Blood-borne parasites Flashcards
(17 cards)
What type of cell is trypanosomes?
Eukaryotics
Cause disease in cattle/horses and some wild animals
What happens in chronic and actute stages in the disease caused by trypanosomes?
Acute stage: fever
Chronic: sleeping sickness: due invasion of the brain but always extracellular
Are all Ab the same in a infection?
IgM is the first contact Ig released by naive B-cells
IgM produced in a t-independent manner, they are not boosted by vaccination or repeated infection (no memory)
Antigen specific IgE and IgE are t-dependent so increase in conc after vaccination and repeated infections (memory)
How do Ab kill parasites?
Ø Neutralise essential antigens
Ø Activate Complement MAC - lyse targets
Ø Act as opsonin’s- facilitates phagocytosis
How is trypanosoma brucei controlled in the body?
IgG
Phagocytes(macrophages/neutrophils)
Express Fcgamma receptor
IgG is better than IgM at clearing trypanosome because
a) Higher conc in blood
b) Also acts as a opsonin
c) Also activates complement
What is IgM action?
IgM is effective at killing trypanosomes
IgM doesn’t act as an opsonin
IgM activates complement MAC
Opsonin is when a protein coats the pathogen/foreign body marking them for other immune systems
IgE is said to be the parasite Ig, but why doesnt this happen in trypanosoma?
Cells involved in such action: eosinophils/mast cells, express Fc3 receptors.
IgE would cause a cytokine storm—> which could lead to anaphylaxis shock in Trypansomes
How does trypanosoma brucei survive?
The surface of the parasite is mostly covered by just one protein
This protein is called the VSG (variable surface glycoprotein)
VSG are approx 60kDa and are densly packed
It is thought the VSG coat protects more important proteins from the hosts Ab
Tought to be less efficient at producing IgG to glycoproteins (specifically glycan epitopes) than to proteins.
Can antibodies kiill T. brucei
For a while the replication rate exceed the ability of the immune system to destroy parasite
Soon the host produce enough Ab to kill parasites faster than the parasite can replicate.
—-> results in the number of parasites to drop.
How can parasites evade Ab-mediated killing?
Parasites escape Ab-mediated killing by antigenic variation
This is different from viral antigenic drift or shift
T-brucei have multiple copies of same gene producing a VSG which acts as a coat
Only expresses 1
T brucei switches expression to a different VSG gene
Ab to previous VSG to a different VSG gene (epigenetics)
Ab to previous VSG do not recognise the new VSG and the parasites can grow unchecked until new Ab are produced
What disease does plasmodia cause?
Gives rise to Malaria
Is associated only with asexual blood stage
Mild fever: related to schizont rupture, fever is every 48 hours
Sever (life threatening): Cerebral malaria (coma), Anaemia
What is Sporozoite?
Ø Do not live for any appreciable time in the blood
Ø Short period to invade hepatocytes (minutes)
Ø Circumsporozoite protein (CSP) main surface antigens
Anti-CSP Ab block invasion
Basically the cell type that can infect new hosts
Describe the liver stage in plasmodia?
Sporozoites infect hepatocytes where they multiply and develop into merozoites
Intracellular environment protects them against Ab
Generates cytotoxic T cells that kill infected liver cells
Vaccine R21/Matrix-M
Targets is circumsporozoite protein which is expressed on sporozoites and live stages
What is the Schizont repture?
Plasmodium parasite’s schizont stage matures inside a red blood cell or liver cell. The schizont bursts, releasing merozoites into the bloodstream or nearby tissues. These merozoites then invade new cells, continuing the infection cycle. In malaria, this process triggers fever and chills due to the release of pro-inflammatory substances.
