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Parasites and infectious disease > Trypanosmiases paper Barret et al 2003 > Flashcards

Trypanosmiases paper Barret et al 2003 Flashcards

1
Q

What is one of the most prevalent diseases in central and south america?

A

Chagas disease

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2
Q

Why is disease containment an achievable goal with trypanosomiases?

A

Because of the life strategy of the arthropod vectors

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3
Q

What has stimulated research into new drug targets for the trypanosomiases?

A

THey are some of the earliest diverging members of the eukaryote and share several biochemical peculiarities.

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4
Q

What have frustrated efforts to design drugs effective against both speceis?

A

Differences in ways in which trypanosome species intercact with their hosts

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5
Q

What is the protozoan order than trypanosomiases are in?

A

Kinetoplastida

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6
Q

Several trypanosome speceis cause important vector diseases but only 2 cause significant human disease, what are they?

A

T.brucei an t.cruzi

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7
Q

What other genus does the Kinetoplastida contain which also causes disease in the tropics and sub tropics?

A

Leishmania

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8
Q

A substantial amount of similarity exists between t.brucei and t.cruzi, list 2 of them

A

both are trasnmitted by insect vectors

both share many aspects of their basic biochemical physiology

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9
Q

There are profound differences at the level of the host parasite interface and what has this caused?

A

frustrated most efforts to use information gained about one species to assist in control of the other

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10
Q

List 3 of the structural similarities between t.brucei and t.cruzi

A

Single celled flagellates
Transmitted by insect vectors
Share phases of local multiplication in their human host followed by dissemintation and localisation in target organs in which they cause potentially lethal damage

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11
Q

What can account for why clinical manifestations and susceptibility to treatment differ?

A

ALthough there are many similarities between the 2 diseases, there are key differences between the organisms which account for why clinical manifestations and susceptibility to treatment differ.

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12
Q

What did Stevens et al 2001 discover about the evolutionary history of the trypanosomes?

A

Comparison of 18S rRNA gene sequences from multiple trypanosome species obtained from diverse hosts, combined with other molecular approaches suggest tje genus Trypanosoma is monophyletic.

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13
Q

How did Stevens et al 1999 show when t.brucei and t.cruzi shared a common ancestor?

A

By superimposing estimates with the molecular clock on vicariance biogeography it is suggested that they shared a common ancestor 100 mya

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14
Q

What does the prehistoric dating suggest about t.brucei?

A

Indicates that human beings were exposed to african trypanosomes concomitantly with their evolution

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15
Q

What does the prehistoric dating suggest about t.cruzi?

A

American typanosomes evolved independenly of their host homo sapiens who probably joined the host range of t.cruzi only within the past 12 000 too 40 000 years when man arrived on the american continent

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16
Q

T.brucei and t.cruzi are both transmitted by biting insects but a fundamental difference between the means of transmission has been incorporated into the classification of these organisms : ?

A

T.brucei are known as salivaria because they are transmitted by the Tsetse fyl saliva
T.cruzi belongs to the stercoraria because transmission is via vector faeces

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17
Q

Transmission of both organisms can also be via 3 things?

A

Blood transfusion, contaminated needles, or the congenital route

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18
Q

Prata 2001 found a rare case of transmission of t.cruzi how?

A

breastfeeding

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19
Q

In 1985 WHO estimates that how many people are at risk of chagas disease in latin america?

A

100 million

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20
Q

What is the vector of t.cruzi?

A

bugs in sub family triatominae and family reduviidae

assassin bugs

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21
Q

the three most important speceis of assasin bugs that are vectors of t.cruzi are what?

A

Triatoma infestans
Rhodrius polixus
Panstrongylus megistus

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22
Q

How many lineages of t.cruzi are there and which one causes chagas disease?

A

two linneages: type 1 and type 2

type 2 is the cause of chagas

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23
Q

Describe a little about type 1 and type 2 linneages of t.cruzi

A

Type 1 is widespread in mammalian hosts within a wild cycle.

Type 2 is more restricted in its host range to only a few mammalian species in a peridomestic habitat

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24
Q

Chagas disease undergoes ____ stages in its natural course, is potentially ____ and there are no _____.

A

distinct
fatal
vaccines

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25
Q

What happens after entry into the host?

A

T.cruzi invades host cells.

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26
Q

What has an important early role in reacting to infection and in carrying parasites to other sites within the body?

A

macrophages

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27
Q

T.cruzi ____ differentiate into replicative ____ within cells before differentiation back to ____ ____ trypomastigotes that leave one cell type and invade others.

A

trypomastigotes
amastigotes
bloodstream form

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28
Q

The surface of the parasite is covered by ____ ___ _____.

A

Mucin type glycoproteins

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29
Q

These mucin type glycoproteins attach to the membrane how?

A

By glycosylphophotidylinositol (GPI) anchors similar to those of the variant surface glycoproteins in african trypanosomes

30
Q

What are the major recipients of the sialic acid transferred by surface trans-sialidase?

A

Mucins

31
Q

T.cruzi has several ____ mucin genes and the exposed _______ moiety of the molecules belonging to one of the mucin families is ______.

A

hundred
n-terminal
hypervariable

32
Q

What can T.cruzi derived GPI anchors activate?

A

host macrophages

33
Q

What is judged imporatnt in control of infection and outcome of chagas disease?

A

T.cruzi is a potent stimulator of cell mediated immunity and induction of macrophage proinflammatory cytokines is judged important.

34
Q

How is t.cruzi usually transmitted?

A

as infected triatomine vectors gorge themselves on blood from sleeping hosts

35
Q

What do the faeces depsotied by the insect during feeding contain?

A

metacyclic trypomastigotes

36
Q

what allow the trypomastigotes to breech the skin and invade host cells?

A

itching produced by the vectors bite induces the individual to scratch causing microabrasions in the skin

37
Q

When do clinical manifestations of the acute stage occur?

how long do they last?

A

6-10 days after infection

last 1-2 months

38
Q

what is a chagoma?

A

symptom

frequent inflammation at the site of infection leads to an oedematous swelling known as a chagoma

39
Q

what is romanas sign?

A

symptom
swelling of the eyelids after infection at this site and allows easy symptomatic diagnosis in up to half of those cases showing overt manifestations of acute disease

40
Q

when do most acute cases arise? age

A

before 15 years

mainly between 1 and 5 years

41
Q

Why does the acute phase usually pass unnoticed?

A

symptoms typical of general malaise in other infections

42
Q

can death occur in the acute phase?

A

yes usulaly with symptoms similar to that seen in T.b.r infection

43
Q

what are 4 other symptoms of the acute stage that are common?

A

rash
fever
heptasplenomegaly
oedema of the face and elsewhere

44
Q

what can electrocardiograms show in the acute stage?

A

abnormalities and primary t-wave changes

45
Q

where can parasties easily be detected in the acute stage?

A

peripheral blood

46
Q

when does the acute stage of the disease end?

A

when the immunological balance between the host and the parasite greatly reduces the number of circulating trypomastigotes, rendering direct parasitological diagnosis impossible

47
Q

what happens after the acute stage?

A

people enter the chronic stage

patients become asymptomatic with typical findings on the electrocardiogrpahy and chest radiography

48
Q

how mnay people contineu in this state known as indeterminate form of chronic chagas disease for hte rest of their lives?

A

70-85%

49
Q

15-30% will develop in the chronic stage manifestations of organ damage producing what?

A

the cardiac, digestive, or nervous forms of chronic chagas diesease 10-25 years after initial infection

50
Q

what are symptoms of the chronic stage manifestation of organ damage?

A

chest pain, palpitations, dizziness, and peripheral oedema

heart failure and sudden death are common

51
Q

what are the 2 drugs for treatment of chagas?

A

two nitroheterocyclic drugs:
nifurtimox
benzindazole

52
Q

when was nifurtimox introduced and what is it used to treat?

A

1960s
acute chagas
drug is trypanocidal mainly against circulating trypanomastigotes and is better tolerated by young patients

53
Q

When was benzindazole introduced?

A

1970

54
Q

What is the problem with both drugs?

A

they occassionally induce serious side effects and neither has high efficacy against chronic chagas disease

55
Q

What did Sasa estanoi et al 1998 and Andrade et al 1996 show in studies on Benznidazole?

A

showed that benznidazole depleted anti t.cruzi reactivity in specific serological tests and lowered prevalence of heart alterations by 62% in school children

56
Q

What did DaSilva 1999 show about treatment?

A

that treatment of the symptomatic complications of chagas disease is also effective improvement of quality of life

57
Q

What did Wang 1995 show have long been regarded as potential drug targets?

A

biochemical pathways general to trypanosomatids but absent from mammalian hosts

58
Q

Croft 1999
Differences between t.brucei and t.cruzi at the level of the host parasite interaction, however, lead to a huge variation in the _____ _____ needed for agents used against the different diseases

A

pharmacological criteria

59
Q

HAT is seldom diagnosed before the late stage so drugs must cross the ___ ___ ___ to be effective

A

blood brain barrier

60
Q

to target t.cruzi amastigotes drugs must also enter many mammalian cell types, which causes what?

A

diminishes the quantity of drug available to interact with the parasites and amplifies risks of host cell toxic effects

61
Q

What has a proportion of research into trypanosomes over the past 20 years been related to?

A

has been related to target identification and development of lead compounds that interact with these targets

62
Q

What are the 4 approaches to control fo chagas disease?

A

vector control
personal prophylaxis
serological control of blood banks
treatment of infected individuals

63
Q

What are the 3 approaches to control of HAT?

A

treatment of infected individuals
vector control
active case finding with mobile teams

64
Q

what is the main way that tsetse flies and triatominae differ ecologically?

A

triatominae usually crawl within peridomestic environments, and bitten while asleep indoors where as tsetse flies are active during the day

65
Q

what is the one important ecological factor that tsetse flies and triatominae share? and this makes them vulnerable to interventions aimed at altering their environment and lowering their reproductive rate

A

k strategists

low reproductive rate, high survival rate, adapted for the efficient exploitation of their habitat

66
Q

triatomine bugs reside where? so what would be a good control prevention?

A

within the hatched roofs and cracked walls of rural huts.

exchanging these for corrugated iron / wood / stone

67
Q

DDT is not effective against triatomine bugs but what is?

A

other organochlorides are effective

68
Q

what occurred before the 1970s?

A

successful insecticide control campaigns in argentina, brazil, chile, and venezuela encouraged other endemic countries to adopt similar methods

69
Q

today acute chagas disease has been eliminated from many __ ____ and the cost benefit initiatives are highly positive

A

rural areas

70
Q

there is some concern about what with the eradication?

A

eradication of the domsetic sp will open a niche for sylvatic triatominae to inhabit

71
Q

Barrat et al 2003 showed what were the priorities for research into trypanosomiases? (4 points)

A
  1. development of sustainable, multicomponent approaches to control of insect vectors
  2. Identification of drug targets with genome data bases and their validation by genetic approaches
  3. Improvement in practical diagnostic techniques capable of detecting infection and staging the disease
  4. Improvement in understanding of the parts played by the parasites and of host responses to them in development of pathophysiology

Parasites and infectious disease (15 decks)

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