Flashcards in Parasitology lecture 4 Deck (11):
what are microparasites and what are their general characteristics?
viruses, protozoa, some bacteria and fungi.
small, multiply profusely in host, often cause long lasting immunity, unstable populations, cause epidemics
what are macroparasites and what are their general characteristics?
generally larger than microparasites and dont multiply in the host, dont induce long lasting immunity (both have exceptions), more stable populations, cause endemic disease.
general differences between bacteria/viruses/protozoa?
bacteria - replicate in animals to cause disease or replicate in media (ie food etc) and not cause disease.
vs malaria and such that require a host to complete their life cycle
vs viruses which also need hosts but will cause generally acute disease and due to their limited genomes will usually have effective immune responses mounted against them.
what distinct assets do vertebrate hosts and parasites have in the evolutionary 'arms race'?
vertebrates = large genome so complex immune system and vast antibody repertoir
parasite = short generation time. P.falciparum marozoites just 48hrs. far higher mutation rate than host. fecundity eg ascaris producing 200,000 eggs a day
generally parasite antigenic variation is poorly understood but it has been extensively studied in which parasite? describe.
1 - trypanosoma brucei, causes african sleeping sickness. infects mammalian blood. flagellated unicellular protozoa.
2 - transmittted by tsetse flies
3 - lots of mammalian animal reservoirs.
4 - remain extracellular during chronic infection.
5 - cells densley coated with variant surface glycoprotein VSG homodimers that protect vs complements mediated lysis.
6 - eventually host produces AB for predominant VSG variant causing antibody mediated lysis. trypanosome then switches to antigenically different VSG.
7 - express one VSG at a time from 20 telomeric expression sites (present at one or both ends of chromosomes)
8 - switching VSG can be switching to a different expression site (in situ switch with concurrent silencing of old site) or via rearrangements such as gene conversion (duplication of silent gene into active expression site) or telomere exhange (DNA crossover between 2 chromosome ends) to insert one of hundreds of silent VSG genes from subtelomeric VSG arrays into the active expression site.
why no parasite vaccines?
effective immune evasion and plsaticity in life cycles.
plasticity - can detect environment ie plasmodium gametocyte prod ifluenced by factors inc physiological and immunological status of host.
evolve in response to changing immune environment - vaccination changes environment and it will adapt.
malaria virulence fundamentally due to growth rate. grow as fast as poss to enhance transmission. upper limit is host death before transmission. if you vaccinate then the host is more resistant and growth rate will increase. this is fine in the vaccinated but will be detrimental in those who aren't. so weak vaccines are a bad idea as they drive this process.
different strageies needed for chronic helminth disease vs acute bacterial and viral
parasite induce harm to hosts
the point of genome sequencing parasites? results with malaria?
1 - to identify genetic loci for intervention targets
2 - to develope monitoring and surveillence tools
3 - found a high density of loci displacing high frequencies of polymorphisms. the immune system strongly drives maintenance of multiple alleles
p.Falciparum is evolving in response to
- host immune system
- mosquito vector
- environmental factors ie drugs and changes in transmission intensity due to interventions
hygiene hypothesis details?
1 - helminth infection and allergic disease associated with Th2 response
2 - several studies found helminth infected rarely have allergies
3 - suggested that exposure to pathogens inc parasites developes an immune system with strong regulatory networks controlling autoimmune and allergic responses
4 - parasites particularly helminths are often long lived and inhabit chronically and it is thus expected that they can modulate host immune responses.
examples of parasite induced behavioural changes
toxoplasma gondii in rats - no longer fear scent of cats, eaten, desireable for predator-prey life cycles
- in humans the infection can cause psychological effects such as personality change to reduce fear that would keep the person from harm.