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)

A fatal case of meningoencephalitis due to a leptomyxid ameba in a patient with the acquired immunodeficiency syndrome is presented. This opportunistic organism has not been previously recognized as a human pathogen. A 36-year-old male intravenous drug abuser died after an 18-day hospital course heralded by fever and headache and followed by nuchal rigidity and hemiparesis. Computed tomography of the head showed multiple hypodense lesions. Neuropathologic examination showed that in addition to human immunodeficiency virus encephalomyelitis, there was multifocal meningoencephalitis with trophozoites and cysts morphologically indistinguishable from those of Acanthamoeba. These organisms were also found in the kidneys and adrenal glands. By immunofluorescence, the parasites showed antigenic identity with a free-living leptomyxid ameba and failed to react with any of a spectrum of antiacanthamoeba antisera. This emphasizes the importance of immunofluorescence identification of morphologically indistinguishable ameba species.
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PMID:Amebic meningoencephalitis in a patient with AIDS caused by a newly recognized opportunistic pathogen. Leptomyxid ameba. 198 9

This paper presents clinical, immunological and post-mortem findings in three family members (husband, wife and daughter) who all died in 1976 after having had chronic and recurrent opportunistic infections for many years. In all of them a progressive, presumably acquired T-lymphocyte defect associated with B-lymphocyte dysfunction had been diagnosed several years before death. The clinical and immunological findings are compatible with those seen in acquired immunodeficiency syndrome (AIDS) caused by HTLV-III/LAV infection, but examinations of stored blood samples from the three patients were negative with regard to the presence of HTLV-III/LAV antibodies. This immunodeficiency may therefore have been caused by an infectious agent of unknown nature. The most remarkable finding on post-mortem examination was the presence of a granulomatous encephalomyelitis with multinucleated giant cells in the husband and his wife. In addition, the wife's CNS revealed scattered microglial nodules. No infectious agents could be demonstrated, and the etiology of this peculiar CNS affection therefore remains obscure.
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PMID:Autopsy findings in three family members with a presumably acquired immunodeficiency syndrome of unknown etiology. 348 98

Encephalomyelitis is a sequela to ovine lentivirus (OvLV) and human immunodeficiency virus infections. Examination of autopsy tissue from 38 naturally infected asymptomatic sheep showed that 7 (18%) had subclinical neurological lesions characterized by perivascular and periventricular infiltrates of lymphocytes and histiocytes in the leptomeninges, cerebral white matter, choroid plexus, and/or cervical spinal cord. Intralesional histiocytes were shown to contain lentiviral capsid proteins or RNA. Infectious virus (2/7), viral proteins (4/7), and antiviral antibody (5/7) were only detected in cerebrospinal fluid (CSF) from animals with central nervous system (CNS) lesions associated with OvLV infection, suggesting that such virologic markers in CSF, when used concurrently, are predictive of pathologic changes specific to the CNS.
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PMID:Virological markers in cerebrospinal fluid are predictive of ovine lentivirus-associated subclinical encephalomyelitis. 755 77

Infection of the central nervous (CNS) system by the human immunodeficiency virus (HIV) depends on the migration of infected hematogenous cells into the brain. We thus used quantitative light and electron microscopic immunocytochemistry to study the homing and turnover of bone marrow derived cells in the CNS in radiation bone marrow chimeras under normal conditions and in experimental autoimmune encephalomyelitis (EAE) as an experimental model of brain inflammation. Our studies suggest the following conclusions. First, the central nervous system is continuously patrolled by a small number of T-lymphocytes and monocytes. Meningeal and perivascular monocytes are slowly replaced by hematogenous cells under normal conditions, and this turnover is accelerated in the course of inflammation. In contrast, resident microglia represent a very stable cell pool, which in adult animals is only exceptionally replaced by hematogenous cells, even after recovery from severe brain inflammation. Second, although in bone-marrow-chimeric animals resident microglia, astrocytes, and ependymal cells are not able to present antigen to Lewis T-lymphocytes, the inflammatory reaction in EAE is qualitatively and quantitatively similar in these animals compared to fully histocompatible Lewis rats. Finally, resident microglia express the macrophage activation antigen ED1. Thus, microglia cells appear to function as effector cells in EAE lesions.
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PMID:Bone marrow derived elements and resident microglia in brain inflammation. 767 81

A number of endogenous mouse mammary tumor virus (MMTV) proviruses encode superantigen that have the ability to stimulate T cells with a certain T cell receptor (TCR) beta-chain variable region (V beta) and to mediate the V beta-specific clonal deletion. The tumorigenic milk-borne MMTV carried by C3H and GR mice also have superantigenic properties in vivo. In the present study we identified and characterized a novel V beta 8.2-specific superantigen of exogenous MMTV carried by FM mice. The open reading frame (ORF) in the 3' long terminal repeat of the MMTV was cloned by polymerase chain reaction with primers corresponding to conserved regions spanning the ORF coding region. Sequence analysis of the ORF revealed that there is no sequence identical to those in other known MMTV in the carboxy terminus implicated in TCR V beta recognition. Subcutaneous injection of the virus into adult BALB/c mice induced an approximately three- to fourfold enlargement of draining lymph nodes and a substantial increase of V beta 8.2+ CD4+ T cells in the lymph nodes within 6 days. The exposure of newborn BALB/c mice to the virus by foster nursing resulted in a marked deletion of V beta 8.2+ cells both in CD4+ and CD8+ T cells. Thus, a novel milk-borne MMTV in FM mice expresses strong superantigenic properties capable of stimulating V beta 8.2+ T cells. V beta 8.2+ T cells have been demonstrated to be frequently involved in recognition of conventional antigens and responsible for autoimmune diseases such as experimental allergic encephalomyelitis. Therefore, the MMTV (FM) may provide a new mouse model system for inducing immunodeficiency or autoimmune disease by retroviral infection.
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PMID:A V beta 8.2-specific superantigen from exogenous mouse mammary tumor virus carried by FM mice. 791 38

A captive-born rhesus monkey (Macaca mulatta) experimentally infected with simian immunodeficiency virus developed neurologic abnormalities approximately seven months postinoculation. A chronic necrotizing encephalomyelitis with intralesional protozoal schizonts was diagnosed histologically. The protozoa was identified as Sarcocystis neurona based on its morphologic characteristics by light and electron microscopic examination, the developmental stages of the schizonts, and positive staining with antisera against Sarcocystis cruzi by immunocytochemical techniques. Although S. neurona may be confused with Toxoplasma gondii by light microscopy, the former lacks rhoptries, is in direct contact with the host cell cytoplasm, and divides by endopolygeny. Sarcocystis neurona has recently been identified as an etiologic agent of encephalomyelitis in horses, raccoons, and mink.
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PMID:Encephalomyelitis due to a Sarcocystis neurona-like protozoan in a rhesus monkey (Macaca mulatta) infected with simian immunodeficiency virus. 794 53

Infectious agents have been postulated as causes of multiple sclerosis for over a century. The possible role of a virus or viruses is supported by data that (1) a childhood exposure is involved and "viral" infections may precipitate exacerbations of disease, (2) experimental infections in animals and natural infections in humans can cause diseases with long incubation periods, remitting and relapsing courses, and demyelination, and (3) patients with multiple sclerosis have abnormal immune responses to viruses. The pathogenesis of three human demyelinating diseases of known viral etiology is discussed. In progressive multifocal leukoencephalopathy, a papovavirus selectively infects oligodendrocytes and causes focal areas of demyelination. In postmeasles encephalomyelitis, the virus is lymphotrophic and disrupts immune regulation that can result in an autoimmune perivenular demyelinating illness without evidence of infection of the central nervous system. In human immunodeficiency virus-encephalopathy and myelopathy virus is present in macrophages and microglia and the myelin abnormalities apparently are caused by soluble factors such as viral proteins, cytokines, or neurotoxins. These findings may have implications on how, when, and where to seek viruses in multiple sclerosis.
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PMID:The virology of demyelinating diseases. 801 89

Severe combined immunodeficient (SCID) C.B-17-scid/scid (H-2d) strain mice are deficient for T and B lymphocytes and lack all of the immune functions associated with these cell types. Experimental autoimmune encephalomyelitis (EAE) was induced in chimeric SCID mice that had been previously reconstituted with allogeneic mouse or xenogeneic rat hematopoietic stem cells from EAE-susceptible donor strains. Encephalitogenic, myelin Ag-specific, T lymphocytes selected from SJL mice, Lewis rats, or Buffalo rats transferred passive EAE into chimeric SCID mice reconstituted with SJL mouse, Lewis rat, or Buffalo rat hematopoietic cells, respectively. SCID mice reconstituted with Lewis rat hematopoietic tissue and thymus were also susceptible to EAE induced by active immunization with the myelin proteolipid protein synthetic peptide PLP S139-151. T lymphocytes recovered from the spleens of SCID mouse-rat chimeras with EAE proliferated upon in vitro stimulation with myelin Ag presented by APC syngeneic to the transplant donor, and rat T lymphocytes selected in vitro from SCID mouse-rat chimeras with EAE transferred EAE back into naive recipient rats. Thus, the immunodeficiency present in SCID mice can be overcome at least partially by hematopoietic tissue transplantation from allogeneic or xenogeneic donors. Furthermore, allogeneic SJL mouse and xenogeneic Lewis or Buffalo rat myelin Ag-specific T cells can transfer EAE between strains and species, respectively, into recipient SCID mouse chimeras.
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PMID:Induction of experimental autoimmune encephalomyelitis in severe combined immunodeficient mice reconstituted with allogeneic or xenogeneic hematopoietic cells. 809 58

Histopathologic lesions in the central nervous system (CNS) of 400 autopsy cases of the acquired immunodeficiency syndrome (AIDS) collected from 1982 to 1990 were studied. Lesions most closely associated with human immunodeficiency virus (HIV) infection in the CNS (perivascular macrophages, nodular encephalomyelitis, diffuse leukoencephalopathy, necrotizing encephalitis, and long-tract degeneration) were found in 20% of the cases. The group of vascular and inflammatory lesions and of opportunistic infections was seen in 25% of cases. These two lesion groups were found together in 32% of cases, and none of these lesions was present in 23% of cases (most of the latter having no significant CNS lesions). Length of survival increased in the last group of 100 cases compared with the first 300 cases. The homosexual and bisexual risk groups showed continuously increasing lengths of survival for each category of HIV-associated CNS lesions throughout the study, while the lengths of survival in the other risk groups varied. Patients in the last group of 100 autopsy cases with any HIV-associated lesion survived longer than patients without these lesions. The AIDS patients with no CNS lesions had the shortest mean length of survival. The results suggest that although survival is prolonged as specific therapy is given, there is an increase in CNS lesions in AIDS patients with longer survival. This may indicate that CNS lesions in AIDS are generally dependent on systemic disease progression over many months as immune function decreases.
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PMID:Histopathologic features in the central nervous system of 400 acquired immunodeficiency syndrome cases: implications of rates of occurrence. 824 20

One rhesus macaque displayed severe encephalomyelitis and another displayed severe enterocolitis following infection with molecularly cloned simian immunodeficiency virus (SIV) strain SIVmac239. Little or no free anti-SIV antibody developed in these two macaques, and they died relatively quickly (4 to 6 months) after infection. Manifestation of the tissue-specific disease in these macaques was associated with the emergence of variants with high replicative capacity for macrophages and primary infection of tissue macrophages. The nature of sequence variation in the central region (vif, vpr, and vpx), the env gene, and the nef long terminal repeat (LTR) region in brain, colon, and other tissues was examined to see whether specific genetic changes were associated with SIV replication in brain or gut. Sequence analysis revealed strong conservation of the intergenic central region, nef, and the LTR. However, analysis of env sequences in these two macaques and one other revealed significant, interesting patterns of sequence variation. (i) Changes in env that were found previously to contribute to the replicative ability of SIVmac for macrophages in culture were present in the tissues of these animals. (ii) The greatest variability was located in the regions between V1 and V2 and from "V3" through C3 in gp120, which are different in location from the variable regions observed previously in animals with strong antibody responses and long-term persistent infection. (iii) The predominant sequence change of D-->N at position 385 in C3 is most surprising, since this change in both SIV and human immunodeficiency virus type 1 has been associated with dramatically diminished affinity for CD4 and replication in vitro. (iv) The nature of sequence changes at some positions (146, 178, 345, 385, and "V3") suggests that viral replication in brain and gut may be facilitated by specific sequence changes in env in addition to those that impart a general ability to replicate well in macrophages. These results demonstrate that complex selective pressures, including immune responses and varying cell and tissue specificity, can influence the nature of sequence changes in env.
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PMID:Analysis of simian immunodeficiency virus sequence variation in tissues of rhesus macaques with simian AIDS. 841 55


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