Vl 5 Entamoeba

Question 1

Describe the principles of tissue invasion by Entamoeba histolytica.

Answer 1

1) sticks to mucus in intestine
2) degrades MUC2 mucins with cystein protease ⇒ inserts amoebapore to destroy the adhered (intestinal epithelial) cell (no receptor required)
3) subversion of the immune reaction: CP cleaves pIL-1 to IL-1 ⇒ activates NFkB in neighboring cells ⇒ produce cytokines and inflammatory mediators
4) Neutrophils barge in between the epithelial cells and and are swallowed by Entamoeba
5) dying neutrophils contain mediators ⇒ further damage the cells and macrophages release TNFalpha ⇒ induces apoptose and inflammation
⇒ invasive amoebiasis of gut epithelium

can also travel to liver (but evolutionary dead end)

Question 2

How does Entamoeba dispar differ from Entamoeba histolytica?

Answer 2

E.histlytica potentially dangerous, E.dispar harmless

2% genetic difference, dispar doesnt have virulence factors

has lost Cystein protease CP5 or just did never have it

Question 3

How is an Entamoeba histolytica infection treated? How do the drugs work?

Answer 3

• NITROimidazolderivate
• activated by reduction in anaerobic milieu, destroy amoeba-DNA ⇒ no replication possible! - highly effective, no resistances known

Question 4

What are the main virulence factors in Entamoeba histolytica and how do they work?

Answer 4

• Surface Gal/GalNAc Lectins: bind to Gal/GalNAc of host cell mucus ⇒ causes cell death by Ca2+-influx in epithelial cells

Cystein proteases: destroy extracellular matrix (mucines)

Amoebapores: very unspecific, adhere to target cell’s membrane ⇒ lead to holes and cell death

• all 3 are used to breach through the epithel cells and lyse the cell-connective

Question 5

Describe the life cycle of Entamoeba

Answer 5

• Entamoeba transfered only between humans, fecal-oral
• 4-nuclei cyst (Dauerform) is infectious
• trophozoit bursts out of cyst, starts eating
• have multiple nuclei ⇒ single nucleus amoeba splits of
• multiplies and encysts