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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