12 - Immunity to Parasites And Fungus (Steph) Flashcards
protozoan parastes
- unicellular, mostly intracellular
- many motile, many free living and found in contaminated water
- others move from arthropod vectors
metazoans
helminth worms, mostly extracellular
what immune response does a protozoan parasite elicit when in bloodstream, gut or interstitial fluids
humoral antibody responce
when a protozoan parasite is in its intracellular life cycle, what immune response does it elicit
cell-mediated immune response
what is malaria caused by
Plasmodium spp. carried by female anopheles mosquitos
plasmodium has what kind of life stages
multiple extracellular and intracellular stages of infection
throught the lifecycle of plasmodium, where does it move within the body
moves through liver/RBCs
what are the intracellular phases of plasmodium able to resist
Ab-based responses
how does plasmodium avoid good immune stimulation
- short blood circulation time free parasite stage prevents good immune stimulation
- Ab responses avoided by outer coat of shedding
T/F: Babesia bovis is multicellular
false
what clinical signs does Babesia bovis cause
hemolytic anemia (cattle fever, piroplasmosis)
how is Babesia bovis transmitted?
by bites from infected larval ticks (ixodes)
leishmaniasis is tranmitted through what?
sandflies
what kind of pathogen is leishmania
obligated intracellular pathogen
2 syndromes caused by leishmania
- Localized cutaneous self-resolving lesion
- Systemic visceral leishaniasis (fatal without treatment)
2 cells that leishmaniasis invade
neutrophils and macrophages
where do leishmaniasis live
in macrophage phagosomes
why does leishmaniasis cause skin inflammation
through tissue damage and sandfly salivary proteins
what response does leishmaniasis elicit
CD4+ and Th1response and Th1 delayed hypersensitivity (chronic exposure), INF-gamma secretion, M1like macrophages (iNOS, nitric oxide), eosinophils may promote unprotective Th2
describe parasitic worms and a few examples
large, multicellular. NEMATODEs, cestodes, trematodes
how do worms contaminate the environement
eggs contaminate food, water and feces
are helminths intracellular or extracellular
exclusively extracellular
how do helminths enter the host
through internal mucosa
why do helminths have limited immune engagement
often do not replicate within host, giving few epitopes
do helminths get phagocytozed
no, they are two large to get phagocytosed
how do helminths hide from immunity
wrap themselves in host proteins and limit immunity
how do helminths get expelled
IgE mediated mast cells and eosinophil degranulation
- release of histamines and leukotrienes that induce muscle contractions and mucus secretion (diarrhea, vomit and coughing)
2 ways helminths get expelled
Ig-mediated past cell and eosinophil degranulation and Th2 type responce
describe the Th2 type response for expelling helminths
IL-4 production, Th2 cell activation and IgE
describe the effective and ineffective mechanism for expelling helminths
Th2 = effective: Includes IgE, mast cell degranulation, influx of eosinophils, antibody dependent cytotoxicity
Th1 = ineffective: macrophages and INF-gamma. Likely inhibited as an invasion mechanism, parasite might survive if this response is activated
how are fungal infections aquired
ubiquitous
how do fungal infections gain access to the host
via mucosae to extracellular spacesw
what causes fungal infections
exogenous or endogenous commensal organisms that become pathogenic
what kind of immunity controls most fungal infections
Innate immunity!
- physical barriers
- commensal microbiota. Antibacterial medications may result in yeast infections
- phagocytosis by neutrophils
what is key for controlling fungal infections
PRRs: C-type lectin receptors sense cell wall components (B glucans, mannans, chitin),
- TLRs 2,4,9 and complement receptor 3
- Th1 response
- Adaptive immunity
what increases susceptibility for fungal infections
Th2 response ??
T cell immunosuppressed patients
Describe Neospora caninum
- obligate intracellular parasite
- affects cattle (abortions) and dogs
- domestic dogs are the host
describe the balance between Th1 + Th2 response for controlling neosporosis
Th1 responce –> INF-gamma –> control of infection but non viable pregancy because severe inflammation
Th2 response –> IL-4 and IL10 –> uncontrolled infection but viable preganancy
what is key for killing neospora
TH1 INF-gamma and macrophages
Immune response to intracellular bacteria, protozoa and viruses
Th1-type response
Triggered by IL-12 by dendritic cells, macrophages and B cells
Th1-type response
Induces pro-inflammatory cytokines including IFNg by T cells and NK cells
TH1-type responce
An antibody-stimulating immune response elicited by helminth parasites
Th2-type response
expression of IL-4 cytokines
Th2-type responce
infiltration of eosinophils and mast cells and IgE production
Th2-type responce
