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AMOEBIASIS. HISTORY. 2yr 10mo girl Main Complaint: 7 days of loose, bloody diarrhoea and vomiting Lethargic and doesn’t feed well Previous history: Uneventful perinatal history No previous admissions to hospital Numerous clinic visits in preceding months for diarrhoea RVD status unknown

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  • 2yr 10mo girl
  • Main Complaint:
    • 7 days of loose, bloody diarrhoea and vomiting
    • Lethargic and doesn’t feed well
  • Previous history:
    • Uneventful perinatal history
    • No previous admissions to hospital
    • Numerous clinic visits in preceding months for diarrhoea
    • RVD status unknown
    • No TB or other infectious contacts
    • No recent travel history / No significant family history
    • DIET: Never breastfed , Feeds on a family diet that includes mainly veg protein and carbohydrates. Denies traditional medicine ingestion.
  • Growth paramoeters:
    • Weight: 11kg - 73% of expected for age
    • Length: 86cm – Below 3rd centile
    • Head Circ: 48cm – On 50th centile
    • Weight for height: Just below 3rd centile
    • Temp: 37.1 HR:135bpm RR:42/m BP:70mmHg syst
    • Distressed, ill-looking, pale, 7.5% dehydrated
    • Chest, CVS & CNS: Normal
  • Abdomen:
    • Soft, distended abdomen with decreased bowel sounds
    • 3cm hepatomegaly – Firm, sharp edge, smooth surface non-displaced and not tender.
    • Fullness possibly a mass lesion extending from R flank across midline & tender to touch.
    • Normal hernial orifices and female genitalia
    • PR: No exterior abnormalities noted

Irregular rectal mucosa

Bloody, foul-smelling diarrhoea mixed with pus noted

special investigations

WCC: 3.12

Hb: 9.5

MCV: 80.1

Platelets: 127

Diff: Neut: 42.7%

Mono: 17.8%

Lymph: 35.7%

Eosino: 1.8%

Smear: Left shift + toxic granulation.

CRP: 337


129 / 2.6 / 91 / 24 / 3.4 / 38


Tbili: 13 Cbili: 1

TP: 46 Alb: 17 Glob: 29

ALP: 54 GGT: 32

ALT: 68 AST:81

Urine culture: Negative

Stool culture: Negative

Blood culture: Negative

RVD Elisa: Positive

CD4: 188 (4.62%)

TB W/Up: Negative

special investigations1

Distended loops of large bowel with air fluid levels

No free air noted

Abd. Sonar:

Aperistaltic thickened loops of bowel in RFI

No mass seen

CT Abdomen:

Fluid-filled large & small bowel loops

Closely related bowel loops in RFI – bowel wall thickening

No definite mass seen


Mass seen at recto-sigmoid junction – biopsy taken


Rectal biopsy with extensive mucosal ulceration.

Marked inflammatory cell infiltrate composed predominantly of chronic inflamm. cells and fibrin deposition

Amoebae noted and confirmed with PAS stain.

summary management
  • 2yr 10mo girl with
    • Immunosuppression
    • Amoebic proctitis and a chronic inflammatory mass at the recto-sigmoid junction consistent with an amoeboma.
  • Treated with oral Metronidazole
  • Optimized general condition in terms of nutrition
  • Referred for initiation of HAART
the organism
The Organism
  • 4 species of Entamoeba:
    • Nonpathogenic: E. dispar, E. coli, E. hartmanni
    • Pathogenic: E. histolytica
  • amoebiasis = A Parasitic infection caused by the protozoon Entamoeba histolytica
    • 2nd to Malaria as protozoan cause of death worldwide
  • 10% of world’s population infected – Increased prevalence in developing countries (up to 25%)
    • In SA – More common in KZN
  • Factors contributing to faecal-oral spread:
    • Poor education
    • Poverty and overcrowding
    • Unsanitary conditions
    • HIV infection
the life cycle
1. Cyst Stage

Infective stage

Survive from –4 to 40 Celcius

Size – 12mm


Ingested by contact with fecally contaminated food

Passes through stomach, excysts in lower small bowel.

Metacystic amoeba with four cystic nuclei from each cyst

8 Small trophozoites from each metacystic amoeba

Trophozoites carried to cecum

The Life Cycle
the life cycle1
The Trophozoite Stage:

10-40 qm, fragile



Reside, feed and multiply by binary fission in lumen of colon

May invade – Lytic & physical mechanisms and metastasize to liver and other extra-intestinal sites

Galactose-containing molecules & receptors regulate cyst formation

Precyst – Cyst – Uninucleate to Quadrinucleate and passed in stool

The Life Cycle
the pathogenesis
The Pathogenesis
  • 10% of infected individuals develop invasive disease
  • Factors contributing to developing invasive disease:
    • Pathogenicity of infecting Entamoeba species
    • Dose of inoculum
    • Host factors: Impaired cell-mediated immunity, on steroids
    • Virulence of infecting species:
      • Presence of surface adhesion factors
      • Release of proteolytic enzymes
      • Release of cytotoxins and inflicting of cytolysis
the pathogenesis1
The Pathogenesis
  • Trophozoites adhere to colonic mucosal glycoproteins via a galactose and N-acetyl-D-galactosamine-specific lectin.
    • (Gal/GalNac) – Lectin is 260kD-surface protein consisting of a 225kD subunit and a 35kD subunit.
  • Adherence results in cell lysis (apoptosis) and PMN invasion
  • PMN’s are then lysed releasing lytic enzymes, causing more tissue destruction
  • Small foci of necrosis in the intestinal wall coalesce to form ulcers (Flask-shaped ulcers)
  • Parasites resist destruction by complement arm of immune system via Gal/GalNac mediated inhibition of the membrane attack complex
  • Cell-mediated immunity is important in clearing infection through generating Ұ-INF and TNF-α to activate macrophages and neutrophils to kill the trophozoite
the pathogenesis2
Area most commonly involved = Cecum, then Recto-sigmoid area

May invade blood vessels causing thrombosis, infarction and dissemination via portal circulation to liver and extra-intestinal sites eg. brain, pleura, pericardium and genito-urinary system.

Flask-shaped ulcers

The Pathogenesis
the clinical features
The Clinical Features
  • Many infections = Asymptomatic ‘cyst passers’
  • Symptomatic infections may have a gradual, acute or rapid, fulminant course.
  • Clinical incubation period = 4 days to several months
  • Oftengradual development of symptoms = Irregular bouts of diarrhoea, abdominal pain, weight loss, nausea, loss of appetite

(amoebic proctocolitis)

  • Less often sudden onset of copious diarrhoea containing mucus and blood.
  • Findings may include low-grade fever, tenderness on palpation of the abdominal wall overlying involved large bowel.
the complications
The Complications
  • Complications of Intestinal amoebiasis:
    • Fulminant Amoebic Colitis with Perforation
      • May have a mortality rate of up to 50%
      • Children less than 2 yrs at increased risk of perforation
    • Massive Haemorrhage
      • Due to vasculitis of large arteries or multiple ulcers leading to small arterial leaks
    • amoebomas
      • A granulomatous thickening of the colon resulting from lytic necrosis followed by secondary pyogenic inflammation, leading to fibrosis and proliferative granulation tissue. Lesions are firm, hard, may resemble a carcinoma.
    • amoebic Stricture
      • Resulting from fibrosis of intestinal wall. Can involve rectum, anus or sigmoid.
the complications1
The Complications
  • Complications of Extra-Intestinal Amoebiasis:
    • Amoebic Liver Abcess
      • Most frequent complication of amoebiasis
      • Male:Female Ratio = 1 in Children and infants
      • In adulthood = More common in young males
      • Third to Half may have no history of diarrhoea
      • Commonly found in Right Lobe of liver
      • Presents acutely with high fever, RUQ tenderness
      • Jaundice an unusual finding
      • Have marked leucocytosis and may have XR abnormalities in 25 to 90% of patients
the complications2
The Complications
  • Complications of Extra-Intestinal amoebiasis:
    • amoebic Peritonitis
      • As a complication of a ruptured hepatic abcess
    • Pleuropulmonary amoebiasis
      • Caused by rupture of Rt. Lobe Liver abcess in 10% of patients
      • Has cough, pleuritic chest pain & dyspnoea
    • amoebic Pericarditis
      • Rare, but most serious complication in 3% of pts. with liver involvement
      • Rupture of Left Lobe liver abcess
    • Cerebral amoebiasis
      • Rare, has altered consciousness and focal neuro signs
      • CT – Irregular lesions without surrounding capsule or enhancement
    • Genito-Urinary Involvement
      • Painful genital ulcers – Punched out appearance & profuse discharge
the diagnosis
The Diagnosis
  • Light Microscopy of Stool
    • Identification of trophozoites / cysts in fresh stool
    • Disadvantages:
      • Not sensitive (miss up to two thirds of infections)
      • Cannot distinguish between E.histolytica and E. dispar
  • Serology:
    • Anti-amoebic antibodies (IgM) 70% sensitive for amoebiccolitis and 90% sensitive for amoebic liver abcess
  • Stool antigen-detection test or PCR
    • Sensitive and Specific
    • Disadvantages:
      • Antigen detection test (EIA) only available from Blacksburg VA
the diagnosis1
The Diagnosis
  • Colonoscopy / Sigmoidoscopy
    • Colonoscopy preferable
    • Wet preps of material from ulcer-base can show trophozoites
    • Biopsies should be taken from edge of ulcers
    • Recommended to evaluate for amoebic colitis even when Ulcerative Colitis considered
the diagnosis2
The Diagnosis
  • amoebic Liver Abcess:
    • Diagnosis relies on:
      • Detection of risk factors for E.histolytica infection
      • Positive Serology
      • Lesion in Liver :
        • Abdominal USS
        • Abdominal CT: Well-rounded, wall enhances
      • Aspiration may yield “anchovy-paste” material
        • More often yellow / gray-green
        • Often odourless and sterile – Highly suggestive of amoebicabcess
the management
The Management
  • Asymptomatic infections
    • Luminal agent only recommended but ?not available in SA
    • In general, not treated in endemic areas
  • Symptomatic infections
    • Oral Metronidazole for 10 days
    • Effective in eradicating amoebae in bowel lumen and wall
    • Effective in eradicating extra-intestinal disease
    • Additional luminal agent not necessary
  • E. dispar infection doesn’t require treatment
  • Improved sanitationandclean water supplyreducefecal-oral transmission
  • Boiling water, Washing veg with vinegar
  • Vaccination:
    • None available currently
    • Prototype subunit vaccines based on the Gal/GalNAc-lectin under study