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)

An 8-yr-old captive, female common wombat (Vombatus ursinus) from Victoria, Australia was euthanased after an illness of 36 days manifested by lethargy, inappetance and terminal coma with respiratory failure. Toxoplasmosis was diagnosed during life by the Toxoplasma direct agglutination test (DAT) which showed a positive initial titre of 1:1,024 at 22 days after onset of illness and a four fold rise in titre to 1:4,098 2 wk later, just prior to death. The Toxoplasma modified agglutination test (MAT) remained negative over this time period. The serological diagnosis was confirmed by histological diagnosis of granulomatous encephalitis, focal myocarditis, interstitial pneumonia and severe adrenal cortical necrosis and the presence of tachyzoites of Toxoplasma gondii in large numbers within the focal necrotic lesions in the brain, myocardium and adrenal cortices. The serological response in the wombat differed from that of the typical eutherian which exhibits a reaction in both the DAT and MAT within 2 wk of infection with T. gondii. An incidental finding was calcification in the media of the ascending aorta and proximal parts of the major arteries.
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PMID:Serodiagnosis of toxoplasmosis in a common wombat. 913 74

A 3-mo-old, male African hedgehog (Atelerix albiventris) was anorectic and lethargic for a period of 3 days prior to death. Necropys revealed lungs that were diffusely firm, dark red, and dorsally adhered by fibrinous tags to the pericardial sac. Histopathology revealed necrosuppurative bronchopneumonia with pulmonary abscesses and suppurative pericarditis and myocarditis. A Corynebacterium sp. was isolated from the lungs. We believe this is the first reported case of corynebacterial pneumonia in an African hedgehog.
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PMID:Corynebacterial pneumonia in an African hedgehog. 957 94

A three-year-old weimaraner was presented with lethargy, anorexia, neck pain and a soft fluctuant swelling in the thoracic inlet. A cough had been noted previously. Clinical examination revealed tachycardia, tachypnoea, pallor and a large subcutaneous swelling, with bruising, suggestive of a haematoma in the thoracic inlet. Thoracic radiographs revealed a cranial mediastinal mass which had the ultrasonographic appearance of fluid, and there was also a marked generalised interstitial lung pattern. Routine haematology revealed severe anaemia and thrombocytopenia, although coagulation tests were within normal limits. A diagnosis of immune-mediated thrombocytopenia was however made on the basis of a positive antiplatelet antibody test and a rapid response to prednisolone therapy. Furthermore, a tentative diagnosis of Angiostrongylus vasorum infection was suggested on the basis of clinical and radiographic findings, although no lungworm larvae were identified on faecal analysis. Despite initiating treatment with fenbendazole, the dog died suddenly. Postmortem examination revealed myocarditis, thrombosing arteritis, pneumonia and chronic membranoproliferative glomerulonephritis associated with A vasorum infection.
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PMID:Immune-mediated thrombocytopenia associated with Angiostrongylus vasorum infection in a dog. 1038 68

The unique clinical and pathological findings in nine Asian (Elephas maximus) and two African (Loxodonta africana) elephants from North American Zoos with a highly fatal disease caused by novel endotheliotropic herpesviruses are described. Identification of the viruses by molecular techniques and some epidemiological aspects of the disease were previously reported. Consensus primer polymerase chain reaction (PCR) combined with sequencing yielded molecular evidence that confirmed the presence of two novel but related herpesviruses associated with the disease, one in Asian elephants and the second in African elephants. Disease onset was acute, with lethargy, edema of the head and thoracic limbs, oral ulceration and cyanosis of the tongue followed by death of most animals in 1 to 7 days. Pertinent laboratory findings in two of three clinically evaluated animals included lymphocytopenia and thrombocytopenia. Two affected young Asian elephants recovered after a 3 to 4 wk course of therapy with the anti-herpesvirus drug famciclovir. Necropsy findings in the fatal cases included pericardial effusion and extensive petechial hemorrhages in the heart and throughout the peritoneal cavity, hepatomegaly, cyanosis of the tongue, intestinal hemorrhage, and ulceration. Histologically, there were extensive microhemorrhages and edema throughout the myocardium and mild, subacute myocarditis. Similar hemorrhagic lesions with inflammation were evident in the tongue, liver, and large intestine. Lesions in these target organs were accompanied by amphophilic to basophilic intranuclear viral inclusion bodies in capillary endothelial cells. Transmission electron microscopy of the endothelial inclusion bodies revealed 80 to 92 nm diameter viral capsids consistent with herpesvirus morphology. The short course of the herpesvirus infections, with sudden deaths in all but the two surviving elephants, was ascribed to acute cardiac failure attributed to herpesvirus-induced capillary injury with extensive myocardial hemorrhage and edema.
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PMID:Clinical and pathological findings of a newly recognized disease of elephants caused by endotheliotropic herpesviruses. 1068 40

The aim of this study was to present neurological complications of influenza infections. Infections caused by influenza viruses can be very serious and may lead even to death resulted from the post-infectious complications. The most often occurring complications are pneumonia, bronchitis, bronchiolitis, myocarditis and otitis media. The other group is neurological post-influenza complications, including dementia, epileptic disorders, cerebrovascular disease, febrile convulsions, toxic encephalopathy, encephalitis, meningitis, subarachnoid hemorrhages, lethargic encephalitis, psychosis or increase in the number of cases of Parkinson's disease. The first way of prevention of influenza is vaccination that results in healthy, social and economic benefits.
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PMID:[Neurological complication of influenza infections]. 1219 26

The nonpoliovirus enteroviruses commonly infect newborns, with consequences ranging from asymptomatic infection and benign illness, to severe, life-threatening disease. Frequently occurring symptoms include fever, irritability, lethargy, anorexia, and rash. Although most illnesses are mild, severe disease develops in a subset of newborns infected in the first 2 weeks of life. Severe disease may consist of sepsis, meningoencephalitis, myocarditis, pneumonia, hepatitis, and/or coagulopathy. Substantial mortality rates have been reported, and long-term sequelae may occur among survivors. Risk factors and clinical features associated with severe disease include absence of neutralizing antibody to the infecting serotype, maternal illness prior to or at delivery, prematurity, illness onset within the first few days of life, multiorgan disease, severe hepatitis, positive serum viral culture, and specific infecting serotype (e.g. group B coxsackieviruses and echovirus 11). Whereas the mainstay of diagnosis has traditionally been viral isolation in tissue culture, the polymerase chain reaction has been demonstrated to be more sensitive than culture, highly specific, and rapid. Immunoglobulin has been used as a therapeutic agent for neonates with enterovirus disease; however, clinical efficacy has not been proven. Specific antiviral therapy for enteroviruses is in development. Pleconaril is an investigational agent that inhibits viral attachment to host cell receptors and uncoating of viral nucleic acid. It has broad and potent anti-enterovirus activity, excellent oral bioavailability, and is well tolerated. Some clinical trials have demonstrated benefit in children and adults with enterovirus meningitis, and in adults with upper respiratory tract infections caused by picornaviruses (rhinoviruses or enteroviruses). Data summarizing compassionate use for severe enterovirus diseases (including neonatal sepsis) also suggest possible benefit. Limited pharmacokinetic data are available in infants and neonates. A multicenter, placebo-controlled, randomized trial of pleconaril in neonates with severe hepatitis, coagulopathy, and/or myocarditis is currently being conducted.
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PMID:Presentation, diagnosis, and management of enterovirus infections in neonates. 1496 66

A male fennec fox (Fennecus zerda) kit was examined for lethargy, inappetence, and weight loss. Clinical findings included respiratory distress, a gallop rhythm, and retinochoroiditis. Radiography indicated pleural effusion and cardiomegaly. Echocardiographic findings included left ventricular dilatation, low left ventricular ejection fraction, and atrioventricular valvular regurgitation. Necropsy findings were compatible with a diagnosis of congestive heart failure caused by myocarditis. Histopathology showed a disseminated infection with Toxoplasma gondii causing myocarditis, skeletal polymyositis, gastrointestinal myositis, and panuveitis. Toxoplasma-induced myocarditis should be included in the differential diagnosis of heart failure and retinochoroiditis in the fennec fox.
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PMID:Heart failure caused by toxoplasmosis in a fennec fox (Fennecus zerda). 1553 72

The present study tested the hypothesis that murine (m)IFN-beta or mIFN-alpha(2) can eliminate cardiac viral load and protect cardiomyocytes from injury in animals infected with coxsackievirus B3 (CVB3). CVB3-inoculated male Balb/c mice exhibited signs of illness, including lethargy, progressive weight loss, and death (10% on day 3 and 100% on day 8). Cardiac viral load was high [4,277 +/- 1,009 plaque-forming units and 25 +/- 5 copies CVB3/hypoxanthine guanine phosphoribosyl transferase 1 mRNA] on day 4. The cardiac tissue exhibited severe inflammatory infiltration and myocyte damage with an average myocarditis integrated pathology score of 2.1 +/- 0.2 on day 7. Most of the mice infected with CVB3 also developed epicarditis, and 55% had intraventricular thrombi present. Treatment with mIFN-beta [2.5 to 10 million international units (MIU)/kg] dose-dependently improved the general health status in CVB3-inoculated mice, as evidenced by reduction in weight loss, prevention of death, elimination of cardiac viral load, protection of myocytes from injury, decrease in inflammatory cell infiltration, and attenuation of intraventricular thrombus formation. Treatment with 10 MIU/kg mIFN-alpha(2) resulted in a similar level of efficacy as that induced by 5 MIU/kg mIFN-beta, with the exception that mIFN-alpha(2) did not reduce cardiac CVB3 mRNA. However, mIFN-alpha(2) , but not any dose group of mIFN-beta, significantly attenuated CVB3-induced epicarditis. These data demonstrate antiviral effects for both mIFN-beta and mIFN-alpha(2), which lead to protection of the mice from CVB3-induced myocarditis. However, the potential mechanisms leading to a differential host response for the two isoforms of mIFN remain to be elucidated.
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PMID:Antiviral and myocyte protective effects of murine interferon-beta and -{alpha}2 in coxsackievirus B3-induced myocarditis and epicarditis in Balb/c mice. 1743 74

West Nile virus (WNV) has affected many thousands of birds since it was first detected in North America in 1999, but the overall impact on wild bird populations is unknown. In mid-August 2002, wildlife rehabilitators and local wildlife officials from multiple states began reporting increasing numbers of sick and dying raptors, mostly red-tailed hawks (Buteo jamaicensis) and great horned owls (Bubo virginianus). Commonly reported clinical signs were nonspecific and included emaciation, lethargy, weakness, inability to perch, fly or stand, and nonresponse to danger. Raptor carcasses from 12 states were received, and diagnostic evaluation of 56 raptors implicated WNV infection in 40 (71%) of these cases. Histologically, nonsuppurative encephalitis and myocarditis were the salient lesions (79% and 61%, respectively). Other causes of death included lead poisoning, trauma, aspergillosis, and Salmonella spp. and Clostridium spp. infections. The reason(s) for the reported increase in raptor mortality due to WNV in 2002 compared with the previous WNV seasons is unclear, and a better understanding of the epizootiology and pathogenesis of the virus in raptor populations is needed.
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PMID:Raptor mortality due to West Nile virus in the United States, 2002. 1749 4

Although acute and chronic cases of canine Chagas disease have been reported from multiple areas in the southern region of the United States, little data are available on current disease occurrence patterns in endemic areas. Therefore, a study to assess frequency, geographic distribution, signalment, and clinical spectrum of Chagas disease in domestic dogs from Texas was conducted. Serology, histopathology, and clinical case records from multiple institutions for the time period 1993-2007 were analyzed. A total of 537 serologically and/or histopathologically confirmed cases were documented. Cases were reported from 48 of 254 counties within Texas, covering all major geographic regions. Forty-eight dog breeds were represented among the cases, primarily in the sporting and working groups. In histopathologically confirmed cases, acute death occurred in 42%, approximately half of which were <1 year of age. Nearly all cases with histopathology data reported myocarditis (97.9%) and observation of Trypanosoma cruzi organisms (81.7%). Predominant clinical observations included enlarged heart, lethargy, anorexia, ascites, cardiac conduction disturbances, and respiratory difficulties. An increasing rate of serologic test submissions was noted over the study period, with an overall positive test prevalence of 20.3%. The study results provide strong evidence that an active canine Chagas disease transmission cycle is present throughout all ecoregions of Texas, affecting a broad range of dog breeds and age groups.
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PMID:Distribution and characterization of canine Chagas disease in Texas. 1825 33


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