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)

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Disseminated infection with Mycobacterium avium complex is described in 3 adult Siamese cats. All cats were the result of father-daughter matings. Clinical signs included anorexia, weight loss, and lethargy. Physical examination revealed pale mucous membranes, lymphadenopathy, splenomegaly, and pyrexia. Nonregenerative anemia was detected in all 3 cats, and macrocytosis was observed in 2. An antemortem diagnosis of mycobacterial infection was made on the basis of identification of acid-fast bacilli in tissue aspirates. The cats died or were euthanatized owing to clinical deterioration, despite antibiotic treatment. Necropsy findings included granulomatous lymphadenitis, enterocolitis, pneumonia, cellulitis, myelitis, and hepatitis. Organisms from the Mycobacterium avium complex were identified in bacteriologic cultures of tissue samples.
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PMID:Disseminated Mycobacterium avium complex infection in three Siamese cats. 812 27

The results of clinical and radiographic examinations of 15 dogs with confirmed malignant histiocytosis (MH) were reviewed. The most common clinical signs were anorexia (14 dogs), weight loss (13 dogs), lethargy (13 dogs), anaemia (11 dogs), and dyspnoea and/or coughing (8 dogs). Radiographs revealed abnormalities in all dogs, either intrathoracic (pulmonary nodules or consolidation [7 dogs], mediastinal masses [10 dogs], and incidentally pleural effusion [3 dogs]) or abdominal (hepatomegaly [6 dogs] and splenomegaly [2 dogs]), or both. MH occurs relatively frequently in Bernese Mountain dogs. Both clinical and radiographic signs are non-specific, but when they are present in a middle-aged Bernese Mountain dog, MH should be included in the differential diagnosis.
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PMID:Clinical and radiographic manifestations of canine malignant histiocytosis. 826 26

We demonstrate that Borrelia burgdorferi infection in the rhesus monkey mimics the early and early disseminated phases of human Lyme disease. Clinical, bacteriological, immunological, and pathological signs of infection were investigated during 13 weeks after inoculation of the spirochete. Three animals were given B. burgdorferi (strain JD1) by needle inoculations, six animals were exposed to the bite of B. burgdorferi-infected Ixodes dammini ticks, and three animals were uninfected controls. B. burgdorferi could be recovered from all animals that were given the spirochete. Bacteria were detectable until week 6 postinoculation (p.i.) in blood, until week 8 p.i. in skin biopsies, and at 10 weeks p.i. in the conjunctiva of one of two animals which developed conjunctivitis. Erythema migrans (EM) appeared in one of the three animals infected by needle inoculation and in five of the six animals infected by ticks. Deep dermal perivascular lymphocytic infiltrations (characteristic of human EM) were observed in all animals showing EM clinically. Both EM and conjunctivitis were documented concomitantly with the presence of the spirochete. Lethargy, splenomegaly, and cerebrospinal fluid pleocytosis were also noted in some animals, but the direct connection of these signs with the infection was not shown. The appearance rate of immunoglobulin M and immunoglobulin G antibodies to B. burgdorferi, as well as the antigen spectra recognized, were remarkably similar to those seen in humans. Serum antibodies from infected animals were able to kill B. burgdorferi in vitro in the presence of rhesus complement. The rhesus monkey model appears to be useful for the investigation of the immunology and pathogenesis of Lyme disease and for the development of immunoprophylactic, diagnostic, and chemotherapeutic protocols.
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PMID:Early and early disseminated phases of Lyme disease in the rhesus monkey: a model for infection in humans. 851 12

Fatal (Panthera tigris) cytauxzoonosis was diagnosed in a 7-year-old female white tiger. The tiger presented with a 2-day history of anorexia and lethargy. She was mildly dehydrated, with a temperature of 105.2 F and a hematocrit of 26%. Over the next day, icterus developed, and her physical condition progressed to recumbency, coma, and death. Hematologic findings obtained shortly before death included icteric plasma, severe thrombocytopenia, mild anemia, hematuria, and parasites consistent with Cytauxzoon felis in circulating erythrocytes. Gross necropsy findings included generalized icterus, generalized petechiae and ecchymoses, splenomegaly, and peribronchial edema. Histologic changes included large numbers of intravascular macrophages containing developmental stages of Cytauxzoon felis that partially or completely occluded blood vessels in the lung, spleen, liver, and bone marrow. Except for an experimental infection of a bobcat, fatal cytauxzoonosis has not previously been diagnosed in felids other than domestic cats. These findings raise questions regarding the pathogenicity of this organism in felids and may impact husbandry and interstate transfer of captive large cats.
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PMID:Fatal cytauxzoonosis in a captive-reared white tiger (Panthera tigris). 882 11

Ninety-five (97%) of 98 black siskins (Carduelis atrata) died within 2 months of arrival in Italy from South America with the following clinical sings: rapid weight loss, breast muscle atrophy, congested and distended abdomen, diarrhea, and lethargy. Macroscopically we observed hepato-splenomegaly, pulmonary congestion, and thickening of the interstinal wall. Histologically, lymphomonocytic transmural enteritis, interstitial mononuclear cell infiltrates in the lungs and in the liver, as well as activation of splenic follicles were common features. Large numbers of protozoa belonging to Isospora sp. were observed in various stages of their life-cycle in the intestinal epithelium, and some zoites were found in the extra-intestinal cellular infiltrate as well. No viral or bacterial pathogens were found.
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PMID:Mortality in black siskins (Carduelis atrata) with systemic coccidiosis. 902 5

Three dogs became lethargic and had poor appetites within 2 months after anticonvulsant treatment was initiated to control seizures. Dogs were neutropenic, thrombocytopenic, and anemic and had splenomegaly. Sensitivity to phenobarbital and related anticonvulsants may induce life-threatening leukopenia, thrombocytopenia, and anemia in dogs. Phenobarbital-induced neutropenia in these 3 dogs may have posed a risk for developing bacteremia. It is important for clinicians to be aware of adverse effects so that adequate precautions can be taken. A baseline hemogram should always be obtained before starting anticonvulsant treatment, and periodic hemograms should be obtained to monitor animals. Furthermore, client education should include instructions on recognizing signs of bacteremia, thrombocytopenia, and anemia.
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PMID:Neutropenia and thrombocytopenia in three dogs treated with anticonvulsants. 952 40

Using three murine tumor models, we compared the antitumor efficacy and certain physiological effects of an in vivo interleukin-12 (IL-12) gene therapy protocol and a systemic IL-12 protein therapy protocol. An IL-12 cDNA gene construct was administered in situ into skin tissue via gene gun delivery, and recombinant IL-12 protein was administered subcutaneously at a dose of 1 microgram/mouse/treatment. Both treatment regimes induced a comparable level of regression of established intradermal MethA sarcomas. In B16 melanoma and P815 mastocytoma models, antitumor efficacy of IL-12 protein therapy appeared to be slightly higher than that of IL-12 gene therapy; however, the protein therapy protocol in this comparative study resulted in a high level of mortality of mice. It was also demonstrated that IL-12 gene therapy, in contrast to the IL-12 protein therapy, was not associated with weight loss, splenomegaly, increased Ly6 antigen expression in the spleen, or visible signs of toxicity, such as fur ruffling and lethargy. Moreover, serum levels of interferon-gamma (IFN-gamma) induced in response to IL-12 gene therapy were 300-1000 times lower than those induced by the systemic IL-12 protein administration. Together, these results suggest that gene gunmediated in vivo delivery of IL-12 cDNA may be considered as a safer alternative to IL-12 protein therapy for certain human cancers.
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PMID:Gene gun-mediated IL-12 gene therapy induces antitumor effects in the absence of toxicity: a direct comparison with systemic IL-12 protein therapy. 1009 38

A 6-mo-old hand-raised male western lowland gorilla (Gorilla gorilla gorilla) was diagnosed with acute lymphocytic leukemia based on complete blood count and bone marrow cytology. Clinical signs of the disease were pyrexia, abdominal distention, splenomegaly, and lethargy. Acute lymphocytic leukemia has rarely been reported in this species, and therapy was based on human oncologic protocols. Remission induction chemotherapy resulted in complete clearing of leukemia cells from the bone marrow. Consolidation and maintenance chemotherapy followed. Therapy was facilitated by the use of an infusion port for i.v. treatments and an indwelling lumbar catheter for intrathecal therapy. Side effects associated with chemotherapy were inappetence, moderate alopecia, pancytopenia resulting in sepsis, and bleeding tendency. In spite of initial success, the leukemia reappeared 120 days into treatment. The gorilla was euthanized 7 days later when respiratory distress developed. Intensive care by the animal staff was a key factor in the treatment of this gorilla.
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PMID:Acute lymphocytic leukemia in a six-month-old western lowland gorilla (Gorilla gorilla gorilla). 1048 44

Toxoplasma gondii is a unicellular protozoan. The definitive hosts, cats, produce hardy oocysts and sporozoites. Ingestion by a nonfeline leads to the formation of tachyzoites acutely, which cause parasitemia and further dissemination, and bradyzoites, which lead to latent infection with the formation of tissue cysts in skeletal muscle, heart muscle, and central nervous system (CNS) tissue. Toxoplasmosis can be transmitted to humans by ingestion of tissue cysts in raw or inadequately cooked infected meat or in uncooked foods that have come in contact with contaminated meat, by inadvertent ingestion of oocysts and sporozoites in cat feces, or transplacentally. Immunocompetent adults and adolescents with primary infection are generally asymptomatic, but symptoms may include mild malaise, lethargy, and lymphadenopathy. Specific treatment for nonpregnant adults and adolescents is not required. Immunosuppressed patients may experience more severe manifestations, including splenomegaly, chorioretinitis, pneumonitis, encephalitis, and multisystem organ failure. These patients are also prone to reactivation of latent infection involving the CNS. All patients with human immunodeficiency virus infection and CD4 counts <100 cells per cubic millimeter should be treated prophylactically with pyrimethamine-sulfonamide. Congenital toxoplasmosis is marked by the classic triad of chorioretinits, intracranial calcifications, and hydrocephalus. Current studies have determined that prolonged treatment (1-2 years) of neonates with fansidar is important to prevent serious sequelae. Diagnosis of acute toxoplasmosis is mainly by antibody detection and generally only undertaken in pregnant patients with risk factors for transplacental transmission. All positive screening tests in pregnant women must be confirmed at a toxoplasma reference laboratory. Recent studies have shown that polymerase chain reaction testing of amniotic fluid is useful for identification or exclusion of fetal T. gondii infection. Ultrasound can be used as an adjunct to serological screening but cannot itself definitively diagnose disease. Early-first-trimester maternal infections are less likely to result in congenital infection, but the sequelae are more severe. Transplacental passage is more common when maternal infection occurs in the latter half of pregnancy, but fetal injury is usually much less severe. Typically, infected pregnant patients are treated with pyrimethamine-sulfonamide for positive PCR-amniotic-fluid testing and with spiramycin for negative PCR-AF testing.
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PMID:Toxoplasmosis. 1137 31


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