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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral toxoplasmosis and cytomegalovirus (CMV) infection are very frequent in AIDS. Biological markers of toxoplasmosis and CMV were studied in blood and cerebrospinal fluid (CSF) of 121 HIV-positive and 35 HIV-negative patients in the Central Hospital of the Congolese Army in Brazzaville. In the case of clinically suspected cerebral toxoplasmosis, the simultaneous presence of specific IgG antibodies in the blood and in the CSF can be considered as having complementary diagnostic value (PPV = 63.3%, NPV = 89.9%). The symptomatology of AIDS is very polymorphous and includes various etiological factors; as a result it is very difficult to estimate the responsibility of cytomegalovirus in the absence of positive viral culture, even with the simultaneous presence of specific IgG antibodies in the blood and CSF (PPV = 75.7%, NPV = 54.6%).
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PMID:[Toxoplasmosis and cytomegalovirus serology in patients infected with HIV in Congo]. 816 59

The pathology of AIDS encephalopathy and its relation to other CNS infections in AIDS was studied in 112 autopsies of AIDS patients and 14 of HIV-positive patients. Special interest was focused on gliomesenchymal nodules (GMNs), a common finding in encephalitis of various etiologies, and on giant cells. GMNs and giant cells were found in 40 patients. These 40 were used for the present study, they were further divided into five groups: I. 21 with AIDS encephalopathy; II. 3 with HIV infection but no AIDS; III. 8 with Toxoplasma encephalitis; IV. 7 with cytomegalovirus encephalitis; and V. 1 with cryptococcus encephalitis. Comparison of the morphological features of GMNs between the five groups revealed parameters which may help distinguish GMNs in HIV infection from opportunistic infections. Small GMN size, low cellular density, ill-defined demarcation from the adjacent brain paraenchyma, minimal tissue rarefaction in the area of GMNs and a strong predilection for the superficial and deep white matter were typical of AIDS encephalopathy. In contrast, opportunistic infections were usually associated with clear demarcation from surrounding brain tissue, high cellular density, strong tissue rarefaction and a predilection for gray matter. Rod cells and macrophages in great numbers were also more commonly found in the AIDS and HIV groups.
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PMID:Cellular composition and distribution of gliomesenchymal nodules in the CNS of AIDS patients. 839 54

The major surface antigen from the proliferative form of Toxoplasma gondii (P-30 of SAG-1) was chosen as a target for exploration of Toxoplasma gondii reactivation in sera from immunocompromised patients. Samples were obtained from 37 HIV-infected subjects with lymphocyte levels of CD4+ < 200/mm3. The prevalence of IgG antibodies to Toxoplasma gondii was 64.9%. Ten patients had clinical symptoms of reactivated toxoplasmosis; eight of these had Toxoplasma encephalitis. The SAG-1 epitopes were found as circulating antigen in five cases with an immunocapture enzyme immunoassay (EIA). The EIA was improved with an IgG1 monoclonal antibody to SAG-1 and a streptavidinbiotin amplification. The sensitivity, specificity and positive predictive value were 30, 92 and 60%, respectively. The SAG-1 levels were compared with different biological parameters such as HIV p24 antigen, beta 2 microglobulin, CD4+ cell count and IgG antibodies to Toxoplasma gondii. The levels of SAG-1 in these patients were significantly higher than those in the 75 healthy control persons with or without a chronic Toxoplasma gondii infection. Therefore, SAG-1 may be involved as a marker of reactivated toxoplasmosis in HIV-infected patients.
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PMID:Toxoplasma gondii surface antigen-1 in sera of HIV-infected patients as an indicator of reactivated toxoplasmosis. 860 4

Cerebral toxoplasmosis is a common, opportunistic, and often life-threatening disease in HIV-infected patients. Diagnosis is supported mainly by clinical evidence and computerized tomography or magnetic resonance imaging scans, but brain images may share features with other brain diseases occurring in HIV-infected patients. To determine the diagnostic value of PCR for the detection of Toxoplasma gondii in blood from HIV-infected patients, we examined 89 blood samples from 59 HIV-infected patients. PCR and Southern blot hybridization were done with DNA extracted from blood samples from 20 patients with confirmed cerebral toxoplasmosis and from 10 patients with suspected but not confirmed cerebral toxoplasmosis. The samples were taken before and 7 to 10 days after the beginning of antiparasitic therapy. For 9 patients who suffered from cerebral toxoplasmosis more than 6 months prior to the study and for 20 patients without any evidence for toxoplasmosis only one blood sample per patient was examined. PCR gave positive results with 5 of the 20 blood samples from patients who suffered from cerebral toxoplasmosis. After 7 to 10 days of therapy PCR results became negative in all these five cases. No amplification was seen with DNA from blood samples from the other 54 patients as the target. The results presented here show that PCR testing of blood samples from HIV-infected patients is of limited value for the diagnosis of cerebral toxoplasmosis. The sensitivity was only 25%, but the specificity was very high (100%), so this technique may be useful for discriminating between cerebral toxoplasmosis and other brain diseases which may be mistaken for toxoplasmosis.
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PMID:Limited value of PCR for detection of Toxoplasma gondii in blood from human immunodeficiency virus-infected patients. 931 22

Reactivation of latent Toxoplasma gondii infection in patients with HIV infection is responsible for life-threatening disease. We present the aetiology, epidemiological data, diagnostic method, signs, symptoms, and therapy of Toxoplasma gondii encephalitis.
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PMID:[Inflammation of the brain caused by Toxoplasma gondii in patients infected with human immunodeficiency virus (HIV)]. 938 Feb 58

Progression from seroconversion to the development of AIDS in Africa may be shorter than in industrialized countries, but there are insufficient data to be certain. Although the data are not always directly comparable, survival after an AIDS diagnosis appears to be substantially shorter in African countries and this may be partly because of later diagnosis of AIDS in Africa, but may also be because of environmental factors such as increased exposure to pathogens of high virulence and lack of access to care. Tuberculosis and bacterial infections are the most important causes of morbidity and mortality among hospitalized patients. Bacteraemia is frequent, particularly due to non-typhoid salmonellae and S. pneumoniae. Cryptosporidia and I. belli are the most frequently isolated pathogens in patients with diarrhoea; non-typhoid salmonellae and Shigella species are also commonly isolated when stool cultures are performed. Cerebral toxoplasmosis, and meningitis due to Cryptococcus, tuberculosis and bacterial pathogens are the most frequent neurological infections and cognitive changes are frequently identified when specifically looked for. Infections with atypical mycobacteria and Pneumocystis carinii are rare, as is CMV retinitis. In women, HIV infection is associated with cervical human papillomavirus and with SIL, although there is currently no evidence for an association with invasive cervical cancer. Individuals infected with HIV-2 progress to AIDS and to death more slowly than those infected with HIV-1, but seem to experience the same spectrum of opportunistic disease when they reach the stage of advanced disease. The limited data available suggest that HIV-infected individuals in Africa develop opportunistic disease at broadly the same level of immunosuppression as do individuals in industrialized countries, but death occurs at a higher range of CD4 counts, although still in the range consistent with advanced disease. Data are still lacking concerning the aetiology of common clinical presentations of HIV disease and the relative frequencies of specific opportunistic diseases in different regions, particularly from southern Africa. Tuberculosis is the single most important HIV-related opportunistic infection in African countries, but diagnosis, particularly of extrapulmonary disease, remains difficult. The lack of laboratory facilities makes the diagnosis of bacterial infections difficult in many parts of the continent and, since this situation is unlikely to change in the near future, clinical algorithms for syndromic management need to be evaluated. More information is needed about gynaecological disease in HIV-infected women. The most important research questions concern the development and evaluation of cost-effective regimes for prophylaxis and treatment of opportunistic disease in order to prolong healthy life in HIV-infected individuals.
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PMID:Natural history and spectrum of disease in adults with HIV/AIDS in Africa. 941 66

There is much hope that HIV-infected patients and AIDS patients can reckon with a prolonged survival in future. The increased survival of AIDS patients with positive Toxoplasma serology is not necessarily associated with an increased risk of developing Toxoplasma encephalitis. For HIV-infected patients with negative Toxoplasma serology, the probability of acquiring a primary Toxoplasma infection in highly endemic areas such as Germany had not been studied to date. One hundred eighty-three HIV-infected patients were followed up between 1987 and 1995 in a retrospective study. Within the cohort, 95% of the patients were male and 83% haemophiliacs. The initial (1987) and final (1995) prevalence rate of Toxoplasma antibodies was 33.3% and 36.6%, respectively. The annual rise of the primary infection rate was calculated as 0.41%. The dye test was used for the detection of Toxoplasma-specific antibodies. This assay proved to be reliable and stable during long-term observation. The rate of primary toxoplasmosis found in this long-term study was not higher than that of pregnant women in Germany. Chemoprophylactic measurements for seronegative HIV-infected patients are therefore not recommended, but regular serological screening to detect seroconverters is.
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PMID:The probability of acquiring primary Toxoplasma infection in HIV-infected patients: results of an 8-year retrospective study. 950 75

Laboratory techniques for the diagnosis of central nervous system (CNS) infections are rapidly improving but at present have limitations that necessitate our guarded enthusiasm. Enteroviruses are the most common infectious agents of viral meningitis for which an etiology can be determined, and it is anticipated that the use of the reverse transcriptase polymerase chain reaction (RT-PCR) technique should significantly improve the identification of the etiologic agent of aseptic meningitis. The combination of the polymerase chain reaction technique with laboratory methods for the determination of intrathecal antibody production to herpes simplex virus and varicella-zoster virus have improved the rapidity with which these viral infections can be diagnosed. The pearls and pitfalls of the use of these laboratory techniques in the diagnosis of viral meningitis, recurrent meningitis, and focal encephalitis are included. Recommendations for the empiric therapy of bacterial meningitis in children and adults have changed because of the emergence of penicillin and cephalosporin-resistant pneumococcal organisms. The currently recommended antibiotics and their dosages are included. The evidence for the efficacy of dexamethasone therapy in bacterial meningitis is provided. Meningitis due to Mycobacterium tuberculosis is increasingly recognized, and the initiation of empiric antituberculous chemotherapy should not await the results of CSF cultures. Toxoplasma encephalitis and primary CNS lymphoma are the most common cause of mass lesions in patients with HIV, and the diagnostic techniques to distinguish between these two infections is reviewed. A short discussion of the best test for the diagnosis of neurosyphilis is provided.
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PMID:Pearls and pitfalls in the diagnosis and management of central nervous system infectious diseases. 960 16

We present a case of the coincidence of progressive multifocal leukoencephalopathy (PML) and central nervous system (CNS) toxoplasmosis in an adult patient, without a detectable cause of cell-mediated immunity impairment. The proper diagnosis was made postmortem on the basis of histological changes typical of both pathological processes. PML was characterized by the presence of subcortical focal demyelination, containing enlarged, densely basophilic oligodendrocyte nuclei, often with intranuclear inclusion, and bizarre astrocytes, mimicking neoplastic cells. PML was confirmed by detecting numerous papova virus particles in oligo- and astroglial nuclei by thin-section electron microscopy. Cerebral toxoplasmosis was characterized by the presence of multiple well-circumscribed necrotizing abscesses. Numerous Toxoplasma gondii (T. gondii) cysts and free, non-encysted protozoan parasites were found among the inflammatory infiltrates. The diagnosis of cerebral toxoplasmosis was further confirmed by immunocytochemistry. In order to detect putative immunosuppressive background underlying both pathological processes, HIV infection was taken into consideration, however, no histopathological changes indicative of AIDS either in the CNS or in the peripheral organs were eventually found. Moreover no HIV provirus genome was identified in the formalin-fixed, paraffin embedded brain tissue by the polymerase chain reaction (PCR). Current view on the selected aspects of the pathogenesis of both disorders were discussed.
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PMID:Progressive multifocal leukoencephalopathy (PML) and cerebral toxoplasmosis in an adult patient, with no symptoms of underlying immunosuppressing illness. 1007 6

Toxoplasmosis has gained particular attention in the AIDS era as the most common opportunistic encephalitis in HIV-infected patients. Since there are important parallels between the human and rodent infection, experimental murine toxoplasmosis is widely used to study the immune reactions to this protozoal parasite. Oral application of low-virulent Toxoplasma (T.) gondii cysts leads to a biphasic disease characterized by an acute, generalized phase followed by a chronic stage confined to the brain, where an encephalitis with persistence of the parasite develops. Immunity to T. gondii is T cell mediated, and there is increasing evidence for a critical role of cytokines for an effective immune response. In order to address the functional role of interferon (IFN)-gamma in toxoplasmosis, we took advantage of mice lacking the IFN-gamma-receptor. Inactivation of the IFN-gamma-receptor rendered mice highly susceptible to T. gondii, and they died of a fulminant acute toxoplasmosis. Among the various organs affected, hepatitis was severe enough to cause death. In contrast to wild type animals, IFN-gamma-receptor-deficient mice were unable to activate their macrophages as evidenced by a lack of major histocompatibility complex (MHC) class II antigen induction and the absence of an upregulation of tumor necrosis factor (TNF)-alpha and inducible nitric oxide synthase (iNOS) mRNA transcripts, two macrophage effector molecules. These observations prompted the investigation of TNF- and TNF-receptor-mediated effects in toxoplasmosis by use of mice deficient in either the TNF-receptor type 1 (TNFR1) and/or the TNF-receptor type 2 (TNFR2). The lethal outcome of T. gondii-infected TNFR1/2- and TNFR1-deficient mice, but not of TNFR2-deficient and wild type animals, illustrated the important role of TNF-alpha and TNFR1-mediated signalling, respectively, in this infection. Histopathology attributed death of TNFR1- and TNFR1/2-deficient mice to a severe, necrotizing encephalitis. Unrestricted intracerebral parasite replication in these strains was associated with reduced numbers of iNOS+ leukocytes and a lack of iNOS mRNA induction in their brains as compared to resistant wild type and TNFR2-deficient mice. To precisely identify the cellular sources of cytokines in the brain, flow cytometry of leukocytes isolated from the brain, in situ hybridization, immunohistochemistry and RT-PCR analysis of cytokine mRNA transcripts of magnetically purified leukocyte populations were performed. These studies disclosed that both CD4+, CD8+ T lymphocytes and macrophages recruited to the brain as well as resident cell populations of the CNS including neurons, astrocytes and microglia contributed to the intracerebral cytokine synthesis. Each population was characterized by a specific cytokine pattern. Interestingly, activation of brain cells is a hallmark of Toxoplasma encephalitis. The marked induction of a variety of immunologically important cell surface molecules as MHC class I and II antigens, cell adhesion molecules and their ligands on microglia points to a particular important role of this cell type for the immune response to T. gondii, since the expression of these molecules is a prerequisite for cellular interactions with T cells. The observation of a prominent interleukin (IL)-10 production in the T. gondii-infected brain initiated studies addressing the function of this powerful immunosuppressive mediator in chronic Toxoplasma encephalitis. Neutralization experiments revealed that IL-10 facilitates persistence of the parasite in the brain by downregulating the intracerebral immune response. On the other hand, IL-10 may exert a regulatory role and may be necessary to prevent immunopathological effects of an uncontrolled immune response. In conclusion, these studies demonstrate the important role of the cytokines IFN-gamma and TNF-alpha and their receptors, respectively, for an effective control of T. gondii. In the CNS, the target organ of the parasite, a
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PMID:[Rudolf-Virchow Prize 1998. Award lecture. Toxoplasmosis: a model infection for studying systemic and intracerebral immune reactions]. 1009 13


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