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AMOEBIASIS
Learning Objectives
• Definition
• Epidemiology
• Epidemiological determinants
• Clinical presentation
• Diagnosis and further investigation
• Prevention and treatment
Amoebiasis
• Amoebiasis is an infection with the intestinal protozoa
Entamoeba histolytica.
• About 90% of infections are asymptomatic
• Remaining 10% produce a spectrum of clinical
syndromes
Amoebiasis
Symptomatic group
Intestinal
Small % - invasive
amoebiasis
Mild abdominal
discomfort,
diarrhea to acute
fulminating
dysentery
Extraintestinal
Liver(liver
abscess), brain,
lung, spleen
Epidemiology
World
• Worldwide in distribution
• 3rd most common parasitic death
• India, China, Mexico, Africa, SouthAmerica
• 2-60% prevalence(based on ELISA and PCR studies from
stool samples)
• 100,000 deaths/yr
• 500 million infections
• 50 million cases/yr Data-2007
Epidemiology
level and
India
• 15% prevalence (3.6-47.4%)
• Variation according to sanitation
clinical diagnostic criteria
Epidemiological determinants
• Agent
• Virulence factor
• Host factor
• Environmental factor
• Mode of transmission
• Incubation period
Agents
• Entamoeba histolytica
 Trophozoites
• 18-40 μm in D
• Cytoplasm – # outer clear ectoplasm
# inner granular endoplasm
# food vacuoles with RBCs, leukocytes & tissue
debris
• Motile by pseudopodia extensions
• Nucleus with central karyosome, surrounded by delicate membrane
lined with chromatin granules
• Non infectious
Agents
• Entamoeba histolytica
Precyst
• Intermediate form
• Oval with blunt pseudopodia
• No food vacuoles
Cysts
• Spherical, 10 - 15 μm in D
• Uninucleate, later bi- or quadri- nucleate
• Thick chitinous wall
• Glycogen mass – not in quadrinucleate
• Chromidial or Chromatoid bars
• Infectious
Invasive x Noninvasive strains
• A zymodem comprises those Entamoeba strains that share the same
electrophoretic pattern and mobility for certain enzymes like – malic
enzyme, phosphoglucomutase, hexokinase, glucose phosphate isomerase,
aldolase etc
• 24 different zymodems – 21 of human strains
• 7 pathogenic zymodems
• The invasive and non invasive strains may appear identical may represent
two distinct species
• Invasive strain – E.histolytica(give rise to fecal cysts)
• Non invasive strains reclassified as E.dispar.
Agent factor
• Source of infection is a case or carrier
-1∙5 X 107 cysts per day
• Reservoir is only human – several years
• Resistant to chlorine in normal conc.
• Readily killed by freezing or heating(55°C)
• Period of communicability- very long
Host factor
• 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
• Men who have sex with men
• All age groups affected
• No gender or racial differences
• Severe if children, old, pregnant, PEM
• Develops antiamoebic antibodies in tissue invasion
Host factor
• Liver abscesses due to amoebiasis are 10 times
more frequent in adults than in children
• Amoebic liver abscess 7 times more in men than
women
• Predominance among men aged 18-50 years
• Increased among postmenopausal women
• Hormonal effect and alcohol can be risk factors
Environment factor
• Low socio-economic status
• Poor sanitation, sewage contamination
• Night soil for agriculture
• Seasonal variation(more in rainy season)
 Faeco -oral route
• Contaminated water and food
• Direct hand to mouth(cysts under finger nails)
• Vegetables irrigated with sewage polluted water
 Agency of flies, cockroaches, rats, etc.
 Sexual contact via oral-rectal route
Modes of transmission
Incubation period
• 2- 4 weeks
Life cycle of E. histolytica
Source:- medical-dictionary.com
Life Cycle of E. histolytica
Clinical presentation
• Most common type of amoebic infection is
asymptomatic cyst passage
• Intestinal amoebiasis – abdominal cramps with mild
diarrhea to colitis and dysentery
• Extra-intestinal amoebiasis – Amoebic liver abscess,
rarely lungs, skin, genitalia and CNS are affected
• Amoeboma – inflammatory and edematous reaction
around trophozoites
Clinical presentation
• Asymptomatic carriers
• 90% without symptoms
• does not damage lumen
How the Amoebiasis Manifests
• Most cases of amoebiasis have very mild symptoms or none.
• Wide spectrum, from asymptomatic infection to luminal
amoebiasis and amoebic colitis
• Clinical symptoms are usually vague
• More severe infection may cause fever, profuse diarrhoea,
vomiting, abdominal pain, jaundice, anorexia, and weight
loss.
• Invasive intestinal amoebiasis (dysentery, colitis,
appendicitis, toxic mega colon, amoebomas)
Clinical presentation
• Amoebic colitis-
• Abdominal cramp to severe pain
• Fever, vomiting, anorexia
• Mucus in stool, dysentery
• Flask shaped ulcer in intestine
Clinical presentation
• Fulminant colitis-
• <0.5%
• Severely ill with high fever
• Intestinal bleeding, perforation
• Paralytic illus
• CFR-40%
• Uncommonly, a chronic form of
amoebic colitis can be confused with
inflammatory bowel disease
Amoeboma
• Pseudotumoral lesion
• Necrosis, edema and inflammatory thickening of mucosa
and submucosa of intestinal wall
• 1% of cases
• Palpable mass with trophozoites
• Always coexists with ulceration
• Single, rarely multiple in different parts of colon, on skin at
site of amoebic liver aspiration
Character Amoebic dysentery Bacillary dysentery
Number 6-8 motions per day > 10 motions per day
Amount Copious Small
Odour Offensive Odourless
Colour Dark red Bright red
Reaction Acidic Alkaline
Consistency Non-adherent Adherent
Difference between amoebic and bacillary
dysentery
Macroscopy
Character Amoebic dysentry Bacillary dysentry
RBCs In clumps Discrete or in Rouleaux
Pus cells Few Numerous
Macrophages Few Numerous, many have
RBCs and may mimic EH
Eosinophils Present Scarce
Charcot-Leyden crystals Present Absent
Pyknotic bodies Present Absent
Ghost cells Absent Present
Parasites Trophozoites of EH Absent
Bacteria Many motile bacteria Few or Absent
Difference between amoebic and bacillary
dysentery
Microscopy
Metastatic lesions in liver
• Amoebic liver abscess- Most common extra-intestinal
presentation
• The parasite reaches liver via portal system
• Occurs within 5 months of dysentery in 95% of cases
• But concomitant active diarrhea is seen in less than a third of
cases
• Pain and point tenderness over right hypochondrium and fever
• Jaundice rare, pleural effusion is common
Amoebic liver abscess
• Older pt. from endemic areas usually have chronic disease
• Right lobe is commonly affected, abscess of left lobe is
more dangerous due to its proximity to heart –> rupture –>
pericardial effusion
• Necrotic cavitary lesion filled with cellular debris and
parasite trophozoites – Anchovy sauce pus
Metastatic lesions in liver
Complications of ALA
• Rupture is the most dreaded complication
• It may spread to pleura, lungs, peritoneum,
pericardium or open outside through the anterior
abdominal wall
• Pulmonary amoebiasis-
I.
II.
III.
Rupture from ALA into pleural space
Hepato-bronchial fistula with necrotic material in sputum
may mimic blood – trophozoites can be present
Serous pleural effusion or contiguous spread from ALA
Metastatic lesions in other organs
Metastatic lesions in other organs
• Cerebral amoebiasis-
• Rare, complication of
hepatic/ pulmonary abscess
• Single small lesion in
cerebral hemisphere
• Cutaneous amoebiasis-
• In areas of drainage of liver abscess/colostomy
wound
• Granulomatous ulcerations
Metastatic lesions in other organs
• Splenic amoebiasis-
• Amoebiasis of penis-
• Amoebic pericarditis-
• Rupture of liver left lobe
abscess
• High fever, epigastric pain
dyspnoea, pericardial rub
Metastatic lesions in other organs
Samples :
I. Stool ( 3 consecutive samples)
II. Biopsy material from the ulcers (colonoscopy or
sigmoidoscopy)
III. Aspirate from liver abscess
IV. Serum
V. Pleural fluid
VI. Pericardial fluid
VII. Sputum
Laboratory diagnosis
Microscopy -
• Both saline and iodine wet mounts are prepared
• Any motile trophozoite is better seen in saline mount
• Iodine mount stains the internal structures and is used to
identify cysts
• Charcot-leyden crystals can be seen
• Permanent stains can also be used to stain smears
Laboratory diagnosis
Laboratory diagnosis
• For amoebic liver abscess and other
metastatic lesions-
I. Radiological examination
II. Radio isotope tracing of liver
III. Ultrasonogrphy of upper abdomen
IV. CT and MRI abdomen
Serology-
• Antibody detection
• ELISA
• IHA
• IFA
Copro-antigen detection by ELISA is another recent and
very useful method
• Antigen detection
• Coagglutination
• ELISA
Laboratory diagnosis
• Symptomatic case:- (amoebic colitis and
amoebic liver abscess)
Treatment
Drug
Tinidazole
Metronidazole
Dose
2g/day
750mg(adult)
30mg/kg(children)
Frequency
tid
tid
Route
oral
Oral/iv
Duration
3 days
5-10
days
• Luminal infections and -(with above)
Treatment
Drug
Parmomycin
Iodoquinol
Dose
30mg/kg
650mg
Frequency
qid
tid
Route
oral
oral
Duration
5-10
days
20 days
Treatment
• Percutaneous radiography guided aspiration of
abscess:- large left lobe liver abscess, bacterial
superinfection, pyogenic abscess, pleuropulmonary
amoebiasis, empyema, amebic pericrditis
Simple aspiration of amoebic liver abscess
• Asymptomatic cases and cyst passers-
Treatment
Drug
Didohydroxyquin
Diloxanide furoate
Dose
650mg(adult), 30-
40mg/kg(children)
500mg
Frequency
tid
tid
Route
oral
oral
Duration
20 days
10 days
Prevention
1.Primary prevention-
a.Sanitation-safe disposal of human excreta, good
sanitary practice like washing hands after defecation and
before eating
b. Water supply-water filtration(sand filters), boiling
c.Food hygiene- prevent fecal contamination of food and
drink, vegetables washed with aqueous acetic acid(5-10%)
d. Health education- food handlers and public
Prevention
2. Secondary prevention-
a. Early diagnosis
b. Treatment
Contd…
• E. dispar is morphologically indistinguishable
from E. histolytica and so is E. moshkovskii
• Most asymptomatic cases of amoebic
infestation are believed to be one of these
two species
• The other species are also non-pathogenic
but can be microscopically differentiated
Summary
• Amoebiasis is an infection with the intestinal protozoa
Entamoeba histolytica.
• About 90% of infections are asymptomatic
• Worldwide in distribution
• Infectious- cyst form
• Poor sanitation, sewage contamination
• Wide spectrum, from asymptomatic infection to luminal
amoebiasis and amoebic colitis
• Invasive intestinal amoebiasis (dysentery, colitis,
appendicitis, toxic mega colon, amoebomas)
• Amoebic liver abscess- Most common extra-intestinal
presentation
• Diagnosis by stool microscopy and other investigations
• Treatment tinidazole is prefered
• Prevention is good sanitary practice
Reference
• PARK’S TEXTBOOK OF PREVENTIVE
AND SOCIAL MEDICINE
• PARASITOLOGY, K. D. Chatterjee
• HARRISON’S PRINCIPLE OF INTERNAL
MEDICINE
• Medscape
• Wikipedia
amoebiasis

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amoebiasis

  • 2. Learning Objectives • Definition • Epidemiology • Epidemiological determinants • Clinical presentation • Diagnosis and further investigation • Prevention and treatment
  • 3. Amoebiasis • Amoebiasis is an infection with the intestinal protozoa Entamoeba histolytica. • About 90% of infections are asymptomatic • Remaining 10% produce a spectrum of clinical syndromes
  • 4. Amoebiasis Symptomatic group Intestinal Small % - invasive amoebiasis Mild abdominal discomfort, diarrhea to acute fulminating dysentery Extraintestinal Liver(liver abscess), brain, lung, spleen
  • 5. Epidemiology World • Worldwide in distribution • 3rd most common parasitic death • India, China, Mexico, Africa, SouthAmerica • 2-60% prevalence(based on ELISA and PCR studies from stool samples) • 100,000 deaths/yr • 500 million infections • 50 million cases/yr Data-2007
  • 6. Epidemiology level and India • 15% prevalence (3.6-47.4%) • Variation according to sanitation clinical diagnostic criteria
  • 7. Epidemiological determinants • Agent • Virulence factor • Host factor • Environmental factor • Mode of transmission • Incubation period
  • 8. Agents • Entamoeba histolytica  Trophozoites • 18-40 μm in D • Cytoplasm – # outer clear ectoplasm # inner granular endoplasm # food vacuoles with RBCs, leukocytes & tissue debris • Motile by pseudopodia extensions • Nucleus with central karyosome, surrounded by delicate membrane lined with chromatin granules • Non infectious
  • 9. Agents • Entamoeba histolytica Precyst • Intermediate form • Oval with blunt pseudopodia • No food vacuoles Cysts • Spherical, 10 - 15 μm in D • Uninucleate, later bi- or quadri- nucleate • Thick chitinous wall • Glycogen mass – not in quadrinucleate • Chromidial or Chromatoid bars • Infectious
  • 10. Invasive x Noninvasive strains • A zymodem comprises those Entamoeba strains that share the same electrophoretic pattern and mobility for certain enzymes like – malic enzyme, phosphoglucomutase, hexokinase, glucose phosphate isomerase, aldolase etc • 24 different zymodems – 21 of human strains • 7 pathogenic zymodems • The invasive and non invasive strains may appear identical may represent two distinct species • Invasive strain – E.histolytica(give rise to fecal cysts) • Non invasive strains reclassified as E.dispar.
  • 11. Agent factor • Source of infection is a case or carrier -1∙5 X 107 cysts per day • Reservoir is only human – several years • Resistant to chlorine in normal conc. • Readily killed by freezing or heating(55°C) • Period of communicability- very long
  • 12. Host factor • 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 • Men who have sex with men • All age groups affected • No gender or racial differences • Severe if children, old, pregnant, PEM • Develops antiamoebic antibodies in tissue invasion
  • 13. Host factor • Liver abscesses due to amoebiasis are 10 times more frequent in adults than in children • Amoebic liver abscess 7 times more in men than women • Predominance among men aged 18-50 years • Increased among postmenopausal women • Hormonal effect and alcohol can be risk factors
  • 14. Environment factor • Low socio-economic status • Poor sanitation, sewage contamination • Night soil for agriculture • Seasonal variation(more in rainy season)
  • 15.  Faeco -oral route • Contaminated water and food • Direct hand to mouth(cysts under finger nails) • Vegetables irrigated with sewage polluted water  Agency of flies, cockroaches, rats, etc.  Sexual contact via oral-rectal route Modes of transmission
  • 17. Life cycle of E. histolytica Source:- medical-dictionary.com
  • 18. Life Cycle of E. histolytica
  • 19. Clinical presentation • Most common type of amoebic infection is asymptomatic cyst passage • Intestinal amoebiasis – abdominal cramps with mild diarrhea to colitis and dysentery • Extra-intestinal amoebiasis – Amoebic liver abscess, rarely lungs, skin, genitalia and CNS are affected • Amoeboma – inflammatory and edematous reaction around trophozoites
  • 20. Clinical presentation • Asymptomatic carriers • 90% without symptoms • does not damage lumen
  • 21. How the Amoebiasis Manifests • Most cases of amoebiasis have very mild symptoms or none. • Wide spectrum, from asymptomatic infection to luminal amoebiasis and amoebic colitis • Clinical symptoms are usually vague • More severe infection may cause fever, profuse diarrhoea, vomiting, abdominal pain, jaundice, anorexia, and weight loss. • Invasive intestinal amoebiasis (dysentery, colitis, appendicitis, toxic mega colon, amoebomas)
  • 22. Clinical presentation • Amoebic colitis- • Abdominal cramp to severe pain • Fever, vomiting, anorexia • Mucus in stool, dysentery • Flask shaped ulcer in intestine
  • 23. Clinical presentation • Fulminant colitis- • <0.5% • Severely ill with high fever • Intestinal bleeding, perforation • Paralytic illus • CFR-40% • Uncommonly, a chronic form of amoebic colitis can be confused with inflammatory bowel disease
  • 24. Amoeboma • Pseudotumoral lesion • Necrosis, edema and inflammatory thickening of mucosa and submucosa of intestinal wall • 1% of cases • Palpable mass with trophozoites • Always coexists with ulceration • Single, rarely multiple in different parts of colon, on skin at site of amoebic liver aspiration
  • 25. Character Amoebic dysentery Bacillary dysentery Number 6-8 motions per day > 10 motions per day Amount Copious Small Odour Offensive Odourless Colour Dark red Bright red Reaction Acidic Alkaline Consistency Non-adherent Adherent Difference between amoebic and bacillary dysentery Macroscopy
  • 26. Character Amoebic dysentry Bacillary dysentry RBCs In clumps Discrete or in Rouleaux Pus cells Few Numerous Macrophages Few Numerous, many have RBCs and may mimic EH Eosinophils Present Scarce Charcot-Leyden crystals Present Absent Pyknotic bodies Present Absent Ghost cells Absent Present Parasites Trophozoites of EH Absent Bacteria Many motile bacteria Few or Absent Difference between amoebic and bacillary dysentery Microscopy
  • 27. Metastatic lesions in liver • Amoebic liver abscess- Most common extra-intestinal presentation • The parasite reaches liver via portal system • Occurs within 5 months of dysentery in 95% of cases • But concomitant active diarrhea is seen in less than a third of cases • Pain and point tenderness over right hypochondrium and fever • Jaundice rare, pleural effusion is common
  • 29. • Older pt. from endemic areas usually have chronic disease • Right lobe is commonly affected, abscess of left lobe is more dangerous due to its proximity to heart –> rupture –> pericardial effusion • Necrotic cavitary lesion filled with cellular debris and parasite trophozoites – Anchovy sauce pus Metastatic lesions in liver
  • 30. Complications of ALA • Rupture is the most dreaded complication • It may spread to pleura, lungs, peritoneum, pericardium or open outside through the anterior abdominal wall
  • 31. • Pulmonary amoebiasis- I. II. III. Rupture from ALA into pleural space Hepato-bronchial fistula with necrotic material in sputum may mimic blood – trophozoites can be present Serous pleural effusion or contiguous spread from ALA Metastatic lesions in other organs
  • 32. Metastatic lesions in other organs
  • 33. • Cerebral amoebiasis- • Rare, complication of hepatic/ pulmonary abscess • Single small lesion in cerebral hemisphere • Cutaneous amoebiasis- • In areas of drainage of liver abscess/colostomy wound • Granulomatous ulcerations Metastatic lesions in other organs
  • 34. • Splenic amoebiasis- • Amoebiasis of penis- • Amoebic pericarditis- • Rupture of liver left lobe abscess • High fever, epigastric pain dyspnoea, pericardial rub Metastatic lesions in other organs
  • 35. Samples : I. Stool ( 3 consecutive samples) II. Biopsy material from the ulcers (colonoscopy or sigmoidoscopy) III. Aspirate from liver abscess IV. Serum V. Pleural fluid VI. Pericardial fluid VII. Sputum Laboratory diagnosis
  • 36. Microscopy - • Both saline and iodine wet mounts are prepared • Any motile trophozoite is better seen in saline mount • Iodine mount stains the internal structures and is used to identify cysts • Charcot-leyden crystals can be seen • Permanent stains can also be used to stain smears Laboratory diagnosis
  • 37. Laboratory diagnosis • For amoebic liver abscess and other metastatic lesions- I. Radiological examination II. Radio isotope tracing of liver III. Ultrasonogrphy of upper abdomen IV. CT and MRI abdomen
  • 38. Serology- • Antibody detection • ELISA • IHA • IFA Copro-antigen detection by ELISA is another recent and very useful method • Antigen detection • Coagglutination • ELISA Laboratory diagnosis
  • 39. • Symptomatic case:- (amoebic colitis and amoebic liver abscess) Treatment Drug Tinidazole Metronidazole Dose 2g/day 750mg(adult) 30mg/kg(children) Frequency tid tid Route oral Oral/iv Duration 3 days 5-10 days
  • 40. • Luminal infections and -(with above) Treatment Drug Parmomycin Iodoquinol Dose 30mg/kg 650mg Frequency qid tid Route oral oral Duration 5-10 days 20 days
  • 41. Treatment • Percutaneous radiography guided aspiration of abscess:- large left lobe liver abscess, bacterial superinfection, pyogenic abscess, pleuropulmonary amoebiasis, empyema, amebic pericrditis Simple aspiration of amoebic liver abscess
  • 42. • Asymptomatic cases and cyst passers- Treatment Drug Didohydroxyquin Diloxanide furoate Dose 650mg(adult), 30- 40mg/kg(children) 500mg Frequency tid tid Route oral oral Duration 20 days 10 days
  • 43. Prevention 1.Primary prevention- a.Sanitation-safe disposal of human excreta, good sanitary practice like washing hands after defecation and before eating b. Water supply-water filtration(sand filters), boiling c.Food hygiene- prevent fecal contamination of food and drink, vegetables washed with aqueous acetic acid(5-10%) d. Health education- food handlers and public
  • 44. Prevention 2. Secondary prevention- a. Early diagnosis b. Treatment
  • 45. Contd… • E. dispar is morphologically indistinguishable from E. histolytica and so is E. moshkovskii • Most asymptomatic cases of amoebic infestation are believed to be one of these two species • The other species are also non-pathogenic but can be microscopically differentiated
  • 46. Summary • Amoebiasis is an infection with the intestinal protozoa Entamoeba histolytica. • About 90% of infections are asymptomatic • Worldwide in distribution • Infectious- cyst form • Poor sanitation, sewage contamination • Wide spectrum, from asymptomatic infection to luminal amoebiasis and amoebic colitis • Invasive intestinal amoebiasis (dysentery, colitis, appendicitis, toxic mega colon, amoebomas) • Amoebic liver abscess- Most common extra-intestinal presentation • Diagnosis by stool microscopy and other investigations • Treatment tinidazole is prefered • Prevention is good sanitary practice
  • 47. Reference • PARK’S TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE • PARASITOLOGY, K. D. Chatterjee • HARRISON’S PRINCIPLE OF INTERNAL MEDICINE • Medscape • Wikipedia