Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851341 (infestation)
 10,121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A healthy young adult with no evidence of immunosuppression presented with a diffuse encephalopathy considered to be due to Toxoplasma gondii. A marked eosinophilia as well as an anamnestic reaction to a previous parasitic infestation was present. The clinical picture and abnormalities on computed tomography were in keeping with the diagnosis, which was supported by serological tests. Treatment with pyrimethamine and sulphadiazine was effective and there were negligible sequelae.
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PMID:Toxoplasma gondii encephalitis in an immunocompetent adult. A case report. 357 8

Human African trypanosomiasis (HAT) is caused by infestation with a flagellate protozoan, the trypanosome which is inoculated by the bite of the tsetse fly Glossina. The particular ecological conditions of parasites and vectors are such that the disease is only found in the intertropical regions of Africa. Although there are many species of trypanosomes, only two, belonging to the brucei group are likely to lead to HAT. These two species are quite similar morphologically but have different pathogenicity. Trypanosoma brucei gambiense found in West and Central Africa leads to a chronic form of the disease or sleeping sickness. T. b. rhodesiense leads to a more virulent and acute condition, although for each species of trypanosome there are strains of different virulence, which account, at least in part, for the interindividual variability in the clinical course. Immediately after penetration into the human organism, the trypanosome multiplies at the point of inoculation, producing a local inflammatory reaction. It then invades the whole organism, and the central nervous system (CNS). The involvement of the CNS leads to an irreversible demyelinating process ending by death without treatment. Apart from the initial stages, it is not easy to determine the phase of the disease that the patient is presenting. The parasite can escape the host immune response by varying the surface glycoprotein coat. Variable surface glycoproteins (VSG) are strongly antigenic and lead to great antibody response with immune lysis. But, some heterologous antigenic variants can survive to repopulate blood and other tissues. This mechanism of antigenic variation is under parasite genetic control. The trypanosome can release numerous pathogenic substances which cause alterations in cytokine/prostaglandin network. A 41-46 kDa molecule termed trypanosome-released lymphocyte trigerring factor may selectively activate CD8+ T cells to produce interferon-gamma which then activates macrophages but also promotes parasite growth. Activated macrophages release tumor necrosis factor alpha and nitric oxide (NO) which are trypanostatic static and other cytokines and prostanglandins. These macrophage relased substances enhance the immunosuppression and alter the blood brain barrier (BBB). So, trypanosomes and inflammatory cells can invade the CNS leading to a progressive meningoencephalitis with typical perivascular cuffings which explain neurological disorders and neuroendocrine alterations. The inflammatory cells (lymphocytes, astrocytes, glial cells) produce cytokines, NO and other mediators and enhance the CNS immunopathological process. The peri-ventricular regions, the tuberoinfundibula and thalamic-hypothalamic regions, are particulary involved. These disturbances lead to a progressively complete disruption of the normal sleep-waking cycle. Antibodies anti-CNS components (galactocerebrosides, neurofilaments, tryptophane) are also described in sera and cerebrospinal fluid (CSF) of HAT patients. Their presence may be due to cross reactions with comon epitopes between host and trypanosomes which can lead to a self-propagating autoimmune reaction, which accounts for the marked demyelination found in the late stage of the disease. The diagnosis of CNS involvement in not easy to establish in the early neurological phase in the absence of neurological signs and in absence of great chnages in CSF. This is an important problem because it is the basis to apply existing available drugs. pentamidine and suramin are effective only in early stages of the disease when CNS is not invaded. Melarsoprol is effective in all-stages: this is the drug of choice when CNS is involved. Unfortunaley, melarsoprol is toxic and, in 5% of treated patients, this drug can lead to arsenical encephalopathy which is often fatal. In the continuing search for new antitrypanosonal drugs, biochemical peculiarities of the trypanosome are used as drug garget, especially glycolysis, trypanothione, sensibil
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PMID:[Human African trypanosomiasis]. 895 90

Eight genotypes of Borrelia burgdorferi are known currently. In Slovakia (Carpathian Euroregion) the most frequent genotypes are B. garini, B. afzelii, as well as B. valaisiana and B. lusitaniae. Infestation of the vector Ixodes ricinus is 3-30%. The most frequent early skin manifestation is erythema migrans (60-70%). Borrelia burgdorferi is suggested to be the causative agent in sclerodermia circumscripta, lichen sclerosus et atrophicus, maybe also in urticaria chronica, granuloma anulare, erythema anulare, erythema nodosum. It can be the causative agent also in neurological diagnoses as e.g. chronic oligosymptomatic encephalopathy, "sclerosis multiplex-like" syndrome and fatigue syndrome, arthralgia, myalgia, seronegative indifferentiated oligoarthritis and fibromyalgies. The serological diagnosis has to be coincide with clinical findings. Used serological examinations are ELISA, Immunoblot, indirect immunofluorescence examination. PCR is an important contribution in examination of synovial fluid (85% detection) and cerebrospinal liquor (24-100%). The importance of PCR is stressed in cases with mixed infections by several borrrelia genotypes. The first line treatment includes doxyciclin, amoxicilin, and erythromycin. The second line includes macrolides, cephalosporines. New perspectives are ascribed to active immunisation with recombined antigen OsA (LYMErix, ImuLyme).
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PMID:[Skin manifestations of Lyme borreliosis--occurrence, diagnosis, therapy]. 1121 59

Infestation with Ascaris lumbricoides in children has a varied manifestation, but encephalopathy is a very rare presentation. This report describes a case of ascariasis-associated encephalopathy in a child. An 18-month-old boy was admitted with altered sensorium. He had a history of vomiting and was passing Ascaris worms in the vomitus. The cerebrospinal fluid analysis did not reveal any abnormality. The patient was treated with an antihelminthic drug and he recovered completely. Worm encephalopathy should be considered as a differential diagnosis for unexplained encephalopathy in tropical areas.
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PMID:Ascariasis-associated worm encephalopathy in a young child. 1929 1

A 13-year-old Standardbred gelding was referred for evaluation of continuous abdominal pain. Rectal examination revealed a dislocated large colon (Dislocatio coli ad dextram). The horse showed muscle fasciculations and appeared lethargic. It was sent to surgery because of persistent colic. In transit the gelding showed an unstable walk and immediately prior to surgery a wide-based stance in the hindlimbs. Laparotomy revealed a retroflexion of the large colon and a secundary mesenterial volvulus. After surgery the horse remained recumbent. Due to the comatose state and poor prognosis the gelding was euthanized after 15 hours of recumbency. Necropsy indicated hyperaemic meninges, edema of gliacells and submeningeal tissue with vacuolization and loss of several cerebellar Purkinjecells as well as multiple conglomerates of Alzheimer type II astrocyte groups within the grey matter. Further findings included marked hepatolipidosis, multiple gastric ulcers, small intestinal hyperaemia with mild mononuclear inflammation, tapeworm-infestation of the caecum and moderate chronic enteritis with eosinophilic component in the large intestine. To the best of our knowledge, this was the first case of a horse with colic and concurrent encephalopathy without primary liver disease described in a German-speaking country.
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PMID:[Encephalopathy and Alzheimer type II astrocytes in a post laparotomy recumbent horse]. 1953 45

We report a case of a 37-year-old patient with Plasmodium falciparum infestation who developed posterior reversible encephalopathy. In cerebral malaria, microscopic studies have shown endothelial dysfunction and disruption of the blood-brain barrier. Data from the literature show that one of the mechanisms of posterior reversible encephalopathy may be capillary leakage and acute disruption of the blood-brain barrier. Our case supports the theory of blood-brain barrier disruption being a key factor in the causation of cerebral malaria.
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PMID:Posterior reversible encephalopathy syndrome in neuro-malaria. 2104 44