Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Murin Cerebral Malaria (MCM) with Plasmodium berghei ANKA and the CBA/Ca mice is the result of an immunopathological process. An overproduction of TNF is implicated in its pathogenesis. Recent datas concerning TNF production during the course of Plasmodium vinckei vinckei infection, and analysis of relationships between MCM and Experimental Allergic Encephalomyelitis (EAE) raise the hypothesis of the involvement of an auto-immune process in the murin disease. The role of cellular immunity in human cerebral malaria remains obscure. Cytokines could majore adherence of parasitized red blood cells to cerebral endothelial cells.
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PMID:[Involvement of cellular immunity in pathology. Neuromalaria]. 132 51

Studies are reviewed in which the role of IFN-gamma in different models of inflammation in mice is examined: LPS-induced generalized Shwartzman reaction, experimental allergic encephalomyelitis (EAE) and experimental cerebral malaria (ECM). The particular role of the cytokine was studied by systemic administration and by blocking the endogenously produced cytokine by the use of neutralizing antibodies. IFN-gamma was found, depending on the model and circumstances, to exert an anti- or a pro-inflammatory effect. In the generalized Shwartzman reaction and ECM this cytokine has a disease promoting role. In EAE, on the contrary, endogenous as well as exogenous IFN-gamma exert a down-regulating effect.
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PMID:The role of cytokines in various animal models of inflammation. 250 97

The biology, veterinary importance and control of certain Nematocera are described and discussed. Culicoides spp. (family Ceratopogonidae) transmit the arboviruses of bluetongue (BT), African horse sickness (AHS), bovine ephemeral fever (BEF) and Akabane. Some other arboviruses have been isolated from these species, while fowl pox has been transmitted experimentally by Culicoides. These insects are vectors of the parasitic protozoans Leucocytozoon caulleryi and Haemoproteus nettionis, and the parasitic nematodes Onchocerca gutturosa, O. gibsoni and O. cervicalis. They also cause recurrent summer hypersensitivity in horses, ponies, donkeys, cattle and sheep. Farm animals can die as a result of mass attack by Simulium spp., which are also vectors of Leucocytozoon simondi, L. smithi and the filariae O. gutturosa, O. linealis and O. ochengi. Venezuelan equine encephalomyelitis (VEE) and Rift Valley fever (RVF) have been isolated from simuliids, and vesicular stomatitis virus New Jersey strain has been replicated in Simulium vittatum. Simuliids are well known as vectors of O. volvulus, the cause of human onchocercosis (river blindness). The family Psychodidae includes the genera Phlebotomus and Lutzomyia (subfamily Phlebotominae), vectors of Leishmania spp. in humans, dogs and other mammals. Vesicular stomatitis virus Indiana strain has been regularly isolated from phlebotomine sandflies. Mass attack by mosquitoes can also prove fatal to farm animals. Mosquitoes are vectors of the viruses of Akabane, BEF, RVF, Japanese encephalitis, VEE, western equine encephalomyelitis, eastern equine encephalomyelitis and west Nile meningoencephalitis, secondary vectors of AHS and suspected vectors of Israel turkey meningoencephalitis. The viruses of hog cholera, fowl pox and reticuloendotheliosis, the rickettsiae Eperythrozoon ovis and E. suis, and the bacterium Borrelia anserina are mechanically transmitted by mosquitoes. These insects also induce allergic dermatitis in horses. They transmit several filarial worms of both animals and humans, and are of great medical importance as vectors of major human diseases, including malaria, yellow fever, dengue fever and many more diseases caused by arboviruses.
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PMID:Nematocera (Ceratopogonidae, Psychodidae, Simuliidae and Culicidae) and control methods. 771 9

Neuropsychiatric complications in the course of plasmodium falciparum infection are usually summarized as cerebral malaria. Heterogeneous clinical symptoms, different courses and inconstant parasitemia, however, suggest different pathogenic mechanisms. We report a case of an acute symptomatic psychosis occurring two weeks after successful therapy of a primary manifestation of plasmodium falciparum infection. The diagnosis of meningoencephalitis was based on lymphocytic pleocytosis of cerebrospinal fluid and hyperintense lesions in cranial magnetic resonance imaging. Due to the lack of plasmodium falciparum parasitemia and of serological evidence of viral infection a final diagnosis was not possible. Considering the pertinent literature, an immune-mediated complication of plasmodium falciparum infection (acute disseminated encephalomyelitis, ADEM) appears to be more probable than a direct viral or plasmodium CNS infection. We propose to reverse the term cerebral malaria for the cases with direct pathogenic influence of plasmodium falciparum, and to distinguish it from cases with possible immune-mediated pathogenesis.
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PMID:[Acute organic psychosis after malaria tropica]. 867 92

A 24-year-old Japanese man showed neurological disturbances 2 weeks after complete recovery from Plasmodium vivax infection. Magnetic resonance (MR) images of the brain showed multiple high-intensity spotty lesions in the left cerebral cortex and subcortex. Cerebrospinal fluid examination, including polymerase chain reaction analysis for viruses, revealed no sign of active infection. Repeated blood smears were negative for malaria. We diagnosed acute disseminated encephalomyelitis (ADEM) following Plasmodium vivax malaria from the clinical course and MR images. ADEM should be regarded as one of the neurological complications after malarial infection.
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PMID:Acute disseminated encephalomyelitis following Plasmodium vivax malaria. 1451 95

Tumor necrosis factor alpha(TNFalpha) is a crucial mediator involved in the communications between immune and nervous systems in physiological conditions, and its relevance is amplified during disease. Considered originally detrimental and a target for therapeutic intervention, recently it has also gained attention for its protective role, especially in central nervous system (CNS) confined diseases. Thus, TNFalpha has become the key molecule illustrating the peculiar and still not completely understood pathways by which inflammatory and immune reactions occur in the brain. Several human pathologies that lack an efficient therapy and that carry enormous social costs rely on these mechanisms. Thus, further research is needed to improve our knowledge and to allow the identification of therapeutic targets or strategies for immune-mediated inflammatory disease of the CNS in which TNFalpha is primarily involved. We describe here how to induce experimental autoimmune encephalomyelitis, cerebral malaria, and brain ischemia in rodents, and some protocols to analyze them. The application of innovative research strategies or original therapeutic approaches to these experimental models may be rewarding in terms of advancement in a field that is crucial for the management of many human patients.
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PMID:TNFalpha in experimental diseases of the CNS. 1506 39

Neurologic complications in the course of Plasmodium falciparum infections are commonly diagnosed as cerebral malaria, but bacterial or viral meningitis may exhibit similar symptoms. One to three weeks after P. falciparum malaria, acute disseminated encephalomyelitis (ADEM) can also mimick the symptoms of cerebral malaria. We describe a 31-year-old woman with life-threatening ADEM five days after successful treatment of P. falciparum malaria. The detection of IgG and IgM antibodies in serum and cerebrospinal fluid (CSF) against multiple viruses and bacteria reflected a non-specific polyclonal B cell activation and was more confusing than helpful for diagnostic decisions. Varicella zoster virus was identified with a reverse transcriptase multiplex polymerase chain reaction in the initially obtained and frozen CSF. This case and findings from the literature indicate that P. falciparum-associated ADEM might not be immune mediated, but of infectious origin. With unclear cerebral complications during or after P. falciparum malaria, prompt initiation of empirical antiviral and antibacterial treatment in addition to antimalarials may reduce mortality.
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PMID:Acute disseminated encephalomyelitis following Plasmodium falciparum malaria caused by varicella zoster virus reactivation. 1582 91

Several neurological complications are associated with severe falciparum malaria. Cerebral malaria is one of the most life-threatening complications. A few patients may experience a neurological syndrome after complete recovery from Plasmodium falciparum infection. In the literature especially the postmalaria neurological syndrome (PMNS), acute disseminated encephalomyelitis (ADEM) and delayed cerebellar ataxia have been reported. We describe a case of a 53-year-old woman who was readmitted after an adequately treated P. falciparum infection with word-finding difficulties, confusion and tremor. Peripheral blood smears were repeatedly negative for malarial parasites. The clinical features best fitted a PMNS. Because of the severity of the syndrome she was treated with high-dose prednisone. She recovered completely. The possibility of ADEM is also discussed. Aetiology of these syndromes is still unknown, but it could be mediated by an immunological mechanism. PMNS or ADEM must be considered when neurological signs and symptoms occur after recovery from a P. falciparum infection.
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PMID:Neurological complications following Plasmodium falciparum infection. 1595 88

Several neurological complications are associated with severe falciparum malaria. Indeed, some patients experience a neurological syndrome after complete recovery from Plasmodium falciparum infection. Particularly, postmalaria neurological syndrome (PMNS) is a self-limiting post-infective encephalopathy that occurs within 2 months after an episode of P. falciparum infection. We describe the case of a 54-year-old Japanese man who was readmitted to our hospital with incoherent speech and markedly disturbed and uncooperative behavior after a high-grade fever that occurred after an earlier adequately treated severe P. falciparum infection. Peripheral blood smears were repeatedly negative for malaria parasites, no organisms were detected in the cerebrospinal fluid, and no hallmark lesions of acute disseminated encephalomyelitis were depicted by brain magnetic resonance imaging. The neuropsychiatric symptoms were thought to be due to PMNS. The etiology of PMNS remains unclear, but it could be mediated by an immunological mechanism and could possibly be caused by mefloquine treatment. PMNS must be considered when characteristic neurological signs and symptoms such as psychotic or acute confusional episodes, general convulsions, and tremor occur after recovery from severe P. falciparum infection treated with oral mefloquine. This is the first reported case of suspected PMNS in Japan.
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PMID:A case of postmalaria neurological syndrome in Japan. 1723 48

Ethyl 2-[4-(12-beta-artemisininoxy)]phenoxylpropionate (SM933) is a novel derivative of artemisinin, an herbal compound approved for the treatment of malaria. In this study, we show that SM933 has unique anti-inflammatory properties through regulation of signaling pathways, leading to amelioration of experimental autoimmune encephalomyelitis. The anti-inflammatory properties of SM933 were characterized by inhibition of encephalitogenic T cell responses that were altered to exhibit a Th2 immune deviation and reduced activity and concentration of NO and inducible NO synthase. The observed effect of SM933 was mediated through regulatory mechanisms involving the NFkappaB and the Rig-G/JAB1 signaling pathways. SM933 was found to inhibit the activity of NFkappaB by up-regulating IkappaB, which accounted for various down-stream anti-inflammatory actions. Furthermore, it up-regulated Rig-G through the action of IFN-alpha and prevented JAB1, a master cell cycle regulator, from entering the nucleus to promote p27 degradation, resulting in down-regulation of CDK2 and cyclin A and cell cycle progression. Regulation of the Rig-G/JAB1 pathway by SM933 led to altered cell cycle activity of encephalitogenic T cells as a result of its selective effect on activated, but not resting, T cells. The study indicates that SM933 is a novel anti-inflammatory agent acting through defined signaling mechanisms and provides regulatory mechanisms required for effective drug targeting in treatment of autoimmune disease and inflammation.
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PMID:Anti-inflammatory properties and regulatory mechanism of a novel derivative of artemisinin in experimental autoimmune encephalomyelitis. 1794 69


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