Pathogenicity of Acanthamoeba.

Page updated 26/5/02

Acanthamoeba is essentially ubiquitous in the biosphere inhabiting every conceivable space from the Antarctic to the Artic.  Naturally, man and Acanthamoeba often cross paths.  In the vast majority of cases there is no conflict, but two factors have lead to problems over the last twenty years; AIDs and contact lenses.  Immunocompromisation as a result of AIDs infection has lead to many secondary Acanthamoeba infections, and contact lens wearers are at risk from Acanthamoeba keratitis.

In a very small number of instances otherwise healthy individuals have been known to succumb to infection by Acanthamoeba. This disease is known as granulatomatous amoebic encephalitis (GAE) or primary amoebic meningoencephalitis (PAM) (Butt, 1966).  Immunity against Acanthamoeba is probably through macrophages (Marciano-Cabral & Toney, 1998), or natural killer cells (Hyun et al, 1992; Kim et al, 1993) although immunization by the administering of Acanthamoeba extract prior to challenge with the sane species of intact Acanthamoeba resulted in a degree of protection (in mice) indicating that an antibody response may also be involved (Ferrante, 1991b).  There is also the suggestion that mice pups may be afforded protection through immunization of their mothers (Kong et al, 1993).

Acanthamoeba cysts have been discovered in human faeces (Zaman et al, 1998), however, there has to date to my knowledge been no indication of the involvement of the amoeba in pathogenesis in the intestinal tract as there is of course with Entamoeba.

Very few Acanthamoeba in the natural environment turn out to be pathogenic to humans. The differentiation between pathogenic and non-pathogenic Acanthamoeba is an important activity but is clouded by the fact that mice seem especially prone to becoming infected with Acanthamoeba.  Many attempts have been made to find "the" difference between the two, and several predisposing properties have been identified for example the ability to grow at temperatures approaching mammalian body has been reported to be important.  Other less obvious characteristics have been suggested including some possibly spurious genetic markers (Howe et al, 1997).  The classification of Acanthamoeba has been problematic relying on morphological features especially of the cysts.  However, not only has the cyst morphology been found to be a function (to some extent) of the conditions under which the amoeba encyst (), but this classification scheme has not been found to reliably reflect possibly more robust genetic efforts based on SSUrDNA sequence analysis (Stothard et al).  See Acanthamoeba Classification.

Acanthamoeba Proteases in Pathogenesis	Acanthamoeba keratitis	Acanthamoeba and AIDS
Acanthamoeba and Pathogenic Bacteria	Acanthamoeba induced apoptosis in vertebrate cells

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Simon Kilvington

Borazjani, R. N., May, L. L., Noble, J. A., Avery, S. V. & Ahearn, D. G. (2000) Flow cytometry for determination of the efficacy of contact lens disinfecting solutions against Acanthamoeba spp.  App.Environ.Microbiol. 66, 1057-1061.

Butt, C.G. (1966) Primary amebic meningoencephalitis. New England J.Med. 274, 1473-1476.

Cao, Z., Jefferson, D. M. & Panjwani, N. (1998) Role of carbohydrate-mediated adherence in cytopathogenic mechanisms of Acanthamoeba.  J.Biol.Chem. 273, 15838-15845.

Dini, L. A., Cockinos, C., Frean, J. A., Niszl, I. A. & Markus, M. B. (2000) Unusual case of Acanthamoeba polyphaga and Pseudomonas aeruginosa keratitis in a contact lens wearer from Gauteng, South Africa.  J.Clin.Microbiol. 38, 826-829.

Howe, D. K., Vodkin, M. H., Novak, R. J., Visvesvara, G. & McLaughlin, G. L. (1997) Identification of two genetic markers that distinquish pathogenic and nonpathogenic strains of Acanthamoeba spp., Parasitol.Res. 83, 345-348.

Hyun, D.-K., Shin, C.-O. & Im, K.-I. (1992) Natural killer cell activity in mice infected with Acanthamoeba culbertsoni.  Korean J. Parasitol. 29, 101-112.

Kim, T.-U., Im, K.-I. & Cho, Y.-D. (1989) A biochemical study on the cytolytic substance of Acanthamoeba culbertsoni. Yonsei Rep.Trop.Med. 20, 32-36.

Leher, H., Silvany, R., Alizadeh, H., Huang, J. & Niederkorn, J. Y. (1998) Mannose induces the release of cytopathogenic factors from Acanthamoeba castellanii. Infection Immunity. 66, 5-10.

Lehmann, O. J., Green, S. M., Morlet, N., Kilvington, S., Keys, M. F., Matheson, M. M., Dart, J. K. G., McGill, J. I. & Watt, P. J. (1998) Polymerase chain reaction analysis of corneal epithelial and tear samples in the diagnosis of Acanthamoeba keratitis., IOVS. 39, 1261-1265.

Macrciano-Cabral, F., Puffenbarger, R. & Cabral, G. A. (2000) The increasing importance of Acanthamoeba infections. J.Eukaryot.Microbiol. 47, 29-36.

Morton, L. D., McLaughlin, G. L. & Whiteley, H. E. (1991) Effects of temperature, amebic strain, and carbohydrates on Acanthamoeba adherence to corneal epithelium in vitro. Infect.Immun. 59, 3819-3822.

Niszl, I. A., Veale, R. B. & Markus, M. B. (1998) Cytophathogenicity of clinical and environmental Acanthamoeba isolates for two mammalian cell lines. J.Parasitol. 84, 961-967.

Zaman, V., Zaki, M. & Manzoor, M. (1998) Acanthamoeba in human faeces from Karachi. Annals Trop.Med.&Parasitol. 93, 189-191.