Harboring(infection) of protozoa Entamoeba histolytica inside the body with or without the disease is called amoebiasis.
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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 2 nd leading cause of death due to parasitic disease ( 1 st 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 factors Trophozoites 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 G Cysts of Entamoeba histolytica / E. dispar , permanent preparations stained with trichrome .
Transmission feco -oral (direct hand-to-mouth contact) Veneral transmission among homosexual males Food or drink contaminated with feces containing the E. histolytica cyst Use of human feces (night soil) for soil fertilizer 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 features Intestinal 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 colitis Symptoms 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 detection 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 1 st 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 agent Fulminant amoebic colitis : add an antibiotic to deal with bowel flora Amoebic liver abscess: tissue amoebicide followed by luminal agent
treatment continued………………… Asymptomatic intestinal carriers : a luminal agent Treatment 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 T reat water(iodine, boiling): NOT chlorine Secondary Early diagnosis Treatment