• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Amoebiasis by datha

Amoebiasis by datha



ameobiasis disease and its structure

ameobiasis disease and its structure



Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

    Amoebiasis by datha Amoebiasis by datha Presentation Transcript

    • By B.Devadatha 123680029 M.Sc BMB 2nd sem Pondicherry university
    •  Introduction  Etiology  Transmission  Lifecycle  Pathogenesis  Virulence factors  Clinical features  Complications  Diagnosis  Treatment and Prophylaxis
    •  Amoebiasis is a protozoan infection of the intestinal tract that occurs due to ingestion of foods or water contaminated with Entamoeba histolytica cysts.  Entamoeba histolytica was described by Lambl in1859 and Losch established its pathogenic nature.  Councilman and Laufler in 1981 described liver abscess  Humans are the only host of E.histolytica and no zoonotic reservoirs .  There are an estimated 50million cases of amebiasis per year upto 10,0000 deaths
    •  species of Entamoeba: ◦ Nonpathogenic: E. dispar, E. coli, E. hartmanni ◦ Pathogenic: E. histolytica , Dientamoeba fragilis, which causes Dientamoebiasis  amoebiasis = A Parasitic infection caused by the protozoan 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%)
    •  Amoebiasis is usually transmitted by the fecal- oral route  indirectly through contact with dirty hands or objects  Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and hardy structure found in feces.  transmitted through contaminated food and water
    • Precysticstage:  Trophozoites living in the intestine undergo binary fission  Round and 10-20µ in size  Store glycogen granules and chromatoid bodies Cystic stage:  Enters by forming a delicate cystwall around itself  Size is 12µ  Quadrinucleated cyst is the infective stage of the parasite  Ingested by human host pass along with food into the small intestine  Wall of cyst dissolved by trypsin  Tetranucleate emerges out from cyst into lumen of large intestine called excystment
    •  Metacystic amoeba with four cystic nuclei from each cyst  8 Small trophozoites from each metacystic amoeba The Trophozoite Stage:  10-40 µm, 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.
    •  The spherical structure (Trophozoites) has one basophilic nuclei about the size of RBC’s. Note some RBC's are phagocytosed by the Trophozoites (erythrophagocytosis).
    •  Trophozoites of E.histolytica interact with host through a series of steps 1. Adhesion of target cell, phagocytosis and cytopathic effect 2. E.histolytica induces both Humoral and cell mediated immune responses. 3. Virulence factors – In many circumstances lumen dwelling Amoeba may be asymptomatic 4. Causes disease only when invade the Intestine 5. Virulence is associated with secretion of Cysteine proteniase which assists the organism in digesting the extracellular matrix and invading tissues
    •  It is observed Cysteine proteinase produced by invasive strains of E.histolytica inactivates the complement factor C3 and are thus resistant to Complement mediated lysis.
    •  Trophozoites adhere to colonic mucosal glycoproteins via a galactose and N-acetyl-D-galactosamine-specific lectin.  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 γ-INF and TNF-α to activate macrophages and Neutrophils to kill the trophozoite.
    •  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
    •  Most cases of amebiasis have very mild symptoms or none.  More severe infection may cause fever, profuse diarrhea, abdominal pain, jaundice, anorexia, and weight loss.  In severe cases, it can lead to development of abscesses (pockets of amoebae and inflammatory cells) in the liver or, more rarely, the brain.
    • 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.
    • Complications of Extra-Intestinal Amoebiasis: ◦ Amoebicliverabscess  Commonly found in Right Lobe of liver  Presents acutely with high fever, RUQ tenderness  Jaundice an unusual findings ◦ 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  Rupture left lobeliverabscess ◦ Cerebral amoebiasis  Rare, has altered consciousness and focal neuro signs o Genito-Urinary Involvement  Painful genital ulcers – Punched out appearance & profuse discharge
    •  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 & 90% ◦ For liverabscess  Stool antigen-detection test ◦ Sensitive and Specific A sample of freshly collected Fecal specimen
    • Luminal Amebicides  Acts on the parasites in the lumen of the bow  Diloxanide Furoate  Iodoquinol Tissue Amoebicides  Acts on the intestinal wall and liver  Emetine  Dehydroemetine  Chloroquine Mixed amoebicides  Metronidazol  Tinidazole
    •  Drink only bottled or boiled (for 1 minute) water, or carbonated (bubbly) drinks in cans or bottles.  Avoid fresh fruit or vegetables that were peeled by someone else.  Avoid milk, cheese, or dairy products that may not have been pasteurized.  Avoid anything sold by street vendors.
    •  Thoroughly cook all raw foods.  Thoroughly wash raw vegetables and fruitchanging diapers, after smoking or after using a tissue or handkerchief. s before eating.  Reheat food until eaches at least 167º Fahrenheit.  Wash your hands before preparing food, before eating, after going to the toilet or