Amoebozoa Lineage - Entamoeba histolytica
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Questions and Answers

Which of the following protozoan parasites is responsible for amoebic dysentery?

  • Leishmania
  • Toxoplasma gondii
  • Plasmodium spp
  • Entamoeba histolytica (correct)
  • Invasive strains of Entamoeba cause symptoms primarily through the invasion of epithelial cells lining the intestine.

    True

    What is the primary mode of transmission for Entamoeba histolytica?

    Through food, fomites, fingers, feces, and flies.

    The cyst wall of Entamoeba histolytica is primarily composed of ______.

    <p>chitin</p> Signup and view all the answers

    Match the following protozoa with their respective lineages:

    <p>Entamoeba = Amoebozoa Plasmodium spp = Alveolata Trypanosoma = Excavata Toxoplasma gondii = Alveolata</p> Signup and view all the answers

    What are the two main stages in the life cycle of Entamoeba histolytica?

    <p>Cyst and Trophozoite</p> Signup and view all the answers

    All strains of Entamoeba histolytica are highly virulent and cause severe gastrointestinal symptoms.

    <p>False</p> Signup and view all the answers

    The trophozoite stage of Entamoeba histolytica is responsible for ______ and ______.

    <p>feeding; replicating</p> Signup and view all the answers

    What is the primary role of E.histolytica's Gal/GalNAc lectin?

    <p>To bind to host mucosal cells, preventing lysis</p> Signup and view all the answers

    E.histolytica can cause serious intestinal ulcers that may be invaded by bacteria.

    <p>True</p> Signup and view all the answers

    What distinguishes E.histolytica from E.dispar in terms of pathogenicity?

    <p>E.histolytica is pathogenic while E.dispar is not.</p> Signup and view all the answers

    The main protein secreted by E.histolytica that disrupts epithelial tight junctions is __________.

    <p>prostaglandin EG (PGE2)</p> Signup and view all the answers

    Match the type of amoebiasis with its corresponding symptoms:

    <p>Hepatic amoebiasis = Liver abscess and right upper quadrant pain Pulmonary amoebiasis = Cough and blood-stained sputum Cutaneous amoebiasis = Perianal ulcers Amebic brain abscess = Vulnerability in immunocompromised hosts</p> Signup and view all the answers

    Which enzyme is involved in the trogocytosis process of E.histolytica?

    <p>Phosphoinositide 3-kinase (PI3K)</p> Signup and view all the answers

    Amoebic granulomas can be mistaken for tumors.

    <p>True</p> Signup and view all the answers

    What is the effect of trogocytosis on the immune recognition of E.histolytica?

    <p>It allows E.histolytica to display host MHC I proteins, evading immune detection.</p> Signup and view all the answers

    Treatment for symptomatic amoebic dysentery often includes __________ or __________.

    <p>Metronidazole, tinidazole</p> Signup and view all the answers

    What happens to the intestinal wall due to the ulcers caused by E.histolytica?

    <p>It develops fibrous scar tissue</p> Signup and view all the answers

    Study Notes

    Amoebozoa Lineage - Entamoeba histolytica

    • Characteristics: Locomotion and feeding via pseudopodia; heterotrophic, consuming bacteria via phagocytosis; asexual reproduction by binary fission; parasitic forms infect humans and primates. Intestinal parasitic forms are anaerobic. Examples include Entamoeba, Endolimax, Balamuthia.

    • Entamoeba histolytica: Causes amoebic dysentery, characterized by bloody or mucus-containing stools, cramping, fever, and weight loss. Common in areas with high population density and poor sanitation. Many cases are asymptomatic.

    Entamoeba Life Cycle

    • Two stages: 

      • Trophozoite: Actively growing, feeding, and replicating stage.
      • Cyst: Transmission stage, resistant to environmental conditions.
    • Transmission: Five Fs (food, fomites, fingers, feces, flies).

    Pathogenesis of E. histolytica

    • Non-invasive (avirulent) strains: Trophozoites remain in intestinal lumen, causing mild GI symptoms or being asymptomatic. Can develop into invasive strains by penetrating the mucosa. These strains ingest bacteria and cellular debris and do not penetrate the mucosal layer.
    • Invasive (virulent) strains: Trophozoites invade intestinal cells, spread to underlying tissues, cause flask-shaped ulcers, and lead to extensive bleeding. Hematophagous trophozoites rapidly replicate, causing ulcer expansion and necrotic colitis. Can cause extraintestinal amebiasis, spreading via the circulatory system. Parasite enzymes further damage the host's extracellular matrix, leading to muscle and serous layer perforation, peritonitis, and extraintestinal infection spread.

    Adherence to Host Mucosal Cells

    • E. histolytica lectin: Binds tightly to host galactose (Gal) and N-acetyl-D-galactosamine (GalNAc) residues, crucial for adherence and virulence.

    Virulence Mechanisms and Factors

    • Virulent vs. Avirulent: E. histolytica is pathogenic, while E. dispar is not. Differences in lectin sequences and protein expression are contributing factors.
    • Inflammation: E. histolytica lectins induce host inflammatory response; disrupt tight junctions, altering paracellular permeability.
    • PGE2: E. histolytica secretes prostaglandin EG (PGE2) that disrupts epithelial tight junctions.
    • Apoptosis: E. histolytica surface lectins trigger host cell apoptosis.
    • Amoebopores: Perforate host membranes; E. histolytica has higher expression than E. dispar, contributing to host-cell lysis.
    • Cysteine Proteases: Break down proteins, degrade the mucosal layer and extracellular matrix.
    • Trogocytosis: E. histolytica ingests host cell fragments, acquiring host cell membrane proteins, potentially evading immune responses (MHC I proteins).

    Immune Evasion

    • Immune cell destruction: E. histolytica directly consumes host immune cells.
    • Suppression of immune molecules: Suppresses IFN-γ and NF-κB.
    • Complement system evasion: Thick impervious layer (LPPG) resists complement attack.
    • Host proteins on parasite surface: Expressed MHC I proteins that inhibit MAC (membrane attack complex) formation, impeding innate immune responses,
    • Anti-oxidative stress enzymes, neutralize host ROS.
    • Cleaving IgA and IgG for inactivation: CPs (cysteine proteases) cleave host intestinal IgA antibodies and circulate IgG.

    Extraintestinal Amebiasis

    • Hepatic amoebiasis: Most common, involving liver abscesses ("anchovy sauce" appearance). Possible rupture to peritonitis, or to the lungs.
    • Pulmonary amoebiasis: Liver abscess rupture through the diaphragm.
    • Cutaneous amoebiasis: Perianal ulcers
    • Amebic brain abscess: Rare, but dangerous in immunocompromised individuals.

    Treatment

    • Asymptomatic: Nitroimidazole, iodoquinol, paromomycin, or diloxanide furoate are options.
    • Symptomatic/Colitis/Extraintestinal: Metronidazole or tinidazole are typical treatments
    • Severe cases (Necrosis/perforations): Dehydroemetine or emetine may be necessary.

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    Description

    Explore the fascinating world of Entamoeba histolytica, a significant parasite responsible for amoebic dysentery. This quiz covers its characteristics, life cycle, and pathogenesis, highlighting the importance of understanding its transmission and effects on human health.

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