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Parasites and Infectious Diseases > Human African Trypanosomiasis - 1b > Flashcards

Human African Trypanosomiasis - 1b Flashcards

1
Q

Human African Trypanosomiasis

is also known as

A

African Sleeping Sickness

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2
Q

Human African Trypanosomiasis

prevalence

A
  • 36 countries in sub-Saharan Africa
  • 60 million people at risk
  • common in rural populations
  • prevalence in villages in Angola, the Democratic Republic of Congo, and Southern Sudan is between 20% and 50%
  • associated wit hpoverty
  • zoonotic (domstic and wild animals) and anthropomorphic transmission cycles
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3
Q

Human African Trypanosomiasis

epidemics

A
  • 1896-1906
  • 1920-1940
  • late 1970s - 2000
  • 3 main epidemics correlate with monitoring for disease
    • stop screening → number of reported cases increased
  • screening by NGOs
    • too dangerous in war/unrest → stop screening and testing
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4
Q

Transmission

A
  • T. brucei transmitted in saliva of tsetse fly (Glossina spp)
  • male and femal flies transmit disease
  • very painful bite
  • 34 different species and sub-species
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5
Q

Tsetse fly split into 3 groups based on

A
  • distribution
  • behaviour
  • molecular
  • morphology
  • riverine flies - associated with water
  • savannah - associated with open land
  • forest
  • different groups have different abilities to tranmit different HAT forms
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6
Q

Female flies are

A

viviparous

  • deposits a fully developd larva
  • burrows into the soil
  • pupates
  • emerges as an adult fly (month later)
  • newly-hatched flies not infected with trypanosomes
    • picks up trypanosome from animal or human host, not born with it

multivoltine

  • typically producing 4 generations per year
  • up to 31 generations over lifespan
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7
Q

Female flies are key to

A

vector control

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8
Q

Distribution of HAT and Tsetse fly

A

wherever you have the tsetse fly you have the disease

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9
Q

HAT is caused by the protozoan parasite

A

Trypanosoma brucei

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10
Q

Major forms of the parasite

(T. brucei)

A
  • 2 mastigote forms but one has 4 variants
  • trypomastigote
    • procyclic trypomastigote
    • bloodstream trypomastigote
    • metacyclic trypomastigote
    • short stumpy trypomastigote
  • epimastigote
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11
Q

Major form of T. brucei

trypomastigote (general)

A
  • common morphology in mammalian and insect hosts
  • common morphology of infective forms
  • the form of the parasite that lives within our blood stream and our lymphatic system
  • also the form of the parasite that lives within the gut of the insect vector
  • form of the parasite that’s transmitted from the insect to us and from us back to the insect

(4 forms - one in us, one in insect, 2 transmissable forms)

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12
Q

T. brucei

procyclic trypomastigote

A

INSECT​

  • divide by binary fission
  • cell coat - procyclin
  • lives in midgut of the tsetse fly
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13
Q

T. brucei

bloodstream trypomastigote

A

mammal

  • found in humans and ungulate animals
  • long, slender, bloostream trypomastigote
  • divide by binary fission
  • cell coat of variant surface glycoproten (VSG) to evade antibody-mediated immune destruction
  • lives in bloodstream (or lymphatic system) - extracellular parasite, kicks RBC out of the way
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14
Q

T. brucei

metacyclic trypomastigote

A

insect → humans

  • unable to divide
    • infectious forms compared to replicative forms is that these infectious forms are pre-adapted for life in the forthcoming host (adapted for life in human)
  • spat out in the saliva of the tsetse fly
  • the form that infects us
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15
Q

T. brucei

short stumpy trypomastigote

A

human → insect​

  • unable to divide
    • infectious forms compared to replicative forms is that these infectious forms are pre-adapted for life in the forthcoming host (adapted for life in insect)
  • form that we infect the tsetse fly
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16
Q

T. brucei

epimastigote

A
  • common morpholog in insect salivary gland
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17
Q

Trypomastigote

(picture)

A
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18
Q

Epimastigote

(picture)

A
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19
Q

Life cycle of T. brucei

(overall picture)

A
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20
Q
A
  • as tsetse fly takes a blood meal, parasites (metacyclic trypomastigotes) injected from salivary gland into victims bloodstream (salivarian)
  • injects saliva into host containing anti-coagulants etc
  • also injects the metacyclic trypomastigote - if the fly is infected - into blood or lymphatic system of host
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21
Q

As tsetse fly takes a blood meal, parasites

A

(metacyclic trypomastigotes) injected from salivary gland into victims bloodstream (salivarian)

  • injects saliva into host containing anti-coagulants etc
  • also injects the metacyclic trypomastigote - if the fly is infected - into blood or lymphatic system of host
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22
Q
A
  • injected metacyclic trypomastigotes transform into bloostream form (BSF) trypomastigotes
  • long-slender bloodstream form
  • trigger = temperature? (unknown)
  • BSF trypomastigotes multiply by binary fission in various body fluids (blood, lymph, spinal fluid)
    • begin dividing and colonizing bodily fluids
    • initally in blood and lymphatic system, but if given enough time, will cross the blood-brain barrier to get into the cererbal-spinal fluid
  • in the human host the long-slender BSF trypomastigotes appear to be able to sense the number of other parasites around them, and through a core sensing mechanism they can talk to each other, get a rough idea of the numbers of parasites, and if the population gets too high they express stumpy induction factor
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23
Q

Injected metacyclic trypomastigotes transform into

A

bloostream form (BSF) trypomastigotes

  • long-slender bloodstream form
  • trigger = temperature? (unknown)
  • BSF trypomastigotes multiply by binary fission in various body fluids (blood, lymph, spinal fluid)
  • begin dividing and colonizing bodily fluids
  • initally in blood and lymphatic system, but if given enough time, will cross the blood-brain barrier to get into the cererbal-spinal fluid
  • in the human host the long-slender BSF trypomastigotes appear to be able to sense the number of other parasites around them, and through a core sensing mechanism they can talk to each other, get a rough idea of the numbers of parasites, and if the population gets too high they express stumpy induction factor
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24
Q
A
  • BSF trypomastigotes differentiate into short stumpy (SS) trypomastigotes
    • trigger unknown - stumpy induction factor
    • in the human host the long-slender BSF trypomastigotes appear to be able to sense the number of other parasites around them, and through a core sensing mechanism they can talk to each other, get a rough idea of the numbers of parasites, and if the population gets too high they express stumpy induction factor
    • stumpy induction factor causes the long slender BSF parasite to shrink and form the short-stumpy trypomastigote
    • stumpy induction factor produced in a density-dependent manner
  • SS trypomastigotes can’t divide
    • pre-adapted for life in insect
  • tsetse fly takes a blood meal and ingests BSF and SS trypomastigotes
    • they pass into the gut of the insect
    • if the SS form isn’t taken up, human immune system will kick in and wipe it out
    • dead-end unless the SS gets into the tsetse form
      *
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25
Q

BSF trypomastigotes differentiate into

A

short stumpy (SS) trypomastigotes

  • trigger unknown - stumpy induction factor
    • in the human host the long-slender BSF trypomastigotes appear to be able to sense the number of other parasites around them, and through a core sensing mechanism they can talk to each other, get a rough idea of the numbers of parasites, and if the population gets too high they express stumpy induction factor
    • stumpy induction factor causes the long slender BSF parasite to shrink and form the short-stumpy trypomastigote
    • stumpy induction factor produced in a density-dependent manner
  • SS trypomastigotes can’t divide
    • pre-adapted for life in insect
  • tsetse fly takes a blood meal and ingests BSF and SS trypomastigotes
    • they pass into the gut of the insect
    • if the SS form isn’t taken up, human immune system will kick in and wipe it out
    • dead-end unless the SS gets into the tsetse form
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26
Q
A
  • in tsetse fly midgut, BSF trypomastigotes die
  • SS trypomastigotes transform into procyclic trypomastigotes
    • SS form survives, go into the midgut of the insect vector where they respond to…
    • trigger - temperature/citrate/cis-aconitate (temp and carbs)
  • procyclic trypomastigotes multiply by binary fission
  • colonize insect gut
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27
Q

in tsetse fly midgut, BSF trypomastigotes die

SS trypomastigotes transform into

A

procyclic trypomastigotes

  • SS form survives, go into the midgut of the insect vector where they respond to…
    • trigger - temperature/citrate/cis-aconitate (temp and carbs)
  • procyclic trypomastigotes multiply by binary fission
  • colonize insect gut
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28
Q
A
  • procyclic trypomastigotes leave themidgut
    • can either get back up through the digestive system and can get back into the salivary gland
    • or the procyclic form somehow can access the hemocyl (insect blood supply) to get into the salivary gland
  • migrate to the salivary gland
  • procyclic trypomastigotes transform into epimastigotes
    • trigger unknown
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29
Q

procyclic trypomastigotes leave themidgut and goes to the

A

salivary gland

  • can either get back up through the digestive system and can get back into the salivary gland
  • or the procyclic form somehow can access the hemocyl (insect blood supply) to get into the salivary gland
  • procyclic trypomastigotes transform into epimastigotes
  • trigger unknown
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30
Q
A

epimastigotes in the salivary gland:

  1. attach to epithelial cells via flagella
  2. divide by binary fission
  3. sexual reproduction can occur (genetic exchange is NOT an essential stage in life cycle, doesn’t involve meiosis - 2 diploid organisms fuse to form a tetraploid, with time lose genetic information to go back toward a diploid state) to colonize that organ
  4. transform into metacyclic trypomastigotes (trigger unknown)
  • some epimastigotes undergo a cell division that will result in one epimastigote and one metacyclic trypomastigote
  • probably density dependent
  • the epithelial cells have changed, and parasite off of epithelial cells into lumen (metacyclic form) that’s ready to be spat out into the next mammalian host
31
Q

2 sub species of T. brucei cause HAT

A
  • Trypanosoma brucei gambiense
    • ​West African trypanosomiasis
  • Trypanosoma brucei rhodesiense
    • East African trypanosomiasis
  • differences between the 2 forms
32
Q

Trypanosoma brucei gambiense

A

West African trypanosomiasis

33
Q

Trypanosoma brucei rhodesiense

A

East African trypanosomiasis

34
Q

Other African trypanosomiasis

A
  • found predominantly in ungulate mammals
  • sub of brucei
  • Trypanosoma brucei brucei
    • ​not infectious to humans
    • restricted to cattle
  • Trypanosoma vivax
  • Trypanosoma congolense
    • above 2 can resist human complement but this form is susceptible to our human complement
35
Q

East African trypanosomiasis

tsetse fly

A

savannah

36
Q

West African trypanosomiasis

tsetse fly

A

riverine

37
Q

East African trypanosomiasis

ecology

A

dry bush/woodland

38
Q

West African trypanosomiasis

ecology

A

rainforest

rivers

lakes

39
Q

East African trypanosomiasis

geographical range

A

East/Southern Africa

40
Q

West African trypanosomiasis

geographical range

A

West/Central Africa

41
Q

Meeting of East and West forms

A
  • East and West forms meet in Uganda
  • because of cattle movement worry that the forms will be brougth into contact
  • worry that in salivary gland of the insect vector epimastigotes can have sex
    • what if the 2 forms get on?
    • may get genetic mixing, what will it produce?
    • over time, as a result of cattle migration the 2 parasite forms are getting closer
42
Q

East African trypanosomiasis

transmission cycle

A

zootic

ungulate → human

involving animals

(animal - human - animal)

43
Q

West African trypanosomiasis

transmission cycle

A

anthropomorphic

human → human

44
Q

East African trypanosomiasis

non-human reservoirs

A

wild and domestic animals

45
Q

West African trypanosomiasis

non-human reservoirs

A

rare

46
Q

East African trypanosomiasis

epidemiology

A

sporadic, safaris

47
Q

West African trypanosomiasis

A

endemic, some epidemics

48
Q

East African trypanosomiasis

disease progression

A

rapid progression to death

49
Q

West African trypanosomiasis

disease progression

A

slow progression (~1 year) leading to death

50
Q

East African trypanosomiasis

parasitaemia

A

high

51
Q

West African trypanosomiasis

parasitaemia

A

low

52
Q

East African trypanosomiasis

asymptomatic carriers

A

rare

53
Q

West African trypanosomiasis

asymptomatic carriers

A

common

(always there at a very low level)

(difficult to detect in the first place by looking at a blood smear)

54
Q

In the west

A
  • low level constantly going on
  • number of asymptomatic cases
  • undersestimate number of cases because it’s there in a lot of people but at a very low level
  • not getting treated because not ill, even though it’s there
  • asymptomatic to life-threatening can take a long time (long-lasting chronic infection)
55
Q

In the east

A
  • nothing - nothing - spikes
  • sporadic outbreaks
  • like wildfire - affect a lot of people then die back very quickly
  • parasite burden is very high
    • humans find it very difficult to suppress parasite numbers
  • low number of asymptomatic cases
    • because if you get this form of the disease you transfer from asymptomatic to symptomatic very quickly (acute infection)
    • infection to death as little as 3-4 weeks
56
Q

Pathology

early stage

blood1

A

blood

  • chancre arises at site of bite in 50%
    • moreso with T. b. rhodesiense infections
      • probably more due to the tsetse fly than the infection
  • can heal leaving altered pigmentation
    • diagnostic, particularly of rhodesiense form
57
Q

Pathology

early stage

blood2

A
  • long slender form begins to divide and colonizes the blood
  • intermittent fever, headache
    • fibrile episodes of feeling hot then cooled down, again by the week
    • because immune system trying to wipe the parasite out
    • body responding to antigen insults being thrown at immune system
58
Q

Pathology

early stage

lymphatics

A
  • spreads to body and starts to invade other fluids - including lymphatic system
  • continued fibrile episodes
  • lymphadenopathy
    • localized edemas - water collection
    • swelling of the lymph glands
    • eg Winterbottom’s sign - enlarged neck gland
  • deteriorating health
59
Q

Pathology

late stage

CNS

A
  • severe sleep disturbance

can still get treated and recover, but if not:

  • severe neurological symptoms
  • convulsions
  • coma
  • personality change
  • death

arsenic treatment in East form, but arsenic is lethal also

60
Q

Comparing pathology

A
61
Q

Diagnosis

A
  • must be cheap, can’t rely on power supply
  • direct methods
    • blood smear
    • enrichment
      • DEAE anion exchange
      • microhaematocrit
    • cerebrospinal fluid
62
Q

Diagnosis

direct

A

blood smear

  • ok for East form where parasitaemia can get very high
  • not good for West form where parasite density doesn’t get very high
63
Q

Diagnosis

direct

enrichment

A

enrichment

  • DEAE anion exchange column
    • RBC stay in column, parasites pass through
    • can use concentration methods - use ion exhchange column to bind out red blood cells and allow parasites to come through
  • microhaematocrit (buffy coat)
    • capillary tubes sealed at one end, suck blood up and put into specialized centrifuge, spin to package out all components of blood
    • RBC at bottom - WBC with buffy coat - plasma on top
    • look at buffy coat for presence or parasite
64
Q

Diagnosis

direct

cerebrospinal fluid

A

lumbar punctures to diagnose people with late stage symptoms

65
Q

Diagnosis

indirect (seriology)

CATT

A

Card Agglutination Test for Trypanosomiasis

drop of blood

+ fixed (dead) parasites on a plastic card

⇒ blue granular deposits = infection

  • looking for antibodies against the parasite in the person’s blood
  • if you have antibodies against the parasite it will agglutinate the parasites together to form a granular deposit
  • not infected = no blue granulation
  • only works for T. b. gambiense BUT is cheap (25cents/test)
    • need diagnostic tests for East form that kills you faster
66
Q

5 licensed drugs

A
  1. Suramin
  2. Pentamidine
  3. Melarsoprol
  4. Eflornithine
  5. NECT (nifurtimox-eflornithine combinational therapy)
67
Q

Prevention and control

A
  1. pre-20th century
  2. land clearing
  3. slaughter of wild animals
  4. pesticide campaigns
  5. trapping
  6. irradiated males
  • control efforts undertaken throughout the African continent long-term sustainable control rarely achieved
  • tsetse control efforts tied to poverty, health, politics
68
Q

Prevention and control

pre-20th century

A

humans didn’t settle or cultivate crops in areas where fly prevalent

69
Q

Prevention and control

land clearing

A
  • removal of brush and woody vegetation from area
  • Tsetse tend to rest on trunks of trees
    • hop around rather than flying

if remove the threat, humans will move into the savannah

70
Q

Prevention and control

slaughter of

A

wild animals

71
Q

Prevention and control

pesticide campaigns

A
  • aerosol sprays (DDT)
    • ecosystems rebelled against
  • pour on formulations (cattle)
72
Q

Prevention and control

trapping

A
  • can trap the flies
  • attracted to dark objects
  • put insecticide in dark object
73
Q

Prevention and control

irradiated males

A
  • try to breed out the disease
74
Q
A

Parasites and Infectious Diseases (8 decks)

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