FREE LIVING AMEBAE

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FREE LIVING AMEBAE

• LECTURER
• SR. NORAZSIDA

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INTRODUCTION

• A large and diverse group of protozoan organisms.
• Inhabit fresh and salt water.
• Decaying organic matter and damp soil.
• 2 potential pathogens r 1) Naegleria fowleri 2)
  Acanthamoeba sp.

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N. fowleri
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Morphology

• Family Vahlkampfiidae
• Ameboflagellates having both an ameboid and
  flagellate stage in their life.
• Agent of primary amebic meningoencephalitis (PAM)
  or Naegleriasis.
• Since 1965, 140 cases have been reported world
  wide.
• Risk group healthy children and young adults
  with a history of swimming or diving in fresh or
  brackish water.
• Sources of infection contaminated swimming
  pools, stagnant ponds, freshwater lakes and
  streams, thermal springs and spas.

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• Drought and elevated temperatures increase
  concentrations of N. fowleri. Why? Bcoz, they
  feed on large populations of bacteria in these
  warmed water souces.
• Transmitted via inhalation of contaminated dust.
• Transmission nasal instillation ? follows
  olfactory nerve ? to CNS
• Trophozoite 7-20µm, large, broad pseudopods,
  single nucleus, large central karyosome.

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Life cycle

• Consists of 3 stages 1) an amebic trophozoite
  (the only stage that exist in human) 2) a
  biflagellate form 3) cyst

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TRANSMISSION
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PATHOGENESIS

• The incubation period is generally 3-7 days
  accompanied by the prodromal symptoms of headache
  and fever.
• Rapidly progress to frank meningitis with the
  onset of nausea and vomiting (stiff neck),
  confusion and coma.
• Death usually occurs in 3-6 days following the
  onset of these serious symptoms.

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Primary amebic meningoencephalitis PAM

• 1-14 days incubation period
• symptoms usually within a few days after swimming
  in warm still waters
• infection believed to be introduced through nasal
  cavity and olfactory neuroepithelium
• symptoms include headache, lethargy,
  disorientation, coma
• rapid clinical course, death in 4-5 days after
  onset of symptoms
• trophozoites can be detected in spinal fluid, but
  diagnosis is usually at autopsy

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LABORATORY DIAGNOSIS

• Finding motile trophozoites in
• -saline and wet preps of fresh spinal fluid
• -nasal discharge
• -Tissue biopsy
• Induced within 2-20 hours by transferring the
  ameboid form from tissue or CSF to water and
  incubating at 370C.
• Cultivation technique
• PCR
• Indirect fluorescent antibody procedures.

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TREATMENT

• Amphotericin B
• Combination treatments
• Amphotericin B miconazole
• Amphotericin B rifambin

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PREVENTION

• Public and private swimming pools, hot tubs, and
  baths should be properly maintained and
  adequately chlorinated to prevent growth of the
  organism.

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Acanthamoeba sp.
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Morphology

• Family of Ancanthamoebidae.
• Never produce flagella.
• Produce a chronic infection of the CNS
  Granulomatous amebic encephalitis (GAE).
• Also caused a keratitis and skin ulcers.
• Risk group immunocompromised, chronically ill.
• Transmission respiratory or skin with
  hematogenous spread to CNS
• Trophozoite 10-45µm, spiny acanthopodia, single
  nucleus, large central karyosome
• Cyst 10-20µm, rounded, double walled (outer wall
  having a wrinkled appearance), single nucleus.

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Life cycle

• Consists of
• 1) trophozoite 2) cyst.
• resistant to dessication and mild chlorination.
• Carried out by water and through the air.

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TRANSMISSION
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PATHOGENESIS

• GAE has an insidious onset.
• CNS infection is acquired hematogenously by the
  inhalation/aspiration of trophozoites and cysts
  caused pneumonitis.
• Or through skin and mucosal ulceration.
• Incubation period questionable, may take weeks
  to months to progress.
• Slow process of tissue invasion tends to
  stimulate granuloma formation.
• Single or multiple focal lesions develop over a
  prolonged period marking the chronic nature of
  the disease.
• Symptoms gradually develop headache, fever,
  fatigue, stiff neck, and altered mental status.

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Granulomatous Amebic EncephalitisGAE

• portal of entry unknown, possibly respiratory
  tract, eyes, skin
• presumed hematogenous dissemination to the CNS
• infection associated with debility or
  immunosuppression
• onset is insidious with headache, personality
  changes, slight fever
• progresses to coma and death in weeks to months
• amebas not yet detected in spinal fluid

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LABORATORY DIAGNOSIS

• By finding motile trophozoite in spinal fluid
  specimen.
• By finding trophozoite and cyst form in
• -brain biopsy tissue ? histological examination
• -scrapings from cutaneous or corneal lesions.
• Indirect immunofluorescent staining techniques.
• Cultured on non-nutrient agar, overlaid with
  viable E.coli bacteria ? stained with Giemsa or
  calcofluor white ? identification of cyst or
  trophozoite.

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TREATMENT PREVENTION

• Sulfamethazine however, most cases are only
  diagnosed at autopsy.
• no human cures documented
• Symptoms develop gradually over a prolonged
  period of time ? the disease may be overlooked.

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AMEBIC KERATITIS

• predisposing factors
• ocular trauma
• contact lens (contaminated cleaning solutions)
• symptoms
• ocular pain
• corneal lesions (refractory to usual treatments)
• diagnosis
• demonstration of amebas in corneal scrapings
• treatment
• difficult, limited success
• corneal grafts often required