Naegleri

• Free-Living Pathogenic Amoeba


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


  • Acantamoeba spp.
  • Naegleria fowleri

  
• Usual exposure


  History of swimming in freshwater lakes or ponds or swimming pools
• Mode of transmission


  1. Inhalation of contaminated water

  2. Ingestion of contaminated water does not cause infection
• Disease


  Primary Amoebic Meningoencephalitis (PAM)
• Free-living amoeba-flagellate


  • Amoeboid: trophozoite form
  • Flagellate: swimming form
  • Transformation from amoeba to flagellate facilitate more rapid movement toward food sources

  
• Cyst


  Dormant form
• Epidemiology


  • Worldwide distribution
  • Thermophilic living in hot spring and other aquatic environment
  • Reproduction rate is directly proportional to temperature
• Amoeboid form (trophozoite)


  • Measures 10 to 35 – 40 um
  • Granular cytoplasm with many vacuoles
  • Locomotory apparatus: Blunt lobose pseudopod, bidirectional motility
  • Single large nucleus with large dense karyosome, lacks peripheral chromatin

  
• Flagellate Form


  • Elongated, pear-shaped
  • Anteriorly-located single nucleus morphologically similar with nucleus of amoeboid form, two free flagella
  • For the purpose of faster migration of the parasite toward food sources

  
• Cyst


  • Round with single nucleus
  • Thick, double cyst wall
  • Found in soil
  • NOT found in tissues
• Life Cycle of Naegleria fowleri


  1. Trophozoite is the infective stage as well as the reproductive stage through binary fission (or promitosis, or mitosis)

  2. Nasal mucosa → olfactory nerves (phagocytose amoeba) → Olfactory bulb → cribriform plate → brain

  3. Amoeboid stages (trophozoites, feeding stage), and flagellated stages can be found in the CSF

  4. Amoeboid stage cause lysis of brain parenchyma causing encephalitis

  5. Lungs – parasite may gain entry to the lungs but would have no tropism to the organ, hence there is no disease manifestation in the lungs

  
• Primary Amoebic Meningoencephalitis (PAM)


  • May occur in previously healthy adults with history of swimming in contaminated water
  • Rare but rapidly destructive and fatal meningoencephalitis

  
• Pathogenesis


  1. Secretion of lytic enzymes

  2. Membrane-pore forming proteins

  3. Factors inducing apoptosis

  4. Direct feeding on cells by the amoebae

  
• Manifestations of PAM


  • fever, nausea, vomiting, headache, nuchal rigidity, mental status changes
  • Rapid progression to coma and death
• CSF in PAM


  elevated WBC count with neutrophilic predominance, high protein, and low glucose
• PAM may be misdiagnosed as bacterial meningitis
• Post-mortem examination


  • Gross: Hemorrhagic necrosis particularly the olfactory bulbs, congestion and edema of neural tissue; inflammation and congestion of leptomeninges
  • Microscopic: fibrinopurulent exudate consisting of neutrophils in leptomeninges and brain tissue, pockets of amoebae in necrotic areas

  
• Diagnosis


  • Suspected in people with compatible history of exposure and rapidly progressive meningoencephalitis
  • Definitive diagnosis: Demonstration of characteristic trophozoites in brain and CSF

  
• Serology


  ELISA is less useful in the diagnosis – healthy individuals in endemic area may show positive antibody titers
• PCR


  For species-specific diagnosis
• Treatment


  1. Combination amphotericin B and Clotrimazole

  2. Others: Azithromycin, Voriconazole
• Most infected persons die even before giving effective treatment in the hospital
• Prevention and Control


  1. Avoidance of immersion of the head and accidental inhalation of water should be practiced in endemic areas and in hot springs

  2. Chlorination of water at 1 ppm or higher

  3. Placing warning signs near bodies of water suspected to harbor the parasite