Cases reported "Amebiasis"

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1/58. Primary amebic meningoencephalitis due to naegleria fowleri: an autopsy case in japan.

    Free-living amebas represented by naegleria fowleri, Acanthamoeba and Balamutia have been known to cause fatal meningoencephalitis since Fowler and Carter (1965) reported the first four human cases. An autopsy case of a 25-year-old female with primary amebic meningoencephalitis (PAM) due to naegleria fowleri is described. headache, lethargy and coma developed in this patient, and her condition progressed to death 8 days after the onset of clinical symptoms. Cerebral spinal fluid examination confirmed clusters of amebas, which were grown in culture and identified as naegleria fowleri. At autopsy, lesions were seen in the central nervous system (CNS) and the ethmoid sinus. The CNS had severe, suppurative meningoencephalitis with amebic trophozoites mingled with macrophages. This case is the first report of PAM due to naegleria fowleri in japan.
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2/58. A case of balamuthia mandrillaris meningoencephalitis.

    balamuthia mandrillaris is a newly described pathogen that causes granulomatous amebic encephalitis, an extremely rare clinical entity that usually occurs in immunosuppressed individuals. We report a case of pathologically proven Balamuthia encephalitis with unusual laboratory and radiologic findings. A 52-year-old woman with idiopathic seizures and a 2-year history of chronic neutropenia of unknown cause had a subacute illness with progressive lethargy, headaches, and coma and died 3 months after the onset of symptoms. Cerebrospinal fluid (CSF) glucose concentrations were extremely low or unmeasurable, a feature not previously described (to our knowledge). Cranial magnetic resonance imaging scans showed a single large temporal lobe nodule, followed 6 weeks later by the appearance of 18 ring-enhancing lesions in the cerebral hemispheres that disappeared after treatment with antibiotics and high-dose corticosteroids. The initial brain biopsy specimen and analysis of CSF samples did not demonstate amebae, but a second biopsy specimen and the postmortem pathologic examination showed Balamuthia trophozoites surrounded by widespread granulomatous inflammation and vasculitis. The patient's neutropenia and antibiotic use may have caused susceptibility to this organism. Amebic meningoencephalitis should be considered in cases of subacute meningoencephalitis with greatly depressed CSF glucose concentrations and multiple nodular lesions on cerebral imaging. Arch Neurol. 2000;57:1210-1212
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3/58. Encephalitis due to a free-living amoeba (balamuthia mandrillaris): case report with literature review.

    BACKGROUND: Amebic infections can spread to the central nervous system with a lengthy but usually fatal course. A typical case is presented to raise awareness of this increasingly reported infectious process that may have a more favorable outcome if diagnosed in its early stages. CASE DESCRIPTION: A 38-year-old male presented with an ulcerating 10 x 8 cm mass on his thigh and smaller skin nodules. In less than 6 months seizures developed due to granulomatous lesions of the brain. Biopsies/excisions of the thigh lesion, a subcutaneous nodule, and a brain lesion were performed. He failed to respond to broad spectrum antibiotics and antineoplastic agents, and died within 6 weeks of the initial MRI scan of the brain.Rare amebic trophozoites were appreciated in the biopsy specimens on post-mortem review, and balamuthia mandrillaris confirmed as the infecting agent on immunofluorescence studies. CONCLUSIONS: Granulomatous amebic encephalitis is a parasitic infection with a lengthy clinical course before rapid deterioration due to extensive brain lesions is noted. Either early treatment with antimicrobials or-in rare cases-excision of the brain lesion(s) may offer the chance of a cure.
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keywords = central nervous system, brain, nervous system
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4/58. Granulomatous amebic encephalitis in a patient with AIDS: isolation of acanthamoeba sp. Group II from brain tissue and successful treatment with sulfadiazine and fluconazole.

    A patient with AIDS, treated with highly active antiretroviral therapy and trimethoprim-sulfamethoxazole, presented with confusion, a hemifield defect, and a mass lesion in the right occipital lobe. A brain biopsy confirmed granulomatous amebic encephalitis (GAE) due to acanthamoeba castellanii. The patient was treated with fluconazole and sulfadiazine, and the lesion was surgically excised. This is the first case of AIDS-associated GAE responding favorably to therapy. The existence of a solitary brain lesion, absence of other sites of infection, and intense cellular response in spite of a very low CD4 count conditioned the favorable outcome. We review and discuss the diagnostic microbiologic options for the laboratory diagnosis of infections due to free-living amebae.
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5/58. An autopsy case of amebic meningoencephalitis. The first Japanese case caused by balamuthia mandrillaris.

    We report here the first case of amebic meningoencephalitis caused by Balamuthia mandrillaris in a 78-year-old Japanese woman with sjogren's syndrome. Fourteen days before her death, she presented with high fever and lost consciousness and later developed neck stiffness and abducens palsy. Computed tomography scans of the brain demonstrated multiple low-density areas throughout the brain. Neuropathologically, hemorrhagic and necrotic lesions with many amebic trophozoites were scattered in the brain and spinal cord. Granulomatous lesions were only rarely found. The amebas were identified as balamuthia mandrillaris based on immunofluorescence assay. Clinicopathologically, our case was thought to be an intermediate between primary amebic meningoencephalitis due to Negleria fowleri and granulomatous amebic encephalitis due to Acanthameba species. Essentially, the case was one of an elderly person with suspected immunodeficiency with fulminant necrotic meningoencephalitis and scanty granulomatous lesions of 14 days course.
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6/58. December 2002: 19-year old male with febrile illness after jet ski accident.

    The December 2002 COM. A 19-year-old healthy male fell into stagnant water of the intercostal waterway (salt water of South florida), following a jet ski accident. He sustained minor superficial injuries but engulfed significant quantities of water and sediment. A few days later he developed bifrontal headaches, vomiting, a stiff neck and a temperature of 102 degrees F. A CT scan on admission without contrast was negative. The CSF had markedly elevated white count but bacterial and fungal cultures were negative. He became progressively lethargic. On the fifth day he developed seizure activity. He expired the next day despite antibiotics. Gross examination of the brain at autopsy revealed edema, cerebellar tonsillar herniation and purulent meningitis. Microscopic examination revealed a massive leptomeningeal inflammatory infiltrate composed of neutrophils, lymphocytes, and numerous histiocyte-like cells. The inflammatory infiltrate extended into the cerebral parenchyma in numerous areas also involving the cerebellum, brainstem and ventricular system. Given the exposure to stagnant water (later confirmed to be a man-made fresh water lake), and the numerous histiocytic-like cells, suspicion for an amebic etiology of the disease process was raised and the CDC identified the ameba as naegleria fowleri. infection by naegleria fowleri, a free-living ameba, occurs after exposure to polluted water in man-made fresh water lakes, ponds, swimming pools, particularly during the warm weather months when the thermophilic ameba grows well. The pathologic substrate of the infection is an acute hemorrhagic, necrotizing meningo-encephalitis mainly at the base of the brain, brainstem and cerebellum occurring in young, healthy individuals.
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7/58. Environmental isolation of balamuthia mandrillaris associated with a case of amebic encephalitis.

    This report describes the first isolation of the ameba balamuthia mandrillaris from an environmental soil sample associated with a fatal case of amebic encephalitis in a northern california child. Isolation of the ameba into culture from autopsied brain tissue confirmed the presence of Balamuthia: In trying to locate a possible source of infection, soil and water samples from the child's home and play areas were examined for the presence of Balamuthia: The environmental samples (plated onto nonnutrient agar with escherichia coli as a food source) contained, in addition to the ameba, a variety of soil organisms, including other amebas, ciliates, fungi, and nematodes, as contaminants. Presumptive Balamuthia amebas were recognized only after cultures had been kept for several weeks, after they had burrowed into the agar. These were transferred through a succession of nonnutrient agar plates to eliminate fungal and other contaminants. In subsequent transfers, axenic Naegleria amebas and, later, tissue cultures (monkey kidney cells) served as the food source. Finally, the amebas were transferred to cell-free axenic medium. in vitro, the Balamuthia isolate is a slow-growing organism with a generation time of approximately 30 h and produces populations of approximately 2 x 10(5) amebas per ml. It was confirmed as Balamuthia by indirect immunofluorescence staining with rabbit anti-Balamuthia serum and human anti-Balamuthia antibody-containing serum from the amebic encephalitis patient. The environmental isolate is similar in its antimicrobial sensitivities and identical in its 16S ribosomal dna sequences to the Balamuthia isolate from the deceased patient.
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8/58. Cerebrospinal acanthamebic granulomas. Case report.

    The authors present the case of a previously healthy 26-year-old man who presented with cerebrospinal acanthamebic granulomas, and they review the literature on acanthamebic granulomas of the central nervous system (CNS). The appearance of the lesion on imaging studies suggested the presence of tuberculous granulomas, which are common in india, and antituberculosis treatment was started. Despite surgical excision of a granuloma located in the right temporoparietal region and an intramedullary granuloma at T7-8, the disease progressed and resulted in death. Unlike other cases, this patient was not immunocompromised, had no history of engaging in water activities, and had no ulcers on his body, leaving in question the mode of entry used by the ameba. Acanthamebic granulomas can cause severe infections in healthy patients as well as in sick ones. This disease should be considered in the differential diagnosis when treating infective granulomas of the CNS.
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9/58. Acanthamoeba meningoencephalitis in a patient with acquired immunodeficiency syndrome.

    Several cases of Acanthamoeba encephalitis (ie, granulomatous amebic encephalitis) have been reported in patients with acquired immunodeficiency syndrome from the united states. To our knowledge, none so far has been reported from europe, and this is the first case of amebic meningoencephalitis due to Acanthamoeba in a patient with acquired immunodeficiency syndrome from italy. The patient was a 24-year-old, human immunodeficiency virus-positive heterosexual man with a 6-year history of intravenous drug use. He was admitted to the hospital because of severe headache, confusion, nuchal rigidity, jaundice, and ascites. He died 5 days later. At autopsy, the brain showed extensive hemorrhagic necrosis with numerous trophic and cyst forms of Acanthamoeba. The amebas were identified as Acanthamoeba divionensis by the indirect immunofluorescence test.
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10/58. Neuropathological and ultrastructural features of amebic encephalitis caused by Sappinia diploidea.

    Here we present the neuropathological, ultrastructural, and radiological features of Sappinia diploidea, a newly recognized human pathogen. The patient was a 38-year-old man with visual disturbances, headache, and a seizure. brain images showed a solitary mass in the posterior left temporal lobe. The mass was composed of necrotizing hemorrhagic inflammation that contained free-living amebae. Immunofluorescence microscopy showed that the organism was not a species of ameba previously known to cause encephalitis. trophozoites had a highly distinctive double nucleus, and transmission electron microscopy confirmed that they contained 2 nuclei closely apposed along a flattened surface. The 2 nuclei were attached to each other by distinctive connecting perpendicular filaments. This and several other unique structural features led to the diagnosis of S. diploidea encephalitis. The patient was treated postoperatively with a sequential regimen of anti-amebic drugs (azithromycin, pentamidine, itraconazole, and flucytosine) and is alive after 5 years. Guidelines to recognize future cases of S. diploidea encephalitis are as follows. 1) It presented as a tumor-like cerebral mass without an abscess wall. 2) It had central necrotic and hemorrhagic inflammation that contained acute and chronic inflammatory cells without granulomas or eosinophils. 3) It contained trophozoites (40-70 microm diameter) that contained a distinctive double nucleus. 4) Cyst forms in the host were not excluded or definitely evident. 5) trophozoites engulfed host blood cells and were stained brightly with Giemsa and periodic acid-Schiff. 6) trophozoites often were present in viable brain parenchyma on the periphery of the mass without inflammatory response. 7) The prognosis after surgical excision and medical treatment was favorable in this instance.
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