1. LECTURER: SR. NORAZSIDA
FREE LIVING AMEBAE
LECTURER:
SR. NORAZSIDA

2. 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.

3. N. fowleri

4. 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.

5. 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.

6. Life cycle
Consists of 3 stages: 1) an amebic trophozoite (the only stage that exist in human) 2) a biflagellate form 3) cyst

7. TRANSMISSION

8. 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.

9. 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

10. 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.

11. TREATMENT Amphotericin B Combination treatments:
Amphotericin B + miconazole
Amphotericin B + rifambin

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

13. Acanthamoeba sp.

14. 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.

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

16. TRANSMISSION

17. 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.

18. Granulomatous Amebic Encephalitis GAE
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

19. 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.

20. 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.

21. AMEBIC KERATITIS predisposing factors symptoms diagnosis treatment
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