AMOEBIC ABCESS

Dr.Hary Bagijo Sp.PD,FINASIM

Bagian Gastro-Entero-Hepatology
FK UHT/RSAL Dr.Ramelan
 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
 Quadrinucleated
 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 Trophozoite Stage:
 10-40 qm, fragile
 Uninucleate
 Erythrophagocytosis
 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 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 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 Pathogenesis
 Area most commonly  Flask-shaped ulcers
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.
 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

 Often gradual 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
 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 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 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
 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 amoebic colitis
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 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 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

amoebic abcess
 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

 Prevention
 Improved sanitation and clean water supply
reduce fecal-oral transmission
 Boiling water, Washing veg with vinegar

 Vaccination:
 None available currently

 Prototype subunit vaccines based on the

Gal/GalNAc-lectin under study