Granulomatous Amebic Encephalitis presenting as a cerebral mass lesion

Martinez, A. J.; García, Cristina Arguedas; Halks-Miller, Meredith; Arce-Vela, R.

doi:10.1007/bf00690448

Cited by 27 publications

(11 citation statements)

References 25 publications

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“…Access to the CNS may be by hematogenous spread from a primary site in the lungs or skin or directly through the olfactory neuroepithelium (282). Symptoms of CNS infection (Table 3) include headache, confusion, nausea, vomiting, fever, lethargy, stiff neck, focal neurologic deficits, or signs of increased intracranial pressure (280,286). Pathological findings generally include severe hemorrhagic necrosis, fibrin thrombi, and inflam- mation.…”

Section: Granulomatous Amebic Encephalitismentioning

confidence: 99%

“…These observations of experimental animals dying from encephalitis led Culbertson et al (99) to predict a role for free-living amebae as agents of human disease. Human cases of amebic encephalitis were reported soon thereafter from Australia, Europe, Africa, South America, and the United States (35,57,58,64,74,142,201,280,284,344,476). However, some of these cases were identified later as primary amebic meningoencephalitis, a rapidly fatal disease of the CNS caused by another free-living ameba, Naegleria fowleri (57,268,286).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Granulomatous Amebic Encephalitismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acanthamoebaspp. as Agents of Disease in Humans

2003

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“…The clinical signs of GAE are not specific. Thus, the disease is often misdiagnosed as bacterial leptomeningitis, tuberculous meningitis, viral encephalitis, toxoplasmosis, fungal infections, neurocysticercosis, or a brain tumor [5, 6, 68–71]. …”

Section: Acanthamoeba Sppmentioning

confidence: 99%

“…Multifocal lesions, edema, and multiple ring-enhancing lesions are commonly observed in GAE patients by MRI. Despite these characteristics, both CT and MRI have limited diagnostic value for GAE [5, 7, 41–43, 68–73]. …”

Section: Acanthamoeba Sppmentioning

confidence: 99%

Diagnosis of Infections Caused by Pathogenic Free-Living Amoebae

Rocha-Azevedo

Tanowitz

Marciano‐Cabral

2009

Interdisciplinary Perspectives on Infectious Diseases

105

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Naegleria fowleri, Acanthamoeba spp., Balamuthia mandrillaris, and Sappinia sp. are pathogenic free-living amoebae. N. fowleri causes Primary Amoebic Meningoencephalitis, a rapidly fatal disease of the central nervous system, while Acanthamoeba spp. and B. mandrillaris cause chronic granulomatous encephalitis. Acanthamoeba spp. also can cause cutaneous lesions and Amoebic Keratitis, a sight-threatening infection of the cornea that is associated with contact lens use or corneal trauma. Sappinia pedata has been identified as the cause of a nonlethal case of amoebic encephalitis. In view of the potential health consequences due to infection with these amoebae, rapid diagnosis is critical for early treatment. Microscopic examination and culture of biopsy specimens, cerebral spinal fluid (CSF), and corneal scrapings have been used in the clinical laboratory. For amoebic keratitis, confocal microscopy has been used to successfully identify amoebae in corneal tissue. More recently, conventional and real-time PCR assays have been developed that are sensitive and specific for the amoebae. In addition, multiplex PCR assays are available for the rapid identification of these pathogens in biopsy tissue, CSF, and corneal specimens.

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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%