Acanthameba meningoencephalitis masquerading as neurocysticercosis

Matson, David O.; Rouah, Emilie; Lee, Rita T.; Armstrong, Dawna L.; Parke, Julie T.; Baker, Carol J.

doi:10.1097/00006454-198802000-00011

Cited by 24 publications

(11 citation statements)

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“…In one case described in the literature, in which neurocysticercosis was initially diagnosed, histologic study after autopsy led to reporting of the case as Acanthamoeba encephalitis [29], and the case was subsequently identified by immunostaining to be Balamuthia encephalitis (G.S.V., unpublished observations). The patient in case 1 in this report was initially treated for tuberculosis before amoebas were identified in brain tissue, and cysticercosis was considered as a possibility in case 2.…”

Section: Discussionmentioning

confidence: 99%

Successful Treatment of Balamuthia Amoebic Encephalitis: Presentation of 2 Cases

Deetz¹,

Sawyer

Billman

et al. 2003

Clinical Infectious Diseases

177

151

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Case histories are presented of 2 individuals (a 5-year-old girl and 64-year-old man) who developed encephalitis caused by the free-living amoeba Balamuthia mandrillaris. Both individuals survived after diagnosis and initiation of effective antimicrobial therapy. Immunostaining for Balamuthia-specific antibody levels identified the causative agent of the infections. Antimicrobial therapy with flucytosine, pentamidine, fluconazole, sulfadiazine, and a macrolide antibiotic (azithromycin or clarithromycin) was initiated. Phenothiazines (thioridazine and trifluoperazine) were also used. Both patients recovered, and there was no evidence of recrudescence of the disease at 2 and 6 years after onset of symptoms. Awareness of Balamuthia as the causative agent of encephalitis and early initiation of antimicrobial therapy were critical to the recovery of both patients. Although optimal antimicrobial therapy for Balamuthia amoebic encephalitis has yet to be determined, the antimicrobials used in these 2 cases effectively controlled the disease. These 2 individuals are the only known survivors of this otherwise fatal type of amoebic encephalitis.

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Section: Discussionmentioning

confidence: 99%

Successful Treatment of Balamuthia Amoebic Encephalitis: Presentation of 2 Cases

Deetz¹,

Sawyer

Billman

et al. 2003

Clinical Infectious Diseases

177

151

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“…These procedures have shown that while enhancing lesions are present in many individuals, nonenhancing lesions are present in others. Computed tomography or magnetic resonance imaging of the brain may reveal multifocal areas of signal intensity or discrete lesions suggestive of abscesses or brain tumors (218, 291,397,408). However, although imaging analysis reveals CNS abnormalities, it does not provide a definitive diagnosis of GAE.…”

Section: Granulomatous Amebic Encephalitismentioning

confidence: 99%

“…However, although imaging analysis reveals CNS abnormalities, it does not provide a definitive diagnosis of GAE. In fact, amebic meningoencephalitis has been misdiagnosed as neurocysticercosis based on neuroimaging findings (291).…”

Section: Granulomatous Amebic Encephalitismentioning

confidence: 99%

Acanthamoebaspp. as Agents of Disease in Humans

2003

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Acanthamoeba spp. are free-living amebae that inhabit a variety of air, soil, and water environments. However, these amebae can also act as opportunistic as well as nonopportunistic pathogens. They are the causative agents of granulomatous amebic encephalitis and amebic keratitis and have been associated with cutaneous lesions and sinusitis. Immuno compromised individuals, including AIDS patients, are particularly susceptible to infections with Acanthamoeba. The immune defense mechanisms that operate against Acanthamoeba have not been well characterized, but it has been proposed that both innate and acquired immunity play a role. The ameba's life cycle includes an active feeding trophozoite stage and a dormant cyst stage. Trophozoites feed on bacteria, yeast, and algae. However, both trophozoites and cysts can retain viable bacteria and may serve as reservoirs for bacteria with human pathogenic potential. Diagnosis of infection includes direct microscopy of wet mounts of cerebrospinal fluid or stained smears of cerebrospinal fluid sediment, light or electron microscopy of tissues, in vitro cultivation of Acanthamoeba, and histological assessment of frozen or paraffin-embedded sections of brain or cutaneous lesion biopsy material. Immunocytochemistry, chemifluorescent dye staining, PCR, and analysis of DNA sequence variation also have been employed for laboratory diagnosis. Treatment of Acanthamoeba infections has met with mixed results. However, chlorhexidine gluconate, alone or in combination with propamidene isethionate, is effective in some patients. Furthermore, effective treatment is complicated since patients may present with underlying disease and Acanthamoeba infection may not be recognized. Since an increase in the number of cases of Acanthamoeba infections has occurred worldwide, these protozoa have become increasingly important as agents of human disease

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“…To identify structural brain lesions, computed tomography and magnetic resonance imaging are widely used (Sell, et al, 1997, Kidney & Kim, 1998. These evaluations can reveal changes such as multifocal areas of signal intensities or ring-like lesions or low-density areas indicating occupying mass of tumor or abscess (Martinez, et al, 1977, Martinez, et al, 1980, OforiKwakye, et al, 1986, Matson, et al, 1988, khan, 2005b, Khan, 2008, da Rocha-Azevedo, et al, 2009. The regions of the brain that are usually affected are midbrain, basal areas of the temporal and occipital lobes, and the posterior fossa (Seijo Martinez, et al, 2000, MarcianoCabral & Cabral, 2003, Khan, 2006.…”

Section: Diagnosismentioning

confidence: 99%