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)

A 6-year-old Bernese Mountain dog was presented with a history of lethargy and weight loss of 2 weeks duration. On physical examination the dog had pale mucous membranes and tachypnea. Ultrasound examination revealed hepatomegaly, splenomegaly, and mesenteric lymphadenomegaly. Results of a CBC included marked normocytic normochromic nonregenerative anemia, marked thrombocytopenia, and moderate leukocytosis with mild neutrophilia and a large population of unclassified round cells (6.2 x 10(3)/microL). The unclassified cells occasionally were bi- or multinucleated and had variably abundant pale basophilic cytoplasm that contained multiple irregular clear vacuoles and occasionally erythrocytes. Fine needle aspirate specimens of the mesenteric lymph nodes and spleen were composed of a population of round pleomorphic cells with the same features as the circulating cells. On flow cytometric analysis of peripheral blood, the unclassified cells expressed CD18, CD45, CD11c, CD1c, and CD14; immunocytochemical analysis of blood smears also indicated the cells were positive for CD1c, CD1a, and CD11c. The dog died a few hours after referral. The histologic interpretation of samples collected from spleen, liver, and lymph nodes was malignant neoplasia of histiocytic origin. Immunohistochemical staining yielded negative results for CD11d, a marker of red-pulp macrophages, ruling out hemophagocytic histiocytic sarcoma. Based on clinical and pathologic findings, the final diagnosis was disseminated histiocytic sarcoma (DHS) with peripheral blood involvement. To our knowledge, DHS in a dog with evidence and immunophenotyping of neoplastic cells in peripheral blood has been reported only rarely.
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PMID:Disseminated histiocytic sarcoma with peripheral blood involvement in a Bernese Mountain dog. 1917 Oct 15

An 11-year-old male castrated Australian Shepherd was presented with a history of lethargy, panting, and weight loss for 1 month. Physical examination revealed a moderately enlarged spleen. Laboratory abnormalities included thrombocytopenia and marked hypercalcemia, with hyperglobulinemia, hypoalbuminemia, and a monoclonal spike in the beta-globulin region on serum protein electrophoresis. Serum total calcium concentration was markedly increased (16.5 mg/dL, reference interval 8.9-11.4 mg/dL) but ionized calcium concentration (1.39 mmol/L) was within the reference interval (1.25-1.45 mmol/L). Isosthenuria was noted, but the dog was not polyuric or polydipsic. Serum parathyroid hormone concentration was within reference limits and parathyroid hormone-related peptide concentration was 0 pmol/L. Radiographic findings were largely unremarkable. Results of cytologic evaluation of a fine-needle aspirate specimen from the spleen indicated plasma cell neoplasia. Based on the results of the electrophoresis, splenic aspirates, radiographs, and hypercalcemia, a diagnosis of splenic multiple myeloma was made. The marked hypercalcemia, normal ionized calcium and parathyroid hormone concentrations, and lack of osteolytic lesions indicated a presumptive increase in protein-bound serum calcium, likely due to binding to molecules of the paraprotein (M protein). Protein binding of calcium in dogs with multiple myeloma should be considered as a potential mechanism of elevated total serum calcium concentration.
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PMID:Presumptive increase in protein-bound serum calcium in a dog with multiple myeloma. 1917 Oct 18

A 5-year-old, female Italian hound dog was presented with progressive weight loss, anorexia, and lethargy. Physical examination abnormalities included poor body condition, abdominal distension, splenomegaly, and areas of crusty alopecia on the head and limbs. Clinicopathologic abnormalities included mild normocytic normochromic anemia, moderate hyperproteinemia and hyperglobulinemia, mild hypoalbuminemia, and hyponatremia, a mild increase in serum alkaline phosphatase activity, and a moderate to marked increase in beta- and gamma-globulins on serum protein electrophoresis. Abdominal ultrasonography revealed peritoneal effusion. Abdominocentesis yielded approximately 200 mL of serosanguinous, slightly turbid fluid with 2.6 x 10(9) nucleated cells/L, and a protein concentration of 32 g/L. Cytologic specimens of the fluid contained a mixed population of inflammatory cells. Intracytoplasmic inclusions identified as Leishmania sp. amastigotes were observed in numerous macrophages and also free in the background. An ELISA for canine Leishmania sp. antibody was positive. The abdominal effusion resolved within a few days of beginning treatment with meglumine antimoniate and allopurinol. Finding Leishmania amastigotes in peritoneal fluid is rare in canine leishmaniasias and allows an easy, quick diagnosis of the disease.
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PMID:What is your diagnosis? Peritoneal effusion from a dog. 1935 38

A 4-year-old intact female American Pit Bull Terrier from Italy descendant of an American-born bitch was evaluated for anorexia, lethargy, weakness, and intermittent vomiting. On physical examination, the dog was dehydrated, had pale mucous membranes, hunched posture and abdominal pain. A moderate anemia was observed. Splenomegaly and hyperechoic regions suspected as infarcts in the spleen were seen on abdominal ultrasound. Based on the suspicion of splenic torsion, splenectomy was performed. After surgery, the clinical condition deteriorated. A follow-up complete blood count demonstrated severe macrocytic normochromic anemia with evidence of marked regeneration, left shift neutrophilia, monocytosis and marked thrombocytopenia. Blood smear evaluation revealed single to multiple, variable sized (1-3 microm in diameter), and round to oval to band-like piroplasms within many red blood cells consistent with small form Babesia spp. or Theileria spp. A partial segment of the 18S rRNA gene was amplified and the PCR product was analyzed by direct sequencing. The nucleotide sequence was completely identical to that of Babesia gibsoni present in GenBank. This is the first molecular detection and characterization of B. gibsoni infection in a sick dog from Italy.
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PMID:Clinicopathological findings, molecular detection and characterization of Babesia gibsoni infection in a sick dog from Italy. 1967 97

All fledgling canaries (Serinum canarius) in a small private aviary died from atoxoplasmosis during a single breeding season. The birds were clinically normal when removed from their parents at 2 mo of age, but by 3 mo of age all had died following an illness characterized by progressive lethargy, anorexia, and debilitation. Cachexia, splenomegaly, and pale foci in the liver were evident at necropsy. Microscopically, there was striking infiltration of the intestinal lamina propria by mononuclear cells that contained intracytoplasmic protozoa. Protozoa were also observed in mononuclear cells in splenic and hepatic sinusoids and in vascular or perivascular spaces of other organs, but were much less numerous. Ultrastructural features of infected enteric mononuclear cells were suggestive of lymphocytes, and the majority of parasitized cells in paraffin sections of intestine were positive for CD-79 antigen, consistent with B lymphocytes. CD-3 staining was minimal, suggesting little or no T-cell infection. The following year, after egg-laying was completed, adults were treated with sulfadimethoxine, and no further fledgling losses occurred.
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PMID:Atoxoplasmosis in canary fledglings: severe lymphocytic enteritis with preferential parasitism of B lymphocytes. 1984 92

Three dogs from Saskatoon, Saskatchewan were diagnosed with acute granulocytic anaplasmosis. Fever, lethargy, inappetence, vomiting, diarrhea, and lameness were reported. Lymphopenia, thrombocytopenia, and splenomegaly were identified in all dogs. Inclusions were identified within the cytoplasm of blood neutrophils, and infection with Anaplasma phagocytophilum was confirmed by polymerase chain reaction.
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PMID:Granulocytic anaplasmosis in three dogs from Saskatoon, Saskatchewan. 1988 21

A 3.5-year-old, male, neutered ferret (Mustela putorius furo) was presented with a 3-day history of lethargy and anorexia. Splenic aspirates revealed high numbers of intermediate-sized lymphocytes and Mott cells interpreted as lymphoma with Mott cells. The ferret was euthanized because of a poor clinical prognosis. Postmortem examination revealed markedly enlarged spleen and lymph nodes, with multifocal white nodules in the liver parenchyma. Histologically, the spleen had multifocal large nodules composed of neoplastic lymphocytes with frequent Mott cells. Similar neoplastic cells were present in the sections of liver, lymph nodes, and bone marrow. These cells were cluster of differentiation (CD)3-negative, CD79alpha-positive, and lambda light-chain-positive. Electron microscopy revealed that the cytoplasm of the neoplastic Mott cells had increased, disorganized, dilated, rough endoplasmic reticulum containing electron-dense immunoglobulin. On the basis of cytologic, histopathologic, immunohistochemical, and electron microscopic findings, a malignant B-cell lymphoma with Mott cell differentiation was diagnosed.
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PMID:Malignant B-cell lymphoma with Mott cell differentiation in a ferret (Mustela putorius furo). 2045 31

A 4-year-old male, castrated Saint Bernard was evaluated for acute onset of lethargy and collapse. Moderately severe anemia and splenomegaly were noted. Immune mediated hemolytic anemia was initially suspected. Abdominal ultrasound demonstrated an absence of splenic blood flow. Splenic torsion was confirmed on exploratory laparotomy and a splenectomy was performed.
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PMID:A case of splenic torsion with progressive anemia and thrombocytopenia. 2067 99

Amblyomma americanum was confirmed as a competent vector in the transmission of Cytauxzoon felis to domestic cats. Infection with C. felis was produced and replicated in four domestic felines by the bite of A. americanum adults that were acquisition fed as nymphs on a domestic cat that survived cytauxzoonosis. Numerous attempts to transmit C. felis with Dermacentor variabilis at the same time were not successful. All cats upon which infected A. americanum were transmission fed exhibited disease typical of cytauxzoonosis, and the eitiologic agent's presence was confirmed. Clinical signs including fever, inappetence, depression, and lethargy were observed beginning 13 d postinfestation. Pale mucus membranes, splenomegaly, icterus, and dyspnea were also observed during the course of the disease. Rectal temperatures of the C. felis-infected principal cats fluctuated from high to subnormal before returning to the normal range. Clinical signs of cytauxzoonsis improved by 24 d postinfestation in all but one cat, with survivors remaining parasitemic and subclinically infected with C. felis. Unengorged A. americanum and D. variabilis were collected from wild habitats to determine the minimum infection rate of C. felis in ticks from an enzootic area. Infection of C. felis was found only in wild-collected A. americanum. The minimum infection rate of C. felis in A. americanum was 0.5% (one of 178) in males, 0.8% (three of 393) in nymphs, and 1.5% (three of 197) in females. We found no wild-collected D. variabilis infected with C. felis. Our results confirm that A. americanum is a primary vector of C. felis.
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PMID:Confirmation of Amblyomma americanum (Acari: Ixodidae) as a vector for Cytauxzoon felis (Piroplasmorida: Theileriidae) to domestic cats. 2093 86

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


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