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Amoebiasis
(Amoebic dysentery)
Amoebiasis
Causal agent: Entamoeba histolytica is well
recognized as a pathogenic amoeba.
History: Loosh was first described in 1875
“Harbouring of protozoa E. histolytica inside the body
with or without disease”
 only 10% of infected develop disease
 two types of infection
-Extra-intestinal
-Intestinal- mild to fulminant
Causative agent:
Entamoeba histolytica
Taxonomic Classification
Kingdom:
Subkingdom
Phylum
Subphylum
Class
Order
Family
Genus
Species
Protista
Protozoa
Sarcomastigophora
Sarcodina
Lobosea
Amoebida
Endamoebidae
Entamoeba
histolytica
Etiology:
Five species of Entamoeba:
E. histolytica (Pathogenic),
E. dispar
E. coli,
E. hartmanni,
E. gingivalis
Life cycle
cyst postcyst
precyst large trophozoite
Morphology
•Different form of E. histolytica;
• 1- trophozoite
• 2- precyst
•3- cyst(1, 2, 4 nuclei)
Trophozoite characteristics
• Size: 12-60μm in diameter;
• Non-invasive form ( minuta) / E. dispare
• Invasive form (magna) contain RBC, E. histolytica
• Pseudopodia:
• Motility:
Ectoplasm:
• Endoplasm: may be contain ingested RBC
• Nucleoplasm:
Non-invasive form
invasive form
Trends of Amoebiasis
Magnitude
Global: - worldwide in distribution
- 3rd most common parasitic death
- India, China, Africa, South America
- 2-60% prevalence
- 100,000 deaths/year
- 500 million infections
- 50 million cases
India: - 15% prevalence (3.6-47.4%)
- variation according to sanitation
Epidemiological determinants
Entamoeba histolytica
 7 zymodemes pathogenic
 two forms –
- trophozoite (vegetative)-fragile
- cyst -this is the infective stage
• -survives for weeks if appropr. envi
• -infective dose can be a single cyst
 source of infection is a case or carrier
-1.5*107 cysts per day
 reservoir is only human –several years
 resistant to chlorine in normal conc.
 readily killed by freezing or heating(55°C)
Incubation period:
3 days in severe
infection;
several months in
sub-acute and chronic
form.
In average case vary
from 3-4 weeks.
Period of
communicability:
For duration of the
illness.
Mode of Transmission
1-driect contact of person to person( fecal-
oral)
2- Veneral transmission among homosexual
males(oral-anal)
3- Food or drink contaminated with feces
containing the E.his. cyst
4- Use of human feces (night soil) for soil
fertilizer
5- contamination of foodstuffs by flies, and
possibly cockroaches, rats, etc.
• Host
 All age groups affected
 No gender or racial differences
 Institutional, community living,
Severe if children, old, pregnant,
Develops antibodies in tissue invasion
• Environment
 Low socio-economic
 Poor sanitation, sewage seepage
 Night soil for agriculture
 Seasonal variation
Host Factor Contributions
•Several factors contribute to influence infection
1 Stress
2 Malnutrition
3 Alcoholism
4 Corticosteroid therapy
5 Immunodeficiency
6 Alteration of Bacterial flora
Risk factors
• People in developing countries that have
poor sanitary conditions
• Immigrants from developing countries
• Travellers to developing countries
• People who live in institutions that have
poor sanitary conditions
• HIV-positive patients
• homosexuals
Clinical features
Intestinal
•Asymptomatic
carriers
• Amoebic colitis
• Fulminant colitis
• Amoeboma
Extra intestinal
• Liver
• Lung
• Brain
• Skin
Non Invasive Forms:
Asymptomatic carriers
- 90% without symptoms
- does not damage lumen
Invasive forms:
Amoebic colitis
- flask shaped ulcers superficial or deep
- abd pain, diarrhoea, blood, fever
- peri-anal ulcers
Fulminant colitis - <0.5%
- severely ill with high fever
- intestinal bleeding
- perforation
- paralytic ileus
Amoeboma
- 1% of cases
- inflammatory thickening of intestinal wall
- palpable mass with trophozoites
Symptoms of amoebic colitis
Symptoms Percentage
1. Diarrhea 100
2. Dysentery 99
3. Abdominal pain 85
4. Fever 68
5. Dehydration 5
6. Length of symptoms 2 to 4 weeks
Symptom Bacillary dysentery Amoebic dysentery
Onset Acute Gradual
General
Condition
Poor Normal
Fever High grade Little fever (adult)
Tenesmus Severe Moderate
Dehydration Frequent Little dehydration
(adult)
Faeces No trophozoites Trophozoites present
Culture Positive Negative
Extra-intestinal
Amoebic liver abscess
- via portal system
- 5% of invasive disease
- 10 times more common in men
Pleuropulmonary
- direct spread from liver abcess (10%)
- haematogenous spread
Brain
- abrupt onset & rapid progression
- death in 12-72 hrs
Virulence factors
•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
Cysteine proteinase - Complement factor C3
•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.
Zymodeme
•Zymodeme: Populations of
parasites with identical isoenzymes.
•Based on Electrophoretic mobility
E.histolytica strains are classified into
22 Zymodemes
•However only 9 are invasive
Invasive x Noninvasive strains
•The invasive and non invasive
strains may appear identical
may represent two distinct
species
•1. Invasive strain –
E.histolytica
•2. Non invasive strains
reclassified as E.dispar.
Pathogenesis
Effective factors:
1- strain virulence:
- classic strain
- non-classic strain; Laredo , Huff, ….
- pathogen zymodemes
2- susceptibility of the host; nutrition status, immune-sys.
3- breakdown of immunologic barrier (tissue invasion)
Pathogenicity mechanisms
• 1- secreting proteolytic enzymes( histolysine )
and cytotoxic substances.
• 2 - contact-dependent cell killing
• 3 – cytophagocytosis
Amebic killing target cell:
• 1- Receptor-mediated adherence of amebae to target cell (adherence
lectin)
• 2- Amebic cytolysis of target cell
• 3- Amebic phagocytosis of killed target cell
Clinical manifestation
A. Acute amoebic dysentery
Slight attack of diarrhea, altered
with periods of constipation and
often accompanied by tenesmus.
Diarrhea, watery and foul-smelling
stools often containing blood-
streaked mucus.
Diarrhea, watery and foul-smelling
stools often containing blood-
streaked mucus.
Nausea, flatulence and abdominal
distension, and tenderness in the
right iliac region over the colon.
B. Chronic amoebic dysentery
Attack of dysentery lasting for several days,
usually succeeded by constipation.
Tenesmus accompanied by the desire to
defecate.
Anorexia, weight loss and weakness.
Liver maybe enlarged.
The stools at first are semi-fluid but soon
become watery, blood, and mucoid.
Vague abdominal distress, flatulence,
constipation or irregularity of the bowel.
Mild anorexia, constant fatigue and lassitude
Abdomen lost its elasticity when picked---up
between fingers.
On sigmoidoscopy, scattered ulceration with
yellowish and erythematous border.
Gangrenous type of stool
Diagnosis
 Diagnosis
- fresh mucus or rectal ulcer swab
- colourless motile trophozoites with RBC
- quadrinucleated cysts
 Serology –IHA, ELISA
- usually negative in intestinal
Quadrinucleated cyst
Drug
Metronidazole Tinidazole Iodoquinol Diloxanide
furoate
Acts
on
Kills
trophozoites in
intestine & tissue
Kills
trophozoites
in intestine &
tissue
Luminal-
Eradicate
cysts
Luminal-
Eradicate
cysts
Dose 500-750 mg PO
tid x 5-10 days
600 mg bd
PO x 5 days
650 mg PO
tid x10days
500 mg PO
tid x10days
Treatment
- symptomatic cases
- asymptomatic in non-endemic areas
- asymptomatic if food handlers
Prevention & Control
Primary prevention
- Safe excreta disposal
- Safe water supply
- Hygiene
- Health education
Secondary
- Early diagnosis
- Treatment
Primary prevention
Sanitation Water Food hygiene H edu.
-excreta -protect -protect food -long
-wash hands -sand filter -acetic acid term
-latrines -boiling -detergent
-food handlers
examine
treat
educate
Amoebiasis

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Amoebiasis

  • 2. Amoebiasis Causal agent: Entamoeba histolytica is well recognized as a pathogenic amoeba. History: Loosh was first described in 1875 “Harbouring of protozoa E. histolytica inside the body with or without disease”  only 10% of infected develop disease  two types of infection -Extra-intestinal -Intestinal- mild to fulminant
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  • 6. Etiology: Five species of Entamoeba: E. histolytica (Pathogenic), E. dispar E. coli, E. hartmanni, E. gingivalis
  • 8. Morphology •Different form of E. histolytica; • 1- trophozoite • 2- precyst •3- cyst(1, 2, 4 nuclei)
  • 9. Trophozoite characteristics • Size: 12-60μm in diameter; • Non-invasive form ( minuta) / E. dispare • Invasive form (magna) contain RBC, E. histolytica • Pseudopodia: • Motility: Ectoplasm: • Endoplasm: may be contain ingested RBC • Nucleoplasm: Non-invasive form invasive form
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  • 13. Magnitude Global: - worldwide in distribution - 3rd most common parasitic death - India, China, Africa, South America - 2-60% prevalence - 100,000 deaths/year - 500 million infections - 50 million cases India: - 15% prevalence (3.6-47.4%) - variation according to sanitation
  • 14. Epidemiological determinants Entamoeba histolytica  7 zymodemes pathogenic  two forms – - trophozoite (vegetative)-fragile - cyst -this is the infective stage • -survives for weeks if appropr. envi • -infective dose can be a single cyst  source of infection is a case or carrier -1.5*107 cysts per day  reservoir is only human –several years  resistant to chlorine in normal conc.  readily killed by freezing or heating(55°C)
  • 15. Incubation period: 3 days in severe infection; several months in sub-acute and chronic form. In average case vary from 3-4 weeks. Period of communicability: For duration of the illness.
  • 16. Mode of Transmission 1-driect contact of person to person( fecal- oral) 2- Veneral transmission among homosexual males(oral-anal) 3- Food or drink contaminated with feces containing the E.his. cyst 4- Use of human feces (night soil) for soil fertilizer 5- contamination of foodstuffs by flies, and possibly cockroaches, rats, etc.
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  • 18. • Host  All age groups affected  No gender or racial differences  Institutional, community living, Severe if children, old, pregnant, Develops antibodies in tissue invasion • Environment  Low socio-economic  Poor sanitation, sewage seepage  Night soil for agriculture  Seasonal variation
  • 19. Host Factor Contributions •Several factors contribute to influence infection 1 Stress 2 Malnutrition 3 Alcoholism 4 Corticosteroid therapy 5 Immunodeficiency 6 Alteration of Bacterial flora
  • 20. Risk factors • People in developing countries that have poor sanitary conditions • Immigrants from developing countries • Travellers to developing countries • People who live in institutions that have poor sanitary conditions • HIV-positive patients • homosexuals
  • 21. Clinical features Intestinal •Asymptomatic carriers • Amoebic colitis • Fulminant colitis • Amoeboma Extra intestinal • Liver • Lung • Brain • Skin
  • 22. Non Invasive Forms: Asymptomatic carriers - 90% without symptoms - does not damage lumen Invasive forms: Amoebic colitis - flask shaped ulcers superficial or deep - abd pain, diarrhoea, blood, fever - peri-anal ulcers Fulminant colitis - <0.5% - severely ill with high fever - intestinal bleeding - perforation - paralytic ileus
  • 23. Amoeboma - 1% of cases - inflammatory thickening of intestinal wall - palpable mass with trophozoites Symptoms of amoebic colitis Symptoms Percentage 1. Diarrhea 100 2. Dysentery 99 3. Abdominal pain 85 4. Fever 68 5. Dehydration 5 6. Length of symptoms 2 to 4 weeks
  • 24. Symptom Bacillary dysentery Amoebic dysentery Onset Acute Gradual General Condition Poor Normal Fever High grade Little fever (adult) Tenesmus Severe Moderate Dehydration Frequent Little dehydration (adult) Faeces No trophozoites Trophozoites present Culture Positive Negative
  • 25. Extra-intestinal Amoebic liver abscess - via portal system - 5% of invasive disease - 10 times more common in men Pleuropulmonary - direct spread from liver abcess (10%) - haematogenous spread Brain - abrupt onset & rapid progression - death in 12-72 hrs
  • 26. Virulence factors •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
  • 27. Cysteine proteinase - Complement factor C3 •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.
  • 28. Zymodeme •Zymodeme: Populations of parasites with identical isoenzymes. •Based on Electrophoretic mobility E.histolytica strains are classified into 22 Zymodemes •However only 9 are invasive
  • 29. Invasive x Noninvasive strains •The invasive and non invasive strains may appear identical may represent two distinct species •1. Invasive strain – E.histolytica •2. Non invasive strains reclassified as E.dispar.
  • 30. Pathogenesis Effective factors: 1- strain virulence: - classic strain - non-classic strain; Laredo , Huff, …. - pathogen zymodemes 2- susceptibility of the host; nutrition status, immune-sys. 3- breakdown of immunologic barrier (tissue invasion)
  • 31. Pathogenicity mechanisms • 1- secreting proteolytic enzymes( histolysine ) and cytotoxic substances. • 2 - contact-dependent cell killing • 3 – cytophagocytosis Amebic killing target cell: • 1- Receptor-mediated adherence of amebae to target cell (adherence lectin) • 2- Amebic cytolysis of target cell • 3- Amebic phagocytosis of killed target cell
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  • 44. Clinical manifestation A. Acute amoebic dysentery Slight attack of diarrhea, altered with periods of constipation and often accompanied by tenesmus. Diarrhea, watery and foul-smelling stools often containing blood- streaked mucus. Diarrhea, watery and foul-smelling stools often containing blood- streaked mucus. Nausea, flatulence and abdominal distension, and tenderness in the right iliac region over the colon.
  • 45. B. Chronic amoebic dysentery Attack of dysentery lasting for several days, usually succeeded by constipation. Tenesmus accompanied by the desire to defecate. Anorexia, weight loss and weakness. Liver maybe enlarged. The stools at first are semi-fluid but soon become watery, blood, and mucoid. Vague abdominal distress, flatulence, constipation or irregularity of the bowel. Mild anorexia, constant fatigue and lassitude Abdomen lost its elasticity when picked---up between fingers. On sigmoidoscopy, scattered ulceration with yellowish and erythematous border. Gangrenous type of stool
  • 46. Diagnosis  Diagnosis - fresh mucus or rectal ulcer swab - colourless motile trophozoites with RBC - quadrinucleated cysts  Serology –IHA, ELISA - usually negative in intestinal
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  • 55. Drug Metronidazole Tinidazole Iodoquinol Diloxanide furoate Acts on Kills trophozoites in intestine & tissue Kills trophozoites in intestine & tissue Luminal- Eradicate cysts Luminal- Eradicate cysts Dose 500-750 mg PO tid x 5-10 days 600 mg bd PO x 5 days 650 mg PO tid x10days 500 mg PO tid x10days Treatment - symptomatic cases - asymptomatic in non-endemic areas - asymptomatic if food handlers
  • 56. Prevention & Control Primary prevention - Safe excreta disposal - Safe water supply - Hygiene - Health education Secondary - Early diagnosis - Treatment
  • 57. Primary prevention Sanitation Water Food hygiene H edu. -excreta -protect -protect food -long -wash hands -sand filter -acetic acid term -latrines -boiling -detergent -food handlers examine treat educate