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)

During an outbreak of a herpesvirus infection in juvenile harbor seals, 11 out of 23 seals died. The duration of the disease in these 11 animals varied from 1-6 days. Nasal discharge, inflammation of the oral mucosa, vomiting, diarrhea and fever up to 40 degrees C were observed in the first days of the disease. In later stages coughing, anorexia and lethargy occurred. Severe necrosis of the liver and interstitial pneumonia were the most striking histopathological findings.
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PMID:An outbreak of a herpesvirus infection in harbor seals (Phoca vitulina). 300 64

Thirty-four, 9- to 11-week-old, male castrated, crossbred, specific pathogen-free derived pigs were exposed to a T-2 toxin aerosol at a nebulized dose of 0 or 9 mg/kg in pairs, each pair consisting of 1 control and 1 T-2 treated pig which were exposed on the same day. Twenty to 30% of the toxin (1.8 to 2.7 mg/kg) was retained by the pigs. Five pairs were killed on each of 1, 3 and 7 days after dosing. Two pairs of pigs were designated as a 0.33-day group when one T-2 treated pig died and the other was killed in a moribund state at 8 to 10 hours after dosing. The pulmonary and systemic immunity and morphologic changes of the lungs and other organs were examined. Bronchoalveolar lavage was performed to obtain alveolar macrophages (AM) and pulmonary lymphocytes (PL). The phagocytic ability of AM and mitogen-induced blastogenic responses of enriched PL and peripheral blood lymphocytes were evaluated. Clinically, all of the T-2 treated pigs vomited and were cyanotic, anorexic, lethargic and laterally recumbent. In the 0.33-, 1-, and 3-day T-2 treated pigs, there was a marked reduction in AM phagocytosis and mitogen-induced blastogenic responses of PL but not of peripheral blood lymphocytes. Mild to moderate, multifocal interstitial pneumonia was seen in the majority of the T-2 treated pigs. In pigs dying following inhalation of T-2 toxin, there was a more severe pneumonia, as well as marked necrosis of lymphoid tissues, severe necrohemorrhagic gastroenteritis and edema of the gall bladder wall, and multifocal necrosis of the heart and pancreas. Thus, inhalation exposure to T-2 toxin can result in clinical signs and morphologic changes resembling those reported previously in pigs given T-2 toxin intravascularly (iv) at a dose of 1.2 mg/kg (approximate LD50) or greater, as well as death. Mild pulmonary injury as well as transient impairment of pulmonary immunity was present in pigs surviving inhalation exposure.
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PMID:Experimental T-2 toxicosis in swine following inhalation exposure: effects on pulmonary and systemic immunity, and morphologic changes. 368 91

Acute toxicosis developed in a group (n = 35) of fattening hogs and replacement gilts that had excessive vitamin D3 inadvertently added to their feed. All of the pigs were lethargic, and emesis was evident in about half of the pigs 1 to 2 days after they consumed the feed. On the 2nd day, 3 of the pigs died. The remaining pigs were given a different ration. Five additional pigs died during the next 2 weeks. Clinical toxicosis also was observed in 1 of 2 feeder pigs fed the suspect feed in the laboratory and in 2 of 2 pigs fed the suspect feed by the company that had mixed the feed. Gross necropsy findings consistently observed were hemorrhagic gastritis and diffuse interstitial pneumonia. Myocardial degeneration and nephrosis were seen in, respectively, 1 of 6 and 4 of 6 pigs necropsied. Histologically, necrosis and mineralization of variable severity were observed in the fundic gastric mucosa, lungs, kidneys, bone, heart, and small blood vessels of the lungs and heart. Less necrosis and more mineralization were observed in pigs that survived longer than 6 days. The 2 pigs fed the suspect feed in the laboratory had increased concentrations of serum calcium from the 3rd to the 9th days or the 1st to the 3rd days, after feeding the suspect feed. Serum phosphorus concentrations were increased from the 1st until the 2nd or 3rd day, and serum magnesium concentrations were increased from the 1st or 2nd to the 3rd day after feeding the suspect feed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute toxicosis in swine associated with excessive dietary intake of vitamin D. 632 15

The clinical signs and gross and microscopic lesions of Lassa virus infection in the rhesus monkey are described. Of 17 monkeys infected with Lassa virus, nine died or were killed when moribund. The clinical signs were lethargy, aphagia, constipation, fever, conjunctivitis, and skin rash. Pulmonary congestion, pleural effusion, pericardial edema, hydropericardium, and a few visceral hemorrhages were present grossly. Major microscopic lesions were necrotizing hepatitis and interstitial pneumonia. Other microscopic changes were present in the heart, small intestine, spleen, lymph nodes, kidney, urinary bladder, adrenal glands, and central nervous system; however, most of these lesions were mild. In fact, death could not always be attributed to the morphologic changes; therefore, function alterations must be examined.
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PMID:Pathology of Lassa virus infection in the rhesus monkey. 712 56

A 2-phase study was conducted to evaluate the ability of the NEB-1 strain of porcine reproductive and respiratory syndrome virus (PRRSV) to potentiate common bacterial pathogens of swine. In phase I, 25 of 50 4-5-week-old specific-pathogen-free (SPF) pigs were exposed to NEB-1 PRRSV (day 0). Seven days after virus inoculation, 8 groups received 1 of 4 bacterial pathogens: Haemophilus parasuis, Streptococcus suis, Salmonella cholerasuis, and Pasteurella multocida. The ability of NEB-1 PRRSV to produce clinical disease, viremia, neutralizing antibody, gross and microscopic lesions and to potentiate bacterial pathogens was assessed. Response to NEB-1 PRRSV was similar among inoculated pigs; prolonged hyperthermia, lethargy, mild to moderate dyspnea, and cutaneous erythema were consistent clinical signs. No clinical differences were observed in groups after bacterial challenge. Virus was isolated from serum at weekly intervals through the end of the study, and all PRRSV-inoculated pigs had seroconverted by study termination. Two of 5 pigs died in non-PRRSV-inoculated groups challenged with H. parasuis and Streptococcus suis. Mortality in PRRSV-infected pigs was limited to 1 of 5 pigs from the Salmonella cholerasuis-challenged group. Gross lesions were seen in pigs dying after inoculation in H. parasuis- and Streptococcus suis-inoculated groups, in Salmonella cholerasuis- and P. multocida-challenged pigs, and in 1 non-PRRSV-inoculated control pig. Microscopic lesions consisted of mild to moderate proliferative interstitial pneumonia, nonsuppurative myocarditis, lymphoid hyperplasia, and nonsuppurative encephalitis in PRRSV-inoculated pigs. Findings in phase I indicated that NEB-1 PRRSV does not potentiate bacterial disease while inducing consistent clinical signs, viremia, seroconversion, and microscopic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Porcine reproductive and respiratory syndrome: NEB-1 PRRSV infection did not potentiate bacterial pathogens. 757 44

An emerging swine disease principally involving periweaning piglets was examined. The disease was clinically characterized by lethargy, fever, emaciation, coughing, and severe abdominal breathing, hence colloquially named "Heko-heko" disease. The consistent lesions in affected piglets were diffuse interstitial pneumonia with pronounced type II pneumocytic proliferation, meningoencephalitis, and regression of the lymphoid tissues. The causal virus was isolated in primary porcine lung cell (PLC) cultures from various organs of affected piglets and showed serological relatedness to the European porcine reproductive and respiratory syndrome (PRRS) virus. Numerous virus particles, measured about 49 nm in diameter, were detected in the cytoplasm of alveolar epithelial cells and pulmonary macrophages in PLC cultures infected with the isolate. The condition could be experimentally reproduced in conventional piglets by intranasal inoculation with the isolate and the virus was reisolated from the infected animals.
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PMID:An outbreak of porcine reproductive and respiratory syndrome in Japan. 786 92

From August 1990 to June 1991, a moderate die-off of 4- to 5-year-old green sea turtles (Chelonia mydas) occurred at Cayman Turtle Farm, Grand Cayman, British West Indies. Clinical signs included lethargy, anorexia, and inability to dive. Many of the ill turtles floated on the surface of their tanks. There was no apparent sex predilection. Complete necropsies, including histopathologic examination of tissues, were performed on eight turtles. Necropsies revealed multiple irregular discrete to patchy 1-10 mm pale gray foci throughout the hearts of four turtles. By light microscopic examination, the most severe and consistent lesions were necrotizing myocarditis, histiocytic to fibrinous splenitis, and hepatic lipidosis and necrosis. A mixed leukocytic infiltrate of acidophils, macrophages, and lymphocytes was present in affected areas of the heart. Other lesions included lymphocytic/plasmacytic interstitial nephritis, subacute interstitial pneumonia, subacute mesenteric vasculitis, chronic/active enteritis of the small intestine, and occasional granulomas associated with spirorchid trematode ova. Chlamydiae could be demonstrated in macrophages in sections of paraffin-embedded heart, liver, and spleen and in myocardial fibers and hepatocytes using a modified Macchiavello's stain. Chlamydial antigen was detected by light microscopic examination in the cytoplasm of myocardial fibers and in occasional hepatocytes using a commercially available genus-specific antichlamydial monoclonal antibody and the avidin biotin peroxidase complex staining method. Electron microscopic examination of the heart of the most severely affected turtle revealed developmental stages of chlamydial organisms. A suspension of heart from this turtle was inoculated into the yolk sacs of chicken embryos.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chlamydiosis in mariculture-reared green sea turtles (Chelonia mydas). 814 Jul 12

This study was designed to examine the effects of a pre-existing, clinically asymptomatic feline immunodeficiency virus (FIV) infection on a primary challenge with Toxoplasma gondii. Parenteral challenge of FIV-infected cats with tachyzoites of the ME49 strain of T. gondii caused a precipitous drop in all lymphocytes (CD4+, CD8+, and B cells) and generalized severe toxoplasmosis. The predominant postmortem lesions included acute and often fatal interstitial pneumonia, dominated histologically by macrophages, and multifocal to coalescing hepatic necrosis. Immunohistochemistry revealed numerous T. gondii antigen and tachyzoites in macrophages and other cell types in the lung lesions. The proliferative response of peripheral blood mononuclear cells to specific (T. gondii antigen) and nonspecific (Concanavalin A) mitogens was defective in the dually infected cats, suggesting marked immunosuppression. In contrast to the dually infected cats, cats infected only with T. gondii developed a transient, mild clinical disease characterized by anorexia, lethargy, and multifocal chorioretinitis. Lymphocyte changes in T. gondii-infected cats included an early pan-lymphopenia followed by reestablishment of all lymphocyte subset profiles. These cats also showed a reduced proliferative response to Concanavalin A at 1 week after challenge, but a measurable in vivo response to T. gondii antigens, as evidenced by in vitro lymphocyte proliferation in the absence of a mitogenic stimulus. These results show that infection of cats with FIV-NCSU, markedly enhances their susceptibility to a primary T. gondii infection and provides a model to study the mechanisms of the underlying immunological defect(s) occurring early after HIV infection that may predispose individuals to development of acquired immunodeficiency syndrome and associated diseases.
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PMID:Feline immunodeficiency virus predisposes cats to acute generalized toxoplasmosis. 823 62

The first case of phocine distemper in a seal from Canadian waters and the first case of clinical phocine distemper in a harp seal, Phoca groenlandica, is reported. A two-month-old female harp seal stranded on Prince Edward Island in May 1991. Significant clinical findings were lethargy and severe conjunctivitis. Pulmonary congestion was the main necropsy finding, and histological lesions included diffuse demyelinating nonsuppurative encephalitis and mild multifocal interstitial pneumonia. Acidophilic intracytoplasmic and intranuclear inclusions were present in cerebral neurons and astrocytes. Immunoperoxidase staining confirmed phocine distemper virus (PDV) antigen in the cytoplasm and nuclei of neurons, bronchiolar gland epithelium and transitional epithelium of the bladder. Infectivity titers of canine distemper virus (CDV) (Onderstpoort strain) and a morbillivirus isolated from a grey seal were significantly reduced by serum from the harp seal.
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PMID:Phocine distemper in a harp seal (Phoca groenlandica) from the Gulf of St. Lawrence, Canada. 844 69

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


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