Lecture 6: Parasitology 1 Flashcards
What is a parasite?
a eukaryotic organism that is using another for a variety of purposes
T/F
all parasites are worms
false
not all parasites are worms. some can be amoebas, protozoa, etc.
T/F
Parasitic infections can manifest in many different ways.
true
Why do the complex life cycles of parasites make diagnostics and treatment challenging?
- there are multiple stages for the parasite, which can target multiple locations within the body
- makes diagnostics, drug and vaccine development challenging
T/F
Most parasitic infections are not clinical.
true
infections are generally ____ –> most effective parasites are only ____ _____. that is to say, they will ____ but not ____
- chronic
- moderately virulent
- infect
- kill
parasites have the biological imperative to ____, ____, and ___, so not killing the host is beneficial to their existence.
reproduce, find nutrients, and shelter
If you are not the right host, how will a parasite respond?
it will try to get out of you by any means. Often kills the incidental host
T/F
parasites have maintained their responses to the host body since their inception.
false
parasites have evolved to manipulate host immune responses and host
routes of parasitic infection
- ingestion
- arthropod bite
- transplacental penetration
- direct penetration
- transmammary
organisms that use ingestion to infect host
- Giardia
- E. histolytica
- Cryptosporidium spp.
- cestodes
- nematodes
organisms that use arthropod vectors to infect host
- Malaria
- Babesia
- filaria
- Leishmania spp.
- Trypanosomes
Organisms that use transplacental penetration to infect host
Toxoplasma gondii
organisms that use direct penetration to infect host
- hookworm
- Strongyloides
- Schistosomes
how can parasites harm their hosts?
toxic products
- proteases, phospolipase, lytic enzymes, collagenase, elastase
mechanical tissue damage
- intestinal and organ blockage, pressure atrophy, tissue migration
immunopathology
- hypersensitivity reactions, autoimmunity, metaplastic changes, chronic inflammatory changes
Type 1 Reaction: ??
Mechanism: ??
Organism: ??
- anaphylactic
- Ag + IgE –> histamine
- helminths, trypanosomes
Type 2 Reaction: ??
Mechanism: ??
Organism: ??
- cytotoxic
- Ab + Ag + C’ (ADCC)
- T. cruzi
Type 3 Reaction: ??
Mechanism: ??
Organism: ??
- immune complex
- Ab + Ag complex
- Malaria, schistosomes, trypanosomes
Type 4 Reaction: ??
Mechanism: ??
Organism: ??
- delayed
- T cells
- Leishmania, Schistosomes, trypanosomes
What can a type 1 reaction result in?
anaphylactic shock, bronchospasms, local inflammation
what can a type 2 reaction result in?
Ab + Ag on cell surface –> complement activation or ab-dependent cellular cytotoxicity. results in the lysis of cell-bearing microbial antigens
What can a type 3 reaction result in?
inflammation and tissue damage; complex deposition in glomeruli, joints, skin vessels, brain; glomerulonephritis and vasculitis
what can a type 4 reaction result in?
sensitized T-cell reaction with antigen, liberation of lymphokines, triggered cytotoxicity –> results in inflammation, mononuclear accumulation, macrophage activation, tissue damage
What is released when a parasite is destroy and what can it cause?
proteases and phospholipases are released
can cause cell destruction, inflammatory response, and gross tissue pathology
differentiate between parasitic infection and parasitic disease.
parasitic infection is the presence of a parasite in the host; parasitic disease results when the parasitic infection damages the cells or body, thereby harming the host
T/F
most parastic infections are acute
False
most parasite infections are sub-acute or chronic
What determines the outcome of parasitic disease?
- route of exposure
- inoculum size and infective dose
- tissue tropism
- disruption, evasion, and inactivation of host immune system
- host age and immune status
- disease progression –> in for the long haul (unless immunocompromised)
How does Chagas disease demonstrate that parasitic complications can occur YEARS after initial infection?
- can initially see minor skin lesions at time of infection, but years later, the infected can develop complications from damage to cardiac muscle and nerve damage, leading to heart disease, GI issues, etc.
How do schistosome infections demonstrate that parasitic complications can occur YEARS after initial infection?
initial infections may have minor bleeding in the GI or urinary tract from beginning, but years of it develops into obstructions, cancer, etc.
How do eosinophils aid in parasite infections?
- these are the leukocytes that help neutralize infection with worms
what occurs in response to parasites’ surface proteins?
- eosinophilia
- -> accompanied by increased levels of IgE and is triggered by increased IL-5
eosinophilia helps to identify parasitic infection with ___, but doesn’t help much with ____
- helminths
- protozoa
T/F parasites are only a type 2 response.
false
parasites can be either type 1 or type 2
Th Group: Th1 Cell products: ?? Cell receptor: ?? Cell target: ?? Infectious agent(s): ??
- interferon-gamma, IL-2
- IL-12R
- macrophages, DCs
- intracellular bacteria, fungi, viruses, INTRACELLULAR PARASITES
Th Group: Th17 Cell products: ?? Cell receptor: ?? Cell target: ?? Infectious agent(s): ??
- IL-17A, IL-17F, IL-21, IL-22
- IL-23R
- Neutrophils
- Extracellular bacteria, fungi, EXTRACELLULAR PARASITES (?)
Th Group: Th2 Cell products: ?? Cell receptor: ?? Cell target: ?? Infectious agent(s): ??
- IL-4, IL-13, IL-5
- IL4R
- Eosinophils, basophils
- parasites
Types of interference/avoidance
- antigenic variation
- molecular mimicry
- concealment of antigenic site (masking)
- intracellular location
- immunosuppression
mechanism of antigenic variation
variation of surface antigens within the host
mechanism of molecular mimicry
microbial antigens mimicking host antigens leads to poor Ab response
mechanism of masking (concealment of antigenic site)
acquisition of coating host molecules
mechanism of intracellular location
- failure to display microbial antigen on host cell curface
- inhibition of phagolysosomal fusion
- escape from phagosome into cytoplasm with subsequent replication
mechanism of immunosuppression
- suppression of parasite-specific B- and T-cell responses
- degradation of immunoglobulins
trophozoite
motile, feeding stage, causes pathogenesis
- these are the ones interfering with cell lining in the gut, blocking absorption
- “out and about,” so the immune response can recognize them
cyst
infectious (immediately), non-motile, passed in feces (or in tissue and consumed to cause infection)
- often very resistant to immune system or to chemicals
- stage isn’t really doing anything
oocyst
protozoan version of egg; passed in feces; often takes 1-2 days to sporulate and be infectious
sporulate
when oocysts develop from undifferentiated cellular material to sporozoites
merozoite
stage that undergoes asexual reproduction; feeding stage (seen with malaria and coccidia)
schizont
whole cell full of multiplying merozoites; schzogeny is the process by which asexual reproduction may occur