Intestinal Amoebae Flashcards
E. histolytica morphology
troph = nucleus and food vacuoles, RBC, granules
cyst = chitin wall, chromatoidal bar, glycogen vacuole
- precyst, metacyst, mature cyst
- mature cyst = thick protective wall= resistant to enzymes and chlorination
resistance to adverse conditions (weeks to months)
temp range = -5C to 40C
helical bodies made of RNA - later aggregating to crystalline array
chromatoidal bars
visible in young cells and disappear once cysts ages
T or F. E. histolytica cysts do not transition in hot climates such as Saudi Arabia
T! temp only ranges from -5 to 40C
process of infection and diseases from E. histolytica
action of trophs that have been released from cysts swallowed by a person
E. histolytica cysts
environmentally hardy; survive journey from stomach to intestine
and then encyst again when leaving body
factors that stimulate E. histolytica encystation
- dehydration of feces
- excess or deficiency of nutrients
- overpopulations
- bacterial metabolic products
- change in pH, O2 tension
life cycle of E. histolytica
- ingestion of cysts
- excystation
> alk pH in small gut, change in osmotic conditions, enzymes of intracystic organisms - chitinases = releases trophs
causes
causes flask-shaped ulcers
E. histolytica
- flask = large cavity where amoeba eat their way through epithelium and tissues (practically full thickness of colon; but narrow point of entry)
what happens when flask-shaped ulcers coalesce?
can connect with each other; still small openings
can peel off entire surfaces of superficial epithelium to reveal large gaping wounds or cavities underneath
lethal complication of this
how does E. histolytica spread?
dissemination gut
dissemination through blood = trophs picked up as they erode blood vessels - spill over and can disseminate to other organs and create abscesses =brain or liver for example
dissemination through continuous spread = “continuous eating”; from transverse colon, through it and then go to diagram and then eat through it and directly invade lungs
acute vs chronic E. histolytica
crowding in the gut = too many trophs = start to encyst = hallmark of chronic stage
acute = excrete trophs in the feces mostly; not infectious bc trophs don’t survive outside gut
BUT once chronic = start passing cysts and can contaminate environment and wait for cysts to be picked up by another host through contaminated food or water
mechanism of invasion of E. histolytica
Step 1. Adherence to colonic mucus layer
Step 2. Disruption of intestinal barriers via proteolytic enzymes and toxins
Step 3. Contact-mediated killing of cells (intestinal epithelium, other cells) by APOPTOSIS
= resulting in ulceration, organ/tissue invasion
what is the essential step for invasion of E. histolytica
adherence (gut epi)
mediated by galactose/n-acetyl-d-galactosamine adherence lectin
must first overcome first layer of defence of gut (thich mucin gel); blocks lectin receptor so cysteine protease (ehcp 5) helps with this
> secretory IgA produced locally on coloinic mucosa = prevent first step
contact-mediated cytolysis
- lethal hit
- galactose/galactosamine lectin & filopodia (acting as triggers for amoebic surface active lysosomes)
phospholipase A
other lysosomal constituents (incl. pore-forming proteins - amoebapores A,B,C)
they disrupt target cell membranes and rendering cell permeable to Ca2+ = when calcium increases inside activate host cells and endogenous DNA proteases, phospholipases, etc. = target cell death
E. histolytica disruption of barriers
hylarunodisae
trypsin, pepsin
gelatinase
collagenase
B-n-acetyl glucosaminases
= disrupt bonds between adjacent intestinal cells and basement membrane
history of E. histolytica
E. dispar - not doing much
E. dysenteriae = bloody diarrhea
lumped together = E. histolytica
zymodees
= electrophorestic enzyme patterns
- over 20 (isoenzyme patterns) recognized, but only 1/3 associated with invasiveness
reclassifiction of Entamoeba after zymodemes
E. histolytica = pathogenic
E. dispar = non-pathogenic
NOTE: problems with differentiation in diagnostic laboratories (morphologically; looks identical in stool)
pathogenesis of Entamoeba
invasiveness also depends on host factors
- malnutrition/young age
- corticosteroids (depresses host immunity)
- pregnancy/puerperium
- genetics/HLA antigens (resistance to infection)
infective dose of E. histolytica
can be 1 cyst or >/= 1000
intestinal lesions caused by E. histolytica
- hallmark = flask-shaped ulcers (cecum, appendix, upper colon)
> coalescence
> perforation through full thickness of gut - dissemination
contiguous or direct spread
T or F. amoebic lesinos can be found outside of the colon
extraintestinal amoebic abscess
location = liver, lung, sometimes brain, skin, and penis
structure = centre- necrotic fluid, outside - liver tissue and active trophozoites
move radially when want to look for amoebae = aspirate edges not middle (just necrotic fluid)
T or F. Amoebic intestinal infections can clear up spontaneously
T! Does not mean that it cannot come back in the form of distant abscess much later
Ex: can just have upset stomach on vacation then come home, several months later = brain abscess from amoebic trophs that managed to get from gut to blood all the way to brain
onset of E. histiolytica
baries but usually 2 wks - 4 months post exposure
dependent on host immune system and other factors
asymptomatic form of E. histolytica
people can be asymptomatic carriers
