Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > protists and human disease > Flashcards

protists and human disease Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

parabasalids

A

The parabasalids are a group of flagellated protists within the supergroup Excavata.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

example of a parabasalid and the disease it causes

A

Trichomonas vaginalis =Trichomoniasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Trichomoniasis

A

Infection of the urogenital tract. it is the most common pathogenic protozoan infection of humans in industrialised countries. More than 160 mill people worldwide are annually infected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diplomonads

A

The diplomonads are a group of flagellates, most of which are parasitic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

example of a diplomands and the disease it causes

A

Guardia lamblia= Giardiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Giardiasis

A

one of the most common parasitic diseases globally. Causes diarrhoea, abdominal pain and weight loss. Occurs in other animals including beavers. Animals are thought to play a role in keeping the infection present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Trypanosomes

A

is a genus of kinetoplastids (class Kinetoplastida), a monophyletic[1] group of unicellular parasitic flagellate protozoa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where do trypanosomes live

A

in vertebrates blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

characteristics of a Trypanosome

A

kinetoplast and single flagellum attached to membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Trypanosomes are most famous for being

A

vector-borne parasite
e.g. a bug will take up the parasite whilst feeding on a cow, then will inoculate a human with it whilst feeding on their blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

excavates

A

ancient group, diverged just after emergence of eukaryotes –> many important parasites of humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

kinetoplastics

A

mitochondria contain kinetoplast (a network of circular DNA inside a large mitochondria that contains many copies of the mitochondrial genome)
-includes important vector-borne parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chagas disease is caused by the parasite

A

Trypanosome cruzi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the vector for chagas disease

A

triatomine bugs- also known as kissing/vampire bugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what guides triatomine bugs to their host

A

CO2 from bath and heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

two forms of Trypanosoma cruzi

A

acute (brief) and chronic (long term)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

host invasion of T.cruzi (s.america)

A
  • feeding wound or mucosa
  • blood
  • muscle
  • nerves
  • macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

host localisation of T.cruzi

A
  • intracellular: cardiac muscle, smooth muscle autonomic nerves, macrophages
  • enter and migrate around host via blog stream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

where is T.cruzi found

A

south america

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

immune response to T.cruzi

A

primarily cellular- T cells etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why is T.cruzi hard for the immune system to cope with

A
  • can grow within macrophages–> enter via phagocytic vacuole and quickly escape the vacuole and move into the cytoplasm where is is safe from enzyme activity. –> now hidden from host immune response within cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

life cycle of T.cruzi

A

1) kissing bug take a blood meal and releases trypomastigotes in its faeces near the site of the wound
2) Trypomastigotess enter the host through the wound or through intact mucosal membranes
3) inside the host the the trypomastigotes invade cells near the site of inoculation, where they differentiate into amstigotes
4) the amastigotes multiply by binary fission and differentiate into trymastigotes
5) then released into circulations bloodstream trypomastigotes
6) these ice again enter cells and differentiate into amstigotes–> new infection
7) ingested trypomastigotes transform into epimastigotes in the vectors midgut. The parasites multiply and differentiate into infect metacyclic typomastigotes in the handgun.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

replication of trypomastiogfs (t.cruzi) can only occur

A

in cells, they cannot multiply in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

life cycle of T.cruzi

A

-trypomastigotes–> amastigotes–> epimastigotes –> metacyclic trypomastigotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

phages and pathology

A
  • cardiopathy- causes cardiac damage which causes rhythm abnormalities.
  • also damage to colon (severe weight loss and swallowing difficulties)
26
Q

Chagas disease: pathology I: acute form

A

lasts for the first few weeks or months and host symptoms can be mild or not exist. symptoms includeL swell gin, fever, fatigue, body aches, muscle pain, headaches, rash, loss of appetite, diarrhoea, nausea and vomiting

27
Q

acute form of chagas is the direct consequence of

A

invasion, amastigote multiplication and cell rupture

28
Q

chagas disease: pathology II- chronic form

A

Infection persists and enters chronic phase (60-80& sufferers will never develop chronic symptoms). Toxins released by intracellular amastigotes cause widespread damage

29
Q

damage caused by chronic chagas

A
  • destruction of autonomic nerve elements
  • muscle denervation leading to inability to contract
  • autoimmune tissue destruction
30
Q

african sleeping sickness is caused by

A

T.brucei

31
Q

vector of african sleeping sickness

A

Tsetse flies

32
Q

two subset of T.brucei that causes sleeping sickness

A

west: Trypansoma brucei gambiense
east: Trypanosome brucei rhodesiene

33
Q

Trypanosoma brucei gambiense

A

invades the NS- chronic

34
Q

Trypanosoma brucei rhodesiense

A

widespread organ damage- acute

35
Q

host invasion by T.brucei

A
  • inoculated by tsetse fly
  • blood
  • lymph
  • lympg nodes
  • cerebrospinal fluid
  • brain
36
Q

host localisation by T. brucei

A

intercellular: blood, lymph, cerebrospinal fluid, brain

37
Q

immune evasion of T.brucei

A

parasite presents a series of variation antigenic types (VATs) by virtue of its surface coat. Coat is made up of variable survive glycoproteins (VSGs). More than 10 mill identical glycoprotein molecules cover parasite surface.

38
Q

more detailed on immune evasion using VSG variability in T.brucei

A

VSG pack tightly preventing immune recognition. VSG produced change throughout the course of infection:

  1. parasite coats itself entirely in a particular VSG (=VSG1)
  2. Host produces antibodies against the corresponding VAT (VAT1)
  3. host antibodies eventually destroy all of the parasite expressing VAT1
  4. Parasitaemia subside (blood count of parasites)
  5. subset of parasite pop begins rto express another VSG gene (VSG2)
  6. parasite coated with the new VSG2 come to predominate the pop
  7. host has no immediate antibody type ready for recognition of VAT2
  8. parasite number increases rapidly… and so on… there are 1000 diff VSGs
39
Q

what is the changing nature of VSG in T.brucei known as

A

classical undulating waves of parasitaemia- malaria also produce classical waves of parasitaemia and symptoms

40
Q

VSG changing in tsetse fly and host

A

in tsetse fly gut, trypanosomes express a single surface antigen (procyclin). In salivary gland - first VSG. In bloodstream of mammalian host there will be a succession of VSG.

41
Q

VSG

A

genome has over 1000 VSG genes.

42
Q

only VSG located in ….. can be expressed

A

telomeric expression sites

43
Q

how many expression sites to VSG have in bloodstream parasites

A

20

44
Q

there is only one active VSG expression site

A

therefore only one VSG expressed at a time

45
Q

2 main methods lead to antigenic variation- expression of new VSG

A

1) use of different VSG expression site- around 20 - in situe switch
2) DNA recombination changes VSG present in active expression site= gene conversion

46
Q

in situe switch

A

use of different VSG expression site- around 20

47
Q

Gene conversion

A

DNA recombination changes VSG present in active expression site- gene conversion

48
Q

life cycle of sleeping sickness

A

1) tsetse fly takes a blood meal- injecting metacyclic trypomastigotes
2) injected metacyclic trypomastiogtes transform into bloodstream trypomastigotes, which are carried to other sites
3) Trypomastigotes multiply by binary fission in various body fluids e.g. blood lymph and spinal fluid
4) trypomastigotres in blood
5) tsetse fly takes a blood meal
6) bloodstream trypomastigotes transform into pro cyclic trypomastigotes in tsetse fly midgut, multiplying by binary fission

ABSENCE OF AMASTIGOTE INTRACELLULAR FORM

49
Q

main difference between life cycle of chagas and sleeping sickness

A

absence of amastigote intracellular form in sleeping sickness

50
Q

sleeping sickness: pathology I–> acute form

A
  • first stageL fever, headaches, joint pains, itching –> attacks lasting a day to a week, separated by intervals of a few days or to a month.
  • untreated diseases can overcomes the hosts defences causing extensive damage- anaemia, cardiac and kidney dysfunction
51
Q

anemia and acute sleeping sickness

A

Parasite antigens absorbs host red blood cells leading to lysis and therefore anaemia.

52
Q

huge lymph nodes and acute sleeping sickness

A

invasion of circulatory and lymphatic systems by parasite is associated with severe swelling of lymph nodes and often to a tremendous size

53
Q

first stage of sleeping sickness is called

A

hemolyphatic

54
Q

chronic phase of sleeping sickness is called

A

meningoencephalitic phase

55
Q

the second stage of sleeping sickness is more

A

neurological

56
Q

where does sleeping sickness get its name from

A

causes fragmented 24-hour rhythm of sleep-wake cycle, daytime sleep and night time wakefulness episodes

57
Q

neurological symptoms of sleeping sickness

A

confusion, tremors, paralysis, speech disorders and psychiatric symptoms

58
Q

why does sleeping sickness cause neurological problems

A

due to invasion f the CNS causing neurological damage- inflammation of brain and spinal cord- lesions in merges and cerebral cortex

-inflammatory reaction leads to myelin destruction

59
Q

treatment of chagas

A
  • target patients early, before major invasion of heart and organs
  • drug targets parasites in bloodstream- long treatment
  • development of drug resistance

worry about raising conc of drug in body high enough to act against amastigotes in muscle cells

60
Q

treatment of sleeping sickness

A
  • target patients early- before invasion of CNS
  • problem with raising conc of drug in the body high enough to act in brain
  • combination of drug used- to avoid high dosage of arsenic based compounds
61
Q

3 main parasites talked about

A

trypanosoma cruz
trypanosoma brucei gambiense
trypanosoma brucei rhodesiense

Microbiology (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions