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
 EPIDEMIOLOGY
World
• Worldwide in distribution

• 3rd most common parasitic death

• India, China, Mexico, Africa, South America

• 2-60% prevalence(based on ELISA and PCR studies from

stool samples)

• 100,000 deaths/yr

• 500 million infections

• 50 million cases/yr
 EPIDEMIOLOGY

India
• 15% prevalence (3.6-47.4%)

• Variation according to sanitation level and

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)

 MODES OF TRANSMISSION

 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
 INCUBATION PERIOD

• 2- 4 weeks
LIFE CYCLE OF E. HISTOLYTICA
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

• 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
 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
 LABORATORY DIAGNOSIS

Samples :
I. Stool ( 3 consecutive samples)
II. Biopsy material from the ulcers (colonoscopy or
sigmoidoscopy)
III. Aspirate from liver abscess
 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
 TREATMENT
• Symptomatic case:- (amoebic colitis and amoebic
liver abscess)

Drug Dose Frequency Route Duration

Tinidazole 2g/day tid oral 3 days

750mg(adult) 5-10
Metronidazole tid Oral/iv
30mg/kg(children) days
 TREATMENT
• Luminal infections and -(with above)

Drug Dose Frequency Route Duration

5-10
Parmomycin 30mg/kg qid oral
days

Iodoquinol 650mg tid oral 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

 TREATMENT
• Asymptomatic cases and cyst passers-

Drug Dose Frequency Route Duration

650mg(adult), 30-
Didohydroxyquin tid oral 20 days
40mg/kg(children)

Diloxanide furoate 500mg tid oral 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