Transcript FREE LIVING AMEBAE

FREE LIVING AMEBAE
LECTURER:
SR. NORAZSIDA
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.
N. fowleri
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.
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.
Life cycle
Consists of 3 stages: 1) an amebic trophozoite (the only
stage that exist in human) 2) a biflagellate form 3) cyst
TRANSMISSION
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.
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
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.
TREATMENT
Amphotericin B
Combination treatments:
- Amphotericin B + miconazole
- Amphotericin B + rifambin
PREVENTION
Public and private swimming pools, hot
tubs, and baths should be properly
maintained and adequately chlorinated to
prevent growth of the organism.
Acanthamoeba sp.
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.
Life cycle
Consists of:
1) trophozoite 2) cyst.
resistant to
dessication and mild
chlorination.
Carried out by water
and through the air.
TRANSMISSION
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.
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
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.
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.
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