Entamoeba histolytica is a protozoan parasite that causes amoebiasis through fecal-oral transmission. It has a lifecycle involving an infective cyst stage and pathogenic trophozoite stage. Trophozoites cause intestinal and extra-intestinal disease through virulence factors like cysteine proteases. Symptoms range from mild diarrhea to severe colitis, liver abscesses, or other extra-intestinal complications. Diagnosis involves microscopy, antigen detection in stool, or serology. Treatment involves luminal agents like diloxanide furoate or tissue agents like metronidazole. Prevention relies on proper hygiene and sanitation practices.

1. By
B.Devadatha
123680029
M.Sc BMB 2nd sem
Pondicherry university

3.  Introduction
 Etiology
 Transmission
 Lifecycle
 Pathogenesis
 Virulence factors
 Clinical features
 Complications
 Diagnosis
 Treatment and Prophylaxis

4.  Amoebiasis is a protozoan infection of the intestinal
tract that occurs due to ingestion of foods or water
contaminated with Entamoeba histolytica cysts.
 Entamoeba histolytica was described by Lambl in1859
and Losch established its pathogenic nature.
 Councilman and Laufler in 1981 described liver
abscess
 Humans are the only host of E.histolytica and no
zoonotic reservoirs .
 There are an estimated 50million cases of amebiasis
per year upto 10,0000 deaths

5.  species of Entamoeba:
◦ Nonpathogenic: E. dispar, E. coli, E. hartmanni
◦ Pathogenic: E. histolytica , Dientamoeba fragilis,
which causes Dientamoebiasis
 amoebiasis = A Parasitic infection caused by the
protozoan Entamoeba histolytica
◦ 2nd to Malaria as protozoan cause of death worldwide
 10% of world’s population infected – Increased
prevalence in developing countries (up to 25%)

6.  Amoebiasis is usually transmitted by the fecal-
oral route
 indirectly through contact with dirty hands or
objects
 Infection is spread through ingestion of the cyst
form of the parasite, a semi-dormant and hardy
structure found in feces.
 transmitted through contaminated food and water

7. Precysticstage:
 Trophozoites living in the intestine undergo binary fission
 Round and 10-20µ in size
 Store glycogen granules and chromatoid bodies
Cystic stage:
 Enters by forming a delicate cystwall around itself
 Size is 12µ
 Quadrinucleated cyst is the infective stage of the parasite
 Ingested by human host pass along with food into the small
intestine
 Wall of cyst dissolved by trypsin
 Tetranucleate emerges out from cyst into lumen of large
intestine called excystment

8.  Metacystic amoeba with four cystic nuclei from each
cyst
 8 Small trophozoites from each metacystic amoeba
The Trophozoite Stage:
 10-40 µm, fragile.
 Uninucleate.
 Erythrophagocytosis.
 Reside, feed and multiply by binary fission in lumen
of colon.
 May invade – Lytic & physical mechanisms and
metastasize to liver and other extra-intestinal sites.
 Galactose-containing molecules & receptors regulate cyst
formation.

10.  The spherical structure (Trophozoites) has one
basophilic nuclei about the size of RBC’s. Note some
RBC's are phagocytosed by the Trophozoites
(erythrophagocytosis).

11.  Trophozoites of E.histolytica interact with host through
a series of steps
1. Adhesion of target cell, phagocytosis and cytopathic
effect
2. E.histolytica induces both Humoral and cell mediated
immune responses.
3. Virulence factors – In many circumstances lumen
dwelling Amoeba may be asymptomatic
4. Causes disease only when invade the Intestine
5. Virulence is associated with secretion of Cysteine
proteniase which assists the organism in digesting the
extracellular matrix and invading tissues

12.  It is observed Cysteine proteinase produced by invasive
strains of E.histolytica inactivates the complement
factor C3 and are thus resistant to Complement
mediated lysis.

14.  Trophozoites adhere to colonic mucosal glycoproteins via a
galactose and N-acetyl-D-galactosamine-specific lectin.
 Adherence results in cell lysis (apoptosis) and PMN invasion.
 PMN’s are then lysed releasing lytic enzymes, causing more
tissue destruction.
 Small foci of necrosis in the intestinal wall coalesce to form
ulcers (Flask-shaped ulcers).
 Parasites resist destruction by complement arm of immune
system via Gal/GalNac mediated inhibition of the membrane
attack complex.
 Cell-mediated immunity is important in clearing infection
through generating γ-INF and TNF-α to activate macrophages
and Neutrophils to kill the trophozoite.

15.  Area most commonly involved = Cecum, then Recto-
sigmoid area.
 May invade blood vessels causing thrombosis,
infarction and dissemination via portal circulation to
liver and extra-intestinal sites eg. brain, pleura,
pericardium and genito-urinary system.
Flask-shaped ulcers

16.  Most cases of amebiasis have very mild symptoms or
none.
 More severe infection may cause fever, profuse
diarrhea, abdominal pain, jaundice, anorexia, and
weight loss.
 In severe cases, it can lead to development of abscesses
(pockets of amoebae and inflammatory cells) in the
liver or, more rarely, the brain.

17. Complications of Intestinal amoebiasis:
◦ Fulminant Amoebic Colitis with Perforation
 May have a mortality rate of up to 50%
 Children less than 2 yrs at increased risk of perforation
◦ Massive Haemorrhage
 Due to vasculitis of large arteries or multiple ulcers leading
to small arterial leaks
◦ Amoebomas
 A granulomatous thickening of the colon resulting from lytic
necrosis followed by secondary pyogenic inflammation,
leading to fibrosis and proliferative granulation tissue.
Lesions are firm, hard, may resemble a carcinoma.
◦ Amoebic Stricture
 Resulting from fibrosis of intestinal wall. Can involve
rectum, anus or sigmoid.

18. Complications of Extra-Intestinal Amoebiasis:
◦ Amoebicliverabscess
 Commonly found in Right Lobe of liver
 Presents acutely with high fever, RUQ tenderness
 Jaundice an unusual findings
◦ amoebic Peritonitis
 As a complication of a ruptured hepatic abcess
◦ Pleuropulmonary amoebiasis
 Caused by rupture of Rt. Lobe Liver abcess in 10% of patients
 Has cough, pleuritic chest pain & dyspnoea
◦ amoebic Pericarditis
 Rupture left lobeliverabscess
◦ Cerebral amoebiasis
 Rare, has altered consciousness and focal neuro signs
o Genito-Urinary Involvement
 Painful genital ulcers – Punched out appearance & profuse
discharge

19.  Light Microscopy of Stool
◦ Identification of trophozoites / cysts in fresh stool
Disadvantages:
Not sensitive (miss up to two thirds of infections)
Cannot distinguish between E.histolytica and E. dispar
 Serology:
◦ Anti-amoebic antibodies (IgM) 70%
◦ Sensitive for amoebic colitis & 90%
◦ For liverabscess
 Stool antigen-detection test
◦ Sensitive and Specific
A sample of freshly collected
Fecal specimen

20. Luminal Amebicides
 Acts on the parasites in the lumen of the bow
 Diloxanide Furoate
 Iodoquinol
Tissue Amoebicides
 Acts on the intestinal wall and liver
 Emetine
 Dehydroemetine
 Chloroquine
Mixed amoebicides
 Metronidazol
 Tinidazole

21.  Drink only bottled or boiled (for 1 minute) water, or
carbonated (bubbly) drinks in cans or bottles.
 Avoid fresh fruit or vegetables that were peeled by
someone else.
 Avoid milk, cheese, or dairy products that may not
have been pasteurized.
 Avoid anything sold by street vendors.

22.  Thoroughly cook all raw foods.
 Thoroughly wash raw vegetables
and fruitchanging diapers, after
smoking or after using a tissue or
handkerchief. s before eating.
 Reheat food until eaches at least
167º Fahrenheit.
 Wash your hands before preparing
food, before eating, after going to
the toilet or