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MMI 426 > Leishmania > Flashcards

Leishmania Flashcards

1
Q

Leishmania

A
  • single celledorganism
  • flagellete that belongs to the Trypanosomatide family
  • Disease manifestation partly due to parasite, presence of a RNA virus in the parasite and the immune response
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2
Q

What are the resovoirs for Leishmania?

A

Canines, rodents, and humans

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3
Q

What is the vector for Leishmania?

A

The (female) sandfly

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4
Q

Describe the lifecycle of Leishmania.

A
  1. Sandfly takes a blood meal and injects promastigotes (infective stage) into the skin
  2. Promastigotes are phagocytoed by macrophages where they turn into intracellular amastigotes (diagnostic phase)
  3. The amastigotes multiply in the cells of macrophages and various tissues
  4. The sandfly takes a blood meal and ingests macrophages infected with amastigotes
  5. The amastigotes transform into motile promastigotes (noninfectious) in the midgut where they multiply/ transfrm into metacyclic promastigotes (infectious) and migrate to the proboscis. The cycle repeats itself with a blood meal.
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5
Q

What are the major species of Leishmania that cause cutaneous/ mucocutaneous disease presentation?

A

L. major, L. tropica, L. aethiopica

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6
Q

What is the species of Leishmania thatcause viseral disease presentation?

A

L. danavani/ L. infantum

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7
Q

How is Leishmania transmitted?

A
  • Biologically via canine, rat and human resovoirs or from the sandfly vector
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8
Q

What are the risk factors for Leishmania?

A
  • poor rural housing conditions (cracked walls/ earthan floors)
  • poor sanitation
  • lack of accessible medicines
  • conflict (warzones, hard to control vectors)
  • People with HIV have increased risk of contracting viseral disease
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9
Q

What makes a good resovoir for infection?

A

Needs to:
- be in close contact to vector
- be suseptible to infection
- allow for replication of infectious agent and ensure delivery of large numbers to next host
- should be the main food source for vector
- disease should develop to chronic to give time for next transmission season

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10
Q

What is the difference between zoonotic leishaniasis and anthropontic leishmaniasis?

A

Zoonotic: animals to humans, typically in rural areas and mostly skin manifestations

Anthroponotic: humans to humans and humans to animals via vectors; typically in densely populated areas and mostly visceral amnifestations

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11
Q

How does Leishamania affect the vector?

A
  • Alters the feeding behaviour by making them “hungrier” by secreting a gel like substance that forms a plug and blocks the stomach and allowing for the multlipication of parasites
  • The timing of blood feedings is correlated to the number of metecylic promastigotes (increased biting when number of parasite increases)
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12
Q

How does the parasite adapt to 2 different hosts in order to complete it’s lifecycle?

A
  • Stage specific virulence determinants such as phosphoglucans which have repeated GalBeta1, 4ManAlpha1-PO4 units
  • LPG important for delaying macrophage phagolysome fusion and for attachment/ detachment from insect midgut epithelium
  • Number of repeating units varies in the differnt functional stages (ex: 15 repeats in promastigotes increases to 30 repeats in metacyclic promastigotes, alongation faciliates steachment from the gut
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13
Q

What causes differenciation to promastigotes vs amastigotes?

A

Different expression of proteins, monocolonial antibodies made from one type do not react with the other form and they have different metabolisms.

Promastigotes: increased surface glycoprotein GP63,flagellated, prefer alkaline pH and high glucose concentration

Amastigotes: decreased surface glycoprotein GP63, rudimentary flagella, prefer acid pH and prefer low glucouse concentration (shifts to metabolizing fats/proteins)

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14
Q

GP63

A

Zn protinase found on the prasites membrane and aids in the internalization of promastigotes.

aka Leishmaniolysin

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15
Q

Macrophage

A

WBC that does receptor mediated phagocytosis using complement receptors CR1, CR3, and monnose fructose receptor to help to help the cell bind to the promastigote

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16
Q

How does the parasite internalize itself into the macrophage?

A
  • LPG (Lipophosphoglycan) is used for attcahment and hinders endosome-lysosome fusion by activating F actin and proteins to delay this process
  • the parasites produce a heat shock protein to protect itself and contribute to resistance to oxidants
17
Q

How does the parasitic macrophage destruction relate to disease presentation?

A
  • when they stay in the lymphatics during macrophage destruction is creates a cutaneous and mucocutaneous presentation
  • when they dissemate through the reticuloendothelial (macrophage) system to rhe liver and sleen it causes further damage and recruits T cells leading to visceral presentation
18
Q

What advantage does macrophage destruction have for the parasite?

A

the decrease in tissue/circulating macrophages causes immunosuppression and shifts the TH2 response (increases infection spread)

19
Q

LCL

A
  • local cutaneous
  • in immunocompitent patients and normally has 1-10 ulcerated leisons
  • well defeined round, painless ulver with raised edges and central crust
  • may heal sponanenously after about 2 months
  • ulcer devlops to a typical epitheloid granuloma
  • prodominance of Th1 response
  • often leaves a hypopigmented smooth scar
20
Q

What is the role of the immune system in our protection from Leishmaniasis?

A
  • control of infection is mediated by CMI (cell mediated immunity) and CD4 cells
  • spleen is a major site for parasitic killing
  • antibodies have no protective effect and are associated with the non-healing type of disease
21
Q

DCL

A
  • Diffuse cutaneous
  • Nodules on at least 2 body parts
  • anergic indivisuals (lifelong)
  • subcutaneous nodules that dont ulcerate unless trauma
  • not cell mediated immunity but might have some antibody production
  • Invasion of nasal mucousa if disease persists
22
Q

DL

A
  • Disseminated leishmaniasis
  • In immunodeficent patients, numerous nodules, plaques, and popules
  • 10-300 pleomorphic leisons in more than 2 areas of the body
  • mucocutaneous leisons found in about 30% of the cases
23
Q

MCL

A
  • Mucocutaneous Leishmanisis
  • Extensive leison prone to relapse
  • upper espiratory tract mucosa is commonly infected (destruction of walls of oral-nasal and pharyngeal cavities)
  • Usually L. braziliensis
  • Can appear years after onset of cutaneous leishmania
24
Q

How does the RNA virus increase pathogenisity of Leishamania infections?

A

Antiviral response to LRV1 exacerbates Leishamania infection

25
Q

Visceral Leishmaniasis

A

Usually “old world leishmanaisis” caused by L. donovani and L. infantum
Systemic and most severe form of Leishmania

26
Q

PKDL

A

Post Kala-azar dissemated Leishmaniasis
Chronic disease disease and some indivisuals get a granulomatous sytrome after a treated VL

27
Q

Why do HIV+ people have increased chance of contracting Viseral Leishmania?

A

VL progresses faster in HIV positive indivisuals
HIV and VL target similar cells and together are much worse then indivisually

28
Q

How do you diagnose Leishmania?

A
  • The disese can mimic malaria, typhoid fever, TB, sporotrichosis, etc making it difficult to diagnose
  • Spleen and lymph node biopsy to find sequestered parasites (direct diagnosis)
  • molecular techniques (reliable but not practical where leishmania is a problem)
  • detect antibodies (serology): indirect dignosis
29
Q

How do you treat Leishmania?

A
  • Clean leisons with topical antiseptics
  • treatment of secondary bacterial infections
  • reconstruction of damaged tissue
  • Antimony compounds dor cutaneous and liposomal amphetericin B for viseral
  • Drugs for treatment have toxicity
    Treatment failure is common due to the complexity of the disease
30
Q

What will a vaccine have to target in a Leihmaniasis vaccine?

A

It will need to activate the Th1 arm (IFN-gamma and IL-12)

MMI 426 (10 decks)

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