African Trypanosmosis Flashcards Preview

PHVTD > African Trypanosmosis > Flashcards

Flashcards in African Trypanosmosis Deck (23):
1

What diseases does T. brucei cause?

Sleeping sickness and nagana

2

How does its life cycle differ to the South American trypanosome?

It is a salivarian parasite, transmitted by the tsetse fly. There is no intracellular life cycle stage. There is also evidence that sexual reproduction occurs in the salivary gland of the fly.

3

What habitats is the tsetse fly found in?

Rivverine and savannah.

4

What aspects of the fly LC would allow it to be targeted by control measures?

It is infected for life but only lays a single egg.

5

What are the two stages of disease in humans?

Lymphadenopathy, fever and headaches. Then is enters the cerebellum/brain which can lead to oedema and hemorrhage. Also see behavioral changes/fatigue.

Can get severe immunosuppression later on.

6

What is the pathogenesis of the disease?

Lymphoid depletion leads to immunosuppression. there is also aneamia and degeneration/inflammation.

7

What are the subspecies of T.brucei and how do their disease dynamics differ?

gambiense - humans are chronically infected with a low parasitaemia and it is endemic. Therefore humans are the main reservoir and domestic animals the minor reservoir.

rhodensiense - humans suffer from acute and fatal disease so are not generally responsible for transmission to other humans. The parasiteamia is high and infections sporadic. The main reservoir are (domestic) and wild animals.

8

Are there any other ways this parasite can be transmitted?

evansi - mechanically (Tabanid spp.) and vertically transmitted

Surra (horses&camels) - mechanical

Dourine (horses and donkeys) - venereal

9

How are flies controlled?

Spraying and trapping
barrier fences and buffer zones to seperate wild and domestic animals

10

How else is the disease spread controlled?

Prophylactic drugs
Using trypano-tolerant animals (act as a reservoir)
Therapeutic drugs

11

Why are there no vaccines?

VSG
Proteinases cleave complement and abs on trypanosome surface
induce immunosuppression - hinder memory responses

12

How can it be diagnosed?

Giemsa staining, heamatocrit tubes, blood film

ELISA IFAT, western blot
PCR
culture

13

What is the most prominent problem encountered by T. brucei as a host?

Surviving within the host/evading the host immune resposne.

14

How does T. brucei avoid the immune response?

Immune suppression and immune evasion (switching surface antigens)

15

How does T. brucei avoid immune killing?

Covers constant antigens (ones that could not be altered) with the variable N-terminal VSG

16

How does the number of M-VSGs compare to the number of blood VSGs?

28 genes for M VSG
roughly 1000 for VSG

17

How often are VSG genes switched?

Every 10^6 divisions. Roughly every millionth trypanomastigote has a different VSG.

18

How does this aid their survival as a species?

Strong IgM response kills most parasites through opsonisation and complement lysis, however, the millionth will survive therefore you get waves of infection.

19

Where are VSG genes located?

Expression sites
Minichromosomes
Subtelomeres

20

What is meant by mono- and polycistronic?

Mono = 1 promoter to 1 gene
Poly = 1 promotor to many genes

21

How can the parasite change its VSG?

In situ switch of the ESB
Telomere exchange (swap in a gene from minichromosome)
Gene conversion (change the gene by adding in some repeats from subtelomeric sites)
Base J - change a ......

22

What covers the parasite stage entering the insect?

Procyclin, which is constant. This covers the procyclic trypanomastigote.

23

What prospects are there for vaccination against T. brucei?

Target hidden C-terminal antigens with nanobodies
Target M-VSG
Target proteins involved with endocytocis. (although not very immunogenic)