Open Access Articles- Top Results for Acanthamoeba


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Scientific classification

Acanthamoeba is a genus of amoebae, one of the most common protozoa in soil, and frequently found in fresh water and other habitats. The cells are small, usually 15 to 35 μm in length and oval to triangular in shape when moving. Acanthamoeba is able to form metabolically inactive cysts which are resistant to fluctuations in temperature and pH levels. Cysts are also resistant to attack by the host immune system and facilitate the recurrence of infection. Most species are free-living bacterivores, but some are opportunists that can cause infections in humans and other animals.

Human pathogen

File:Acanthamoeba pathology.jpg
Acanthamoeba encephalitis. Scale bar: 10 μm

Diseases caused by Acanthamoeba include amoebic keratitis and encephalitis (more specifically the Granulomatous amoebic encephalitis) (GAE).[1] The latter is seen in immunocompetent hosts, with an intact T-cell immunity.[2] GAE is caused by the Acanthamoeba entering the body through wounds, nasal air sinuses and lungs, that eventually spreads to the brain.[3] The combination of host immune response and amoebal proteases causes the brain damage[4] resulting in death in over 95% of the patients.

Acanthamoeba granulomatous encephalitis

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.[5] 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.[6] 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.[7]

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% [8] 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.


Methicillin-resistant Staphylococcus aureus (MRSA) is an important pathogen in the hospital setting due to its resistance to many antibiotics. Recent findings from the University of Bath demonstrate that MRSA can infect and replicate inside Acanthamoeba polyphaga cells; this species is 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."[9][citation needed] Acanthamoeba has been observed to increase MRSA numbers by up to 1000-fold.[10] The Acanthamoeba gets into the body either through the skin or up the nose. It then travels through the nervous system to the brain; once there, it eats brain cells. After feeding, it divides rapidly, causing sudden and massive inflammation, killing the human host in just a few days.

Campylobacter spp. are Gram-negative bacteria that are recognized worldwide as a common cause of acute bacterial enteritis in humans. Acanthamoeba castellanii is a protozoan suspected to serve as a reservoir for bacterial pathogens such as Campylobacter jejuni.[citation needed] . A serious complication of Campylobacter jejuni infection is the development of Guillain–Barré syndrome (GBS). There is increasing evidence that what is diagnosed as Guillain–Barré syndrom may include conditions originating from a variety of underlying pathogenic mechanisms.[citation needed] . For the record, survival of Campylobacter jejuni in co-culture with Acanthamoeba castellanii has been reported in the literature.[citation needed] .

Importance in soil ecology

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,[11] and probably contributes to the breakdown of organic matter in soil, contributing to the microbial loop.


Species of Acanthamoeba are distinguished mainly on the form of cysts, and include the following; those marked with an asterisk are known to cause infections.

File:Free-living amebic infections.png
Life cycle of the parasitic agents responsible for causing "free-living" amebic infections
  • A. astronyxis*
  • A. byersi*
  • A. castellanii*
  • A. comandoni
  • A. culbertsoni*
  • A. divionensis
  • A. griffini
  • A. hatchetti*
  • A. healyi
  • A. jacobsi
  • A. keratitis*
  • A. lenticulata
  • A. lugdunensis*
  • A. mauritaniensis
  • A. palestinensis*
  • A. pearcei
  • A. polyphaga*
  • A. pustulosa
  • A. quina*
  • A. rhysodes*
  • A. royreba
  • A. terricola (renamed A. castellanii Poussard)
  • A. triangularis
  • A. tubiashi

Endosymbiontes of Acanthamoeba

Acanthamoeba spp. contain diverse bacterial endosymbionts that are similar to human pathogens, so they are considered to be potential emerging human pathogens.[12] 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.[13]

Role as a model organism

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 [14] and cancer cell dormancy by in-depth exploration of the process of encystation[15]

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 Dr. 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. Dr. 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.

Acanthamoebic keratitis

When present in the eye, Acanthamoeba strains can cause acanthamoebic keratitis, which may lead to corneal ulcers or even blindness.[16] 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.[17][18]

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.[19]

Giant viruses

The giant viruses Mimivirus, Megavirus and Pandoravirus infect Acanthamoeba.[20]

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).

See also


  1. ^ 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. 
  2. ^ Baig AM. Granulomatous amoebic encephalitis: ghost response of an immunocompromised host? J Med Microbiol. 2014 Dec;63(Pt 12):1763-6.
  3. ^ Baig AM, Iqbal J, Khan NA. In vitro efficacies of clinically available drugs against the growth and viability of an Acanthamoeba castellanii keratitis isolate
  4. ^ Baig AM. Pathogenesis of Amoebic Encephalitis: Are the Amoebas being credited to an 'Inside job' done by the Host Immune response? Acta Trop. 2015 Apr 27. pii:
  5. ^ Khan, N (November 2006). "Acanthamoeba invasion of the central nervous system". International Journal for Parasitology 37 (2): 131–8. PMID 17207487. doi:10.1016/j.ijpara.2006.11.010. 
  6. ^ 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. PMID 18445961. doi:10.4103/0255-0857.40539. 
  7. ^ 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. 
  8. ^ (Baig AM et al).
  9. ^ "MRSA use amoeba to spread, sidestepping hospital protection measures, new research shows" (Press release). University of Bath. 2006-02-28. Retrieved 2007-02-12. 
  10. ^ "Single Cell Amoeba Increases MRSA Numbers One Thousand Fold" (Press release). Blackwell Publishing. 2006-03-01. Retrieved 2007-02-12. 
  11. ^ 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. PMID 16171187. doi:10.1016/j.protis.2005.04.001. 
  12. ^ Horn, M; Wagner, M (Sep–Oct 2004). "Bacterial Endosymbionts of Free-living Amoebae". Journal of Eukaryotic Microbiology 51 (5): 509–14. PMID 15537084. doi:10.1111/j.1550-7408.2004.tb00278.x. 
  13. ^ 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. PMID 15072770. doi:10.1016/j.drup.2004.01.002.  edit
  14. ^ Khan N (2009). Acanthamoeba: Biology and Pathogenesis. Caister Academic Press. ISBN 978-1-904455-43-1. 
  15. ^ 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
  16. ^ Lorenzo-Morales, Jacob; Khan, Naveed A.; Walochnik, Julia (2015). "An update on Acanthamoeba keratitis: diagnosis, pathogenesis and treatment". Parasite 22: 10. ISSN 1776-1042. PMID 25687209. doi:10.1051/parasite/2015010.  open access publication - free to read
  17. ^ 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. PMID 18580265. doi:10.1097/QAI.0b013e31815e7251. 
  18. ^ 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. PMC 2708465. PMID 19403771. doi:10.1128/JCM.00575-09. 
  19. ^
  20. ^ 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. PMID 23869018. doi:10.1126/science.1239181. 

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