1991
DOI: 10.1111/j.1365-3024.1991.tb00261.x
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Free‐living amoebae: pathogenicity and immunity

Abstract: Free-living amoebae causes three well-defined disease entities: (i) primary amoebic meningoencephalitis, caused by Naegleria fowleri, (ii) granulomatous amoebic encephalitis and (iii) chronic amoebic keratitis, caused by species of Acanthamoeba. Both Naegleria infections and chronic amoebic keratitis occur in healthy individuals while granulomatous amoebic encephalitis is often associated with patients with acquired immunodeficiencies. The different pathogenic behaviour of these organisms is associated with di… Show more

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Cited by 63 publications
(44 citation statements)
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“…Conversely, amoebae can evade immune mechanisms by binding to a C1q component, as shown in the case of A. culbertsoni, and the parasite-derived serine proteases can degrade IgG and IgA , Kong, et al, 2000, Na, et al, 2002, Marciano-Cabral & Cabral, 2003. Neutrophils, macrophages, and microglia can destroy amoebae, and their amoebicidal effects are mediated in part by respiratory burst and nitric oxide under the influence of IL-1 , IL-1 , TNF-and/or IFN- (Ferrante, 1991a, Ferrante, 1991b, MarcianoCabral & Toney, 1998, Marciano-Cabral, et al, 2000, Benedetto & Auriault, 2002a, Benedetto & Auriault, 2002b, Dudley, et al, 2007, Khan, 2008. Affected patients, including healthy individuals upto 90%, carry the Acanthamoeba-reactive antibodies of IgM, IgG, and IgA isotypes with no significant differences between males (86.2%) and females (89.2%), indicating that humans are regularly exposed to Acanthamoeba and become sensitized with the amoebic antigens (Chappell, et al, 2001, McClellan, et al, 2002, Schuster, 2002, Khan, 2005a, Brindley, et al, 2009, da Rocha-Azevedo, et al, 2009.…”
Section: Immune Responses To Acanthamoebamentioning
confidence: 99%
“…Conversely, amoebae can evade immune mechanisms by binding to a C1q component, as shown in the case of A. culbertsoni, and the parasite-derived serine proteases can degrade IgG and IgA , Kong, et al, 2000, Na, et al, 2002, Marciano-Cabral & Cabral, 2003. Neutrophils, macrophages, and microglia can destroy amoebae, and their amoebicidal effects are mediated in part by respiratory burst and nitric oxide under the influence of IL-1 , IL-1 , TNF-and/or IFN- (Ferrante, 1991a, Ferrante, 1991b, MarcianoCabral & Toney, 1998, Marciano-Cabral, et al, 2000, Benedetto & Auriault, 2002a, Benedetto & Auriault, 2002b, Dudley, et al, 2007, Khan, 2008. Affected patients, including healthy individuals upto 90%, carry the Acanthamoeba-reactive antibodies of IgM, IgG, and IgA isotypes with no significant differences between males (86.2%) and females (89.2%), indicating that humans are regularly exposed to Acanthamoeba and become sensitized with the amoebic antigens (Chappell, et al, 2001, McClellan, et al, 2002, Schuster, 2002, Khan, 2005a, Brindley, et al, 2009, da Rocha-Azevedo, et al, 2009.…”
Section: Immune Responses To Acanthamoebamentioning
confidence: 99%
“…Since the early 1960s, Acanthamoeba has been recognized as an opportunistic human pathogen capable of causing infections in both immunocompetent and immunocompromised hosts [14,15]. In particular, Acanthamoeba spp.…”
Section: Introductionmentioning
confidence: 99%
“…PAM, caused by Naegleria fowleri, is a fast progressing disease (lasting 7-14 days), affecting both immunocompromised and immunocompetent hosts. N. fowleri gains entry into the central nervous system (CNS) through the olfactory neuroepithelium, producing necrotizing and haemorrhagic meningoencephalitis, and is associated with stiff neck, headache, vomiting, fever and nausea (Barnett et al, 1996;Ferrante, 1991;Ma et al, 1990;Martinez & Visvesvara, 1997). In contrast, GAE can be caused by both Balamuthia mandrillaris and Acanthamoeba species and is thought to be initiated by the entry of amoebae through the lower respiratory tract or skin lesions, followed by haematogenous spread (reviewed by Khan, 2003;Marciano-Cabral & Cabral, 2003).…”
Section: Introductionmentioning
confidence: 99%