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Medical Microbiology > Parasites > Flashcards

Parasites Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What are the 2 main subgenres of leishmaniases?

A

Leishmania (old world) and Leishmania (viannia)

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2
Q

What are the 3 main disease conditions of leishmaniasis?

A

Cutaneous = found in exposed body parts
Mucocutaneous = several species of leishmania viannia
Visceral = parasites invade liver and spleen causing organ enlargement

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3
Q

Explain the life cycle of leishmaniasis?

A

1 - sandfly takes a blood meal and injects promastigote into the skin of the host
2 - parasites are taken up by phagocytic cells of the host immune system
3 - promastigotes transform into amastigotes and start to multiply
4 - amastigotes multiply in various tissues and infect other cells
5 - sandfly takes blood meal from infected host and ingests macrophages infected with amastigotes
6 - parasitised cell is ingested
7 - amastigotes transform into promastigote stage in the gut
8 - promastigotes divide in the gut and migrate to the proboscis

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4
Q

What is the vector for leishmaniasis and how many species transmit infection?

A

Sandflies, ~70 species out of 1000 transmit infection

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5
Q

How do promastigotes enter mammalian cells?

A
  • promastigotes have GP63 on their surface
  • GP63 converts C3 into C3b
  • C3b binds complement receptor 1 CR1
  • CR1 cleaves C3b into 1C3b
  • 1C3b facilitates binding to CR3
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6
Q

What interactions take place with amastigotes and host cell?

A
  • amastigotes have much less LPG on the surface, so less GP63
  • decreased GP63 allows for opsonisation, and also antibody and fibronectin detection
  • leads to ligation of Fc gamma receptors and fibronectin receptors
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7
Q

What is the effect of sandfly saliva material?

A
  • increases lesion size
  • promote a Th2 response when injected with parasites
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8
Q

Results of footpad swelling between BALB/c mice and IL-10 knockouts?

A

Footpad swelling occurs in BALB/c mice, but IL-10 knockouts can control swelling

Th1 plays a role in controlling infection

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9
Q

Results of footpad thickness between BALB/c, BALB/c + anti-IL-4, and BALB/c + anti-IL-4 + anti IFNY?

A

BALB/c control mice showed increased footpad thickness, while both other mice were able to control swelling of footpad thickness

Swelling response is unlikely to be caused by IFNY

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10
Q

What do C57 and BALB/c mice show about Th1 and Th2 response within infection?

A

C57 mice show Th1 delayed type hypersensitivity response which reduces parasitaemia and controls infections, meaning Th1 is important for parasite clearance

BALB/c mice present a strong antibody Th2 response which results in disseminating disease

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11
Q

How does IFNy affect C57 and BALB/c?

A

C57 mice control infection through IFNy
BALB/c mice cannot control infection under natural conditions, but when IL-4 is reduced mice control infection but do not rely on IFNy

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12
Q

What are the issues with using BALB/c and C57 mice?

A
  • inbred within laboratory conditions, so may not represent natural populations within genetically diverse species
  • results may vary to how humans react to parasites
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13
Q

Main points of acute disease immune response and parasites?

A
  • low Th1 response IFNy
  • increased Th2 response IL-4
  • moderate Treg response IL-10 & TGFB
  • low IL-17 and IL-22
    = many parasites
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14
Q

Main points of chronic disease immune response and parasites?

A
  • mixed immune response
  • high Th1 response
  • reduction of IL-4 and IL-10
  • high production of IL-17 and IL-22
    = few parasites
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15
Q

What is localised cutaneous leishmaniasis?

A
  • incubation 2-4 weeks, begins as asymptomatic papules which enlarge and form well circumscribed ulcers with violaceous border due to epidermal breakdown
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16
Q

What is chronic relapsing cutaneous leishmaniasis? What species causes this?

A

Has been some healing but parasite is still present and continues to reappear and cause lesions, generally caused by L. tropica

17
Q

What is diffuse cutaneous leishmaniasis?

A

Rare, appears as painless nodules which progress to affect nearly entire cutaneous surface

18
Q

What is the causative agent of mucocutaneous leishmaniasis?

A

L. Braziliensis

19
Q

What are the 2 main causative species of visceral leishmaniasis? Where do they cause issues and what are their vectors?

A
  • L. donavani, found in Africa and Asia, mostly human to human transmission via a vector
  • L. infantum, found in Mediterranean and South America, canines are implicated as reservoirs
20
Q

How does visceral leishmaniasis affect the body?

A
  • usually asymptomatic, typically 2-8 months after infection
  • Infected macrophages move to internal organs
  • liver dysfunction as kupffer cells are invaded causing inflammation and fibrosis
  • infected bone marrow may cause anaemia due to issues with blood cell production
21
Q

What is the life cycle of malaria?

A

1 - mosquito takes a blood meal and injects sporozoites which travel to the liver of the host
2 - sporozoites divide in the liver forming merozoites which infect red blood cells
3 - once RBCs are infected, the parasite undergoes cyclical growth in erythrocytes which is the stage responsible for disease symptoms
4 - a small proportion of parasites exit the life cycle and form gametocytes required for transmission
5 - gametocyte goes into mosquito when feeding, where it divides further to produce sporozoites, which travel to the salivary gland

22
Q

How do plasmodium sporozoites interact with the liver?

A
  • They are released into the dermis and migrate to cross blood vessel walls
  • Circumsporozoite protein CSP is released during migration
  • sporozoites reach liver and glide over endothelium, binding with heperan sulphate proteoglycans (HSPG)
  • after binding they then cross the sinusoidal layer via kupffer cells
23
Q

What happens to plasmodium in the liver cycle stage?

A
  • parasite stops moving in the liver and divides
  • merozoites are made and released from exoerythrocytic schizonts into the blood stream in meronts
  • escape and invade RBCs
24
Q

What are the 3 methods of sequestering in malaria?

A
  • cytoadherance to endothelial cells
  • rosetting, by binding to other non infected RBCs
  • platelet mediated clumping
25
Q

How does PfEMP1 mediate cytoadherance?

A
  • localised to knobs and binds to endothelial receptors
  • PfEMP1 is already exposed to immune system, so parasite can avoid detection and being killed through antigenic variation
26
Q

Consequences of blood cells binding to capillary endothelium?

A
  • physical blockage of venules and accumulation of infected cells
  • once bound, signal cascade is induced recruiting immune cells
  • pro inflammatory cytokines are released leading to alteration in endothelial cell function such as increased permeability and apoptosis
27
Q

How does cerebral malaria occur?

A

Infected erythrocytes line cerebral capillaries in the process of cytoadherance to endothelial cells

Through receptors ICAM1 and PCAM1

28
Q

What are the main triggers for gametocytogenesis?

A
  • Change in temperature
  • Gametocyte activating factor (xanthurenic acid)
29
Q

What happens within the gametogenesis stage?

A

Merozoites form into either male or female gametocytes, with males undergoing exflagellation. Male and female fertilize to produce ookinetes which infect mosquito. Once in mosquito, ookinetes divide in the gut to form oocysts, which release sporozoites

30
Q

In what ways does immunity to malaria develop with repeated exposure?

A

Immune to severe disease THEN immune to uncomplicated disease (illness/ symptoms) THEN immune to infection

31
Q

How does RTSS vaccine work?

A
  • is multi component
  • CSP is fused to hepatitis B virus surface antigen
  • parts of molecule attract T cells

Medical Microbiology (13 decks)

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