The available clinical diagnostic markers were: 56 cases of herpes, 26 cases of generalized adenopathy, 25 cases of inflammatory infiltration of paraganglionic zones, 13 abscesses and phlegmons, 8 cases of chronic proctitis, 8 prurigo cases, 7 cases of chronic pneumonia and bronchitis, 4 cases of paresis of the facial nerve, 4 cases of Kaposi's sarcoma, 2 cases of fresh syphilis, 2 cases of anemia, asthenia, dizziness, and weight loss. Tomo- and zonographical X-ray study of the thorax of 80 patients aged 20-65 (51 men and 29 women) was performed. In 62 patients changes in the lungs were evident. In 2 patients tuberculosis of the lungs was diagnosed: miliary TB in a 26-year woman and disseminated TB in a 31-year man. 2 chronic and 3 bronchial, and 10 interstitial pneumonia cases were diagnosed in 15 patients with average age of 30 years. 4 patients had peribronchial and pneumonic infiltrations. In a group of 45 patients magnified picture showed no deformation in the lungs; and only 5 had respiratory organ pathology. Interstitial pneumonia was the most often diagnosed ailment by X-ray inpatients infected with HIV.
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PMID:[X-ray pulmonary manifestations in patients infected with the human immunodeficiency virus]. 196 22


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