Amebiasis
-bhanu chalise
• Harboring(infection) of protozoa Entamoeba histolytica inside the body with or without the disease is called amoebiasis.
• Associated with high mortality and morbidity
• Major public health problem globally• 2nd leading cause of death due to parasitic
disease ( 1st being malaria )
Epidemiology• 10% of population infected globally• About 100,000 deaths occur every year globally• High prevalence in tropics and subtropics• Risk factors: Developing countries Developed countries
travelers immigrants homosexual men HIV positive immunodeficiency states
poverty
Ignorance
overcrowding
Poor sanitation
malnutrition
Causative organism
3 species of entamoeba: E. dispar : E. moshkovskii : E. histolytica
Only E. histolytica is pathogenic. Other two species are apparently non-pathogenic and cause most of the asymptomatic cases.
Morphology• Different form of E. histolytica: 1- trophozoite 2- precyst 3- cyst(1, 2, 4 nuclei)• Quadrinucleated cyst is the infective stage
oval/round resistant to chlorination destroyed above 55 degree celsious and with disinfectants
• Trophozoite stage is feeding vegetative form which is destructive to tissue
Trophozoites of Entamoeba histolytica with ingested erythrocytes (trichrome stain)
The ingested erythrocytes appear as dark inclusions. Erythrophagocytosis is the only morphologic characteristic that can be
used to differentiate E. histolytica from the nonpathogenic E. dispar.
F E
Virulence factorsTrophozoites of E. histolytica interact with host through a series of steps:
Adhesion of target cell, cytopathic effect E.histolytica induces both Humoral and cell
mediated immune responses Causes disease only when invade the
Intestine Virulence is associated with secretion of
Cysteine proteinase (histolysin) which assists the organism in digesting the extracellular matrix and invading tissues
Cysts of Entamoeba histolytica /E. dispar
• GHI
I H GCysts of Entamoeba histolytica/E.
dispar, permanent preparations stained with trichrome.
Transmission1) feco-oral(direct hand-to-mouth contact)2) Veneral transmission among homosexual males3) Food or drink contaminated with feces containing the E.
histolytica cyst4) Use of human feces (night soil) for soil fertilizer5) contamination of foodstuffs by flies, and possibly
cockroaches
a single cyst is sufficient to cause the disease Asymptomatic human( the only host) cyst
carriers are the principle reservoir of infection.
Pathogenesis Ingestion of
cysts Excystation in small intestine
Production of 8 trophozoites
Multiplication and Colonization in large intestine
Tissue invasion and destruction
Flask – shaped ulcers(mostly in
caecum, transverse and sigmoid colon
Encystation and exit from
host in the stool
Migrate via Blood
stream( portal circulation) to
the liver Amoebic liver abscess
Clinical featuresIntestinal • Asymptomatic
carriers(90%)• Amoebic colitis• Fulminant colitis• Amoeboma
Extraintestinal• Liver • Lung • brain • skin
Incubation period : varies from weeks to months : average= 3-4 weeks
Asymptomatic carriers -90% without symptoms(non-invasive) - lumen not damaged(cyst passers)Invasive forms: Amoebic colitis/dysentery - flask shaped ulcers superficial or deep - abd.pain, watery/mucoid blood-streaked foul-smelling diarrhoea - fever, tenesmus, peri-anal ulcers - sometimes intermittent diarrhoea alternating constipation Fulminant colitis - <0.5% - severely ill with high fever - profuse bloody diarrhea - perforation(diffuse tenderness) - paralytic ileus -pronounced leukocytosis
• ulcers with raised borders• little inflammation between lesions
Amoeboma- 1% of cases- inflammatory thickening of intestinal wall- palpable mass with trophozoites
Symptoms of amoebic colitisSymptoms Percentage
Diarrhea 100 Dysentery 99 Abdominal pain 85 Fever 68 Dehydration 5
Complications: toxic megacolon, amoeboma, cutaneous amoebiasis, rectovaginal fistula
Amoebic v^s Bacillary Dysentery symptoms Amoebic dysentery Bacillary dysentery Occurrence Usu. In the form of sporadic cases Usu. In the form of outbreaks
Onset gradual Acute
Fever Usu. Low grade (may be high in case of liver abscess)
High grade
Tenesmus/Abd. Cramps Moderate Very severe
Stool Foul- smelling Not foul-smelling
RBCs In clumps Discrete
Pus cells Scanty Numerous
Eosinophils Present Absent or rare
Bacteria Numerous, motile Scanty, non-motile
E. histolytica Trophozoites + Absent
Growth on culture Negative Positive
Extra-intestinal
Amoebic liver abcess(most common) - 5% of invasive disease - 10 times more common in men -Usually no bowel symptoms except sometimes -right upper quadrant tenderness - hepatomegaly - jaundice(10- 15%)Pleuropulmonary/pericardial
- direct spread(transdiaphragmatic rupture) from liver abscess (10%) - hematogenous spread -cough with crepitation
Similarly infection can spread to brain, skin and genitourinary system
Investigation
Parasite detection Antibody detection
Antigen detection PCR and other tests
Investigation
Parasite detection1. Direct saline(wet) mount of feces:
- most common microscopic technique-sample examined within 1 hour of collection-3 stool samples taken on consecutive day ( since
sensitivity increased from 60% to 90%)-presence of ingested erythrocytes within trophozoites is
pathognomic for E. histolytica-carriers have only cysts in their stool Misidentification: macrophages v^s trophozoites : PMN v^s cysts : other entamoeba
2. Various culture techniques are available but not done routinely
Antibody detection tests
• Routinely employed for extra-intestinal dz– Positive(75%)- at presentation and 90%- beyond
1st week of symptoms– ELISA is most sensitive – IHA– Latex agglutination– Immunoelectrophoresis and immunodiffusion
Antigen detection• ELISA kits( sensitivity>90%): used in
epidemiological studies ; useful in endemic areas
• Antigen detection by ELISA: is the ideal test – distinguishes current from past infection.
PCR OTHER TESTS: chest radiograph
: CT , MRI : sigmoidoscopy : peripheral blood- leukocytosis without eosinophillia, mild anemia : Alp, ESR are common lab findings.
• raised immobile right diaphragm• Other imaging modalities show
– A single abscess in the right or left lobe
– Multiple lesions can be present
Imaging
None of these modalities can
differentiate amebic abscess from pyogenic
or malignant one
Treatment of amebiasis -combination of a luminal and a tissue amoebicide is advocated for complete parasite clearance in Invasive disease
Luminal amoebicides• Diloxanide furoate• diiodoquinol• paromomycin
Tissue amoebicides• 5-nitroimidazoles(DOC) -metronidazole -tinidazole -secnidazole• Chloroquin• Dehydroemetine
Amoebic colitis: metronidazole followed by a luminal agentFulminant amoebic colitis: add an antibiotic to deal with bowel floraAmoebic liver abscess: tissue amoebicide followed by luminal agent
treatment continued…………………
Asymptomatic intestinal carriers : a luminal agentTreatment for only E. dispar is not nessary Most patients show a response to a treatment( reduced
fever and abdominal pain) within 72-96 hrs.Percutaneous therapeutic aspiration guided by ultrasound
or CT is reserved for: -when lesion in the left lobe of liver -when diagnosis is uncertain - no response to metronidazole( persistent fever and abd. pain) after 4 days of treatment -large(>8-10 cm) ie. >300 ml of fluid -severly ill patients
Amoebicide Pediatric dose Adult dose
Metronidazole 35-50 mg/kg/day for 7-10 days( in 3 divided doses)
750 mg 8 hourly
Tinidazole 50 mg/kg/day for 3 days(once daily)
2 g once a day
Paromomycin 25-35mg/kg/day for 7 days(in 3 divided doses)
25-35mg/kg/day (in 3 divided doses)
Diloxanide furoate 20mg/kg/day for 7 days(in 3 divided doses)
500mg 8 hourly
Iodoquinone 30-40mg/kg/day for 20 days(in 3 divided doses)
650mg 8 hourly
DRUGS AND DOSES
PREVENTION & CONTROL Primary prevention
Safe excreta disposal Safe water supply Hygiene Health education Treat symptomatic carriers Treat water(iodine, boiling): NOT
chlorine Secondary
Early diagnosis Treatment
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