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Amebiasis
-bhanu chalise
• Harboring(infection) of protozoa Entamoeba
histolytica inside the body with or without the
disease is called amoebiasis.
• Associated with high mortality and morbidity
• Major public health problem globally
• 2nd leading cause of death due to parasitic
disease ( 1st being malaria )
Epidemiology
• 10% of population infected globally
• About 100,000 deaths occur every year globally
• High prevalence in tropics and subtropics
• Risk factors:
Developing countries Developed countries
 travelers
 immigrants
 homosexual men
 HIV positive
 immunodeficiency states
poverty
Ignorance
overcrowding
Poor sanitation
malnutrition
Causative organism
3 species of entamoeba: E. dispar
: E. moshkovskii
: E. histolytica
Only E. histolytica is pathogenic. Other two
species are apparently non-pathogenic and
cause most of the asymptomatic cases.
Morphology
• Different form of E. histolytica:
1- trophozoite
2- precyst
3- cyst(1, 2, 4 nuclei)
• Quadrinucleated cyst is the infective stage
oval/round
resistant to chlorination
destroyed above 55 degree celsious and with disinfectants
• Trophozoite stage is feeding vegetative form which is
destructive to tissue
Trophozoites of Entamoeba histolytica with ingested
erythrocytes (trichrome stain)
The ingested erythrocytes appear as dark inclusions.
Erythrophagocytosis is the only morphologic characteristic that can be
used to differentiate E. histolytica from the nonpathogenic E.
dispar .
FE
Virulence factors
Trophozoites of E. histolytica interact with host
through a series of steps:
 Adhesion of target cell, cytopathic effect
 E.histolytica induces both Humoral and cell
mediated immune responses
 Causes disease only when invade the
Intestine
 Virulence is associated with secretion of
Cysteine proteinase (histolysin) which assists
the organism in digesting the extracellular
matrix and invading tissues
Cysts of Entamoeba histolytica
/E. dispar
• GHI
IHG
Cysts of Entamoeba histolytica/E.
dispar ,permanent preparations stained
with trichrome.
Transmission
1) feco-oral(direct hand-to-mouth contact)
2) Veneral transmission among homosexual males
3) Food or drink contaminated with feces containing the
E. histolytica cyst
4) Use of human feces (night soil) for soil fertilizer
5) contamination of foodstuffs by flies, and possibly
cockroaches
 a single cyst is sufficient to cause the disease
 Asymptomatic human( the only host) cyst
carriers are the principle reservoir of infection.
Pathogenesis
Ingestion of
cysts
Excystation in
small intestine
Production of 8
trophozoites
Multiplication
and Colonization
in large intestine
Tissue
invasion and
destruction
Flask – shaped
ulcers(mostly in
caecum, transverse
and sigmoid colon
Encystation
and exit from
host in the
stool
Migrate via
Blood stream(
portal
circulation) to
the liver Amoebic liver
abscess
Clinical features
Intestinal
• Asymptomatic
carriers(90%)
• Amoebic colitis
• Fulminant colitis
• Amoeboma
Extraintestinal
• Liver
• Lung
• brain
• skin
Incubation period : varies from weeks to months
: average= 3-4 weeks
Asymptomatic carriers
-90% without symptoms(non-invasive)
- lumen not damaged(cyst passers)
Invasive forms:
Amoebic colitis/dysentery
- flask shaped ulcers superficial or deep
- abd.pain, watery/mucoid blood-streaked foul-smelling diarrhoea
- fever, tenesmus, peri-anal ulcers
- sometimes intermittent diarrhoea
alternating constipation
Fulminant colitis - <0.5%
- severely ill with high fever
- profuse bloody diarrhea
- perforation(diffuse tenderness)
- paralytic ileus
-pronounced leukocytosis
• ulcers with raised borders
• little inflammation between lesions
Amoeboma
- 1% of cases
- inflammatory thickening of intestinal wall
- palpable mass with trophozoites
Symptoms of amoebic colitis
Symptoms Percentage
Diarrhea 100
Dysentery 99
Abdominal pain 85
Fever 68
Dehydration 5
Complications: toxic megacolon, amoeboma,
cutaneous amoebiasis, rectovaginal fistula
Amoebic v^s Bacillary Dysentery
symptoms Amoebic dysentery Bacillary dysentery
Occurrence Usu. In the form of sporadic cases Usu. In the form of outbreaks
Onset gradual Acute
Fever Usu. Low grade (may be high in case
of liver abscess)
High grade
Tenesmus/Abd. Cramps Moderate Very severe
Stool Foul- smelling Not foul-smelling
RBCs In clumps Discrete
Pus cells Scanty Numerous
Eosinophils Present Absent or rare
Bacteria Numerous, motile Scanty, non-motile
E. histolytica Trophozoites + Absent
Growth on culture Negative Positive
Extra-intestinal
Amoebic liver abcess(most common)
- 5% of invasive disease
- 10 times more common in men
-Usually no bowel symptoms except sometimes
-right upper quadrant tenderness
- hepatomegaly
- jaundice(10- 15%)
Pleuropulmonary/pericardial
- direct spread(transdiaphragmatic rupture)
from liver abscess (10%)
- hematogenous spread
-cough with crepitation
Similarly infection can spread to
brain, skin and genitourinary system
Investigation
Parasite detection
Antibody detection
Antigen detection PCR and other tests
Investigation
Parasite detection
1. Direct saline(wet) mount of feces:
- most common microscopic technique
-sample examined within 1 hour of collection
-3 stool samples taken on consecutive day ( since
sensitivity increased from 60% to 90%)
-presence of ingested erythrocytes within trophozoites is
pathognomic for E. histolytica
-carriers have only cysts in their stool
 Misidentification: macrophages v^s trophozoites
: PMN v^s cysts
: other entamoeba
2. Various culture techniques are available but
not done routinely
Antibody detection tests
• Routinely employed for extra-intestinal dz
– Positive(75%)- at presentation and 90%- beyond
1st week of symptoms
– ELISA is most sensitive
– IHA
– Latex agglutination
– Immunoelectrophoresis and immunodiffusion
 Antigen detection
• ELISA kits( sensitivity>90%): used in
epidemiological studies ; useful in endemic
areas
• Antigen detection by ELISA: is the ideal test –
distinguishes current from past infection.
 PCR
 OTHER TESTS: chest radiograph
: CT , MRI
: sigmoidoscopy
: peripheral blood- leukocytosis
without eosinophillia, mild anemia
: Alp, ESR are common lab findings.
• raised immobile right diaphragm
• Other imaging modalities show
– A single abscess in the right or left
lobe
– Multiple lesions can be present
Imaging
None of these
modalities can
differentiate amebic
abscess from pyogenic
or malignant one
Treatment of amebiasis
-combination of a luminal and a tissue
amoebicide is advocated for complete parasite
clearance in Invasive disease
Luminal amoebicides
• Diloxanide furoate
• diiodoquinol
• paromomycin
Tissue amoebicides
• 5-nitroimidazoles(DOC)
-metronidazole
-tinidazole
-secnidazole
• Chloroquin
• Dehydroemetine
Amoebic colitis: metronidazole followed by a luminal agent
Fulminant amoebic colitis: add an antibiotic to deal with bowel flora
Amoebic liver abscess: tissue amoebicide followed by luminal agent
treatment continued…………………
Asymptomatic intestinal carriers : a luminal agent
Treatment for only E. dispar is not nessary
Most patients show a response to a treatment( reduced
fever and abdominal pain) within 72-96 hrs.
Percutaneous therapeutic aspiration guided by
ultrasound or CT is reserved for:
-when lesion in the left lobe of liver
-when diagnosis is uncertain
- no response to metronidazole( persistent fever
and abd. pain) after 4 days of treatment
-large(>8-10 cm) ie. >300 ml of fluid
-severly ill patients
Amoebicide Pediatric dose Adult dose
Metronidazole 35-50 mg/kg/day for 7-10
days( in 3 divided doses)
750 mg 8 hourly
Tinidazole 50 mg/kg/day for 3 days(once
daily)
2 g once a day
Paromomycin 25-35mg/kg/day for 7 days(in
3 divided doses)
25-35mg/kg/day (in 3
divided doses)
Diloxanide furoate 20mg/kg/day for 7 days(in 3
divided doses)
500mg 8 hourly
Iodoquinone 30-40mg/kg/day for 20
days(in 3 divided doses)
650mg 8 hourly
DRUGS AND DOSES
PREVENTION & CONTROL
 Primary prevention
 Safe excreta disposal
 Safe water supply
 Hygiene
 Health education
 Treat symptomatic carriers
 Treat water(iodine, boiling): NOT
chlorine
 Secondary
 Early diagnosis
 Treatment
Amoebiasis by bhanu chalise, iom maharajgunj

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Amoebiasis by bhanu chalise, iom maharajgunj

  • 2. • Harboring(infection) of protozoa Entamoeba histolytica inside the body with or without the disease is called amoebiasis. • Associated with high mortality and morbidity • Major public health problem globally • 2nd leading cause of death due to parasitic disease ( 1st being malaria )
  • 3. Epidemiology • 10% of population infected globally • About 100,000 deaths occur every year globally • High prevalence in tropics and subtropics • Risk factors: Developing countries Developed countries  travelers  immigrants  homosexual men  HIV positive  immunodeficiency states poverty Ignorance overcrowding Poor sanitation malnutrition
  • 4. Causative organism 3 species of entamoeba: E. dispar : E. moshkovskii : E. histolytica Only E. histolytica is pathogenic. Other two species are apparently non-pathogenic and cause most of the asymptomatic cases.
  • 5. Morphology • Different form of E. histolytica: 1- trophozoite 2- precyst 3- cyst(1, 2, 4 nuclei) • Quadrinucleated cyst is the infective stage oval/round resistant to chlorination destroyed above 55 degree celsious and with disinfectants • Trophozoite stage is feeding vegetative form which is destructive to tissue
  • 6. Trophozoites of Entamoeba histolytica with ingested erythrocytes (trichrome stain) The ingested erythrocytes appear as dark inclusions. Erythrophagocytosis is the only morphologic characteristic that can be used to differentiate E. histolytica from the nonpathogenic E. dispar . FE
  • 7. Virulence factors Trophozoites of E. histolytica interact with host through a series of steps:  Adhesion of target cell, cytopathic effect  E.histolytica induces both Humoral and cell mediated immune responses  Causes disease only when invade the Intestine  Virulence is associated with secretion of Cysteine proteinase (histolysin) which assists the organism in digesting the extracellular matrix and invading tissues
  • 8. Cysts of Entamoeba histolytica /E. dispar • GHI IHG Cysts of Entamoeba histolytica/E. dispar ,permanent preparations stained with trichrome.
  • 9. Transmission 1) feco-oral(direct hand-to-mouth contact) 2) Veneral transmission among homosexual males 3) Food or drink contaminated with feces containing the E. histolytica cyst 4) Use of human feces (night soil) for soil fertilizer 5) contamination of foodstuffs by flies, and possibly cockroaches  a single cyst is sufficient to cause the disease  Asymptomatic human( the only host) cyst carriers are the principle reservoir of infection.
  • 10. Pathogenesis Ingestion of cysts Excystation in small intestine Production of 8 trophozoites Multiplication and Colonization in large intestine Tissue invasion and destruction Flask – shaped ulcers(mostly in caecum, transverse and sigmoid colon Encystation and exit from host in the stool Migrate via Blood stream( portal circulation) to the liver Amoebic liver abscess
  • 11.
  • 12.
  • 13. Clinical features Intestinal • Asymptomatic carriers(90%) • Amoebic colitis • Fulminant colitis • Amoeboma Extraintestinal • Liver • Lung • brain • skin Incubation period : varies from weeks to months : average= 3-4 weeks
  • 14. Asymptomatic carriers -90% without symptoms(non-invasive) - lumen not damaged(cyst passers) Invasive forms: Amoebic colitis/dysentery - flask shaped ulcers superficial or deep - abd.pain, watery/mucoid blood-streaked foul-smelling diarrhoea - fever, tenesmus, peri-anal ulcers - sometimes intermittent diarrhoea alternating constipation Fulminant colitis - <0.5% - severely ill with high fever - profuse bloody diarrhea - perforation(diffuse tenderness) - paralytic ileus -pronounced leukocytosis
  • 15. • ulcers with raised borders • little inflammation between lesions
  • 16.
  • 17. Amoeboma - 1% of cases - inflammatory thickening of intestinal wall - palpable mass with trophozoites Symptoms of amoebic colitis Symptoms Percentage Diarrhea 100 Dysentery 99 Abdominal pain 85 Fever 68 Dehydration 5 Complications: toxic megacolon, amoeboma, cutaneous amoebiasis, rectovaginal fistula
  • 18. Amoebic v^s Bacillary Dysentery symptoms Amoebic dysentery Bacillary dysentery Occurrence Usu. In the form of sporadic cases Usu. In the form of outbreaks Onset gradual Acute Fever Usu. Low grade (may be high in case of liver abscess) High grade Tenesmus/Abd. Cramps Moderate Very severe Stool Foul- smelling Not foul-smelling RBCs In clumps Discrete Pus cells Scanty Numerous Eosinophils Present Absent or rare Bacteria Numerous, motile Scanty, non-motile E. histolytica Trophozoites + Absent Growth on culture Negative Positive
  • 19. Extra-intestinal Amoebic liver abcess(most common) - 5% of invasive disease - 10 times more common in men -Usually no bowel symptoms except sometimes -right upper quadrant tenderness - hepatomegaly - jaundice(10- 15%) Pleuropulmonary/pericardial - direct spread(transdiaphragmatic rupture) from liver abscess (10%) - hematogenous spread -cough with crepitation Similarly infection can spread to brain, skin and genitourinary system
  • 20. Investigation Parasite detection Antibody detection Antigen detection PCR and other tests Investigation
  • 21. Parasite detection 1. Direct saline(wet) mount of feces: - most common microscopic technique -sample examined within 1 hour of collection -3 stool samples taken on consecutive day ( since sensitivity increased from 60% to 90%) -presence of ingested erythrocytes within trophozoites is pathognomic for E. histolytica -carriers have only cysts in their stool  Misidentification: macrophages v^s trophozoites : PMN v^s cysts : other entamoeba 2. Various culture techniques are available but not done routinely
  • 22. Antibody detection tests • Routinely employed for extra-intestinal dz – Positive(75%)- at presentation and 90%- beyond 1st week of symptoms – ELISA is most sensitive – IHA – Latex agglutination – Immunoelectrophoresis and immunodiffusion
  • 23.  Antigen detection • ELISA kits( sensitivity>90%): used in epidemiological studies ; useful in endemic areas • Antigen detection by ELISA: is the ideal test – distinguishes current from past infection.  PCR  OTHER TESTS: chest radiograph : CT , MRI : sigmoidoscopy : peripheral blood- leukocytosis without eosinophillia, mild anemia : Alp, ESR are common lab findings.
  • 24. • raised immobile right diaphragm • Other imaging modalities show – A single abscess in the right or left lobe – Multiple lesions can be present Imaging None of these modalities can differentiate amebic abscess from pyogenic or malignant one
  • 25. Treatment of amebiasis -combination of a luminal and a tissue amoebicide is advocated for complete parasite clearance in Invasive disease Luminal amoebicides • Diloxanide furoate • diiodoquinol • paromomycin Tissue amoebicides • 5-nitroimidazoles(DOC) -metronidazole -tinidazole -secnidazole • Chloroquin • Dehydroemetine Amoebic colitis: metronidazole followed by a luminal agent Fulminant amoebic colitis: add an antibiotic to deal with bowel flora Amoebic liver abscess: tissue amoebicide followed by luminal agent
  • 26. treatment continued………………… Asymptomatic intestinal carriers : a luminal agent Treatment for only E. dispar is not nessary Most patients show a response to a treatment( reduced fever and abdominal pain) within 72-96 hrs. Percutaneous therapeutic aspiration guided by ultrasound or CT is reserved for: -when lesion in the left lobe of liver -when diagnosis is uncertain - no response to metronidazole( persistent fever and abd. pain) after 4 days of treatment -large(>8-10 cm) ie. >300 ml of fluid -severly ill patients
  • 27. Amoebicide Pediatric dose Adult dose Metronidazole 35-50 mg/kg/day for 7-10 days( in 3 divided doses) 750 mg 8 hourly Tinidazole 50 mg/kg/day for 3 days(once daily) 2 g once a day Paromomycin 25-35mg/kg/day for 7 days(in 3 divided doses) 25-35mg/kg/day (in 3 divided doses) Diloxanide furoate 20mg/kg/day for 7 days(in 3 divided doses) 500mg 8 hourly Iodoquinone 30-40mg/kg/day for 20 days(in 3 divided doses) 650mg 8 hourly DRUGS AND DOSES
  • 28. PREVENTION & CONTROL  Primary prevention  Safe excreta disposal  Safe water supply  Hygiene  Health education  Treat symptomatic carriers  Treat water(iodine, boiling): NOT chlorine  Secondary  Early diagnosis  Treatment