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Infection and Immunity > Human African trypanosomiasis and Leishmaniasis > Flashcards

Human African trypanosomiasis and Leishmaniasis Flashcards

1
Q

Kinetoplastida (the order)

A

-parasitic protozoa
-named after the “kinetoplast” a network of circular DNA molecules within the single mitochondrion
-genera which infect man include:
-leishmania spp
-trypanosoma spp
-

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2
Q

Human African trypanosomiasis (HAT)

A
  • man and animals

- trypanosoma brucei gambiense and T.b rhodesiense cause disease in man

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3
Q

Sleeping sickness facts:

A

vector= tsetse fly (moist savanna and woodlands)
natural host=
ungulates &other mammals (rhodesinse)
mainly man only (gambiense)
genus= Glossina

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4
Q

Who first recognised that trypanosomes caused sleeping sickness?

A

Sir David Bruce (Edinburgh)

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5
Q

Muriel Robertson

A

-life cycle of the trypanosome, cycling between humans and tsetse flies

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6
Q

Transmission of trypanosomes:

A

Via bite of tsetse fly

  • Inoculation of parasites in saliva
  • ingestion of parasites with blood meal
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7
Q

Trypanosoma brucei gambiense

A
  • causes chronic form of the disease

- this form = endemic in West and Central Africa

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8
Q

Trypanosoma brucei rhodesiense

A
  • causes acute form of the disease (just weeks between infection and death)
  • East and Southern Africa
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9
Q

Stages:

A
  • parasites injected by tsetse fly invade the blood and lymphatic systems
  • they later invade the CNS and brain
  • brain disorders in late stage include sleep wake patterns (hence sleeping sickness)
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10
Q

Weeks after infection

A

successive waves of parasitaemia

  • due to timing of immune reaction
  • parasites grow for about a week before immune system mounts fatal antibody response
  • a small number of parasites change their coat and can now grow while immune system needs to check their foreign status again
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11
Q

Structure of trypanosome:

A

-surface is covered in densely packed “VARIANT SURFACE GLYCOPROTEIN” (Vsg) coat

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12
Q

Structure of trypanosome: (ii)

A
  • single coat protein expressed at one time
  • proteins form homodimers
  • they anchor to the membrane via a glycosyl phosphatidyl inositol (gpi) anchor
  • coat prevents complement proteins fixing at the trypanosomes plasma membrane
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13
Q

Structure of trypanosome: (iii)

A
  • they have potential to express over 1000 VSGs, but express only one at a time
  • complex gene expression regulation
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14
Q

Process of antigenic variation in trypanosomes

A

-affects ability to produce vaccine against African trypanosomiasis

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15
Q

Chemotherapy of human African trypanosomiasis (HAT)

A
  • 5 drugs
  • Suramin and pentamidine useful against early stage disease (before invasion of the CNS)
  • melarsoprol and eflornithine useful against late stage of disease (after CNS invasion)
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16
Q

5 DRUGS useful in chemotherapy of HAT

A
  • Suramin
  • Pentamidine
  • Melarsoprol
  • Eflornithine
  • Nifurtimox
17
Q

Vector control:

A
  • insecticide spraying
  • tsetse trapping
  • sterile male release
18
Q

The Leishmaniases:

A
  • parasites of different species affect different parts of the body - They invade macrophages
  • after macrophage invasion they become amastigote forms proliferating inside the macrophages
19
Q

Vector for Leishmania parasites:

A

-sandflies

20
Q

Who first described Leishmania parasites? in 1900

A

William Leishman (Glasgow uni)

21
Q

New world Leishmaniasis:

A

L. mexicana (cutaneous)
L. braziliensis (mucocutaneous)
L. infantum (visceral)

22
Q

Leishmaniasis = zoonotic

A

dogs represent key reservoir host

23
Q

Sandfly/human stages (LEISH)

A
  1. sandfly takes blood meal (and injects promastigote stage into skin of human)
  2. Promastigotes are phagocytized by macrophages
  3. Promastigotes transform into amastigotes inside macrophages
  4. Amastigotes multiply in cells of various tissues
  5. Sandfly takes a blood meal (and ingests macrophages infected with amastigotes)
  6. Ingestion of parasitized cell
  7. Amastigotes transform into promastigote stage in midgut
  8. Divide in midgut and migrate to proboscis
24
Q

Amastigotes

A

inside macrophage

25
Q

Promastigotes

A

more developed parasites

26
Q

Cutaneous leishmaniasis

A

painless but unsightly skin lesions
- usually self-heal, but can develop into mucocutaneous Leishmaniasis, (MCL)
self-healing of CL lesions can take months, but a variety of drug treatments can speed up this process & reduce complications eg progression to MCL

27
Q

mucocutaneous Leishmaniasis, (MCL)

A

-MCL destroys the mucous membranes of the nose & mouth

28
Q

visceral Leishmaniasis (VL) is the most serious form

A
  • fatal without treatment
  • fevers, weight loss, enlargement of spleen and liver
  • anaemia
  • opportunistic infection in HIV patients
29
Q

Treatments for visceral Leishmaniasis

A 
-intravenous pentavalent antimonials (but some
parasites are resistant to these),
- amphotericin B 
- oral miltefosine 
-no current vaccine

Infection and Immunity (20 decks)

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