Cases reported "Encephalitis"

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1/17. Treatment of toxoplasma brain abscess with clindamycin and sulfadiazine in an AIDS patient with concurrent atypical pneumocystis carinii pneumonia.

    toxoplasmosis is the most common opportunistic infection of the central nervous system in patients with AIDS. The standard treatment for toxoplasmic encephalitis is pyrimethamine and sulfadiazine. There have been few reports of concurrent toxoplasma brain abscess and cavitary pneumocystis carinii pneumonia (PCP) in taiwan. We report the case of a 26-year-old homosexual man with coexisting infection with toxoplasma gondii and P. carinii who was successfully treated for brain abscess with clindamycin and sulfadiazine. The cavitary lung lesions, initially diagnosed as pulmonary tuberculosis, were proved to be PCP by lung biopsy. HIV infection and syphilis had been diagnosed 1 year before admission. He presented with general weakness, ataxia, nausea, blurred vision and fever for 2 weeks. magnetic resonance imaging of the brain revealed multiple ring-enhanced lesions over the cerebrum and cerebellum. Chest roentgenography showed a 3-cm lesion with cavitation over the right upper lung field. Diagnostic computerized tomography-guided lung biopsy revealed P. carinii cysts. clindamycin, sulfadiazine and trimethoprim (TMP)-sulfamethoxazole (20 mg/kg/day TMP) were given with good response. His CD4 count rose from 40 to 280/microL 4 months later. All antibiotics were discontinued after 4.5 months due to the development of a skin rash. He was well at follow-up 1 year later. This case suggests that the combination of clindamycin and sulfadiazine is an effective treatment for toxoplasma brain abscess and highlights the importance of diagnostic lung biopsy for cavitary lung lesions, particularly in a region endemic for tuberculosis.
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2/17. sulfadiazine-induced crystalluria in AIDS patients with toxoplasma encephalitis.

    toxoplasma encephalitis is the most common opportunistic infection of the central nervous system in patients with AIDS. The treatment of choice is a combination of sulfadiazine and pyrimethamine. We present here four patients with AIDS treated for toxoplasmic encephalitis who developed sulfadiazine-induced crystalluria. This complication was rapidly reversible with rehydration and urine alkalinization. patients with AIDS treated with high doses of sulfadiazine should be adequately hydrated, and their urinary pH maintained above 7.5 to prevent sulfadiazine-induced crystalluria.
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3/17. Pathogenesis of HIV encephalitis.

    A wide spectrum of infectious agents attack the central nervous system (CNS) of acquired immunodeficiency syndrome (AIDS) patients. Human immunodeficiency virus (HIV) itself, infects the CNS of a subgroup of these patients. The mechanism behind why HIV enters the CNS is unclear. We have observed an interesting association between HIV and opportunistic viral infections that may explain why HIV enters the brain. Infection of the CNS by opportunistic agents results in recruitment of latently HIV-infected monocytes. Upon differentiation into macrophages these cells produce abundant HIV. Latent HIV-infection of monocytes/macrophages provides a unique opportunity for cooperativity between opportunistic infections and HIV in mediating CNS damage.
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4/17. sulfadiazine crystalluria revisited. The treatment of toxoplasma encephalitis in patients with acquired immunodeficiency syndrome.

    toxoplasma gondii encephalitis is an important opportunistic infection in the acquired immunodeficiency syndrome, estimated to occur in 20,000 to 40,000 patients with acquired immunodeficiency syndrome in the united states by 1991. The combination of sulfadiazine and pyrimethamine is regarded as the treatment of choice. Acute renal failure due to crystal deposition in the urinary tract was well described 30 to 40 years ago and is likely to resurface as a clinical entity if appropriate prophylactic measures are not taken. We describe two cases of sulfadiazine-induced crystalluria and renal failure in patients with acquired immunodeficiency syndrome, review the pertinent literature, and discuss the pathogenesis. Recommendations are made for the prophylaxis and treatment of sulfadiazine-related renal toxic reaction. physicians using this "new" drug must be aware of the potential danger of sulfonamide-induced injury to the urinary tract.
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5/17. Human immunodeficiency virus (HIV) leukoencephalopathy and the microcirculation.

    We studied the brains of three patients with acquired immune deficiency syndrome (AIDS), all of whom developed subacutely progressive dementia unassociated with opportunistic infection or neoplasm in the central nervous system. Computed tomographic (CT) scans of the head revealed cortical atrophy, ventricular dilation, and diffuse hypodensity of the centrum semiovale. On microscopic examination, the cerebral and cerebellar white matter in all cases showed diffuse and focal, angiocentric regions of myelin pallor, focal vacuolization, and extensive gliosis. Variable axonal loss and axonal spheroids were evident. The microvasculature showed striking changes, including mural thickening, increased cellularity, and enlargement and pleomorphism of endothelial cells with variable numbers of macrophages and multinucleated giant cells (MNGC), which often contained hemosiderin pigment. Human immunodeficiency virus type 1 (hiv-1) antigens were identified immunocytochemically within perivascular macrophages and MNGC and in some microglial cells. We suggest that the morphologic abnormalities of the microcirculation may be associated with an alteration of the blood-brain barrier. The increased vascular permeability could contribute to damage and loss of the white matter including both myelin and axons, and result in subcortical cerebral atrophy. The hiv-1 infected cells present in relation to the microvasculature may play a role in mediating the vascular injury.
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6/17. A case of acute encephalopathy caused by the human immunodeficiency virus apparently responsive to zidovudine.

    A case of acute encephalopathy, which apparently was caused by the human immunodeficiency virus and occurred late in the course of this infection yet before any opportunistic infections occurred, is presented. The encephalopathy was considered to be responsive to zidovudine and dexamethasone; this therapy resulted in an excellent, sustained clinical remission. Magnetic resonance images and the histopathological findings also are described.
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7/17. The neurological features of early and 'latent' human immunodeficiency virus infection.

    Neurological manifestations of unknown cause occurring in patients who become or are HIV antibody positive with presumed normal immune function have been described recently. This report adds a further six cases, all of whom had normal CD4 cell counts either throughout the period of observation or after the episode of seroconversion. Three had an acute presentation, two in the context of documented seroconversion consisting of one of the following: an encephalitis, an ataxia, and confusion with neuralgic amyotrophy. Three had a subacute disorder occurring at a later phase of HIV infection but before opportunistic infections or neoplasms, and marked by a static mild cognitive deficit. This report extends the range of abnormalities that may be seen at seroconversion and documents the presence of a non-progressive cognitive deficit occurring in the latent phase of HIV infection.
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8/17. Massive neuronal destruction in human immunodeficiency virus (HIV) encephalitis. A clinico-pathological study of a pediatric case.

    Human immunodeficiency virus (HIV) encephalitis in children with AIDS includes a diffuse white matter disease associated with an inflammatory cell infiltrate that features multinucleated giant cells. cerebral cortex is relatively preserved and only focal loss of purkinje cells in the cerebellum has been observed. We describe a case of encephalitis in a child with AIDS in which there was massive and diffuse destruction of the cerebral cortex with severe neuronal loss, marked inflammatory perivascular infiltrate with abundant multinucleated cells and large pleomorphic reactive astrocytes. Similar findings were present in the basal ganglia. Moreover, the cerebellum disclosed a complete loss of Purkinje and granule cells. These findings could not be related to an ischemic mechanism or to an associated opportunistic infection. Electron microscopy showed numerous HIV particles. This case illustrates a different pattern of CNS involvement by HIV and emphasizes the destructive capacity of this neurotropic virus for neural tissue.
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keywords = opportunistic infection
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9/17. Pathologic features of AIDS encephalopathy in children: evidence for LAV/HTLV-III infection of brain.

    The neuropathologic findings in 11 children with a new CNS disorder that occurs in children with the acquired immunodeficiency syndrome (AIDS) and is postulated to be due to LAV/HTLV-III, the virus that causes AIDS, are reported. The children, who ranged in age from 4 months to 11 years, died of AIDS complicated by progressive encephalopathy. Ten of the children either had positive serum antibody for LAV/HTLV-III or had received blood products from donors later found to be antibody-positive. Examination of the brains of these children at autopsy revealed a unique constellation of findings, including varying degrees of diminished brain weight in all cases, inflammatory cell infiltrates in nine brains, multinucleated cells in eight, three of which also contained multinucleated giant cells, vascular calcification in ten, vascular and perivascular inflammation in five, and white matter changes in nine. Inflammatory and vascular lesions were most prominent in basal ganglia and pons. LAV/HTLV-III retroviral particles, associated with multinucleated giant cells, were observed in two brains on electron microscopic examination. These two and one additional brain had evidence of the LAV/HTLV-III genome by hybridization studies. Only one brain had a recognizable opportunistic infection.
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keywords = opportunistic infection
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10/17. Opportunistic intracranial infection in AIDS detection by technetium-99m DTPA brain scintigraphy.

    Radionuclide brain scintigraphy and computed tomography (CT) demonstrated cerebral lesions in two patients with acquired immunodeficiency disease syndrome (AIDS) complicated by opportunistic infection of the brain. In the detection of these cerebral lesions, [99mTc]DTPA radionuclide scintigraphy was as reliable as CT. Since malignant lymphoma involving the brain has been seen with increasing frequency in patients with AIDS, the positive brain scan alone is nonspecific and should be correlated appropriately with the clinical setting.
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