Free Living Amoebae Flashcards
free living amoebae all belong in this group
Sarcodina
free living amoebae genera that are potentially pathogenic to humans + other vertebrates
Acanthamoeba
Naegleria
Balamuthia
Sappinia
Hartmannella
amphizoic
amoebae’s ability to exist within a host or in environment as free-living forms
T or F. Most free-living amoebaes are bacteriophagous inhabitants of soil, water, and sewage
T
most amoebae exist in two basic forms
trophozoite
cyst
some amoebae are diphasic:
ameboid (binary fission)
flagellated stage
when does amoebae encystment occurs
under adverse environmental conditions and allow for survival outside host
amoebic trophozoites
pseudopods
adhesion essential for locomotion and feeding
movement enhanced by higher temps (30C)
amoebastomes/”food cups” = cytoplasmic extension
- ingestion of bacteria and cell debris
- attachment to surfaces
*NO correlation w pathogenicity
the flagellated tage of amebae
- cell changes shape = synthesizes new flagellar apparatus
> more rigid cell, pear-shaped, sturdy shape, faster movement - induced by nutritional deprivation, temp or osmotic shock
- lasts from 2 to several hrs
cyst stage of amoebae
- environmentally hardy form
- mucopolysaccharide double wall, resistant to biocides
- Ostioles (pores) sealed by mucus plugs
- cysts not formed in tissue, left behind when trophozoite emerge
ostioles
pores that allow communication that allow communication inside and outside of amoeboid cyst
not formed in tissue; left behind when trophozoites emerge
when trophozoites come out of cyst, they squeeze through this which leave intact cyst = easily seen in microscope
Naegleria fowleri
diphasic amoeba
- exist in amoeboid and flagellate form (2 to several hours)
- agent of amoebic encephalitis
lifecycl of Naegleeri fowleri
invasion via nasal passages on contact w water (ex: water slides without plugging nose)
> amoebae travel along olf nerves
> cribriform plate to brain
INHALING infested water is how you get infected; ingestion of water does nothing
virulence of Naegleria depends on:
- Nfa1 protein (mediates amebic attachment to target cells; first step to cell invasion)
- Feeding cups (help directly phagocytose the brain cells).
- Nitric oxide production
- Pore-forming proteins.
- Cytolytic molecules like cysteine proteases, phospholipases, and phospholipolytic enzymes
epidemiology of N. fowlerii
- ubiquitous = freshwater lakes, hot water springs, poorly chlorinated pools (NOT in seawater)
- worldwide
- growth enhancement at high temps (42C); thermophilic organism
- protection = calination and chlorination (cysts more fragile than Acanthamoeba)
primary amoebic meningioencaphalitis
(PAM) FAST AND DEADLY!
N. fowleri
- extensive cell necrosis caused by amoebic trophozoites = significant hemorrhages = severe destruction of meninges, olf nerves, and brain tissue
- inflammatory exudate, edema (swelling of brain => DEATH)
where is amoebic meningitis common?
new zealand/australia
how to diagnose Naegleria fowlerii
- microscopy of brain biopsy, CSF
- in vitro culture on lab media (plain agar w lawn of bacterial growth = amoeba food)
- molecular detection (PCR)
Acanthamoeba culbertsoni morphology
troph = spine like acanthopodia; lobopodia (thick pseudopodia)
cyst = double walled
NO FLAGELATE FORM
other Acanthamoeba species
A. polyphaga
A. castellani
A. astronyxis
life cycle of Acanthamoeba
- entry via resp tract, broken skin, eye, maybeee genitourinary tract
- invasion of CNS, eye, other organs
some nasopharyngeal carriers are completely healthy
pathogenesis of Acanthamoeba
slow tissue invasion (weeks to months)
- adhesion (mannose binding proteins/mannose glycoprotein receptors on cornea
- destruction of corneal epithelium/upregulation of MMPs (matrix metalloproteinases) w release of mannose induced protein 133 + activation of phospholipases and release of collagenases and other proteases = APOPTOSIS
- breaching Bowman’s capsule and destruction of corneal stroma
= usually does not become intraocular
pathology of infections caused by Acanthamoebaspecies
Granulomatous Amebic Encephalitis (GAE) = necrotizing lesions/focal hemorrhages; MOST severe, most fatalities; slow
Eye lesions =
- inflammation
- full thickness corneal ulcers and keratitis (inflammation of the cornea)
- necrosis and full thickness destruction of the eye
Granuloma formation (skin, kidneys, liver, uterus, prostate) = necrotizing lesions/focal hemorrhages
clinical presentation of GAE
granulomatous amoebic encephalitis, or meningoencephalitis
- slow (weeks – months); unlike Naegleria
- progressive tissue invasion and destruction in immunocompromised host
- RARE but serious! almost always leads to death of human
- treatment ineffective
