5. Microorganisms: parasites Flashcards

1
Q

Define parasites

A

Parasite - organism that lives on / in a host organism - gets its food from / at the expense of its host

Three main classes of parasites that cause disease in humans:
- protozoa
- helminths
- ectoparasites

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2
Q

What are the types of parasites based on their host exploitation?

A
  • Obligate parasites: need to spend at least a part of life cycle in parasitic relationship - ex: Ascaris lumbricoides, Plasmodium falciparum
  • Facultative parasites: generally free living but can become parasitic if enter a suitable host - ex: Naegleria fowleri
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3
Q

What are the types of hosts?

A
  • Definitive host: parasite reaches sexual maturity
  • Intermediate host: required for parasite development but no sexual development occurs
  • Incidental host: can be infected but doesn’t play a role in parasite lifecycle
  • Paratenic host: no development takes place but parasite remains alive + infective to another host

DIPI

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4
Q

What are the main routes that parasites use to enter the host?

A
  • Broken skin barrier - wounds
  • Oral pathway
  • Unprotected sex
  • Vector’s bite
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5
Q

What are helminth parasites?

A

Helminths - parasitic worms, usually intestinal

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6
Q

What are the 3 taxonomically important helminth groups?

A

3 taxonomically important helminth groups:
- nematodes (roundworms)
- cestodes (tapeworms)
- trematodes (flukes)

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7
Q

What are the challenges for combating helminth infections?

A

Helminths are good at evading + supressing immunity:
- long-lived - don’t kill the host
- large size - difficult for immunity to kill
- takes long to develop immunity + protective memory
- suppress immunity - reduced pathology

Co-evolved with humans - good at manipulating the immune system

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8
Q

Explain the hygiene hypothesis

A

Hygiene -> allergies - untrained immunity

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9
Q

What are protozoan parasites?

A

Protozoan parasites - microscopic, one-celled parasites - Apicomplexa disease causing - ex: malaria, cryptosporidiosis

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10
Q

Explain malaria as a protozoan parasite disease

A

Malaria:
- Plasmodium spp parasite - 5 species infect humans
- Anopheles mosquitos - definitive hosts
- Parasite migrates and invades a variety of host tissues in their lifecycle
- Malaria - acute disease: rapid parasite replication in the liver

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11
Q

Explain Taxoplasma parasites

A

Taxoplasma:
- unicellular protozoan parasites
- definitive hosts - cats
- intermediate hosts - warm-blooded animals, including humans
- infects brain, eyes, heart, lungs - flu-like symptoms, usually imm system fights on its own

Humans can be infected by:
- contaminated cat faeces
- eating infected meat

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12
Q

What is the host defense against microbial infection?

A

Innate immunity:
- External: skin, mucous, secretion
- Internal: phagocytic cells, NK cells, antimicrobial peptides, inflammatory response, Complement system

Adaptive immunity:
- Humoral response (B cells)
- Cell-mediated response (T cells)

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13
Q

Why parasites don’t kill the host?

A

Parasites (like some other microorg) don’t kill the host too quickly / at all - to fully exploit the host

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14
Q

What are the main environments where parasites reside in human hosts?

A
  • live freely in bloodstream
  • live in protected areas (ex gut, brain)
  • hide in host cells
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15
Q

What are the modes of parasite living inside hosts?

A
  • extracellularly - outside of the cell (ex bloostream)
  • intracellulary - inside of the cell (ex in RBC)
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16
Q

What are the challenges encountered by protozoal parasites while invading human hosts?

A

Challenges encountered by protozoal parasites:
- parasite migration and motility to infect specific cells / hosts
- transmission from one host to other hosts
- gaining nutrients - may need to adapt to new environment while at different lifecycle stages
- avoiding being killed by immune system
- maintaining balance between different life cycle stages: proliferation / forming long-term infection / undergoing transmission

17
Q

Describe the lifecycle of Plasmodium parasite

A

Plasmodium - intracellular parasites - invade RBCs

18
Q

What are the advantages and disadvantages of Plasmodium invading host cells?

A

Plasmodium - intracellular parasite - invades RBCs

Advantages:
- gain nutrients
- shielded from immune system
- RBCs - host cells - readily available and accessible to mosquito vector
=> Plasmodium transmission is very effective

Disadvantages:
- must convert terminally differentiated RBCs into cells with nutrient uptake systems
- remodelling RBC membrane by parasite - increased cell rigidity
=> infected RBCs can be detected -> removed by spleen

19
Q

How do Apicomplexan parasites migrate and invade host cells?

A

Apicomplexan parasites used gliding motility - in motile stages of lifecycle - substrate-dependent cell motility (conc sensing - not flagella / cilia / shape-shifting) - migrate to host - propel themselves into the host

Use host cell receptors - attach - use actin-myosin for forward / backward movement

20
Q

What is the sequence of RBC invasion by Plasmodium?

A
  1. Recognition and attachment: recognises RBC - attaches to surface - mediated by both surface proteins
  2. Reorientation and junction formation: one merozoite attached to RBC reorientates - forms tight junction - allows entry into RBC
  3. Entry and replication: merozoite anters RBC forming parasitophorous vacuole inside - replicates within the vacuole
  4. Exit: bursts out of RBC / released in exoerythrocytic vesicles without RBC lysis
21
Q

What must intracellular parasites avoid when escaping host immune system in host cells?

A

Intracellular parasites - when invade host cells must:
- evade host cell killing mechanism
- prevent host cell apoptosis

22
Q

How do RBCs create a protected niche for Plasmodium?

A

RBCs provide niche for Plasmodium:
- abundant + accessible to mosquito vectors
- contain many nutrients
- no MHC for antigen presentation

HOWEVER - infected RBCs may be detected - because parasite alters surface proteins -> destroyed in spleen => Plasmodium destroyed together

23
Q

What is the Plasmodium membrane protein used in ivading RBCs?

A

Plasmodium falciparum Erythrocyte Membrane Protein 1 (PfEMP1) - encoded by ~60 genes in var gene family - for one protein 1 gene is expressed at a time + var genes show high levels of recombination => high PfEMP1 variation

PfEMP1 composed of building blocks: DBL + CIDR binding domains with variable sequences and binding specificities for host endothelial cells

24
Q

What are the clinical outcomes of Plasmodium infection?

A

Clinical outcomes of Plasmodium infection - malaria disease -> slows down blood flow + damages liver

25
Q

What is the trade-of strategy used by Plasmodium in malaria development?

A

Trade-of between survival and reproduction - to maximise transmission while maintaining infection

26
Q

What is the lifecycle of African trypanosomes?

A

African trypanosomes -> African trypanosomiasis - sleeping sickness

27
Q

What is the main adaptation of African trypanosomes?

A

African trypanosome parasite can change its coating protein - variant surface glycoprotein (VSG) coat - hides invariant proteins - changes -> evades immune system

28
Q

What are the mechanisms used for coat changing in African trypanosomes?

A

Mechanisms:
1. Gene converison: uses a special DNA repair mechanism to replace genes encoding for VSG with a silent version of the same gene - rapidly generate new VSG variants
2. Segmental gene conversion: replaces a part of VSG gene with a silent copy - more VSG variants
3. Telomere exchange: swaps the ends of two different chromosomes - new combination of genes for VSGs - higher variety
4. Transcriptional switch: changes which VSG gene is actively transcribed - rapidly switch to a new protein coat

29
Q

How do African tryponosomes have an inexhaustible repertoire of antigen variants?

A

High antigen variability - different coatings - because VSG protein vsg genes undergo high rates of recombination => parasites can establish long-term chronic infection because adapt every time the immune system fights

30
Q

What is the trade of in African trypanosomes?

A

Trade of between slender (proliferation) - stumpsy (transmission) forms

31
Q

How do African trypanosomes differentiate from their proliferative to transmissive form?

A

Use quorum sensing of stumpy indication factor (sif) - at high sif slender -changes to-> stumpy

32
Q

What are the three African Trypanosome subspecies infecting humans?

A
  • Trypanosoma brucei brucei
  • Trypanosoma brucei rhodesiense (susceptible)
  • Trypanosoma brucei gambiense (susceptible)
33
Q

To which African trypanosome species humans are susceptible? Which genes are responsible?

A
  • Trypanosoma brucei rhodesiense - parasite has serum resistance - associated (SRA) gene
  • Trypanosoma brucei gambiense - T. b. gambiense-specific glycoprotein (TgsGP)

=> genes allow escape human immune system, Trypanosoma brucei brucei is lysed by human immune system

34
Q

What are the main hosts of Trypanosoma species?

A

Trypanosoma - zoonosis: cows / bores -> mosquito -> human

35
Q

Why are humans susceptible to certain Trypanosoma species?

A

APOL1 - human protein - lyses Trypanosome species:
- T. b. brucei: lysed by APOL1 -> humans not susceptible
- T. b. rhodesiense: use serum resistance associated (SRA) proteins - degrade APOL1 -> humans susceptible
- T. b. gambiense: some lysed by APOL1 - TgsGP degrade some APOL1 -> humans susceptible