Intestinal Amoebae

Question 1

E. histolytica morphology

Answer 1

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

Question 2

helical bodies made of RNA - later aggregating to crystalline array

Answer 2

chromatoidal bars
visible in young cells and disappear once cysts ages

Question 3

T or F. E. histolytica cysts do not transition in hot climates such as Saudi Arabia

Answer 3

T! temp only ranges from -5 to 40C

Question 4

process of infection and diseases from E. histolytica

Answer 4

action of trophs that have been released from cysts swallowed by a person

Question 5

E. histolytica cysts

Answer 5

environmentally hardy; survive journey from stomach to intestine

and then encyst again when leaving body

Question 6

factors that stimulate E. histolytica encystation

Answer 6

• dehydration of feces
• excess or deficiency of nutrients
• overpopulations
• bacterial metabolic products
• change in pH, O2 tension

Question 7

life cycle of E. histolytica

Answer 7

• ingestion of cysts
• excystation
  > alk pH in small gut, change in osmotic conditions, enzymes of intracystic organisms - chitinases = releases trophs

causes

Question 8

causes flask-shaped ulcers

Answer 8

E. histolytica
- flask = large cavity where amoeba eat their way through epithelium and tissues (practically full thickness of colon; but narrow point of entry)

Question 9

what happens when flask-shaped ulcers coalesce?

Answer 9

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

Question 10

how does E. histolytica spread?

Answer 10

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

Question 11

acute vs chronic E. histolytica

Answer 11

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

Question 12

mechanism of invasion of E. histolytica

Answer 12

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

Question 13

what is the essential step for invasion of E. histolytica

Answer 13

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

Question 14

contact-mediated cytolysis

Answer 14

• 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

Question 15

E. histolytica disruption of barriers

Answer 15

hylarunodisae
trypsin, pepsin
gelatinase
collagenase
B-n-acetyl glucosaminases

= disrupt bonds between adjacent intestinal cells and basement membrane

Question 16

history of E. histolytica

Answer 16

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

Question 17

reclassifiction of Entamoeba after zymodemes

Answer 17

E. histolytica = pathogenic

E. dispar = non-pathogenic

NOTE: problems with differentiation in diagnostic laboratories (morphologically; looks identical in stool)

Question 18

pathogenesis of Entamoeba

Answer 18

invasiveness also depends on host factors
- malnutrition/young age
- corticosteroids (depresses host immunity)
- pregnancy/puerperium
- genetics/HLA antigens (resistance to infection)

Question 19

infective dose of E. histolytica

Answer 19

can be 1 cyst or >/= 1000

Question 20

intestinal lesions caused by E. histolytica

Answer 20

• hallmark = flask-shaped ulcers (cecum, appendix, upper colon)
  > coalescence
  > perforation through full thickness of gut
• dissemination
  contiguous or direct spread

Question 21

T or F. amoebic lesinos can be found outside of the colon

Answer 21

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)

Question 22

T or F. Amoebic intestinal infections can clear up spontaneously

Answer 22

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

Question 23

onset of E. histiolytica

Answer 23

baries but usually 2 wks - 4 months post exposure

dependent on host immune system and other factors

Question 24

asymptomatic form of E. histolytica

Answer 24

people can be asymptomatic carriers

Question 25

non-dysenteric form of E. histolytica

Answer 25

diarrhea/constipation, cramps
depression, loss of weight

Question 26

dysenteric form of E. histolytica

Answer 26

10-20+ stools/day
blood, mucus, pus
cramps, painful defecation, fever

Question 27

extraintestinal amoebiasis symptoms

Answer 27

dependent on where the abscess is

hepatic = fever, pain, liver enlargement, someitmes jaundice

lungs = chest pain, fever cough

brain = pressure effects ; varies (ex: optic nerve = vision problems)

skin/genital ulcers

Question 28

epidemiology of E. histolytica

Answer 28

• predominantly human but believed that old world monkeys can serve as reservoir
• 10% of worlds population
• risk groups = institutionalized, MSM (up to 40%), recent immigrants from endemic areas

Question 29

highest prevalence of E. histolytica found in this age gorup

Answer 29

20-30 y/o

Question 30

Transmission of E. histolytica

Answer 30

fecal-oral (does not include torphs)

can also be: direct (incl. sexual), food + drink, mechanical vectors, fomites

Question 31

T or F. amoebic cysts survive nicely in ice cubes

Answer 31

T!

Question 32

E. histolytica prevention

Answer 32

• eradicating fecal contamination of food and water = improved hygiene, sanitation, water treatment, etc.
• amoebic cysts are not killed by soap or lowcencration chlorine/iodine so water should be BOILED for more than 1 minute & veggies should be washed with detergent soap and soaked in acetic acid for 10-15 mins or COOKED
• non-endemic areas = disease transmission can be reduced by early treatment of carriers

Question 33

diagnosis of E. histolytica

Answer 33

• stool microscopy (does not distinguish bw E. histolytica and dispar)
• biopsy (extraintestinal)
• serology = can distinguish
• PCR = can distinguish

Question 34

anchovie paste appearance

Answer 34

liver abscess from E. histolytica = brownish thick paste (lots of trophs)