haemoflagellates Flashcards
What is the difference between a trypomastigote and an epimastigote?
trypomastigote= mammalian form epimastigote= vector form
What parasites causes african trypanosomiasis and where are they found?
Humans:
T.brucei rhodesiense (e.africa) and T.brucei. gambiense (w.africa)
Animals:
T.brucei brucei (need PCR to identify)
Describe the life cycle of T.brucei
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.
What are the clinical symptoms of HAT
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.
What is the difference between gambiense and rhodesiense sleeping sickness?
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.
What does pleomorphic mean and which tryps are?
T. brucei. Take more than one form: slender and stumpy
What can we label on a trypomastigote?
Kinetoplast at posterior end stained purple, tip of flagellum at anterior end, central nucleus stained purple, shape
What tsetse species are the vector of gambiense and rhodesiense?
G: Palpalis (riverine)
R: Mortisans (savannah)
What is the initial symptom of HAT
Chancre on skin which contains multiple trypomastigotes.
What are VSGs in tryps and what do they do?
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.
Why do tsetse flies have to bite numerous times if infected with tryps?
The tryps in salivary glands damages muscles important for pumping blood so the fly must bite ore times to blood feed.
What causes chagas disease and whats the vector?
trypanosoma cruzi, triatomine bugs
How does cruzi look different to brucei?
larger kinetoplast, c-shape, monomorphic, never dividing
What method of control do chagas and hat rely on?
vector control- currently no drug or vaccine
What are the possible modes of transmission of chagas?
insect vector bites, blood transfusion, sugar cane juice, congenital, organ transplant
Describe the life cycle of t.cruzi
- triatomine bug takes a blood meal and passes metacyclic trypanomastigotes in faeces which enter bite wound or mucosal membranes.
- transform into amastigotes inside cells
- amastigotes multiply by binary fission in infected tissue cells
- amastigotes transform into trypomastigotes, burst out of cell and enter bloodstream.
- bug takes blood meal (ingests tryps)
- epimastigotes in gut of bug and multiply
- metacyclic tryps in hindgut
Describe the clinical symptoms of chagas
acute: inflammatory lesion ‘chagoma’, fever, chest pain
chronic: if left untreated- enlarged heart / colon, constipation, abdominal pain
Why should you keep chickens away from houses?
Attract chagas but chicken blood lyses trypanosomes.
What are the control methods for chagas?
Improved housing, insecticides, bed nets, screen blood donors, Southern Cone Initiative
What diagnosis methods are there for chagas?
peripheral blood, xenodiagnosis, serological tests (antibodies present after 1 month), in vitro cultures, biopsy for amastigotes
What is the vector of leishmania?
Sandflies (Phlebotomine)
What morphological stages of Lesihmania are there?
promastigote (long and slender) found in the sandfly
amastigote found in human phagocytic cells
Describe the life cycle of Leishmania
- Sandfly takes blood meal and injects promastigote into skin
- promastigotes phagocytozed by macrophages
- promastigotes transform into amastigotes inside macrophages
- amastigotes multiply in cells of various tissues
- sandfly takes a blood meal and ingests macrophages infected with macrophages
- cell ruptures and releases amastigotes
- amastigotes transform into promastigotes in midgut
- divide in midgut and migrate to proboscis
How does leishmania evade immune system of human host?
stays in a vacuole that occupies cytoplasm of host cell
What types of leishmaniasis are there and what symptoms do they present?
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)
What Leishmania species cause VL?
L. donavani complex consisting of:
L.donavanii
L.infantum (old world)
L.chagasi (new world)
What countries is VL common in?
Brazil, Sudan, Bangladesh, India
What is Post-kala-azar dermal leishmaniasis?
Complication of VL. Extensive facial lesions, hypopigmentation.
How would you diagnose Leishmaniasis?
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
Do we feel the bite of a triatomine bug?
No, it has an anaesthetic in its saliva. It sense where capillary is, injects saliva and pumps blood directly from capillary.
Describe the blocked fly hypothesis
‘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.
