Immunopathology and Electron Microscopy of Acanthamoeba Keratitis

Mathers, William D.; Stevens, Garth; Rodrigues, Merlyn; Chan, Chi Chao; Gold, Joseph B.; Visvesvara, Govinda S.; Lemp, Michael A.; Zimmerman, Lorenz E.

doi:10.1016/s0002-9394(14)74321-1

Cited by 74 publications

(40 citation statements)

References 18 publications

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“…Clinically, conjunctival hyperemia, corneal inflammation, episcleritis, and scleritis occur. Trophozoites can infiltrate corneal nerves, causing neuritis and necrosis (150,288). In rare circumstances, Acanthamoeba can spread from the cornea to the retina, causing chorioretinitis (208,319).…”

Section: Acanthamoeba Spp As Nonopportunistic Pathogens Amebic Keratmentioning

confidence: 99%

“…Macrophages and neutrophils are the major inflammatory cell types found in tissues surrounding amebae or cysts. In one set of studies, corneal buttons from two AK patients with chronic inflammation were examined using electron microscopy and immunohistochemistry to identify cell types involved in the inflammatory response (288). The use of monoclonal antibodies to cell surface markers demonstrated that the corneal (248,249).…”

Section: Role Of the Immune System In Amebic Keratitismentioning

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: Acanthamoeba Spp As Nonopportunistic Pathogens Amebic Keratmentioning

confidence: 99%

Section: Role Of the Immune System In Amebic Keratitismentioning

confidence: 99%

Acanthamoebaspp. as Agents of Disease in Humans

2003

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“…Воз-можно использование и других флюоресцирую-щих окрасок, в частности -акридинового оран-жевого [42]. Трансмиссивная электронная микро-скопия позволяет достаточно четко дифференци-ровать цисты и трофозоиты АК [43].…”

Section: морфологическая диагностика акunclassified

Diagnosis of Acanthamoeba keratitis

Marchenko

Kasparova

2016

Vestn. oftal'mol.

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“…Acanthamoeba binds to the corneal surface and produces epithelial thinning and necrosis. Eventually, the parasite invades the corneal stroma, resulting in necrosis, edema, disruption of the stromal lamellae, and an intense polymorphonuclear in ammatory response (7). These considerable damages are known to induced by cytopathogenic substances, such as oxygen radicals and several different enzymes, released by Acanthamoeba trophozoites (8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Purification and Characterization of an Extracellular Serine Proteinase from Acanthamoeba castellanii

Cho

Kim

et al. 2000

IUBMB Life

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SummaryAn extracellular proteinase of Acanthamoeba castellanii was puri ed and its biochemical and pathological properties were characterized. The molecular mass of the puri ed enzyme was » 42 kDa as estimated by sodium dodecyl sulfate -polyacrylamide gel electrophoresis and Sephacryl S-200 HR gel-ltration chromatography. Therefore, its structure seemed to be monomeric with a single polypeptide. Its activity was inhibited by the serine proteinase inhibitors diisopropyl uorophosphate and phenylmethanesulfonyl uoride. Its activity was optimum at 30 to 50 ± C with a maximum at 50 ± C; optimal pH was 8.0. As much as 70% of the enzyme activity was maintained at 50 ± C for at least 12 h but was rapidly inactivated thereafter. The puri ed enzyme degraded collagen and rabbit corneal extract. Furthermore, it exhibited strong cytopathic effects on human corneal epithelial cells and broblast cells. These suggest the possible role of this enzyme in the pathogenesis of Acanthamoeba.

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Immunopathology and Electron Microscopy of Acanthamoeba Keratitis

Cited by 74 publications

References 18 publications

Acanthamoebaspp. as Agents of Disease in Humans

Acanthamoebaspp. as Agents of Disease in Humans

Diagnosis of Acanthamoeba keratitis

Purification and Characterization of an Extracellular Serine Proteinase from Acanthamoeba castellanii

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