Immunity To Bacteria And Fungi Flashcards
Examples of indirect mechanisms of tissue damage from pathogens
- almost all caused by the immune system/response*
- immune complex aggregation
- autoimmune antibodies
- cell-mediated immunity (hyper inflammation)
Examples of direct mechanisms of tissue damage by pathogens
- caused directly by the pathogen itself*
- exotoxins production
- Endotoxins
- Direct cytopathic effects on cells (viruses only)
Extracellular bacteria
Replicate outside of host cells in the circulation, connective tissues, mucosal surfaces
- cause bacteremia*
- leads to septicemia
Bactermeia vs septicemia
Bacteremia = bacterial pathogen itself without toxins or products
Septicemia = bacterial pathogen itself and the presence of its toxins/ products
- actually produces the acute inflammatory response
Toxic shock
Produced by certain extracellular bacteria that cause two things
- massive acute inflammation
- production of various toxins
Types of extracellular toxins
Exotoxins: heat-liable toxin that is extracellular
Enterotoxin: type of exotoxins that affects only GI mucosal surfaces
Endotoxins: intracellular toxin within the physcial bacterial cell wall and is heat stable.
hall mark of septic shock is what? And what are other affects of High TNF
intravascular coagulation and vascular collapse caused by high concentrations of TNF
- causes macrophages to release IL-1 and IL-6 which, w/ TNF, produces fevers.
Suppression of bone marrow and cachexia
- most common pathogen that is notorious for produce high fevers via large TNF release is endogenous pyrogens*
Normal numeral immune response steps with extracellular bacteria
1) bacterial proteins are taken up by APCs and process for MHC via extrinsic pathway
2) leads to MHC 2 up-regulation and activation fo C4 helper T cells
3) C4 helper T cells then activate B cells via CD40:CD40L interaction and cytokine productions
4) B cells then secrete large amounts of antibodies against the pathogenic antigen(s)
Functions of antibodies against extracellular bacteria
IgG enhances phagocytosis
- usually via opsonization
Opsonization can inhibit bacterial motility and invasion as well as stimulate its
IgG and IgM neutralizes toxins and activates complements
IgA neutralize mucosal toxins
Innate immunity to extracellular bacteria
Phagocytosis by neutrophils and macrophages
Complement begins usually via lectin-mannose pathway
C3B opsonizes the bacteria and MAC lysis the bacteria
Cell mediate immune responses
Designed to fight intracellular pathogens and tumors
- T cells macrophages and NK cells
All three cells cooperate with each other in order to eliminate intracellular antigens but is tailored based on what pathogen is present.
Granulomatous inflammation
Granuloma: lesion that develops as a result of prolonged chemotaxis
- “building a wall” around the pathogen
Consists of epitheloid cells, multinucleated giant cells and fibroblasts
- if untreated , becomes necrotic in the center
Because macrophages cannot completely eliminate the pathogen, macrophage enzymes are releasing extracellularly causing nearby cell damage
Valley fever and TB are the most common pathogens to cause granulomas
Cell-mediation immune steps
1) pathogens and their products found in cytosol are processed for MHC presentation by the intrinsic pathway
2) leads to presentation by Class 1 MHC and activation of CD 8 T cells
3) kills infection via FAS/FasL, TNF a and b, and perforin/granzymes activities
4) infected cells can also secrete large amount of cytokine which further activates CD8 T cells.
Fungi
Opportunistic pathogens that are usually difficult to phagocytosis
- too big to phagocytosis
Alternative and lectin C cascade are triggered almost all the time on fungi
- this leads to inflammation visa degranulation of granulocytes
IL 17
Decreased by H17 T cells and does the following
- induces strong inflammation and neutrophils
- stimulates production of antimicrobial substances from many cell types
- up-regulates defensins
