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)

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

The Lelystad virus or one of two US isolates (VR2385, VR2431) of porcine reproductive and respiratory syndrome virus were given intranasally to 25 4-week-old cesarian-derived colostrum-deprived pigs. Pigs from these groups were necropsied at 1, 2, 3, 5, 7, 10, 15, 21, or 28 days postinoculation. The Lelystad virus and VR2431 induced mild transient pyrexia, dyspnea, and tachypnea. VR2385 induced labored and rapid abdominal respiration, pyrexia, lethargy, anorexia, and patchy dermal cyanosis. All three isolates induced multifocal tan-mottled consolidation involving 6.8% (n = 9; SEM = 3.4) of the lung for Lelystad, 9.7% (n = 9, SEM = 2.7) of the lung for VR2431, and 54.2% (n = 9, SEM = 4.4) of the lung for VR2385 at 10 days postinoculation. Characteristic microscopic lung lesions consisted of type 2 pneumocyte hypertrophy and hyperplasia, necrotic debris and increased mixed inflammatory cells in alveolar spaces, and alveolar septal infiltration with mononuclear cells. Lymphadenopathy with follicular hypertrophy, hyperplasia, and necrosis was consistently seen. Similar follicular lesions were also seen in Peyer's patches and tonsils. Lymphohistiocytic myocarditis and encephalitis were reproduced with all three isolates. Clinical respiratory disease and gross and microscopic lung lesion scores were considerably and significantly more severe in the VR2385-inoculated pigs. All three viruses were readily isolated from sera, lungs, and tonsils throughout the 28 days of the study. The lymphoid and respiratory systems have the most remarkable lesions and appear to be the major site of replication of these viruses. This work demonstrated a marked difference in pathogenicity of porcine reproductive and respiratory syndrome isolates.
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PMID:Comparison of the pathogenicity of two US porcine reproductive and respiratory syndrome virus isolates with that of the Lelystad virus. 859

We present the case of a 38-year-old patient who developed symptoms are parkinsonian syndrome at the age of 14, after meningoencephalitis meeting the criteria for a diagnosis of lethargic encephalitis (LE). The extrapyramidal symptoms are asymmetric are quiescent and have responded successfully to levodopa therapy for over 20 years. This is the first such case of parkinsonism secondary to LE to have been described in the Spanish medical literature in recent decades.
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PMID:[Parkinsonism after lethargic encephalitis: possibly the first Spanish case in the second half of the century]. 871 76

In 1954, when he was five years old, a patient suffered from encephalitis with a prolonged lethargic state. Following this episode, he presented a severe parkinsonian syndrome which was associated, after a few years, with an axial dystonia and stereotyped involuntary movements of the upper limbs. These abnormal movements were particular by their coordinated appearance, their rhythmicity and their relative slowness. Treatment with L-dopa suppressed all akinetic, dystonic and dyskinetic symptoms. At age of 40 years, all the akinetic, dystonic and dyskinetic symptoms reappeared after drug withdrawal. Cerebral computed tomography, magnetic resonance imaging and fluorodeoxyglucose positron emission tomography were normal. Fluorodopa positron emission tomography revealed a significant bilateral reduction of tracer accumulation in the posterior part of both putamen, similar to that observed in patients with idiopathic Parkinson's disease. In this patient, pharmacological tests revealed that effectiveness of L-dopa was abolished by administration of a D2 antagonist, and was fully reproduced by a D2 agonist. Clinical signs, pharmacological data and past-medical history strongly suggested a limited lesion of the zona compacta of substantia nigra induced by viral agression. This complex and progressive extrapyramidal syndrome had strong similarities with the lethargic encephalitis of Von Economo and its late symptoms. Other diseases associating akinesia and dyskinesia or dystonic phenomena, like dopa-sensitive dystonia and juvenile Parkinson's disease, are very unlikely. Thus, the persistance of sporadic forms of Von Economo's encephalitis could be discussed.
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PMID:[Parkinsonian syndrome and post-encephalitic stereotyped involuntary movements responsive to L-dopa]. 876 55

In 1954, at the age of 5 years, our patient had an encephalitic syndrome associated with a prolonged lethargic state. After this episode, he developed a severe parkinsonian syndrome that, after a few years, was associated with axial dystonia and stereotyped abnormal movements of the upper limbs. This complex and progressive extrapyramidal syndrome had many similarities to the encephalitis lethargica as described by von Economo. Results of cerebral computed tomography and magnetic resonance imaging were normal. Fluorodopa positron emission tomography showed a significant bilateral reduction of tracer accumulation in both putamen, similar to that observed in patients with idiopathic Parkinson's disease. However, in this patient, treatment with L-Dopa suppressed all akinetic, dystonic and dyskinetic symptoms. The effectiveness of L-Dopa was abolished by administration of a D2 antagonist and was fully reproduced by a D2 agonist. In conclusion, this patient presented a complex postencephalitic, extrapyramidal syndrome, with akinetic symptoms and involuntary movements. These symptoms appeared to be related to a limited lesion of the dopaminergic neurons of the zona compacta of the substantia nigra.
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PMID:Postencephalitic stereotyped involuntary movements responsive to L-Dopa. 886 99

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

Naegleria fowleri, Acanthamoeba spp., and Balamuthia mandrillaris are known to cause fatal central nervous system (CNS) disease in human beings. N. fowleri causes acute, fulminating primary amebic meningoencephalitis (PAM), which generally leads to death within 10 days. Acanthamoeba spp. and B. mandrillaris cause chronic granulomatous amebic encephalitis, which may last for 8 weeks. Acanthamoeba spp. and B. mandrillaris also cause CNS disease in animals. N. fowleri, however, has been described only in human beings. This report is the first of PAM in an animal, a South American tapir. Dry cough, lethargy, and coma developed in the animal, and its condition progressed to death. At necropsy, lesions were seen in the cerebrum, cerebellum, and lungs. The CNS had severe, suppurative meningoencephalitis with many neutrophils, fibrin, plasma cells, and amebas. Amebas were 6.5 microns to 9 microns in diameter and had a nucleus containing a large nucleolus. Amebas in the sections reacted with a monoclonal antibody specific for N. fowleri in the immunofluorescent assay and appeared bright green.
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PMID:Primary amebic meningoencephalitis due to Naegleria fowleri in a South American tapir. 916 83

The spiroplasmas are mollicutes characterized by motility and helical morphology. They were discovered through studies on corn stunt and citrus stubborn diseases. The stubborn agent was the first mollicute of plant origin to be obtained in culture and the first cultured mollicute to possess a helical morphology. The citrus pathogen has been known as Spiroplasma citri since 1973. The corn stunt agent was cultured in 1975 and fully characterized as Spiroplasma kunkelii by 1986. The third and only other phytopathogenic spiroplasma is Spiroplasma phoeniceum, cultured from naturally infected periwinkle plants in Syria and described in 1986. These three spiroplasmas are restricted to the phloem sievetubes of the infected plants and are transmitted from plant by various phloem feeding leafhopper vectors in which the spiroplasmas multiply. Following the pioneering work on S. citri and S. kunkelii, close to fifty other spiroplasma species or proposed species have been discovered. All spiroplasmas have been isolated from insects, ticks and plants. Insects are particularly rich sources of spiroplasmas. Some insect-derived spiroplasmas are entomopathogens. S. melliferum and S. apis are honey bee pathogens. They cross the insect-gut barrier and reach the hemolymph, where they multiply abundantly and kill the bee. Spiroplasma floricola is the agent of lethargy disease of Melolontha melolontha (cockchafer). Spiroplasma poulsonii infects the neotropical species of Drosophila, is transmitted transovarially and kills the male progeny of an infected female fly, hence the name sex ratio spiroplasma. Some insect-derived spiroplasmas are also found on plant (flower) surfaces. For instance, S. apis was cultured from the surfaces of flowers growing in the vicinity of affected beehives. This suggests that the plant surface spiroplasmas are deposited on these surfaces by contaminated insects. Many insect spiroplasmas are not pathogenic, are often restricted to the gut and may be regarded as mutualists or incidental commensals. Of the three known tick spiroplasmas, only Spiroplasma mirum obtained from rabbit ticks is pathogenic to the vertebrate animal (chick embryo, new-born rodents, adult rabbit), but only upon experimental inoculation of the spiroplasma. Strain SMCA induces high incidence of cataracts in new born rodents. With strain GT-48 no cataracts are observed, but fatal encephalitis occurs. Spiral membranous inclusions resembling spiroplasmas have been seen in brain biopsies taken from patients with Creutzfeldt-Jakob disease. However, failure to detect spiroplasmas by serology and culture points to the absence of spiroplasmal involvement in spongiform encephalopathies. Transposon Tn 4001 mutagenesis has been applied for the first time to Spiroplasma citri, and pathogenicity can now be studied at the genetic level. One Tn 4001 mutant does not multiply in the leafhoppers and is, therefore, not transmitted to the plant. Another mutant multiplies well in the plant and is transmitted to the plant, where it reaches high titers, but without inducing symptoms in the plant. In this non-phytopathogenic mutant, Tn 4001 is inserted in the spiroplasmal fructose operon, and the mutant is unable to use fructose. Finally, to study involvement of spiroplasmal motility in pathogenicity, a non-motile mutant has been obtained. Motility was restored by complementation with the wild type genes. This is the first time that successful complementation has been reported, not only in the spiroplasmas but in the mollicutes in general. Undoubtedly, studies on pathogenicity have entered a new era.
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PMID:Spiroplasmas: infectious agents of plants, arthropods and vertebrates. 928 68

Influenza viruses rarely cause acute encephalopathy. Post-influenzal encephalitis, which occurs a few weeks after recovery from influenza is thought to be an autoimmune process associated with demyelination and vasculopathy. It has been suggested that Economo lethargic encephalitis followed by postencephalitic Parkinsonism was associated with the influenza A epidemic of 1918 (Spanish flu). The incidence of Reye's syndrome has markedly decreased due to the avoidance of salicylates in the treatment of influenza or varicella. One inactivated flu vaccine is thought to have caused Guillain Barre syndrome due to molecular mimicry between viral protein and myelin, which triggered autoimmune responses. The persistence of influenza virus genes in neural cells as one of the causes of chronic degenerative diseases of the central nervous system by inducing apoptosis of the host cells is yet to be proven.
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PMID:Influenza virus and neurological diseases. 931 61

A 76-year old woman was affected by lethargic encephalitis in 1918, at the age of 3 months. Long-term clinical follow-up with late neuropsychological evaluation revealed post-encephalitic parkinsonism, which worsened very slowly and was improved by levodopa. Obsessive and compulsive disorders (OCD) were associated to nosophobia. Neuropsychological evaluation showed mild visuocontructional memory deficit, which was isolated. 18 Fluoro-Dopa PET demonstrated a severe bilateral and symmetrical reduction in fluoro-dopa uptake, which was more marked in the putamen than in the caudate. Thus, the pattern of dopaminergic denervation was similar to the one observed in idiopathic Parkinson's disease.
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PMID:PET study and neuropsychological assessment of a long-lasting post-encephalitic parkinsonism. 972 Sep 76


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