Acantha

• Free-Living Pathogenic Amoeba


  • Acanthamoeba spp.
  • Naegleria fowleri

  
• General Characteristics of Free-Living Pathogenic Amoeba


  • World-wide distribution in soil and water
  • No major reservoir host
  • Generally opportunistically parasitic
  • Free-living → Facultative parasites

  
• Members of Acanthamoeba spp

  • Acanthamoeba castellani
  • Acanthamoeba culbertsoni
  • Acanthamoeba polyphaga
  • Acanthamoeba hatchetti
  • Acanthamoeba rhysodes
  • Acanthamoeba divionensis
  • Acanthamoeba lugdunensis
  • Acanthamoeba lenticulate

  
• Differentiation of Acanthamoeba species is unnecessary because all Acanthamoeba spp. cause the same disease manifestations and requires the same treatment

  
• Both cyst and trophozoite stages can enter the body of the host
• The trophozoite is the infective stage that penetrates into the body, while the cyst generally dies inside the body upon entry, unless they manage to excyst to release trophozoite
• Cyst stages are found in abundance in the tissue, while trophozoites can be found but not in abundance
• Acanthamoeba spp. are implicated reservoir hosts of medically important bacteria like Legionella spp, Mycobacteria spp, Gram negative bacilli such as Escherichia coli

  
• Epidemiology of Free-Living Pathogenic Amoeba


  • Ubiquitous, free-living amoeba, hence, exposure is unavoidable
  • Found in lakes, swimming pools, tap water, heating and air conditioning units, sewage, dental treatment units, dialysis machines, even survive in contact lens cleaning solutions

  
• Diseases caused by Free-Living Pathogenic Amoeba


  • Acanthamoeba keratitis (AK)
  • Granulomatous amoebic encephalitis (GAE)

  
• Trophozoite


  • Single large nucleus, centrally-located, densely staining nucleolus
  • Large endosome
  • Finely granulated cytoplasm
  • Large contractile vacuole
  • With acanthopodia: "Thorn-like" appendages more evident under phase contrast microscopy

  
• Replication of Trophozoite


  Mitosis - cell division without production of another organism; production of daughter cells
• The better term to be used for the replication of Acanthamoeba trophozoite is fission (binary fission - division of the cell with the production of another organism)
• Feeding of Trophozoite


  • Feed on gram-negative bacteria, blue-green algae, or yeasts
  • Corneal epithelial cells and brain tissues through phagocytosis and production of lytic enzymes
• Cyst


  • Polygonal, spherical, or star-shaped
  • Double-walled: Outer smooth irregular ectocyst, Inner rough polyhedral endocyst with many pores (ostioles)
  • Formed when conditions are not favorable
  • Highly resilient cyst
• Life Cycle of Acanthamoeba spp.


  1. The cystic and trophozoite stage of the parasite can enter the host, but only the trophozoite causes disease

  2. It may enter the eyes causing corneal keratitis, or through the nasal tract and respiratory system, migrating throughout the body and may infect the brain causing chronic granulomatous amebic encephalitis

  3. It may also penetrate in skin lesions, enter the blood vessels and into the circulation

  
• Acanthamoeba keratitis (AK)


  • Associated with improperly disinfected soft contact lenses especially those rinsed with tap water or contaminated lens solution
  • Manifestations: sever ocular pain and blurring of vision, corneal ulceration with progressive infiltration, hypopyon, scleritis, iritis, or even vision loss

  
• Granulomatous Amoebic Encephalitis (GAE)


  • Usually fatal within 3 – 40 days
  • Usually among immunocompromised individuals: Chronically ill, debilitated, on immunosuppressive agents, chemotheraphy, HIV-AIDS
  • Pathway: From skin or lungs to brain via hematogenous route, or direct infection through the olfactory valves
  • Manifestations: Systematic signs in the early course (fever, malaise, anorexia), Related to destruction of brain tissues and meningeal irritations (Increased sleeping time, severe headache, mental status changes, epilepsy, hemiparesis, blurring of vision, diplopia, ataxia, or even coma and death)

  
• CT scan is not specific for Granulomatous Amoebic Encephalitis and may be mistaken as cancer, toxoplasma, tuberculosis, and the likes
• Granulomatous Amoebic Encephalitis is usually diagnosed after the death of the patient because of the rareness of its incidence that often times it is not considered for diagnosis

  
• Trophozoites are rarely seen in cerebrospinal fluid analysis for Granulomatous Amoebic Encephalitis
• Granulomatous Amoebic Encephalitis may be misdiagnosed as a viral or autoimmune encephalitis leading to improper course of treatment

  
• Diagnosis of Acanthamoeba infections


  1. Demonstration of typical cyst and or trophozoite in tissues like epithelial biopsy, corneal scrapings, or contact lens and lens solution

  2. Species-specific identification via culture and molecular analysis like PCR

  
• Granulomatous Amoebic Encephalitis is usually diagnosed post-mortem due to the rarity of the disease and unfamiliarity of most doctors with the pathogen leading to missed diagnosis

  
• Treatment of Acanthamoeba keratitis


  1. Clotrimazole with pentamidine, isethionate, and Neosporin

  2. Other agents: Polyhexamethylene biguanide, propamidine, dibromopropamidine isetheionate, neomycin, paromomycin, polymyxn B, ketoconazole, miconazole, and itraconazole

  3. Avoid topical steroids – may retard the immune response

  4. Advanced AK: debridement, or deep lamellar keratectomy
• Treatment of Granulomatous Amoebic Encephalitis

  1. Combination of amphotericin B, pentamidine isethionate, sulfadiazine, fluocytosine, fluconazole or itraconazole

  2. Surgery: decompressive lobectomy
• Prevention and Control


  • Keep the immune system strong to prevent disseminated infection
  • Meticulous contact lens hygiene. Avoidance of rinsing contact lens with tap water
  • Prolonged heating and boiling of water kills amoebic trophozoites and cysts
  • Awareness among immunocompromised patients of risk of infection