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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Of 29 neonatal harbor seals that had been abandoned, separated from their mothers, or stranded in the wild, 22 succumbed during hospitalization at the California Marine Mammal Center in the spring of 1982. Compared with standard reported harbor seal pup measurements, 8 of the nonsurviving pups were premature (ie, creamy-white lanugo coat, early pupping season birthdate, and decreased body size [6 to 10 cm shorter and 2.3 to 4.5 kg less than normal]). The premature pups and the young pups (less than or equal to 10 days old) had at least two of the following findings: jaundice, emaciation, labored respiration, hyperbilirubinemia, hypoglobulinemia, or leukopenia. Most of the nonsurviving pups died within 96 hours after admission. Macroscopic and microscopic findings indicated that a high percentage of these pups had pulmonary congestion and edema (72.7%), alveolar squamous cells/debris (27.3%), and/or congenital cardiac anomalies (ie, patent ductus arteriosus [63.6%] and patent foramen ovale [45.4%]). Two older pups (greater than 10 days old) died from chronic bacterial infections, accompanied by adrenal cortical hyperplasia. The 7 surviving pups had adult spotted pelage, normal body weights (9 to 11 kg), normal globulin concentrations (3.0 to 5.1 g/dl), and normal WBC counts (7 to 9 X 10(3)/microliters) and did not have clinical signs of icterus or respiratory distress.
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PMID:Survival versus nonsurvival determinants for neonatal harbor seals. 350 18

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

A seven-year-old male elk (Cervus elaphus nelsoni) was euthanized and necropsied after having a 3-week history of body weight loss, emaciation, excessive salivation, teeth grinding, fever, anorexia, and respiratory distress. The elk was imported into Korea from Canada on March 9, 1997. Gross pathologic findings were restricted to a diffuse fibrinous pneumonia. Microscopic lesions included mild neuronal vacuolation and spongiform change in the neuropil of selected brain stem nuclei and generalized astrocytosis. Immunohistochemistry for protease-resistant prion protein (PrP(res)) was positive in all brain sections but more pronounced in the section of the obex of the medulla. And the PrP(res) was also detected by western immunoblotting in the brain and spinal cord. All the remaining elk and deer that had been in contact with this elk were destroyed and negative for chronic wasting disease (CWD). To our knowledge, this is the first case of CWD occurring outside of the U.S.A. and Canada.
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PMID:A case of chronic wasting disease in an elk imported to Korea from Canada. 1239 15

A case of tuberculosis is reported in an eight-year-old, male, elk (Cervus elaphus nelsoni). The elk showed severe coughing, respiratory distress, abdominal breathing, anorexia, and severe progressive emaciation in the elk farm. At necropsy, the elk appeared in poor body condition. Mild enlargement of retropharyngeal and submandibular lymph node was observed in the head. Diffuse fibrinous pleuritis and purple red lobar pneumonia were found in the thorax. Well demarcated numerous dark yellow discrete or confluent nodules from 0.3 to 2 cm in diameter were scattered in the whole lung. Bronchial and mediastinal lymph nodes were also enlarged. Histopathologically, lungs had typical classical tuberculous granulomas, multiple abscesses, and numerous macrophages and Langhans giant cells infiltration in alveolar lumen. In the lymph nodes, there were small clusters of necrosis and infiltration of numerous macrophages, epithelioid cells, and Langhans giant cells. With the acid-fast staining, numerous mycobacteria were revealed in the lung and lymph nodes. According to this study, there are differences of the histopathologic lesions and the numbers of acid-fast bacilli in the lesions between this elk and cattle. Mycobacterium bovis was confirmed as a causative agent in this elk using bacterial isolation, biochemical characteristics, and PCR technique. The isolate was negative for niacin test, nitrate reductase, and pyrazinamidase. This is a first report for bovine tuberculosis of farmed elk in Asia.
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PMID:Mycobacterium bovis infection in a farmed elk in Korea. 1251 26

An 8-year-old Brown Swiss dairy cow was presented with unilateral epistaxis and mild inspiratory stridor. At that time endoscopic examination revealed a smooth-surfaced mass within the left nasal cavity. Biopsy samples were collected and a diagnosis of fibrosarcoma was made. Eighteen months later the animal developed severe respiratory distress that led to difficulties in feeding and consequently to emaciation and a dramatic drop in milk production. The cow was humanely destroyed and submitted for post-mortem examination. The head was subject to further investigation by radiography, computed tomography and magnetic resonance imaging. These techniques revealed a non-infiltrative, well-circumscribed mass of both radiodense and heterogeneously intense structures. Histopathological examination revealed a mass consisting of well-differentiated and interlacing bone trabeculae lined by osteoblasts and multinucleated osteoclasts. In contrast to the initial diagnosis, the later diagnostic approaches supported the diagnosis of osteoma.
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PMID:Nasal osteoma in a dairy cow: a combined clinical, imaging and histopathological approach to diagnosis. 1953 51

This study describes the pathologic findings of 24 humpback whales (Megaptera novaeangliae) found stranded along the Brazilian coast from 2004 to 2016. Eighteen (75%) animals evaluated were found stranded alive. From these, 13 died naturally on shore and five were euthanized. Six died at sea and were washed ashore. Of the 24, 19 (79.2%) were calves, four (16.7%) were juveniles, and one (4.2%) was an adult. The most probable cause of stranding and/or death (CSD) was determined in 23/24 (95.8%) individuals. In calves, CSD included neonatal respiratory distress (13/19; 68.4%), infectious disease (septicemia, omphaloarteritis and urachocystitis; 3/19; 15.8%), trauma of unknown origin (2/19; 10.5%), and vehicular trauma (vessel strike; 1/19; 5.3%). In juveniles and adult individuals, CSD was: emaciation (2/5; 40%), sunlight-thermal burn shock (1/5; 20%); and discospondylitis (1/5; 20%). In one juvenile, the CSD was undetermined (1/5; 20%). This study integrates novel findings and published case reports to delineate the pathology of a South-western Atlantic population of humpback whales. This foundation will aid in the assessment of the population health and establish a baseline for development of conservation policies.
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PMID:Pathology and causes of death in stranded humpback whales (Megaptera novaeangliae) from Brazil. 2976 5

The clinical importance of heartworm infection in cats has indeed increased in recent years. Dirofilaria immitis infection has been reported worldwide in cats and continues to be regularly diagnosed in endemic areas. The diagnosis can be overlooked easily, especially in Brazil, where there is not a specific feline immunodiagnostic test, forcing the veterinarians to use a test made for the canine host. In 2015, a 10-year-old female neutered cat was diagnosed with D. immitis using an antigen serological test, based on imunocromatography and designed for dogs. The modified Knott test was negative. As the disease progressed, the cat showed clinical signals of respiratory distress, such as dyspnoea and polypnea in addition to prostration and emaciation, and died a few weeks after the diagnosis. During necropsy, one adult nematode was found in the pulmonary artery. D. immitis infection was confirmed by molecular amplification, performed in the worm fragment. This is the first report of serological diagnosis of feline dirofilariasis in Brazil. A chemoprophylaxis routine in cats should be done, as is done in dogs from endemic areas.
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PMID:Feline heartworm (Dirofilaria immitis) infection: first case report of serological diagnosis in Brazil, confirmed by molecular assay. 3006 43

A 5-y-old male Poodle mix was presented with intermittent vomiting, anorexia, and weight loss. Physical examination revealed emaciation, lethargy, dehydration, hypothermia, respiratory distress, and splenomegaly. Based on clinicopathologic, serologic, and parasitologic findings, diagnoses of severe leishmaniosis and dirofilariasis were made. Extracellular, intraneutrophilic, and intramonocytic Leishmania amastigotes were observed on blood smear and buffy coat smear examination. In blood smears, 0.2% of neutrophils were observed to be infected; in buffy coat smears, 0.5% of neutrophils and 0.1% of monocytes were found to be infected. Leishmania amastigotes were also found engulfed by eosinophils and neutrophil precursors in bone marrow aspiration cytology. The detection of Leishmania amastigotes in blood smears is rare, and the clinical significance is uncertain. In circulating blood, Leishmania amastigotes are primarily found phagocytized by neutrophils. Although debatable, there is growing evidence that neutrophils are used as carriers enabling the "silent entry" of the protozoa into macrophages ("Trojan horse" theory). To date, cytologic screening of blood smears for the diagnosis of canine leishmaniosis is not a routine practice. Clinical pathologists and practitioners should be aware that Leishmania amastigotes may be present in neutrophils and less frequently monocytes during blood smear evaluation; neutrophil precursors and eosinophils may also be parasitized in bone marrow specimens.
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PMID:Circulating and bone marrow myeloid cells containing Leishmania amastigotes in a case of advanced canine leishmaniosis. 3127 98