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Parasitology > Week 9 > Flashcards

Week 9 Flashcards

1
Q

Indeterminate Phase of Chaga’s Disease

A
  • Parasites no longer in the blood
  • Parasites present in amastigote nests in involuntary muscle (they have replicated and are waiting)
  • Patient has sero-converted: circulating IgG (developing antibodies in the blood)
  • Tissue destruction
  • Pseudocysts
  • Hosts don’t clear parasite without treatment
  • phase can last years/decades
  • most people in this phase with no symptoms
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1
Q

Acute Phase of Chaga’s Disease

A
  • disease is caused by T.cruzi
  • Chagoma or Romaña’s sign
  • Localized inflammation at the site of infection
  • Only in a minority of cases
  • Many unaware of infection
  • One to two weeks of incubation time (parasite still localized to initial site of infection)
  • Trypomastigotes in the blood
  • Hepatosplenomegaly (Enlarged liver and spleen)
  • Parasites are replicating and finding their way to their tissue of choice (Involuntary muscle of the heart or digestive tract)
  • lasts 2-8 weeks
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2
Q

Chronic Phase of Chaga’s disease

A
  • Characterized by tissue damage and the mega syndromes (enlargement of organs)
  • Different T. cruzi strains have different tissue specificities
  • Destruction of ganglia, loss of signaling
  • Eventually loss of organ function and
    enlargement
  • can lead to chagasic cardiomyopathy and/or megacolon
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3
Q

Chagasic cardiomyopathy

A
  • chronic phase of the disease
  • Heart becomes dilated
  • cells become hypertrophied (bigger) - muscular wall thins
  • function stops due to enlargement
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4
Q

Megacolon

A
  • chronic phase of Chaga’s disease
  • Loss of nerves stops peristalsis (muscle contractions that move things through)
  • no more transit causes colon to enlarge, it gets filled with waste
  • Also in esophagus: Painful swallowing, regurgitation
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5
Q

what are the three transmission cycles of T.cruzi?

A
  1. Sylvatic (wild)
  2. Domestic
  3. Peridomestic
    - also non vector transmission: transfusion, transplant, food/drink
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6
Q

Sylvatic (wild) transmission cycle

A
  • wildlife-insect transmission
  • human infections rare
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7
Q

Domestic transmission cycle

A
  • human-insect transmission
  • major source
  • parasite lives inside
  • Some insect species have evolved to inhabit adobe (mud huts) and thatch shelters
  • Domestic only occurs in areas with such housing
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8
Q

Peridomestic transmission cycle

A
  • cycles between insects and domesticated animals
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9
Q

vectors of T.cruzi

A
  • Triatomine insects
  • different species are specialized for the different cycles
  • they feed on blood at all life stages
  • stercorarian (passed in the feces) parasite
  • the bug has a life long infection
  • epimastigotes replicate in the stomach (midgut)
  • they change into metacyclic (present in hindgut)
  • get deposited into the feces
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10
Q

Salivarian vectors

A
  • anterior station: transmit via mouthparts
  • efficient when transmitting to other host
  • vector infection rare: do not get many transmission opportunities
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11
Q

Stercorarian vectors

A
  • posterior station: transmit via feces or ingestion
  • ineffecient when transmitting to other hosts
  • vector infection is widespread: get many transmission opportunities
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12
Q

what is limiting the spread of T.cruzi?

A
  • it is only endemic in areas where the insect vector occurs
  • domestic cycle is only in areas with suitable houses for infection
  • it can be found in non-endemic areas bc infected people moved there or bc of mechanical transmission
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13
Q

control measures for T.cruzi

A
  1. Improve housing stock – metal roofs, block houses (domestic)
  2. Separate housing from animal shelters (peridomestic)
  3. Insecticides
  4. Screening and treatment of blood donations
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14
Q

Life stages of T.cruzi

A

Trypomastigote:
- Blood stream form
- infectious
- or replicative
Epimastigote:
- insect form
- replicative
Amastigote:
- non-motile
- intracellular
- replicative: inside host

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15
Q

Key differences between T.cruzi and T.brucei

A
  • T.cruzi is stercorarian: More vector infection, less efficient
  • T.cruzi is intracellular: Hides inside the host cell, avoids parts of the
    immune response
  • Forms pseudocysts and stays dormant
  • T.brucei is extracellular
16
Q

What are the key requirements for T.cruzi to survive?

A
  1. Escape from site of initial infection into the blood
  2. Evade host immune system while in the blood
  3. Transit to site of long-term infection
  4. Enter into host cells to replicate
  5. Enter indeterminate phase
17
Q

What are the mechanisms T.cruzi uses to deal with the host immune system in the blood?

A
  1. Cell surface molecules and clearance.
  2. Complement inactivation.
  3. Immunodominance
18
Q

Complement inactivation in T.cruzi

A
  • complement system is part of the innate immune system that targets pathogens for destruction
  • Calreticulin: binds and stops lectin pathway, can bind to also stop classical pathway, no C3 means no alternative pathway
  • Complement regulatory protein (CRP) – binds C3b and C4b
  • Complement C2 receptor inhibition trispanning (CRIT) – blocks C2 cleavage
  • Decay-accelerating factor (T-DAF) and Gp58– interfere with C3 convertase assembly
  • Induces host microvesicle (part of immune response) release
19
Q

Immunomodulation in T.cruzi

A
  • doesn’t have large gene regulatory effect on host early (host cell doesn’t know what’s going on, has no reaction)
  • No immune response until after the first replicative cycle 4-5 days post infection
  • After several rounds of replication immune activation occurs
  • Reduces parasite numbers, but no clearance
  • Cell surface has a large range of immunogenic proteins, expresses them all at the same time
  • by expressing so many
    antigens, T. cruzi induces the host to raise a series of non-productive Ab responses, delaying the protective response
20
Q

Antibody production and T.cruzi

A
  • parasite expresses a mitogen (a protein that stimulates B cells and induces immune response)
  • sheds a large number of immunodominant epitopes (easy for immune system to make antibodies against)
  • Induces polyclonal B cell activation
    immediately
  • Non-protective Ab production
  • Delays the parasite specific protective Ab response
21
Q

Main mechanisms of blood stage evasion in T.cruzi

A
  1. Stealth – grows slowly and doesn’t leave evidence initially
  2. Smoke screen – once it is seen by the host, it induces Ab production and provides lots of great epitopes, that aren’t important to the parasite
  3. Defense – sticky cell surface that cleans host factors, interferes with multiple steps of complement killing
  4. Escape into the cell to avoid
22
Q

How does T.cruzi get into the host cell? (cell invasion)

A
  • Cell surface receptors bind to the host cell
  • Signaling molecules induce uptake by the host cell
  • Either by recruiting lysosomes directly, or invasion followed by maturation
23
Q

Lysosome-dependent cell entry

A
  • enter directly into lysosome at cell surface
  • binding to surface receptor triggers Ca2+ signalling
  • brings lysosomes from the nucleus to fuse with the plasma membrane
  • parasite can then directly enter the lysosome
24
Q

Lysosome independent cell entry

A
  • enters plasma membrane derived vesicle or an endosome
  • recruits lysosomes to fuse with them
  • endosome or vesicle mature into a lysosome
25
Q

How do the parasites survive in the lysosome?

A
  • Expresses a range of antioxidant molecules (get rid of toxic substance)
  • low pH induces the trypomastigote to make pore forming protein that makes pores in the lysosomal membrane and breaks it open
  • they can then escape into the cytosol
26
Q

Why does the parasite enter a lysosome?

A

low pH of the lysosome is the signal they use to know they are in a host cell and should turn into an amastigote

27
Q

What happens after T.cruzi leaves the lysosome?

A
  • once in cytosol, they transform into an amastigote
  • undergo replication
  • With each replicative cycle the parasite is transiting, looking for its niche
  • Wants to end up in the involuntary muscle of the heart or digestive tract
  • host immune system eventually catches up and suppresses parasite numbers
  • amastigotes form pseudocysts and wait for a vector without killing the host
28
Q

Molecular mimicry in T.cruzi

A
  • T. cruzi has some cell surface epitopes that look incredibly like proteins on nerve cells
  • In late infection, hosts often have circulating Ab against these epitopes that are autoimmune
  • thought to be the cause of the nerve
    damage seen in chronic phase disease
  • unclear why this has evolved
29
Q

Phytomonas spp

A
  • infects plants
  • genomes are quite small compared to other trypanosomes
  • cell surface has a variety of glycolipids, just like other kinetoplasts (Probably plays the same roles)
  • Expresses gp63 – same as leishmania (cleavage of many immune related proteins to interfere with cell signaling)
  • Shares some antigens with T. cruzi (Might be able to infect animals)

Parasitology (12 decks)

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