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⦿Amoeba are structurally simple protozoans which have
no fixed shape.
⦿ Phylum : Sarcomastigophora
⦿ Subphylum :Sarcodina
⦿ Super class: Rhizopoda
⦿ Order : Amoebida
⦿Amoeba
Free living
Intestinal
⦿ Entamoeba histolytica is an intestinal amoeba
⦿All intestinal amoebae are non pathogenic except
Entamoeba histolytica
⦿All free living amoeba are oppurtunistic pathogens.
⦿ E. histolytica was discovered by Losch in 1875
⦿Demonstrated the parasite in the dysenteric feces of a
patient in St.Petersburg in Russia.
⦿ Morphology
⦿ Life Cycle
⦿ Pathogenesis & Clinical Features
⦿ Laboratory Diagnosis
⦿ Treatment
⦿ Prevention
 E.histolytica occurs in 3 forms
 Trophozote
 Precyst
 Cyst
⦿ Vegetative or growing stage of the parasite
⦿ Only form present in tissues
⦿ Irregular in shape
⦿ Size: 12-60 μm(Average 20μm)
⦿ Large and actively motile in freshly passed dysenteric
stool, while smaller in convalescents and carriers.
⦿ In the lumen, commensal and small in size(15-
20 μm)-MINUTAFORM
Cytoplasm
Outer ectoplasm-clear, transparent, refractile. Inner
endoplasm-finely granular (ground glass
appearance),with nucleus, food vacuoles, Erythrocytes
leucocytes(occasionally) tissue debris.
⦿ Pseudopodia
 Fingerlike projections formed by sudden jerky
movements of ectoplasm in one direction, followed by
the streaming in of the whole endoplasm
 Typical amoeboid motility is a Crawling or Gliding
 Pseudopodia formation and motility are inhibited
at low temperature.
Nucleus
 It is spherical 4-6μm in size contains central
karyosome,surrounded by clear halo and anchored to
the nuclear membrane by fine radiating fibrils called
the Linin network , giving a cartwheel appearance
 Nuclear membrane is lined by a rim of
chromatin distributed evenly as small
granules
⦿Trophozoites from acute dysentric stools often contain
phagocytosed erythrocytes- diagnostic feature ,these are
not found in any other commensal intestinal amoeba
⦿ These divided by binary fission in every 8 hours
⦿ These are killed by drying, heat ,and chemical
sterilization
⦿ Infections are not transmitted by these- destroyed in
stomach and cannot initiate infection
⦿Trophozoites undergo encystment in the lumen
⦿ Before encystment,the trophozoites extrudesits food
vacuoles and become round or oval,10-20µm in size-
precyst
⦿ Contains a large glycogen vacuole and two chromatid
bars
⦿ It then secretes a highly retractile cyst wall around it
and become cyst
⦿ Spherical ,10-20µm
⦿ 3 types of cyst
Early cyst Binucleate cyst
mature quadrinucleate cyst
Early cyst
contains a single nucleus and two other structures-a mass of
glycogen and 1-4 chromatid bodies or chromadial bars
⦿ As the cyst mature, the glycogen mass and chromidial
bars disappear and the nucleus undergoes 2 succesive
mitotic divisions to form 2 and then 4 nuclei .
⦿The cyst wall is a highly resistant to gastric juice and
unfavorable environmental conditions.
⦿Infective form :Mature quadrinucleate cyst passed in
feces of convalscents and carriers.
⦿Mode of transmission : Man acquires infection by
swallowing food and water contaminated with cyst .
⦿ Stomach –cyst wall is resistant to gastric juice
⦿ Exystation :cyst reaches the caecum or lower part of
ileum ,due to alkaline medium ,cyst wall damaged by
trypsin ,leading to exystation
⦿ E.histolytica causes intestinal and extra intestinal
amoebiasis
Intestinal amoebiasis - Pathogenesis Lumen dwelling
amoeba do not cause any illness .They causes disease
only when they invade the intestinal tissues .
10 % -symptomatic
90% -asymptomatic
⦿Not all strains of E.histolytica are pathogenic or invasive .
⦿Differentiation between pathogenic and non
pathogenic strains can be made by





susceptibility to complement-mediated lysis
Phagocytic activity
by the use of genetic markers
monoclonal antibodies Zymodeme
analysis
 The metacystic trophozoites penetrate the columnar epithelial
cells of crypts of Liberkuhn
 Penetration is facilitated by
motility of the trophozoites tissue lytic
enzyme –histolysin
amoebic lectin -mediate adherence
 Mucosal penetration by amoeba produce discrete ulcers with
pinhead center and raised edges .
 Sometimes invasion remains superficial and heal
spontaneously.
 More often, the amoeba penetrates to submucosal layer and
multiplies rapidly- lytic necrosis- abscess- ulcer
⦿Ulcer appear initially on the mucosa as raised nodules
with pouting edges .
⦿ They breakdown discharging brownish necrotic
material contains large numbers of trophozoites.
⦿ The typical amoebic ulcer –flask shaped
⦿ Multiple ulcers may coalesce to form large necrotic
lesions with ragged and undermined edges,covered
with brownish slough
⦿The ulcers generally do not extend deeper than
submucosal layer.
⦿ Occassionally, a granulamatous pseudotumoral growth
may develop on the intestinal wall from a chronic
ulcer.This amoebic granuloma or amoeboma may be
mistaken for are malignant tumor
⦿ Small superficial ulcers involving only the mucosa
⦿ Round or oval shaped with ragged and undermined
margin and flask-shaped in cross section
⦿ Marked scarring of intestinal wall with thining ,dilatation
,and sacculation
⦿ Extensive adhesions with neighboring viscera
⦿ Formation of tumor-like masses of granulation tissue
amoeba
⦿The incubation period is highly variable from 1-4 months
⦿ The clinical course is characterized by prolonged
latency,relapses and intermissions.
⦿ Typical manifestation is amoebic dysentry
⦿ Compared to bacillary desentry ,it is usually insidious in
onset and the abdominal tenderness is less and localised.
⦿ The stools are large, foul-smelling,and brownish
black, often with bloodstreaked mucus intermingled
with feces.
⦿ The RBCs in stools are clumped and reddish brown in
color.
⦿ Cellular exudate is scanty.
⦿Charcot-leyden crystals are often present.
⦿ The patient is usually afebrile and non toxic.
⦿ In fulminant colitis, there is confluent ulceration and
necrosis of colon-patient is febrile and toxic.
⦿ Intestinal amoebiasis not always result in
dysentry.quite often there may be only diarrhea or
vague abdominal symptoms popularly called
uncomfortable belly or growling abdomen.
⦿ Chronic involvement of the caecum causes a condition
simulating appendicitis.
⦿Fulminant amoebic colitis
toxic megacolon perianal ulceration Amoebae
⦿ Extra intestinal Amebiasis
amoebic hepatitis amoebic liver abscess amoebic
appendicitis and peritonitis pulmonary Amebiasis cerebral
Amebiasis splenic abscess cutaneous Amebiasis genitourinary
Amebiasis.
⦿ HepaticAmoebiasis
⦿ PulmonaryAmoebiasis
⦿ MetastaticAmoebiasis
⦿ CutaneousAmoebiasis
⦿ GenitourinaryAmoebiasis
⦿ Most common extra intestinal amoebiasis .
⦿ The history of amoebic dysentry is absent in more than 50%
cases
⦿Several patients with amoebic colitis develop an enlarged tender
liver without detectable impairment of liver function or fever.
⦿ This acute hepatic involvement (amoebic hepatitis) may be due
to repeated invasion by amoeba from an active colonic
infection or to toxic substance from the colon reaching the liver.
⦿ In about 5-10% of person with intestinal amoebiasis
,liver abscesses may ensue.
⦿ The center of the abscess contains thick chocolate brown
pus(anchovy pus),which is liqeefied necrotic liver tissue.
⦿At the periphery, there is almost normal liver tissue,which
contain invading amoeba.
⦿ Liver abscess may multiple solitary
⦿Usually located on right lobe of liver
⦿ Jaundice develops
only when lesions are multiple OR when they
press on the biliary tract
 Incidenca of liver abscess is less common in women
and rare in children under age of 10
⦿ It may occure by direct hematogenous spread from colon
bypassing the liver,but it most often follows extension of
hepatic abscess through the diaphragm
⦿ Hepatobronchial fistula usually results with expectoration
of chocolate brown sputum
⦿ Patient presents with
severe pleuritic chest pain dyspnea
non-productive cough
⦿ Involvement of distant organs is by
hematogenous spread and through lymphatics
⦿Abscess in
Kidney Brain
Spleen
Adrenals
Spread to brain leads to severe destruction of brain tissues
and is fatal
⦿ It occurs by direct extension around anus,
colostomy site,or discharging sinuses from
amoebic abscess .
⦿ Extensive gangrenous destruction of the skin occurs .
⦿ The lesion may be mistaken for condyloma or
epithelioma
⦿ Penile amoebiasis
prepuce and glans are affected
acquired through anal intercourse
In females
⦿ vulva ,vagina, or cervix by
spread from perineum
destructive ulcerative lesions resemble
carcinoma
⦿
⦿
Laboratory Diagnosis of Intestinal
Amebiasis
Treatment
Prophylaxis
 General prophylaxis is as for all fecal-oral infections.
 Food and water have to be protected from contamination with
human excreta.
 Detection and treatment of carriers and their exclusion from
food handling occupations will help in limiting the spread of
infection.
 Health education and inclusion of healthy personal habits
helps in control.
THANK OU

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Entamoeba histolytica. Medical parasitology pptx

  • 1.
  • 2. ⦿Amoeba are structurally simple protozoans which have no fixed shape. ⦿ Phylum : Sarcomastigophora ⦿ Subphylum :Sarcodina ⦿ Super class: Rhizopoda ⦿ Order : Amoebida
  • 3. ⦿Amoeba Free living Intestinal ⦿ Entamoeba histolytica is an intestinal amoeba ⦿All intestinal amoebae are non pathogenic except Entamoeba histolytica ⦿All free living amoeba are oppurtunistic pathogens.
  • 4. ⦿ E. histolytica was discovered by Losch in 1875 ⦿Demonstrated the parasite in the dysenteric feces of a patient in St.Petersburg in Russia.
  • 5. ⦿ Morphology ⦿ Life Cycle ⦿ Pathogenesis & Clinical Features ⦿ Laboratory Diagnosis ⦿ Treatment ⦿ Prevention
  • 6.  E.histolytica occurs in 3 forms  Trophozote  Precyst  Cyst
  • 7. ⦿ Vegetative or growing stage of the parasite ⦿ Only form present in tissues ⦿ Irregular in shape ⦿ Size: 12-60 μm(Average 20μm) ⦿ Large and actively motile in freshly passed dysenteric stool, while smaller in convalescents and carriers. ⦿ In the lumen, commensal and small in size(15- 20 μm)-MINUTAFORM
  • 8.
  • 9. Cytoplasm Outer ectoplasm-clear, transparent, refractile. Inner endoplasm-finely granular (ground glass appearance),with nucleus, food vacuoles, Erythrocytes leucocytes(occasionally) tissue debris.
  • 10. ⦿ Pseudopodia  Fingerlike projections formed by sudden jerky movements of ectoplasm in one direction, followed by the streaming in of the whole endoplasm  Typical amoeboid motility is a Crawling or Gliding  Pseudopodia formation and motility are inhibited at low temperature.
  • 11. Nucleus  It is spherical 4-6μm in size contains central karyosome,surrounded by clear halo and anchored to the nuclear membrane by fine radiating fibrils called the Linin network , giving a cartwheel appearance  Nuclear membrane is lined by a rim of chromatin distributed evenly as small granules
  • 12. ⦿Trophozoites from acute dysentric stools often contain phagocytosed erythrocytes- diagnostic feature ,these are not found in any other commensal intestinal amoeba ⦿ These divided by binary fission in every 8 hours ⦿ These are killed by drying, heat ,and chemical sterilization ⦿ Infections are not transmitted by these- destroyed in stomach and cannot initiate infection
  • 13. ⦿Trophozoites undergo encystment in the lumen ⦿ Before encystment,the trophozoites extrudesits food vacuoles and become round or oval,10-20µm in size- precyst ⦿ Contains a large glycogen vacuole and two chromatid bars ⦿ It then secretes a highly retractile cyst wall around it and become cyst
  • 14.
  • 15. ⦿ Spherical ,10-20µm ⦿ 3 types of cyst Early cyst Binucleate cyst mature quadrinucleate cyst Early cyst contains a single nucleus and two other structures-a mass of glycogen and 1-4 chromatid bodies or chromadial bars
  • 16. ⦿ As the cyst mature, the glycogen mass and chromidial bars disappear and the nucleus undergoes 2 succesive mitotic divisions to form 2 and then 4 nuclei . ⦿The cyst wall is a highly resistant to gastric juice and unfavorable environmental conditions.
  • 17. ⦿Infective form :Mature quadrinucleate cyst passed in feces of convalscents and carriers. ⦿Mode of transmission : Man acquires infection by swallowing food and water contaminated with cyst . ⦿ Stomach –cyst wall is resistant to gastric juice ⦿ Exystation :cyst reaches the caecum or lower part of ileum ,due to alkaline medium ,cyst wall damaged by trypsin ,leading to exystation
  • 18.
  • 19. ⦿ E.histolytica causes intestinal and extra intestinal amoebiasis Intestinal amoebiasis - Pathogenesis Lumen dwelling amoeba do not cause any illness .They causes disease only when they invade the intestinal tissues . 10 % -symptomatic 90% -asymptomatic
  • 20. ⦿Not all strains of E.histolytica are pathogenic or invasive . ⦿Differentiation between pathogenic and non pathogenic strains can be made by      susceptibility to complement-mediated lysis Phagocytic activity by the use of genetic markers monoclonal antibodies Zymodeme analysis
  • 21.  The metacystic trophozoites penetrate the columnar epithelial cells of crypts of Liberkuhn  Penetration is facilitated by motility of the trophozoites tissue lytic enzyme –histolysin amoebic lectin -mediate adherence  Mucosal penetration by amoeba produce discrete ulcers with pinhead center and raised edges .  Sometimes invasion remains superficial and heal spontaneously.  More often, the amoeba penetrates to submucosal layer and multiplies rapidly- lytic necrosis- abscess- ulcer
  • 22. ⦿Ulcer appear initially on the mucosa as raised nodules with pouting edges . ⦿ They breakdown discharging brownish necrotic material contains large numbers of trophozoites. ⦿ The typical amoebic ulcer –flask shaped ⦿ Multiple ulcers may coalesce to form large necrotic lesions with ragged and undermined edges,covered with brownish slough
  • 23. ⦿The ulcers generally do not extend deeper than submucosal layer. ⦿ Occassionally, a granulamatous pseudotumoral growth may develop on the intestinal wall from a chronic ulcer.This amoebic granuloma or amoeboma may be mistaken for are malignant tumor
  • 24. ⦿ Small superficial ulcers involving only the mucosa ⦿ Round or oval shaped with ragged and undermined margin and flask-shaped in cross section ⦿ Marked scarring of intestinal wall with thining ,dilatation ,and sacculation ⦿ Extensive adhesions with neighboring viscera ⦿ Formation of tumor-like masses of granulation tissue amoeba
  • 25. ⦿The incubation period is highly variable from 1-4 months ⦿ The clinical course is characterized by prolonged latency,relapses and intermissions. ⦿ Typical manifestation is amoebic dysentry ⦿ Compared to bacillary desentry ,it is usually insidious in onset and the abdominal tenderness is less and localised. ⦿ The stools are large, foul-smelling,and brownish black, often with bloodstreaked mucus intermingled with feces.
  • 26.
  • 27. ⦿ The RBCs in stools are clumped and reddish brown in color. ⦿ Cellular exudate is scanty. ⦿Charcot-leyden crystals are often present. ⦿ The patient is usually afebrile and non toxic. ⦿ In fulminant colitis, there is confluent ulceration and necrosis of colon-patient is febrile and toxic.
  • 28. ⦿ Intestinal amoebiasis not always result in dysentry.quite often there may be only diarrhea or vague abdominal symptoms popularly called uncomfortable belly or growling abdomen. ⦿ Chronic involvement of the caecum causes a condition simulating appendicitis.
  • 29. ⦿Fulminant amoebic colitis toxic megacolon perianal ulceration Amoebae ⦿ Extra intestinal Amebiasis amoebic hepatitis amoebic liver abscess amoebic appendicitis and peritonitis pulmonary Amebiasis cerebral Amebiasis splenic abscess cutaneous Amebiasis genitourinary Amebiasis.
  • 30.
  • 31.
  • 32. ⦿ HepaticAmoebiasis ⦿ PulmonaryAmoebiasis ⦿ MetastaticAmoebiasis ⦿ CutaneousAmoebiasis ⦿ GenitourinaryAmoebiasis
  • 33. ⦿ Most common extra intestinal amoebiasis . ⦿ The history of amoebic dysentry is absent in more than 50% cases ⦿Several patients with amoebic colitis develop an enlarged tender liver without detectable impairment of liver function or fever. ⦿ This acute hepatic involvement (amoebic hepatitis) may be due to repeated invasion by amoeba from an active colonic infection or to toxic substance from the colon reaching the liver.
  • 34. ⦿ In about 5-10% of person with intestinal amoebiasis ,liver abscesses may ensue. ⦿ The center of the abscess contains thick chocolate brown pus(anchovy pus),which is liqeefied necrotic liver tissue. ⦿At the periphery, there is almost normal liver tissue,which contain invading amoeba. ⦿ Liver abscess may multiple solitary
  • 35. ⦿Usually located on right lobe of liver ⦿ Jaundice develops only when lesions are multiple OR when they press on the biliary tract  Incidenca of liver abscess is less common in women and rare in children under age of 10
  • 36. ⦿ It may occure by direct hematogenous spread from colon bypassing the liver,but it most often follows extension of hepatic abscess through the diaphragm ⦿ Hepatobronchial fistula usually results with expectoration of chocolate brown sputum ⦿ Patient presents with severe pleuritic chest pain dyspnea non-productive cough
  • 37. ⦿ Involvement of distant organs is by hematogenous spread and through lymphatics ⦿Abscess in Kidney Brain Spleen Adrenals Spread to brain leads to severe destruction of brain tissues and is fatal
  • 38. ⦿ It occurs by direct extension around anus, colostomy site,or discharging sinuses from amoebic abscess . ⦿ Extensive gangrenous destruction of the skin occurs . ⦿ The lesion may be mistaken for condyloma or epithelioma
  • 39. ⦿ Penile amoebiasis prepuce and glans are affected acquired through anal intercourse In females ⦿ vulva ,vagina, or cervix by spread from perineum destructive ulcerative lesions resemble carcinoma ⦿ ⦿
  • 40. Laboratory Diagnosis of Intestinal Amebiasis
  • 41.
  • 43. Prophylaxis  General prophylaxis is as for all fecal-oral infections.  Food and water have to be protected from contamination with human excreta.  Detection and treatment of carriers and their exclusion from food handling occupations will help in limiting the spread of infection.  Health education and inclusion of healthy personal habits helps in control.