Summary Parasitology

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Summary - Parasitology

  • 1.6 Malaria transmission to mosquitoes

  • Why are low-density infections interesting?
    1. Many people have them
    2. No symptoms & not found with diagnostics
  • For falciparum (deadliest), gametocyte production largely goes invisible. Evidence has been found that they sequester in the spleen and bone marrow
  • The parasite has knobs that allow them to stick to RBC -> results in massive deformability of RBC. With gametocytes you don't see these knobs, but they still reside in bone marrow
  • How do gametocytes sequester in the bone marrow?
    At the beginning they are stiff and can't get out of the bone marrow. When they mature, they lose their rigidity and can be flushed out of the bone marrow.
  • Why do you need RNA diagnostics to qualify the stages that can be detected in blood?
    Gametocytes have the same DNA as asexual parasites, you with RNA diagnostics, you can detect transcripts that are indicative of gametocytes.
  • 8.5-12 days after injecting the parasite into the vein, you see the first male and female gametocytes appearing. More female than male, as 1 male gametocyte can make 8 male gametes that can find a female. The blood stage group had 10-100x higher gametocyte production than the mosquito bite group.
  • Higher infection rates in direct skin feeding, but no evidence for higher gametocyte density/fraction
  • How can a Ugandan study report 90% of infections coming from asymptomatic cases, while a Cambodian study reports >95% came from clinical cases?
    In Africa, there are many asymptomatic infections, but also a much higher parasite density. It takes 10-12 days to become infectious, but symptoms develop quite soon. In a perfect health system, once you get sick, you still have 10 days to go to a health facility before you become infectious. So immunology and health seeking behaviour are important
  • What is the Entomologic Inoculation Rate?
    The number of infected bites per person in a time period
  • In Nagongera, Uganda, the EIR was very high. After insecticide sprays, the EIR went from 310 infected bite p.p.p.y to 1. Parasite density went down even more, so people were still infected ut with very low density.
  • What happens with an increasing density?
    The likelihood of infecting the mosquitoes goes up. The proportion of infected mosquitoes also increases, but a weaker association.
  • There was a small group of super-infectors. Just 4 children were responsible for 62.6% of infections. 
  • How can naturally acquired immune responses affect transmission?
    1. You can have immunity that stops the gametocyte development in bone marrow
    2. You can have immunity that affects transmission when you start producing antibodies when RBCs are being cleared as the immune system sees antigens. So when female and male gametes are taken up by mosquito, the gametocyte antibodies may recognize the gametes and inhibit their development
  • 1.8 Survival strategies

  • Which interesting features do trypanosomatids have?
    1. They have 1 mitochondrion per cell
    2. It has a kinetoplast (mini+maxi circle DNA)
    3. It has mitochondrial RNA editing 
  • What are difficulties with covering the entire surface with one single protein (VSG)?
    1. Limited flexibility. To overcome this, VSG is anchored to membrane via GPI (lipid anchor)
    2. You need a molecular mechanism for antigenic varianten. To overcome this, the parasite has 1. In situ switch, 2. Telomere exchange and 3. Gene conversion
  • What are survival strategies of ascaris?
    Both the eggs and larvae are resistant to acidic environment
  • 1.9 Hygiene hypothesis

  • What is the hygiene hypothesis?
    Children with many siblings have less hay fever because they are exposed to germs.
  • Which changes in lifestyle led to a change in microbial exposure?
    1. Rural to urban living
    2. Slow food to fast food
    3. Physical labour to sitting professions
    4. Outdoors to indoors
    5. More isolation, central heating and less humid in houses
    6. Prevention and treatment of infectious diseases (improved sanitation)
  • In the 20th century, they thought as most microbes cause disease, the absence of microbes is key to health. This lead to increased personal hygiene, home cleanliness, antimicrobial agents and preventative strategies in healthcare
  • What is the Old Friends hypothesis?
    Microorganisms , Old Friends, that were once abundant, trained out immune system. Our immune system has evolved in their continuous presence.
  • Almost 1/3 of the world population has a chronic parasite infection. Helminth infections do not kill, but infect up to 100% of children in rural areas. They are often non-inflammatory, but can sometimes cause immunopathological reactions.
  • What did studies show on the association between helminths and atopy/asthma?
    For atopy, helminth infections show a protective association. For asthma, different worms show different associations. However, there is a lot of inconsistency in human studies.
  • In the acute stage of infection you see a type 2 immunity peak. After time, you see regulatory populations like T cells developing. This leads to spill over suppression to 1. Helminth antigens (ensures their survival in the host and 2. Spill over suppression to bystander antigens such as the allergens and therefore also immune responses to the allergens are being reduced.
  • What can regulatory T cells do?
    1. Downregulate effector T-cell responses
    2. Affect antigenpresentation
    3. Work on B-cells
    4. Inhibit cells of innate immune system
  • In what different ways can regulatory Tcells work?
    1. By inhibitory cytokines, such is IL10 IL35 en TFG-B
    2. In a contact dependent manner, by molecules such as CTLA4 (checkpoint inhibitor, can inhibit DCs) and LAG3
    3. They can induce cytolysis or apoptosis by the expression of Granzime B of Perforin
    4. Block T cell proliferation by metabolic deprevation
  • The function of Treg. They are important in inhibiting autoimmune diseases, blocking responses to auto-antigens. They can also be found at eg mucosal tissues, where they block immune responses to harmless antigens. They can express cytokines that drive repair responses to heal tissue.
  • In the acute stage, you get a type 2 response, which is the pro-allergic/pro-inflammatory response. In the chronic stage and infections during infancy, you get type 1 response, which (induction of IL10, increased regulatory responses etc), which are the anti-allergic/anti-inflammatory responses.
  • Why is the early time window important?
    In this time, the immune system is still susceptible to modulation and microbial signals.
  • Commensal bacteria may act positively on immune system. Pathobionts may cause inflammation in gut. They are rare and based on competition of niches and nutrients.
  • How do gut microbiota influence digestion?
    Bacteria help digest indigestible fibers. They also produce metabolites, such as SCFAs (acetate, butyrate &propionate). They result from fermentation of dietary fibers.
  • Why are SCFAs important for the immune system?
    1. They play an important role on the epithelial cells, making the barrier more tight
    2. They act on the mucous production and the tight junction molecules between epithelial cells
    3. They act on effector T-helper cells, such as TH1 and Th17 that make sure there is an increased immunity towards pathogens
    4. They act on dendritic cells and macrophages, which produce more tolelogenic factors that lead to the regulation of more regulatory T-cells and the production of anti-inflammatory cytokines such as IL10
  • The gut-lung axis
    SCFA can migrate through blood to become more available systemic. They act on bone marrow compartment where immune cells are being generated. This leads to generation of DCs that are linked to regulatory responses. Immune cells can also migrate from gut to lung compartment, where they can impact respiratory immunity.
  • Interaction between helminth and microbiota
    You have a certain microbial composition that interacts with the helminth, which may lead to compositional changes. These bacteria produce SCFA., that can act on DCs and drive regulatory Tcells. Helminths produce excretory-secretory products that can drive regulatory Tcells. Tcells migrate to draining lymphnode where they can inhibit housedustmite-induced Type2 airway inflammation. 
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What are survival strategies of ascaris?
Both the eggs and larvae are resistant to acidic environment
What are difficulties with covering the entire surface with one single protein (VSG)?
1. Limited flexibility. To overcome this, VSG is anchored to membrane via GPI (lipid anchor)
2. You need a molecular mechanism for antigenic varianten. To overcome this, the parasite has 1. In situ switch, 2. Telomere exchange and 3. Gene conversion
Which interesting features do trypanosomatids have?
1. They have 1 mitochondrion per cell
2. It has a kinetoplast (mini+maxi circle DNA)
3. It has mitochondrial RNA editing 
How is the bloodstream form protected against complement mediated lysis?
Its cells are densely coated with VSG homodimers that continuously switch
What are control measures for echinococcus multilocularis?
1. Education and information about risk factors (focus on risk groups/regions)
2. Control in dogs (regular praziquantel in high risk region)
3. Control of wildlife (difficult, no vaccine, maybe baiting with praziquantel)
What are control measures?
1. Education for pregnant people
2. Prevention of exposure (Short term: via meat consumption, long term:via environment)
Which complications can be seen as a result of toxoplasma infection?
1. Congenital toxoplasmosis (especially 1st trimester, can become blind)
2. Acquired toxoplasmosis
What is the burden of toxoplasmosis in NL?
1903 DALYs per year, mostly congenital
In NL we don't have screening programs so we don't know exact numbers
How can the burden of foodborne diseases be ranked?
1. Multicriteria Decision Analyses (weighing of values)
2. Disease Burden Estimation (DALY = YLL+YLD)
How does preventative chemotherapy work?
MDA for multiple ND reduces morbidity. The early and regular treatment of risk groups reduces current infection and the development of late-stage severe disease.