Acanthamoeba

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Acanthamoeba
Acanthamoeba polyphaga cyst.jpg
Phase contrast micrograph of an Acanthamoeba polyphaga cyst.
Acanthamoeba.jpg
Acanthamoeba in active stage
Scientific classification
Domain: Eukaryota
Kingdom: Amoebozoa
Family: Acanthamoebidae
Genus: Acanthamoeba

Acanthamoeba is a genus of amoebae, one of the most common protozoa in soil, and frequently found in fresh water and other habitats. Acanthamoeba has two evolutive forms, the metabolically active trophozoite and a dormant, stress resistant cyst. Trophozoites are small, usually 15 to 35 μm in length and amoeboid in shape. In nature, Acanthamoeba species are free-living bacterivores, but in certain situations they can cause infections in humans and other animals.[1]

Distribution[edit]

Acanthamoeba spp. are among the most prevalent protozoa found in the environment.[citation needed] They are distributed worldwide, and have been isolated from soil, air, sewage, seawater, chlorinated swimming pools, domestic tap water, bottled water, dental treatment units, hospitals, air-conditioning units, and contact lens cases. Additionally, Acanthamoeba have been isolated from human skin, nasal cavities, throats, and intestines, as well as plants and other mammals.[2]

Role in disease[edit]

Acanthamoeba encephalitis. Scale bar: 10 μm

Diseases caused by Acanthamoeba include keratitis and granulomatous amoebic encephalitis (GAE).[3] The latter is often but not always seen in immunosuppressed patients.[4] GAE is caused by the amoeba entering the body through an open wound then spreading to the brain.[5] The combination of host immune response and amoebal proteases causes massive brain swelling[6] resulting in death in ~95% of those infected.

Granulomatous amoebic encephalitis[edit]

This is an opportunistic protozoan pathogen that rarely causes disease in humans. Approximately 400 cases have been reported worldwide, with a survival rate of only two to three percent. Infection usually occurs in patients with immunodeficiency, diabetes, malignancies, malnutrition, systemic lupus erythematosus, or alcoholism.[citation needed] The parasite's portal of entry is via lesions in the skin or the upper respiratory tract or via inhalation of airborne cysts.[citation needed] The parasite then spreads hematogenously into the central nervous system. Acanthamoeba crosses the blood–brain barrier by means that are not yet understood. Subsequent invasion of the connective tissue and induction of pro-inflammatory responses leads to neuronal damage that can be fatal within days. A post mortem biopsy reveals severe oedema and hemorrhagic necrosis.[7] A patient who has contracted this illness usually displays subacute symptoms, including altered mental status, headaches, fever, neck stiffness, seizures, focal neurological signs (such as cranial nerve palsies and coma), all leading to death within one week to several months.[8] Due to the rarity of this parasite and a lack of knowledge, there are currently no good diagnoses or treatments for Acanthamoeba infection. Acanthamoeba Keratitis cases in the past, when were managed by Atropine, given as an adjuvant therapy without anti-parasitic drugs added to the regime, had been reported to halt the vision loss. Recent publications debate these successes related to an action of Atropine on muscarinic receptors on Acanthamoeba spp.[9]

Infection usually mimics that of bacterial leptomeningitis, tuberculous meningitis, or viral encephalitis. The misdiagnosis often leads to erroneous, ineffective treatment. In the case that the Acanthamoeba is diagnosed correctly, the current treatments, such as amphotericin B, rifampicin, trimethoprim-sulfamethoxazole, ketoconazole, fluconazole, sulfadiazine, or albendazole, are only tentatively successful. Correct and timely diagnosis, as well as improved treatment methods and an understanding of the parasite are important factors in improving the outcome of infection by Acanthamoeba. A recent paper published in 2013, has shown substantial effects of some FDA approved drugs with a kill rate above 90%.[4] These results were in-vitro effects, but as the drugs are already approved, human infections can be targeted after dose calculations in clinical trials with them.

Acanthamoebic keratitis[edit]

Acanthamoeba causing keratitis

When present in the eye, Acanthamoeba strains can cause acanthamoebic keratitis, which may lead to corneal ulcers or even blindness.[10] This condition occurs most often among contact lens wearers who do not properly disinfect their lenses, exacerbated by a failure to wash hands prior to handling the lenses. Multipurpose contact lens solutions are largely ineffective against Acanthamoeba, whereas hydrogen peroxide-based solutions have good disinfection characteristics.[11][12]

In May 2007, Advanced Medical Optics, manufacturer of Complete Moisture Plus Contact Lens Solution products, issued a voluntary recall of their Complete Moisture Plus solutions. The fear was that contact lens wearers who used their solution were at higher risk of acanthamoebic keratitis than contact lens wearers who used other solutions. The manufacturer recalled the product after the Centers for Disease Control in the United States found that 21 individuals had possibly received an Acanthamoeba infection after using Complete Moisture Plus in the month prior to diagnosis.[13]

MRSA[edit]

Recent findings from the University of Bath demonstrate that methicillin-resistant Staphylococcus aureus can infect and replicate inside Acanthamoeba polyphaga cells, which are widespread throughout the environment. Since A. polyphaga can form cysts, cysts infected with MRSA can act as a mode of airborne dispersal for MRSA.[citation needed] Additionally, it is noted that "evidence with other pathogens suggests that pathogens that emerge from amoeba are more resistant to antibiotics and more virulent."[14][citation needed] Acanthamoeba has been observed to increase MRSA numbers by up to 1000-fold.[15]

Acanthamoeba castellanii is suspected to serve as a reservoir for bacterial pathogens such as Campylobacter jejuni.[citation needed]. Survival of Campylobacter jejuni in co-culture with Acanthamoeba castellanii has been reported in the literature.[citation needed] .

Ecology[edit]

A. castellanii can be found at high densities in various soil ecosystems. It preys on bacteria, but also fungi and other protozoa.

This species is able to lyse bacteria and produce a wide range of enzymes, such as cellulases or chitinases,[16] and probably contributes to the breakdown of organic matter in soil, contributing to the microbial loop.

Physiology[edit]

Role as a model organism[edit]

Because Acanthamoeba does not differ greatly at the ultrastructural-level from a mammalian cell, it is an attractive model for cell biology studies. Acanthamoeba is important in cellular microbiology, environmental biology, physiology, cellular interactions, molecular biology, biochemistry, and evolutionary studies, due to the organisms' versatile roles in the ecosystem and ability to capture prey by phagocytosis, act as vectors and reservoirs for microbial pathogens, and to produce serious human infections. In addition, Acanthamoeba has been used extensively to understand the molecular biology of cell motility[17] and cancer cell dormancy by in-depth exploration of the process of encystation[18]

The recently available Acanthamoeba genome sequence revealed several orthologs of genes employed in meiosis of sexual eukaryotes. These genes included Spo11, Mre11, Rad50, Rad51, Rad52, Mnd1, Dmc1, Msh and Mlh.[19] This finding suggests that Acanthamoeba is capable of some form of meiosis and may be able to undergo sexual reproduction. Furthermore, since Acanthamoeba diverged early from the eukaryotic family tree, these results suggest that meiosis was present early in eukaryotic evolution.

Owing to its ease and economy of cultivation, the Neff strain of A. castellanii discovered in a pond in Golden Gate Park in the 1960s, has been effectively used as a classic model organism in the field of cell biology. From just 30 liters of simple medium inoculated with A. castellanii, approximately one kilogram of cells can be obtained after several days of aerated culture at room temperature. Pioneered in the laboratory of Edward D. Korn at the National Institutes of Health (NIH), many important biological molecules have been discovered and their pathways elucidated using the Acanthamoeba model. Thomas Dean Pollard applied this model at the NIH, Harvard Medical School, Johns Hopkins University School of Medicine, and the Salk Institute for Biological Studies to discover and characterize many proteins that are essential for cell motility, not only in amoebas, but also in many other eukaryotic cells, especially those of the human nervous and immune systems, the developing embryo, and cancer cells.

Endosymbionts of Acanthamoeba[edit]

Acanthamoeba spp. contain diverse bacterial endosymbionts that are similar to human pathogens, so they are considered to be potential emerging human pathogens.[20] The exact nature of these symbionts and the benefit they represent for the amoebal host still have to be clarified.

These include Legionella and Legionella-like pathogens.[21]

Giant viruses[edit]

The giant viruses Mimivirus, Megavirus and Pandoravirus infect Acanthamoeba.[22]

Currently Acanthamoeba is the only species that is a host for such huge viruses (who have more than 1000 protein-coding genes; for instance, Pandoravirus has about 2500 protein-coding genes in its genome).

Diversity[edit]

Acanthamoeba can be distinguished from other genera of amoeba based on morphological characteristics.[23] However, differentiating one species of Acanthamoeba from another by morphology has proven difficult. Based on 18S rDNA sequencing, known Acanthamoeba strains can be organized into 12 groups, denoted T1-T12.[23] Most disease-causing isolates belong to type T4.[23]

Below is a list of described species of Acanthamoeba, with sequence types noted where known. Species which have been identified in diseased patients are marked with *.

  • A. astronyxis* (T7)
  • A. byersi*
  • A. castellanii* (T4)
  • A. comandoni (T9)
  • A. culbertsoni* (T10)
  • A. divionensis (T4)
  • A. griffini (T3)
  • A. hatchetti* (T11)
  • A. healyi (T12)
  • A. jacobsi
  • A. keratitis*
  • A. lenticulata (T3)
  • A. lugdunensis* (T4)
  • A. mauritaniensis (T4)
  • A. palestinensis* (T1)
  • A. paradivionensis (T4)
  • A. pearcei
  • A. polyphaga* (T4)
  • A. pustulosa (T2)
  • A. quina*
  • A. rhysodes* (T4)
  • A. royreba
  • A. stevensoni (T11)
  • A. terricola (renamed A. castellanii Poussard)
  • A. triangularis (T4)
  • A. tubiashi (T8)

See also[edit]

References[edit]

  1. ^ Marciano-Cabral, Francine; Cabral, Guy (2003-04-01). "Acanthamoeba spp. as Agents of Disease in Humans". Clinical Microbiology Reviews 16 (2): 273–307. doi:10.1128/CMR.16.2.273-307.2003. ISSN 0893-8512. PMC 153146. PMID 12692099. 
  2. ^ Johan F De Jonckheere (1991). "Ecology of Acanthamoeba". Reviews of Infectious Diseases 13: S385–S387. PMID 2047667. 
  3. ^ Di Gregorio, C; Rivasi F; Mongiardo N; De Rienzo B; Wallace S; Visvesvara GS (December 1992). "Acanthamoeba meningoencephalitis in a patient with acquired immunodeficiency syndrome". Archives of Pathology & Laboratory Medicine 116 (12): 1363–5. PMID 1456885. 
  4. ^ a b Baig AM (2014). "Granulomatous amoebic encephalitis: ghost response of an immunocompromised host?" (PDF). J Med Microbiol 63 ((Pt 12)): 1763–6. doi:10.1099/jmm.0.081315-0. PMID 25239626. 
  5. ^ Baig AM, Iqbal J, Khan NA (2013). "In vitro efficacies of clinically available drugs against the growth and viability of an Acanthamoeba castellanii keratitis isolate". Antimicrob Agents Chemother 57 (8): 3561–7. doi:10.1128/AAC.00299-13. PMC 3719691. PMID 23669391. 
  6. ^ Baig AM (April 27, 2015). "Pathogenesis of Amoebic Encephalitis: Are the Amoebas being credited to an 'Inside job' done by the Host Immune response?". Acta Trop: pii. doi:10.1016/j.actatropica.2015.04.022. PMID 25930186. 
  7. ^ Khan, N (November 2006). "Acanthamoeba invasion of the central nervous system". International Journal for Parasitology 37 (2): 131–8. doi:10.1016/j.ijpara.2006.11.010. PMID 17207487. 
  8. ^ Kaushal, V; Chhina DK; Kumar R; Pannu HS; Dhooria HPS; Chhina RS (March 2007). "Acanthamoeba Encephalitis". Indian Journal of Medical Microbiology 26 (2): 182–4. doi:10.4103/0255-0857.40539. PMID 18445961. 
  9. ^ Baig, AM; et al. (2014). "Recommendations for the management of Acanthamoeba keratitis". Journal of Medical Microbiology 63: 770–1. doi:10.1099/jmm.0.069237-0. 
  10. ^ Lorenzo-Morales, Jacob; Khan, Naveed A.; Walochnik, Julia (2015). "An update on Acanthamoeba keratitis: diagnosis, pathogenesis and treatment". Parasite 22: 10. doi:10.1051/parasite/2015010. ISSN 1776-1042. PMID 25687209.  open access publication - free to read
  11. ^ Shoff ME, Joslin CE, Tu EY, Kubatko L, Fuerst PA (July 2008). "Efficacy of contact lens systems against recent clinical and tap water Acanthamoeba isolates". Cornea 27 (6): 713–9. doi:10.1097/QAI.0b013e31815e7251. PMID 18580265. 
  12. ^ Johnston SP, Sriram R, Qvarnstrom Y, Roy S, Verani J, Yoder J, Lorick S, Roberts J, Beach MJ, Visvesvara G (July 2009). "Resistance of Acanthamoeba cysts to disinfection in multiple contact lens solutions". J Clin Microbiol 47 (7): 2040–5. doi:10.1128/JCM.00575-09. PMC 2708465. PMID 19403771. 
  13. ^ Abbott Medical Optics
  14. ^ "MRSA use amoeba to spread, sidestepping hospital protection measures, new research shows" (Press release). University of Bath. 2006-02-28. Retrieved 2007-02-12. 
  15. ^ "Single Cell Amoeba Increases MRSA Numbers One Thousand Fold" (Press release). Blackwell Publishing. 2006-03-01. Retrieved 2007-02-12. 
  16. ^ Anderson, I. J.; Watkins, R. F., Samuelson, J., Spencer, D. F., Majoros, W. H., Gray, M. W. and Loftus, B. J. (August 2005). "Gene Discovery in the Acanthamoeba castellanii Genome". Protist 156 (2): 203–14. doi:10.1016/j.protis.2005.04.001. PMID 16171187. 
  17. ^ Khan N (2009). Acanthamoeba: Biology and Pathogenesis. Caister Academic Press. ISBN 978-1-904455-43-1. 
  18. ^ Baig AM, Khan NA, Abbas F. Eukaryotic cell encystation and cancer cell dormancy: is a greater devil veiled in the details of a lesser evil? Cancer Biol
  19. ^ Khan NA, Siddiqui R (2015). "Is there evidence of sexual reproduction (meiosis) in Acanthamoeba?". Pathog Glob Health 109 (4): 193–5. doi:10.1179/2047773215Y.0000000009. PMID 25800982. 
  20. ^ Horn, M; Wagner, M (Sep–Oct 2004). "Bacterial Endosymbionts of Free-living Amoebae". Journal of Eukaryotic Microbiology 51 (5): 509–14. doi:10.1111/j.1550-7408.2004.tb00278.x. PMID 15537084. 
  21. ^ Schuster, F.; Visvesvara, G. (2004). "Opportunistic amoebae: challenges in prophylaxis and treatment". Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy 7 (1): 41–51. doi:10.1016/j.drup.2004.01.002. PMID 15072770. 
  22. ^ Nadège Philippe, Matthieu Legendre, Gabriel Doutre; et al. (July 2013). "Pandoraviruses: Amoeba Viruses with Genomes Up to 2.5 Mb Reaching That of Parasitic Eukaryotes". Science 341 (6143): 281–6. doi:10.1126/science.1239181. PMID 23869018. 
  23. ^ a b c Hyun Hee Kong (October 2009). "Molecular Phylogeny of Acanthamoeba". Korean Journal of Parasitology 47: S21–S28. doi:10.3347/kjp.2009.47.S.S21. PMC 2769217. 

External links[edit]