haemoflagellates

Question 1

What is the difference between a trypomastigote and an epimastigote?

Answer 1

trypomastigote= mammalian form
epimastigote= vector form

Question 2

What parasites causes african trypanosomiasis and where are they found?

Answer 2

Humans:
T.brucei rhodesiense (e.africa) and T.brucei. gambiense (w.africa)
Animals:
T.brucei brucei (need PCR to identify)

Question 3

Describe the life cycle of T.brucei

Answer 3

Human
1. Tsetse inject metacyclic trypomastigotes.
2. Dissemination in bloodstream and multiplication by binary fission
3. tsetse takes a blood meal and ingests bloodstream trypomastigotes
Tsetse
4. Transform into procyclic trypomastigotes in midgut and multiply
5. leave midgut and transform into epimastigotes
6. epimastigotes multiply in salivary gland and transform into metacyclic trypomastigotes.

Question 4

What are the clinical symptoms of HAT

Answer 4

Parasites multiplying in lymph and blood cause headaches, fever, weakness etc. overtime the parasite cross the BBB and migrates to CNS which causes changes in behaviour, disrupts sleep cycle and can be fatal.

Question 5

What is the difference between gambiense and rhodesiense sleeping sickness?

Answer 5

G: human to human transmission. Common in W.Africa in riverine sites.
R: rapid onset. zoonotic disease where animals in savannah are hosts. typically affects people working near animals. Common in E. Africa.

Question 6

What does pleomorphic mean and which tryps are?

Answer 6

T. brucei. Take more than one form: slender and stumpy

Question 7

What can we label on a trypomastigote?

Answer 7

Kinetoplast at posterior end stained purple, tip of flagellum at anterior end, central nucleus stained purple, shape

Question 8

What tsetse species are the vector of gambiense and rhodesiense?

Answer 8

G: Palpalis (riverine)
R: Mortisans (savannah)

Question 9

What is the initial symptom of HAT

Answer 9

Chancre on skin which contains multiple trypomastigotes.

Question 10

What are VSGs in tryps and what do they do?

Answer 10

Variant surface glycoproteins which allows tryp survival in bloodstream. The tryps periodically undergo antigenic variation to express different VSGs so they can’t be cleared by antibodies.

Question 11

Why do tsetse flies have to bite numerous times if infected with tryps?

Answer 11

The tryps in salivary glands damages muscles important for pumping blood so the fly must bite ore times to blood feed.

Question 12

What causes chagas disease and whats the vector?

Answer 12

trypanosoma cruzi, triatomine bugs

Question 13

How does cruzi look different to brucei?

Answer 13

larger kinetoplast, c-shape, monomorphic, never dividing

Question 14

What method of control do chagas and hat rely on?

Answer 14

vector control- currently no drug or vaccine

Question 15

What are the possible modes of transmission of chagas?

Answer 15

insect vector bites, blood transfusion, sugar cane juice, congenital, organ transplant

Question 16

Describe the life cycle of t.cruzi

Answer 16

1. triatomine bug takes a blood meal and passes metacyclic trypanomastigotes in faeces which enter bite wound or mucosal membranes.
2. transform into amastigotes inside cells
3. amastigotes multiply by binary fission in infected tissue cells
4. amastigotes transform into trypomastigotes, burst out of cell and enter bloodstream.
5. bug takes blood meal (ingests tryps)
6. epimastigotes in gut of bug and multiply
7. metacyclic tryps in hindgut

Question 17

Describe the clinical symptoms of chagas

Answer 17

acute: inflammatory lesion ‘chagoma’, fever, chest pain
chronic: if left untreated- enlarged heart / colon, constipation, abdominal pain

Question 18

Why should you keep chickens away from houses?

Answer 18

Attract chagas but chicken blood lyses trypanosomes.

Question 19

What are the control methods for chagas?

Answer 19

Improved housing, insecticides, bed nets, screen blood donors, Southern Cone Initiative

Question 20

What diagnosis methods are there for chagas?

Answer 20

peripheral blood, xenodiagnosis, serological tests (antibodies present after 1 month), in vitro cultures, biopsy for amastigotes

Question 21

What is the vector of leishmania?

Answer 21

Sandflies (Phlebotomine)

Question 22

What morphological stages of Lesihmania are there?

Answer 22

promastigote (long and slender) found in the sandfly

amastigote found in human phagocytic cells

Question 23

Describe the life cycle of Leishmania

Answer 23

1. Sandfly takes blood meal and injects promastigote into skin
2. promastigotes phagocytozed 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 macrophages
6. cell ruptures and releases amastigotes
7. amastigotes transform into promastigotes in midgut
8. divide in midgut and migrate to proboscis

Question 24

How does leishmania evade immune system of human host?

Answer 24

stays in a vacuole that occupies cytoplasm of host cell

Question 25

What types of leishmaniasis are there and what symptoms do they present?

Answer 25

cutaneous: lesions that self heal
diffuse cutaneous: nodules on skin full of amastigotes
mucocutaneous: skin ulcer that heals, parasite reappears on nasal and mouth mucosa years later
visceral: enlargement of spleen and liver (hepatosplenomegaly)

Question 26

What Leishmania species cause VL?

Answer 26

L. donavani complex consisting of:
L.donavanii
L.infantum (old world)
L.chagasi (new world)

Question 27

What countries is VL common in?

Answer 27

Brazil, Sudan, Bangladesh, India

Question 28

What is Post-kala-azar dermal leishmaniasis?

Answer 28

Complication of VL. Extensive facial lesions, hypopigmentation.

Question 29

How would you diagnose Leishmaniasis?

Answer 29

Formal gel test, serology, histopathology (look at amastigotes in tissues), cultures of organism from spleen, marrow, lymph, leishmanin skin test (negative in VL and DCL), PCR

Question 30

Do we feel the bite of a triatomine bug?

Answer 30

No, it has an anaesthetic in its saliva. It sense where capillary is, injects saliva and pumps blood directly from capillary.

Question 31

Describe the blocked fly hypothesis

Answer 31

‘Promastigotes in the gut formed a physical obstruction that had to be removed by regurgitation’
Promastigote secretory gel (PSG) mixed with sandfly saliva, Lesihmania attach to valve in sandfly, PSG obstruct midgut, forces open the valve and promastigotes can be injected into host.