Cases reported "Meningitis, Cryptococcal"

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1/29. Midbrain infarction: a rare presentation of cryptococcal meningitis.

    A 20-year-old farmer who had headache and fever for 1 month, suddenly developed left hemiplegia, tremor in left arm and titubation followed by deep coma. Cranial CT scan revealed an infarction in right crus of midbrain. His CSF revealed 66 mg/dl protein, 10 lymphocytes/mm3, and 70 mg/dl glucose. CSF was positive for cryptococcal antigen. He improved following i.v. amphotericin 0.5 mg/kg and fluconazole 200 mg daily, continued for 6 and 12 weeks respectively. Infarctions though rare in cryptococcal meningitis should be considered in patients with chronic meningitis with vasculitis.
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2/29. Massive pleural effusions in cryptococcal meningitis.

    Cryptococcal infection uncommonly presents with pulmonary manifestations and even more rarely so as massive bilateral effusions. Pleural involvement is usually associated with underlying pulmonary parenchymal lesions and is unusual while on antifungal therapy. We report a patient with cryptococcal meningitis who, while on intravenous 5-flucytosine and amphotericin b, developed life-threatening bilateral massive pleural effusions with evidence of spontaneous resolution, consistent with prior hypothesis of antigenic stimulation as the cause of pleural involvement.
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3/29. Successful medical treatment of multiple cryptococcomas: report of a case and literature review.

    We report a 35-year-old man diagnosed as having CNS cryptococcosis with multiple cryptococcomas, presenting with headache, papilloedema and impaired mental function in a previously healthy man. cerebrospinal fluid (CSF) examination revealed lymphocytic pleocytosis with low glucose level. Gram's stain, acid fast bacilli stain and Indian ink examination were all negative. CSF cryptococcal antigen was positive, however, several fungal cultures were negative. Early cranial CT scan showed focal cerebritis over the right temporal lobe while subsequent imaging studies showed multiple contrast-enhancing masses with severe surrounding brain oedema over bilateral frontoparietal areas. brain biopsy showed cryptococcal granulomatous lesions. Treatment was successful with antifungal agents and steroids without surgical removal.
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4/29. The changing face of AIDS-related opportunism: cryptococcosis in the highly active antiretroviral therapy (HAART) era. case reports and literature review.

    Only nine cases of AIDS-related cryptococcosis have been reported until now in patients receiving highly active antiretroviral therapy (HAART), all of them with abnormal clinical features. Two hiv-infected patients who experienced an atypical relapse of cryptococcosis shortly after the start of HAART and despite maintenance antifungal treatment, are described. Six different relapses of cryptococcal meningitis were observed in a 28-month period in a patient who obtained a poor immune recovery after HAART (as shown by a CD4 lymphocyte count ranging from 78 to 149 cells/microL, opposed to a baseline level of 98 cells/microL). On the other hand, a patient with favorable immunological response to HAART (as expressed by a CD4 count growing from 7 to 186 cells/microL), experienced isolated multiple indolent cryptococcal abscesses involving head, neck, the anterior thoracic wall, and regional lymph nodes, with repeatedly negative cultures, and diagnosis obtained by both histopathologic study and positive serum antigen assay. Both our case reports are representative of novel correlations between opportunistic pathogens and immune reactivity, descending from the introduction of HAART. The first episode describes an exceedingly elevated number of disease relapses despite HAART and antifungal maintenance treatment, which may descend from an incomplete immune response to antiretroviral therapy, possibly responsible for failure in obtaining eradication of yeasts, but also for lack of disease dissemination (usually leading to a lethal multivisceral involvement in the pre-HAART era). The abnormal disease course and localization of second reported patient well depicts an "immune reconstitution syndrome" probably representing a flare-up of a latent fungal infection, caused by a rapidly effective HAART. In patients treated with HAART, AIDS-related cryptococcosis cannot therefore be ruled out by the absence of neurological involvement, and by persistingly negative cultures.
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5/29. Cryptococcal meningoencephalitis presenting with an unusual magnetic resonance imaging appearance--case report.

    A 61-year-old female with a past history of gastric cancer presented with altered mental status, a few seizures, and low-grade fever. Lumbar puncture revealed elevated cerebrospinal fluid (CSF) pressure, lymphocytic pleocytosis, elevated protein level, remarkably decreased glucose level, and presence of cryptococcal antigen. cryptococcus neoformans was identified by india ink staining and culture of CSF. The patient was given antifungal agents intravenously and intrathecally. CSF findings improved and C. neoformans could not be detected in CSF one month after the onset. Cerebral sulcal hyperintensity was identified in the bilateral frontal and parietal lobes on fluid-attenuated inversion recovery (FLAIR) magnetic resonance (MR) imaging one month after the onset, but no leptomeningeal enhancement was detected in the affected sulci on T1-weighted MR imaging. The sulcal hyperintensity on FLAIR imaging developed in the bilateral temporal and occipital lobes 2 months after the onset. CSF findings obtained by lumbar puncture were within the normal range except for pressure. However, neurological deterioration and reconfirmation of C. neoformans in CSF indicated recurrent cryptococcal inflammation. The sulcal hyperintensity on FLAIR imaging may indicate a high CSF protein concentration in the subarachnoid space. Such cerebral sulcal hyperintensity is an unusual MR imaging finding of cryptococcal meningoencephalitis, and may be an early sign of procrastinating process or recurrent inflammation even if the findings of CSF obtained by lumbar puncture are normal.
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6/29. Pathogenesis of cerebral cryptococcus neoformans infection after fungemia.

    The pathogenesis of cerebral infection after cryptococcus neoformans fungemia in outbred mice was investigated. Confocal microscopy and cultures on ficoll-hypaque gradient-separated blood cells were used to detect yeasts in the cytoplasms of monocytes. In semithin brain sections, poorly capsulated yeasts were seen in macrophages in the leptomeningeal space, in monocytes circulating in leptomeningeal capillaries, or in the endothelial cells themselves, strengthening the hypothesis that monocytes and endothelial cells play key roles in the pathogenesis of cryptococcal meningitis. Similar fungal loads and cellular reactions were seen in mice and in 1 patient with acquired immune deficiency syndrome (AIDS), all with acute cryptococcal meningoencephalitis, and in mice and in 1 patient with AIDS, all with cured cryptococcal infection. Immunostaining revealed both the presence of cryptococcal polysaccharide in various brain cells and antigenic variability both from yeast cell to yeast cell and over time. Thus, our data established the relevance and interest that this experimental model has for investigation of the pathogenesis of human cryptococcal meningitis.
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7/29. Cryptococcal meningitis in a neonate.

    A case of cryptococcal meningitis in a neonate born to an hiv-negative women is described. The cryptococcal infection was proved using standard microbiological and antigen detection techniques. Although cryptococcal meningitis has previously been described in both immunocompromised and immunocompetent children, the present case represents youngest case of cryptococcosis reported to date.
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8/29. Cryptococcal meningitis in pediatric systemic lupus erythematosus.

    Cryptococcal meningitis is an uncommon but often fatal complication of systemic lupus erythematosus (SLE). We report on a 13-year-old girl with SLE using high-dose prednisolone for several months, presented to us with low grade fever, intermittent vomiting and headache. physical examination, including papilloedema and meningeal irritation, was unremarkable. serum and cerebrospinal fluid (CSF) cryptococcal antigen titer was 1: 128 by latex agglutination method. CSF culture yielded cryptococcus neoformans. We used amphotericin b deoxycholate (a cumulative dose of 1.95 gm) and fluconazole (200 mg day-1) for 6 weeks. Clinical response was good. Then, we continued fluconazole 200 mg per qd as suppressive therapy for thirty-four months. There were no neurological sequelae or relapse after 20-month follow-up. Timely diagnosis and effective antifungal therapy could improve the prognosis of cryptococcal meningitis in SLE patients.
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9/29. Cryptococcal meningitis in two apparently immunocompetent Maltese patients.

    Two cases of cryptococcal meningitis occurring in immunocompetent men are described. The first case involves a farmer in whom cryptococcal meningitis was rapidly diagnosed using direct microscopy, latex antigen tests and culture of cerebrospinal fluid (CSF). In the second case, initial mycological tests on CSF (direct microscopy and culture) were repetitively negative and latex antigen tests gave unconvincing results. The patient was started on triple antituberculosis therapy, on which he improved immediately; therapy was continued for 1 year with the patient remaining well. However, within 1 week of stopping therapy, he had to be readmitted with neurological signs and symptoms. culture of CSF this time yielded cryptococcus neoformans and the antigen test was consistently positive. These are the first reported cases of cryptococcal meningitis in immunocompetent patients in malta.
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10/29. cerebral infarction related to cryptococcal meningitis in an hiv-infected patient: case report and literature review.

    Neurological dysfunction as the first manifestation of AIDS has been found in 10 to 20% of symptomatic human immunodeficiency virus infections. However, stroke has rarely been reported in AIDS patients. The most common causes of cerebral infarction in AIDS are central nervous system infections: toxoplasmosis, cryptococcal meningitis and tuberculosis. Potential vascular mechanisms for cerebral infarction and transient neurological deficits among AIDS patients include deposition of antigen-antibody complexes with vasculitis and infarction, and a direct toxic effect of a viral antigen or infectious agent on vascular endothelium. The role of cryptococcal meningitis in vasculopathy is still not clear. We report a case of cerebral infarction in an hiv-infected patient, with cryptococcal meningitis as the first manifestation of AIDS.
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