Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Viral myocarditis is the result of a viral infection that produces myocardial necrosis and triggers an immune response to eliminate the viral agent. Many pathogenic mechanisms may contribute to myocardial cell loss including the following: cytokine production contributing to disease severity; viral persistence, which may produce an autoimmune response to cardiac myosin; and viral invasion of vascular endothelium causing vascular spasm with reperfusion injury. The compensatory response of the myocardium to these mechanisms of cell loss is hypertrophy, which results in fibrosis, scarring, and dilation. The myocardial cell loss and physiological response produces a child with fever, lethargy, symptoms of congestive heart failure, cardiogenic shock, or new onset arrhythmias. The initial presentation may be subtle, but if left untreated will go on to produce severe symptoms. The focus of diagnostic studies is to evaluate cardiac function, identify the viral agent, and eliminate other causes of global cardiac dysfunction. Treatment must provide for support of cardiac function through inotropic and afterload-producing agents while providing rest for the stressed cardiac muscle. The nursing care of children with viral myocarditis must focus on continual assessment of the cardiovascular system while supporting the recovery of myocardial function.
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PMID:Viral myocarditis in children. 885 48

Recently we conducted the molecular characterization of Rangelia vitalii, a protozoan with high pathogenicity for young dogs in southern Brazil. To date, the descriptions of the disease have been restricted to natural infection cases. Therefore, this study aimed to evaluate the parasitemia, biological cycles and clinical-pathological findings in dogs experimentally infected with R. vitalii in the acute phase of disease, and also aimed to test a therapeutic protocol based on the diminazene aceturate. For this study, we used 12 young dogs (females), separated into two groups. Group A was composed of healthy dogs, not-infected (n=5), and Group B consisted of animals infected with R. vitalii (n=7). After infection, the animals were monitored by blood smear examinations, which showed intra-erythrocytic forms of the parasite 5 days post-infection (PI). Parasitemia increased progressively in these animals and had the highest peak of circulating parasites between 9 and 11 days PI. Subsequently, the parasitemia reduced and the protozoan was seen inside the leukocytes in days 17, 19 and 21 PI. The most prominent clinical signs observed at the 20 day PI of experiment were lethargy, fever and anorexia. We observed a decrease of hematocrit of infected animals compared with not-infected dogs, featuring a moderate anemia. Pathological evaluation of one dog in Group B at day 21 PI revealed splenomegaly, hepatomegaly, lymphadenopathy, and hemorrhages at necropsy. Histological examination showed only follicular hyperplasia in the spleen and lymph nodes, and the etiologic agent in the vascular endothelium. At 21 days PI, it was performed the treatment of dogs in Group B (n=6) with a single dose of diminazene aceturate, which showed a curative efficacy of 100% in cleaning R. vitalii from blood of infected dogs.
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PMID:Experimental infection with Rangelia vitalii in dogs: acute phase, parasitemia, biological cycle, clinical-pathological aspects and treatment. 2157 Sep 66