1. Dept. of Infectious Diseases
Amebiasis
PENG JIE
Associate Professor
Dept. of Infectious Diseases
Nanfang Hospital, SMU.

2. Prologue Parasite: amebiasis
Infectious diarrhea：pathogenic microorganism
Bacteria: bacillary dysentery
Virus: rotavirus, Infantile Diarrhea
Parasite: amebiasis ……
Noninfectious diarrhea: no pathogenic microorganism, toxic chemical, toxic mushroom

3. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

4. Outlines
Amoebiasis is a parasitic protozoan disease that affects the gut mucosa and liver, resulting in dysentery, colitis and liver abscess.
The causative agent, Entamoeba histolytica, is a potent pathogen that is spread via ingestion of contaminated food and water.
Globally, amoebiasis is highly prevalent, and is the second leading cause of death to parasitic disease. (second to malaria)

5. Outlines
In many cases, the parasite lives in a person's large intestine without causing any symptoms.
But sometimes, it invades the lining of the large intestine, causing bloody diarrhea, stomach pains, cramping, nausea, loss of appetite, or fever.
In rare cases, it can spread into other organs such as the liver, lungs, and brain.

6. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

7. Etiology
The causative organism is parasitic protozoan, called Entamoeba histolytica.
What was once thought to be a single entity, is now recognised as two morphologically identical but genetically distinct forms; E. histolytica (pathogen) and E. dispar (commensal).
The WHO recommendes that E. histolytica colonisation should be treated, however, treatment is unnecessary for E. dispar colonisation.
E. Histolytica

8. E. histolytica: morphology
15-50 mm
10-15 mm
The active trophozoite stage exists only in the host and in the fresh loose stool.
Cysts often found in the stool survive outside of the host, in water, soil and foods.

9. Fecal-oral life cycle Excystation Trophozoite Cyst Encystment
Passed in feces
Non motile
Resistant to hostile environment
Does not multiply
Metabolically active
Motile
Multiplies by binary fission

10. Entamoeba histolytica acute amoebic hepatitis
Life Cycle of
Entamoeba histolytica
acute amoebic hepatitis
amoebic liver abcess
amoebic dysentery

11. E. histolytica: life cycle
Ingestion of cyst in the contaminated water and food
Excystation occurs in the small intestine. Eight trophozoits produced from one cyst.
Trophozoits migrate to large intestine where they multiply or may encyst for excretion
Cysts exit hosts in the stool

12. Life cycle and transmission
Cysts are ingested via contaminated food or water. A refractile wall containing chitin, allows the cyst to survive stomach acid.
In the terminal ileum or colon, the parasite excysts and begins the trophozoite stage.
Trophozoites are highly motile and pleomorphic. They are unable to survive outside the human gut.
Energy is derived from the ingestion of bacteria and food particles. No mitochondria are present in trophozoites.
Trophozoites reproduce by binary fission and encyst in the colonic wall. Cysts are passed in the stool and may remain viable for weeks or months in an appropriately moist environment where they become infectious.

13. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

14. Epidemiology Sources of Infection
Human beings, and perhaps some non-human primates, are the only natural hosts.
symptomatic or asymptomatic carrier
Routes of Infection
Mostly by ingestion of food or water contaminated with faeces containing E. histolytica cysts.
Other risk factors include oral and anal sex, and contact with contaminated enema apparatus.
Susceptible Population
Although anyone can have this disease, it is more common in people who live in tropical areas with poor sanitary conditions.

15. Epidemiology Epidemiologic Feature
E. histolytica is distributed throughout the world, and is a substantial health risk in almost all countries where the barriers between human faeces and food or water are inadequate.
Amoebiasis is found primarily in developing tropical and subtropical countries where sanitation is poor, leading to a direct link between faeces and ingestion.

16. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

17. Pathogenesis and pathology
Amoebic trophozoites invade the colon causing colitis. They may also invade the portal circulation and travel to the liver, causing liver abscess.
The spectrum of colitis in amoebiasis ranges from mucosal thickening, to diffuse Inflammation / edema, to necrosis and perforation of colonic wall.
Trophozoites invade through to the submucosa causing flask shaped ulcers.
Most frequently involves the cecum and ascending colon followed by sigmoid, rectum, appendix.
Amebas establish hepatic infection by ascending the portal venous system. The adjacent liver parenchyma is often completely unaffected.

18. Pathogenesis and pathology
Amoebic liver abscess
Histological cross section of classical flask shaped amoebic ulcer in colonic mucosa.
Amoebic colitis with multiple ulcer formation

19. This slide shows Amebiasis of the rectosigmoid junction
This slide shows Amebiasis of the rectosigmoid junction. Small superficial ulcerations are covered with white exudate and surrounded by an erythematous rim. Amebiasis caused by Entamoeba histolytica has a predilection for the cecal and rectosigmoid area.

20. Numerous eosinophilic spherical structure within necrotic area

21. The spherical structure (trophozoites) has one basophilic nuclei about the size of RBC’s. Note some RBCs are phagocytized by the trophozoites (erythrophagocytosis).

22. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

23. Clinical manifestations of intestinal amebiasis
Some individuals carry E. histolytica asymptomatically % will go on to develop the disease within a year. Incubation is 4 days to 1 year, average 3 weeks
Gradual onset (weeks) of bloody diarrhoea, occasionally with small volumes of mucoid stool.
If blood is not visible, stool is usually ‘haem’ positive due to the breach of the mucosa. Leucocytes and pus may be present in stool.
Abdominal pain and tenderness. Fever, Weight loss and anorexia

24. Clinical manifestations of intestinal amebiasis
In more severe cases fulminant amoebic colitis develops. Liver involvement is more common in these cases, along with paralytic ileus, toxic megacolon and mucosal sloughing. Over 75% of patients with fulminant colitis develop intestinal perforation. It is a predisposition for occurring in malnourished pregnant women, recipients of corticosteroids
Local inflammatory masses, amoebomas, may cause obstructive symptoms.

25. Clinical manifestations of amebic liver abscess
More common in men
Liver abscess pan present in conjunction with bowel symptoms (10% of cases), or in isolation.
Sudden onset of upper abdominal pain with fever. Pain may radiate to right shoulder or be exacerbated by respiratory movements.
Hepatic tenderness may be present. Jaundice is unusual.
Complicated liver abscess may develop if abscess ruptures into the peritoneal, pericardial or pleural cavity. Morbidity and mortality is high.
Rarely, trophozoites may also invade the respiratory tract, brain and GU (genitourinary) tract

26. Symptoms of acute amebiasis
Organ involved
Symptoms
Abdominal pain; frequent bloody dysentery with necrotic mucosa
Small and large intestine

27. Symptoms of chronic amebiasis
Organ involved
Symptoms
Recurrent bloody and mucoid dysentery with intervening constipation; appendicitis; pseudopolyps; perforation
Small and large intestine
Liver
Abscess; hepatitis
Lung
Abscess; pneumonia
Brain
Abscess; encephalitis

28. Chronic amebiasis: mucosal erosion and crater formation

29. Chronic amebiasis: drainage of a liver abscess

30. Chronic amebiasis: drainage of a lung abscess

31. Chronic amebiasis: brain abscess

32. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

33. Amebiasis
A 37 years old businessman complains of central abdominal pain, diarrhea and flatulence of 10-days duration which started 2 days after returning from a trip to Central-South America. His wife and children who did not travel with him have no GI complaints. He has no fever and the physical examination is otherwise normal. The stool contains mucus and blood (leucocytes and monocytes).

34. Diagnosis
Clinical history is important. In low resource settings this may be the means of diagnosis. A good travel history is important as disease may develop years after a visit to an endemic area.
Primary diagnosis can be made by epidemiology history, clinical presentations including mucous and bloody, strawberry jam-like diarrhea. Definitive diagnosis should be confirmed by Laboratory Examinations.

35. Laboratory Examinations
Demonstration of E. histolytica in stool by microscopy (old), or ELISA assay for antigen detection. Trophozoites only survive for short periods of time, therefore, fresh stool samples should be used
Colonoscopy to confirm colitis and tissue biopsy for amoeba
Liver abscess; space occupying lesion on CT/USS with positive amoebic serology

36. E. Histolytica: the diagnostic features
When amebic dysentery is suspected, a fresh fecal sample or a swab should be examined under microscope.
If examined quickly the colorless motile trophozoite can be seen.
The motile trophozoite has one nucleus
H/E stained
Fresh sample

37. Amebiasis is different from giardiasis and bacterial dysentery
Amebiasis: Differential diagnosis
Amebiasis is different from giardiasis and bacterial dysentery
Mucus and blood in stool
No granulocytosis
No high fever
Appropriate culture of stool for bacterial pathogens and obtaining an amebic serologic examination can be definitive.

38. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

39. Treatment
Amoebiasis, in particular with liver involvement, can be fatal if not treated. Chemotherapy can effectively cure ameobiasis.
Iodoquinol and diloxanide furoate, paromomycin act on organisms in the intestinal lumen. Metronidazole, tinidazole, ornidazole, chloroquine, and dehydroemetine, are effective in the treatment of invasive amebiasis but less so against the organisms in the bowel lumen
Nitroimidazole (e.g.metronidazole) is used to treat the invasive pathogens.This is followed by a luminal agent (e.g.diloxanide furoate) to eliminate colonisation. Complicated liver abscesses should be drained surgically.

40. Drugs used to treat amoebiasis depend upon severity of disease

41. Prophylaxis
Better hygiene. Education for the general public in personal hygiene, particularly in sanitary disposal of feces, and in hand washing after defecation and before preparing or eating food
Efficient sewage treatment and disposal Protect public water supplies from fecal contamination

42. Contents Outlines Etiology Epidemiology Pathogenesis and pathology
Clinical manifestations
Diagnosis and differential diagnosis
Treatment and prophylaxis

43. Summary
Amoebiasis is a major global cause of mortality and morbidity, due to dysentery. The causative organism, E. histolytica.
E. histolytica has a biphasic life cycle and exists as an infective cyst and pathological trophozoite.
The disease is spread via contaminated food and water, usually due to poor sanitation.
The disease is found in tropical and sub-tropical parts of the world.
Patients usually present with abdominal pain, bloody stools and fever. Hepatic symptoms are more acute with upper abdominal pain and radiation to the right shoulder.
Treatment is with Nitroimidazole (e.g.metronidazole) and a luminal agent. Spread can be prevented by better hygiene.