Immunoparasitology Flashcards
Ectoparasite vs endoparasite
Ectoparasite: lives on surface of host (lice, ticks, mites)
Endoparasite: lives inside host (Toxoplasma gondii)
Obligate vs Facultative parasite
Obligate: completely dependent on host during part/ all of its life cycle (Plasmodium sp.)
Facultative: exhibits both parasitic + free-living stages (doesn’t completely depend on host for survival ie. Naglaria fowleri)
Accidental vs Erratic parasites
Accidental: infects an unnatural host and survives (Hymenolepis diminuta)
Erratic: migrates improperly and ends up in host tissues where it is not usually found (Trichinella spiralis)
Direct impacts on host
- mechanical injury (migration, growth = blockage)
- toxic substances (waste + immunological distractions)
- nutrient deprivation (competes for iron, energy, water)
- anemia (consumption/ destruction of RBCs
Indirect impacts on host
- inflammation (parasite presence or released molecules)
- encapsulation (granuloma formation)
- reduced cognitive capability
3 stages of immune response to parasites
- Initial exposure
- complement targets parasite for encapsulation + phagocytosis
- previous exposure may have resulted in circulating antibodies
- parasites can encounter immune cells during migration - Establishment of Infection
- tissues: cellular defence + inflammation
- blood: cellular defences, antibody, circulating defence molecules, complement
- gastrointestinal: IgA, antimicrobial peptides, physical environment - Chronic
- long-term infections usually evades immune system
Neutrophil response to parasites
- same functions as macrophages (respiratory burst)
- cytotoxic proteins released with granules:
— Primary: Myeloperoxidase, bacteriacidal, permeability-in
— creasing protein, defensins, elastase
— Secondary: alkaline phosphatase, lysosome, collagenases
Tertiary
Eosinophil response to parasites
- associated with worm infections too large for phagocytosis
- degranulate when surface Fc receptors recognize IgE (enhanced by cytokines ie. TNF-a)
- often acts with Mast cells bc of IgE detection
Phagocytosis response to parasites
- tissue macrophages, monocytes, and granulocytes have basal defence capacity that can be engaged before cytokine production or antibody response is generated
- phagocytic cells remove protozoans and encapsulate small multicellular parasites
- results in inflammation + production of cytokines that regulate the subsequent immune response
- facilitates breakdown of pathogen material so it can be presented to cells of adaptive response (MHC II)
Inflammation response to parasites
Inflammation and intracellular killing occur via production of reactive oxygen and nitrogen species + cytokines that initiate a signalling cascade = activation of immune cells during migration+ production of further general anti-pathogen effectors
IgE
- shortest half-life (2.5 days) = least common serum antibody
- high affinity with mast cell, basophil, and eosinophil Fc receptors
- DOES NOT BIND COMPLEMENT
= immunity to helminth (Schistosoma mansoni, Trichinella spiralis) + protozoan parasites (Plasmodium sp.)
= associated with allergy and hypersensitivity = anaphylaxis
IgE interaction with Mast Cells
Mast cell: critical for helminth defence
- tissue + mucosal
IgE-activated:
- degranulation = serine proteases, histamines, serotonin, anticoagulant (heparin), platelet activating factor, cytokine, eosinophil chemotactic factor
= extensive swelling, vasodilation, inflammation and pain/ itching
= allergic response = anaphylaxis if primed by high IgE
Antibody-Dependent Cell-mediated Cytotoxicity
- innate effector cells (NK, eosinophil, neutrophil) recognizes antigen-bound antibodies on parasite surface
- mediated through recognition of Fc portion of an antibody by a cell-surface Fc receptor with IgG or IgE = cytokine release (IFN-y, perforin, granzymes) = apoptosis
- important for defence against larger helminth parasites (too large for phagocytosis)
