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)

From 2001 to 2003, tilapia (Oreochromis sp.) farms in Florida, California, and South Carolina experienced epizootics of a systemic disease causing mortality. The fish exhibited lethargy, occasional exophthalmia, and skin petechia. The gills were often necrotic, with a patchy white and red appearance. Grossly, the spleen and kidneys were granular with whitish irregular nodules throughout. Granulomatous infiltrates were observed in kidney, spleen, testes, and ovary tissues, but not in the liver. The granulomas contained pleomorphic coccoid bacteria, measuring 0.57 +/- 0.1 x 0.8 +/- 0.2 microm, that were Giemsa-positive, acid-fast-negative, and Gram-negative. The bacteria had a double cell wall, variable electron-dense and -lucent areas, and were present in the cytoplasm and within phagolysosomes. The syndrome was associated with cold stress and poor water conditions. These findings are consistent with an infectious process caused by a Piscirickettsia-like bacterium described previously in tilapia in Taiwan and Hawaii. This report involves the first identified cases of a piscirickettsiosis-like syndrome affecting tilapia in the continental United States.
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PMID:Occurrence of Piscirickettsiosis-like syndrome in tilapia in the continental United States. 1647 24

This manuscript reports on five cases of spontaneous myelogenous leukemia, similar to human disease, occurring within highly inbred, histocompatible sublines of Massachusetts General Hospital (MGH) MHC-defined miniature swine. In cases where a neoplasm was suspected based on clinical observations, samples were obtained for complete blood count, peripheral blood smear, and flow cytometric analysis. Animals confirmed to have neoplasms were euthanized and underwent necropsy. Histological samples were obtained from abnormal tissues and suspect lesions. The phenotype of the malignancies was assessed by flow cytometric analysis of processed peripheral blood mononuclear cells and affected tissues. Five cases of spontaneous myeloid leukemia were identified in adult animals older than 30 months of age. All animals presented with symptoms of weight loss, lethargy, and marked leukocytosis. At autopsy, all animals had systemic disease involvement and presented with severe hepatosplenomegaly. Three of the five myelogenous leukemias have successfully been expanded in vitro. The clustered incidence of disease in this closed herd suggests that genetic factors may be contributing to disease development. Myelogenous leukemia cell lines established from inbred sublines of MGH MHC-defined miniature swine have the potential to be utilized as a model to evaluate therapies of human leukemia.
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PMID:Myelogenous leukemia in adult inbred MHC-defined miniature swine: a model for human myeloid leukemias. 2007 39

A six-year-old female entire German shepherd dog was investigated for polyuria, polydipsia and lethargy. Investigations revealed a mild azotaemia and abdominal ultrasound revealed marked bilateral dilation of the renal pelves with echogenic material and proximal left hydroureter. Urine cytological examination and aspirates from the right renal pelvis revealed mats of fungal hyphae consistent with fungal bezoar formation. Fungal cultures revealed a profuse growth of Paecilomyces variotii. Initial treatment with oral itraconazole was unsuccessful, leading to bilateral nephrotomies to remove the fungal material. Postoperatively the Paecilomyces infection persisted despite continued itraconazole therapy. Treatment was commenced with amphotericin B, leading to resolution of the dog's clinical signs. To the authors' knowledge this is the first report of canine Paecilomyces pyelonephritis, without disseminated systemic disease, which documents its successful treatment.
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PMID:Successful treatment of bilateral Paecilomyces pyelonephritis in a German shepherd dog. 2389 7

A four-year-old Japanese Akita was referred for investigation of lethargy, exercise intolerance, and an irregular heart rhythm. He was diagnosed with atrial fibrillation, a complex ventricular arrhythmia, and hypothyroidism. Echocardiography identified a nest of anomalous vessels surrounding the heart and shunting into the pulmonary artery. Computed tomography confirmed a coronary arteriovenous malformation consisting of a coronary-to-pulmonary arterial communication and an associated complex nest of tortuous vessels, which was thought to be an incidental finding. Clinical signs improved with levothyroxine and antiarrhythmic treatment. Describing an unusual coronary artery anomaly as well, this case serves as a reminder to critically evaluate the hemodynamic significance of structural cardiac disease and to screen for systemic disease in patients with arrhythmias.
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PMID:Coronary arteriovenous malformation in a dog with a complex arrhythmia and hypothyroidism. 3117 28

Metabolism is a tightly regulated sequence of events, supported by key reactions between enzymes and enzyme-specific substrates. These reactions have the potential to produce metabolic side products that can have deleterious effects to further key metabolic reactions. The nicotinamide repair system consists of two partner enzymes, NAD(P)HX epimerase (NAXE) and NAD(P)HX dehydratase (NAXD). These enzymes regulate the levels of metabolic side products. Here we present a case of an 11-month old child who presented to our paediatric department with pyrexia, lethargy and multiple cutaneous lesions on the background of NAXD deficiency, a lethal neurometabolic disorder of early childhood. Despite early intervention with intravenous antibiotics, the patient failed to improve and subsequently passed away. The skin lesions were thought to be a consequence of systemic disease rather than a propagator of infection. Clinicians should be aware of this incredibly rare metabolic disease, its potential to cause widespread systemic dysfunction and the developing avenues for management.
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PMID:Cutaneous manifestations of NAXD deficiency - A case report. 3322 89


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