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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rise of the AIDS epidemic made the requirement for T cells in our continuous protection from pathogens critically apparent. The striking frequency with which AIDS patients exhibited profound neurological pathologies brought attention to many chronic infections that are latent within the immune-privileged CNS. One of the most common lethal opportunistic infections of these patients was with the protozoan parasite, Toxoplasma gondii. Reactivation of Toxoplasma cysts within the brain causes massive tissue destruction evidenced as multiple ring-enhancing lesions on MRI and is called toxoplasmic encephalitis (TE). TE is not limited to AIDS patients, but rather is a risk for all severely immunocompromised patients, including recipients of chemotherapy or transplant recipients. The lessons learned from these patient populations are supported by T cell depletion studies in mice. Such experiments have demonstrated that CD4+ and CD8+ T cells are required for protection against TE. Although it is clear that these T cell subsets work synergistically to fight infection, much evidence has been generated that suggests CD8+ T cells play a dominant role in protection during chronic toxoplasmosis. In other models of CNS inflammation, such as intracerebral infection with LCMV and experimental autoimmune encephalomyelitis (EAE), infiltration of T cells into the brain is harmful and even fatal. In the brain of the immunocompetent host, the well-regulated T cell response to T. gondii is therefore an ideal model to understand a controlled inflammatory response to CNS infection. This review will examine our current understanding of CD8+ T cells in the CNS during T. gondii infection in regards to the (1) mechanisms governing entry into the brain, (2) cues that dictate behavior within the brain, and (3) the functional and phenotypic properties exhibited by these cells.
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PMID:Characteristics and critical function of CD8+ T cells in the Toxoplasma-infected brain. 2589 88

Toxoplasmosis is a parasitic disease that affects man and animals worldwide. The primary hosts and major reservoir for Toxoplasma gondii are felids and the intermediate hosts are most warm-blooded animals including man. This report describes fatal toxoplasmosis in three different rodent species in Germany: a female red squirrel (Sciurus vulgaris) and a male Swinhoe's striped squirrel (Tamiops swinhoei), both kept as pets, and a female New World porcupine (Erethizontidae sp.) from a zoo. All three animals had multifocal necrotizing hepatitis. Additional findings included lymphohistiocytic and necrotizing myocarditis in the New World porcupine and the Swinhoe's striped squirrel, lymphohistiocytic encephalomyelitis in the New World porcupine and suppurative lymphadenitis in the red squirrel. Numerous tachyzoites were identified associated with the lesions. The diagnosis was confirmed by Toxoplasma. gondii immunohistochemistry and electron microscopy. This is the first report of toxoplasmosis in a New World porcupine and a Swinhoe's striped squirrel.
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PMID:Fatal Systemic Toxoplasma gondii Infection in a Red Squirrel (Sciurus vulgaris), a Swinhoe's Striped Squirrel (Tamiops swinhoei) and a New World Porcupine (Erethizontidae sp.). 2698 9

This manuscript describes an outbreak of fatal toxoplasmosis in wallabies. Ten adult red necked wallabies (Macropus rufogriseus) were imported from New Zealand to the Virginia Zoo. Agglutination testing upon admission into quarantine showed all animals to be negative for antibodies to Toxoplasma gondii. Nine of these wallabies died from acute toxoplasmosis within 59-565 (average 224) days after being moved onto exhibit. Clinical signs included lethargy, diarrhea, tachypnea, and ataxia that progressed rapidly; death without premonitory signs occurred in one case. Histopathologic examination revealed interstitial pneumonia, encephalomyelitis, myositis, enteritis, and myocarditis. The diagnosis was confirmed through serologic, histopathologic, and polymerase chain reaction (PCR) testing. Multilocus PCR-RFLP (restriction fragment length polymorphism) genotyping revealed that the first six animals were infected by a previously undiscovered Toxoplasma gondii genotype, designated as ToxoDB PCR-RFLP genotype No. 263. These six cases survived for an average of 118 days on exhibit before succumbing to toxoplasmosis. The other three wallabies were infected with a Toxoplasma gondii strain of ToxoDB PCR-RFLP genotype No. 4, which is a common strain type circulating in wild animals in North America. These three cases survived for an average of 435 days on exhibit before succumbing to toxoplasmosis. The outbreaks of toxoplasmosis in these wallabies are likely from two different sources. Furthermore, the results highlight Toxoplasma gondii PCR-RFLP genotyping in parasite diagnosis and understanding parasite transmission and potential mitigation procedures.
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PMID:NEWLY DESCRIBED TOXOPLASMA GONDII STRAIN CAUSES HIGH MORTALITY IN RED NECKED WALLABIES (MACROPUS RUFOGRISEUS) IN A ZOO. 2892 Aug 10

Toxoplasma gondii is an opportunistic parasite that infects a broad range of hosts including humans. The chronic latent phase of the disease manifests as intra-neuronal cerebral cysts tightly controlled by the host immune system. In immunocompromised patients, reactivation of cerebral toxoplasmosis can have severe neurological outcomes that may sometimes lead to death. Despite the efficient prophylactic and treatment measures taken against the rare reactivation of cerebral toxoplasmosis, many reports including several recent ones revealed the still occurrence of this spectrum of disease. We present the case of a 4 years-6 months old apparently immunocompetent child whose premortem clinical presentation and investigations were highly consistent with severe acute disseminated encephalomyelitis (ADEM). The patient received all appropriate medications with initial improvement followed by rapid deterioration and death. Postmortem brain autopsy revealed a wide reactivation of cerebral toxoplasmosis. This is a peculiar case presentation as such medical treatment for ADEM (i.e. steroids) may worsen the Toxoplasma infection with ominous consequences. This case highlights the importance to rule out the possibility of such infections in apparently immunocompetent hosts by performing the appropriate investigations to prevent complications.
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PMID:Acute disseminated encephalomyelitis and reactivation of cerebral toxoplasmosis in a child: Case report. 3012 90

Toxoplasma gondii is a major protozoan parasite and infects human and many other warm-blooded animals. The infection leads to Toxoplasmosis, a serious issue in AIDS patients, organ transplant recipients and pregnant women. Neospora caninum, another type of protozoa, is closely related to Toxoplasma gondii. Infections of the protozoa in animals also causes serious diseases such as Encephalomyelitis and Myositis-Polyradiculitis in dogs or abortion in cows. Both Toxoplasma gondii and Neospora caninum have similar nucleoside triphosphate hydrolases (NTPase), NcNTPase and TgNTPase-I in Neospora caninum and Toxoplasma gondii, respectively. These possibly play important roles in propagation and survival. Thus, we targeted the enzymes for drug discovery and tried to establish a novel high-standard assay by a combination of original biochemical enzyme assay and fluorescent assay to determine ADP content. We then validated whether or not it can be applied to high-throughput screening (HTS). Then, it fulfilled criterion to carry out HTS in both of the enzymes. In order to identify small molecules having inhibitory effects on the protozoan enzyme, we also performed HTS using two synthetic compound libraries and an extract library derived from marine bacteria and then, identified 19 compounds and 6 extracts. Nagasaki University collected many extracts from over 18,000 marine bacteria found in local Omura bay, and continues to compile an extensive collection of synthetic compounds from numerous drug libraries established by Japanese chemists.
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PMID:Establishment of Novel High-Standard Chemiluminescent Assay for NTPase in Two Protozoans and Its High-Throughput Screening. 3218 21

This article discusses mimics of multiple sclerosis (MS). Excluded in this discussion are neuromyelitis optica and vasculitis, discussed in other articles in this journal. Covered entities include posterior reversible encephalopathy syndrome, reversible vasoconstriction syndrome, acute disseminated encephalomyelitis, Sussac's Syndrome, and chronic idiopathic demyelinating polyneuropathy. There are also multiple infectious entities that mimic MS including; progressive multi-focal leukoencephalopathy (PML), Toxoplasmosis, Tuberculosis, Herpes Simplex Virus, Cytomegalovirus, Varicella zoster virus, Epstein Barr virus, Cryptococcus and Human immunodeficiency virus. In addition, there are leukoencephalopathies that can present in adulthood including Adrenoleukodystrophy, Metachromatic leukodystrophy, Cerebral autosomal dominant idiopathic leukoencephalopathy, Leigh's and Alexanders disease that could be mistaken for MS.
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PMID:What Can Mimic Multiple Sclerosis? 3244 85

Experimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis (MS), a demyelinating autoimmune disease caused by the infiltration of a harmful autoreactive Th1 and Th17 cells. To mitigate MS, which is impossible to cure with medication only, immunomodulatory interventions that prevent Th17 cell activation are ideal. The objective of the present study was to analyze the effect of Toxoplasma gondii infection on the onset of EAE. Our results found that Toxoplasma gondii infection in the brain increases SOCS3 expression and decreases the phosphorylation of STAT3, resulting in reducing IL-17A and IL-23, which suppress the differentiation and expansion of pathogenic Th17 cells, an important factor in MS development. These immune responses resulted in a reduction in the clinical scoring of EAE induced by myelin oligodendrocyte glycoprotein 35-55 immunization. In the EAE group with T. gondii infection (Tg + EAE group), Th17-related immune responses that exacerbate the onset of EAE were reduced compared to those in the EAE group. This study suggests that the alleviation of EAE after T. gondii infection is regulated in a SOCS3/STAT3/IL-17A/blood-brain barrier integrity-dependent manner. Although parasite infection would not be permitted for MS treatment, this study using T. gondii infection identified potential targets that contribute to disease attenuation.
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PMID:Chronic Toxoplasma gondii Infection Alleviates Experimental Autoimmune Encephalomyelitis by the Immune Regulation Inducing Reduction in IL-17A/Th17 Via Upregulation of SOCS3. 3320 83


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