amoebiasis presentation by Gatere joram ward 3 pgh Nakuru

1. Amoebiasis
Ward 3 group
Presenter Gatere Joram
EGERTON UNIVERSITYS
MBChB YR IV /14

2. Background
• Entamoeba histolytica infects hundred of millions of people worldwide
• Endemic foci are particularly common in the tropics, especially in areas with low
socioeconomic and poor sanitary standards(Kenya meets the criteria)
• E. histolytica parasitizes the lumen of the gastrointestinal tract and causes few or no
symptoms or sequelae.
• Commonly manifest into two forms
Intestinal (amoebic colitis-parasitic invasion of interstinal mucosa
Extra-intestinal-amebic liver abscess with dissemination of the parasite to the
liver

3. Cnt…
• Trophozoites themselves are not infective
• Trophozoites are invasive (invade host tissues) and multiply within the human host
by cell division
• Cysts can be killed by boiling water –@55 degree Celsius
• Cysts are resistant to water treatments such as chlorination
• Cysts can survive for long periods in faeces – upto10/7
• Cysts are killed by dessication
• Transmission is by contaminated water, food, vegetable / fruits, by human faeces
(extement) i.e faeco-oral route
• Also contamination from a leaking sewage
• Flies can be vectors
•

4. Etiology
• Two morphologically identical but genetically distinct species of Entamoeba
Entamoeba dispar –more prevalent species assoc only with an asymptomatic
carrier state
E. histolytica, the pathogenic species, can become invasive, causing symptomatic
disease.
Many patients previously described as asymptomatic carriers of E. histolytica based on
microscopy findings were probably infected with E. dispar
• Other include non pathogenic E. coli, E. hartmanni, E. gingivalis, E. moshkovskii,
and E. polecki
• - Also there is Naegleria and acanthamoeba, causing fulminating meningitis and
granulomatous encephalitis

5. • Infection is established by ingestion of parasite cysts, which measure 10–18
mm in diameter and contain 4 nuclei
• After ingestion, the cyst, which is resistant to gastric acidity and digestive
enzymes, excysts in the small intestine to form 8 trophozoites.

6. EPIDEMIOLOGY.
• E. histolytica leads to 50 million cases of symptomatic disease and 40,000–
110,000 deaths annually
• Amebiasis is the 3rd leading parasitic cause of death worldwide
• 4–10% of individuals infected with E. histolytica develop amebic colitis, and
<1% of individuals develop disseminated disease- amebic liver abscess
• Amebic liver abscesses are rare in children and occur equally frequently in
male and female children, whereas in adults, amebic liver abscesses occur
predominantly in men.
• Amebiasis is highly endemic in Africa, Latin America, India, and Southeast
Asia

7. • Food or drink contaminated with Entamoeba cysts and direct fecal-oral
contact are the most common means of infection.
• Untreated water and human feces used as fertilizer are important sources of
infection.
• Food handlers carrying amebic cysts can play a role in spreading the
infection.
• Direct contact with infected feces also may be responsible for person-to-
person transmission

8. PATHOGENESIS
• Trophozoites, which are responsible for tissue invasion and destruction, attach to
the colonic epithelial cells by a galactose and N-acetyl-D-galactosamine
(Gal/GalNac)-specific lectin. This lectin is also thought to be responsible for
resistance to complement-mediated lysis
• Attachment to colonic mucosa>enzymes(cysteine-rich proteinase)>penetrate
epithelial layer. Host cell are destroyed by cytolysis and apoptosis
• Cytolysis mediated by trophozoites release amoebapores( pore forming
protein),phospholipases,hemolysins. Amoebapores also partially responsible for the
induction of apoptosis
• Muscular layer of colon relatively resistant to amoebic invasion -- lateral
spread of Amoebae
Flask shaped ulcers - Lateral spread destroy the blood supply to overlying
mucosa resulting in sloughing and large ulcerations

9. Role of intestinal flora
• i)E. Histolytica requires nutrients produced by E. coli and enterobacteria
aerogenes
• ii) After E. Histolytica infection, secondary bacterial infections e.g.
shigella, clostridia are very common

10. CLINICAL MANIFESTATIONS
A: Chronic carriers are u 90% -has the potential to become invasive and
should be treated
• Asymptomic
• Mild abdominal discomfort
• Flatulence
• Occasional diarrhea
• Constipation

11. B AMOEBIC COLITIS
• may occur within 2/52 of infection or be delayed for months. The onset is usually
gradual with colicky abdominal pains and frequent bowel movements (6–8/day).
Diarrhea is frequently associated with tenesmus. Stools are blood stained and
contain a fair amount of mucus with few leukocytes. constitutional symptoms and
signs - absent, with fever documented in only ⅓ of patients.
• Amebic colitis affects all age groups, but its incidence is strikingly high in children
1–5 yr of age. Severe amebic colitis in infants and young children tends to be
rapidly progressive with frequent extraintestinal involvement and high mortality
rates, particularly in tropical countries.
• Occasionally, amebic dysentery is associated with sudden onset of fever, chills, and
severe diarrhea, which may result in dehydration and electrolyte disturbances.

12. C Amebic Liver Abscess.
• Amebic liver abscess, a serious manifestation of disseminated infection, is
uncommon in children. Although diffuse liver enlargement has been
associated with intestinal amebiasis, liver abscess occurs in <1% of infected
individuals and may appear in patients with no clear history of intestinal
disease.
• Amebic liver abscess may occur months to years after exposure, so
obtaining a careful travel history is critical.
• In children, fever is the hallmark of amebic liver abscess and is frequently
associated with abdominal pain, distention, and tender hepatomegally.
Changes at the base of the right lung, such as elevation of the diaphragm
and atelectasis or effusion, may also occur.

13. • D: AMOEBIC APPENDICITIS
• _ There is proceeding amoebic diarrhea and dysentry
• - There is periumbilical pain – radiating to the right iliac fossa
• -Nausea and vomiting
• - Fever
• NB: Should be treated before surgery

14. E AMOEBIC GRANILOMA
• - Proceeding S+S of amoebic diarrhoea
• - Tender mass in left iliac region
• - R/o carcinoma
• - Secondary infection of the granuloma

15. DIAGNOSIS
• Amoebic colitis –Elisa (enzyme-linked-immunosorbent-assay> 90%
sensitivity and specificity for E.histolytica.
• Microscopic examination of 3 fresh stool samples (within 30 min of
passage) by experienced laboratory personnel has a sensitivity of 90% for
detecting Entamoeba, but microscopy cannot differentiate between E.
histolytica and E. dispar unless phagocytosed erythrocytes, which are specific
for E. histolytica, are seen

16. • serum antiamebic antibody tests
• Serologic results are positive in 70–80% of patients with invasive disease
(colitis or liver abscess) at presentation, and in >90% of patients after 7 days
of disease symptoms
• The most sensitive serologic test, indirect hemagglutination, yields a positive
result years after invasive infection.
• UTRA SOUND IN LIVER ABSCESS
- Pushed up one side of the diaphragm (hemidiaphroagm) and immobile---
Sigmoidoscopy and Mucosal scrapping
- Abscess Aspirate – microcopy -- Aspirate 8th – 9th rib

17. ddx
For amebic colitis includes:
Colitis due to bacterial (Shigella, Salmonella, enteropathogenic Escherichia
coli, Campylobacter, Yersinia, Clostridium difficile)
viral (cytomegalovirus) pathogens, as well as noninfectious causes such as
inflammatory bowel disease.
Pyogenic liver abscess due to bacterial infection, hepatoma,

18. • complications
• amebic colitis include necrotizing colitis, ameboma, toxic megacolon, extraintestinal
extension, or local perforation and peritonitis.
• rarely chronic form of amebic colitis develops, which can mimic inflammatory bowel disease
with bouts of abdominal pain and bloody diarrhea, often recurring over several years.
• An ameboma is a nodular focus of proliferative inflammation sometimes developing in
chronic amebiasis, usually in the wall of the colon. Chronic amebiasis should be excluded
before initiating corticosteroid treatment for inflammatory bowel disease, as corticosteroid
therapy inadvertently given during amebic colitis has been associated with high mortality
rates.
• Amebic liver abscess may be associated with rupture into the peritoneum, pleural cavity, skin,
or, rarely, pericardium when diagnosis and therapy are delayed. Cases of amebic abscesses in
extrahepatic sites, including the lung and brain, have been reporte

19. MEDICATION ADULT DOSAGE (ORAL) PEDIATRIC DOSAGE (ORAL)[*]
INVASIVE DISEASE
Metronidazole Colitis or liver abscess: Colitis or liver abscess:
or 750 mg tid for 7–10 days 35–50 mg/kg/day in 3 divided doses for
7–10 days
Tinidazole Colitis:2 g once daily for 3 days Colitis:50 mg/kg/day once daily for 3
days
Liver abscess:2 g once daily for 3–5 days Liver abscess:50 mg/kg/day once daily
for 3–5 days
Followed by:
Paromomycin (preferred) or 25–35 mg/kg/d in 3 divided doses for 7
days
25–35 mg/kg/day in 3 divided doses for
7 days
Diloxanide furoate[†] or 500 mg tid for 10 days 20 mg/kg/day in 3 divided doses for 7
days
Iodoquinol 650 mg tid for 20 days 30–40 mg/kg/day in 3 divided doses for
20 days
ASYMPTOMATIC INTESTINAL
COLONIZATION
Paromomycin (preferred) or As for invasive disease As for invasive disease
Diloxanide furoate[†] or
Iodoquinol

20. 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

21. reference
Kliegman: Nelson Textbook of Pediatrics, 18th ed.
Copyright © 2007 Saunders, An Imprint of Elsevier
Chapter 278 – Amebiasis
Chandy C. John Robert A. Salata