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Human Parasitology > Protozoa, Trypanosoma, & Antigenic Variation > Flashcards

Protozoa, Trypanosoma, & Antigenic Variation Flashcards

1
Q

What is the kinetoplast, where is it found, and what function does it have?

A 
what - disk of interlocking DNA circles (kDNA)
where - along inner surface in mitochondria
function - mitochondrial
transformation between life cycle forms
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2
Q

What are the 2 components of kDNA and how are they arranged?

A
  1. maxi-circles: ~50 copies
  2. mini-copies: 5000-10000 copies
    arrangement - concatenated mass of interconnected complex networks
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3
Q

What is a basal body and where is it found?

A

what - anchors flagellum
where - outer surface of mitochondrial membrane
always close to kinetoplast

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4
Q

What are the 3 major kinetoplastid infections in humans?

A
  1. human African Trypanosomiasis (HAT)
  2. Chagas’ disease
  3. Leishmaniasis
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5
Q

What 4 morphological forms can occur in the various kinetoplastid life cycles?

A
  1. amastigote - no flagellum
  2. promastigote - flagellum, in vector
  3. epimastigote - undulating membrane
  4. trypomastigote
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6
Q

What is the function of the glycosome?

A

glycolysis

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7
Q

How do the functions of the glycosome and mitochondrion change as the parasite switches between hosts?

A

mammals - environment is rich in glucose so ATP only through glycolysis
mitochondria repressed
lacks components of CAC & ETC
no oxidative phosphorylation
insects - low glucose so mitochondria is activated
glycosomes decrease enzymes

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8
Q

Does the amastigote have a flagellum?

A

no

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9
Q

Does the amastigote have a nucleus?

A

yes

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10
Q

Does the promastigote have a flagellum?

A

yes

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11
Q

Does the promastigote have an undulating membrane?

A

no

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12
Q

Where is the promastigote found?

A

insect vector

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13
Q

Are the kinetoplast/basal body anterior or posterior to the nucleus in the promastigote?

A

kinetoplast/basal body at anterior end in front of nucleus

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14
Q

Does the epimastigote have a flagellum?

A

yes

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15
Q

Does the epimastigote have an undulating membrane?

A

yes

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16
Q

Are the kinetoplast/basal body anterior or posterior to the nucleus in the epimastigote?

A

kinetoplast/basal body at anterior end in front of nucleus

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17
Q

Does the trypomastigote have a flagellum?

A

yes

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18
Q

Does the trypomastigote have an undulating membrane

A

yes

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19
Q

Are the kinetoplast/basal body anterior or posterior to the nucleus in the trypomastigote?

A

posterior to nucleus

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20
Q

What are the 4 basic types of trypomastigote?

A
  1. long and slender - mammals
  2. stumpy - in mammal, infective to host
  3. procyclic - insect
  4. metacyclic - in insect, infective to mammal
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21
Q

Into what 2 sections is the genus Trypanosoma divided?

A
  1. Salivaria

2. Stercoraria

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22
Q

Section Salivaria is also known as

A

Anterior Station Development

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23
Q

Species in Salivaria develop in what part of the vector?

A

anterior

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24
Q

Section Stercoraria is also known as

A

Posterior (Hindgut) Station Development

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25
Q

Species in Stercoraria develop in what part of the vector?

A

posterior/hindgut

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26
Q

Trypansosoma brucei is found in which section?

A

salivaria

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27
Q

What is the vector for Trypansosoma brucei?

A

Glossina - Tsete fly

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28
Q

What stage of Trypansosoma brucei is infective to humans?

A

metacyclic

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29
Q

What stage of Trypansosoma brucei lives in the blood of humans?

A

slender tryps

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30
Q

Where do the tryps multiply?

A

Slender Tryps: Body Fluids
Stumpy Tryps: Do not multiply
Procyclic Tryps: Fly’s gut
Epimastogotes: Salivary Gland

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31
Q

What does the posterior end of Trypansosoma brucei look like?

A

blunt

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32
Q

What stage of Trypansosoma brucei si infective to Glossina?

A

metacylci tryps

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33
Q

How many subpsecies of T. brucei are there?

A

3

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34
Q

How can the subspecies of Trypansosoma brucei be differentiated?

A

DH
pathology
morphologically identical

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35
Q

What is the common name of Glossina? What does that name mean?

A

Tsetse

“fly distructive to cattle”

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36
Q

How can Glossina be identified?

A

“meat cleaver” cell in wing

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37
Q

Where in Africa is Glossina most prevalent?

A

tropical Africa

between 15 deg N & 15 deg S = fly belt

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38
Q

What disease is caused by T. brucei brucei?

A

Nagana

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39
Q

What animals are infected with Nagana?

A

antelope & livestock

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40
Q

What 2 subspecies of T. brucei cause African Sleeping Sickness in humans?

A

1) T. brucei rhodesiense (Tbr) - East African Sleeping Sickness
2) T. b. gambiense (Tbg) - West African Sleeping Sickness

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41
Q

What are the differences in Tbr & Tbg morphology?

A

identical

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42
Q

What are the geographical distributions of Tbg & Tbr?

A

Tbr - Eastern/Southeastern African

Tbg - West and Central Africa

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43
Q

Does Tbg or Tbr infect native game reservoir hosts?

A

Tbr infects cattle and antelope

44
Q

Does Tbg or Tbr cause most cases of sleeping sickness?

A

Tbg

45
Q

What are the 2 stages of human African trypanosomiasis?

A
  1. hemolymphatic - parasite is found in the peripheral circulation and lymph system, entering tissue fluid, but does not invade the CNS
  2. meningo-encephalitic - parasite crosses BB and enters CNS
46
Q

What happens in either stage of human African trypanosomiasis if it is not treated?

A

Death within a few months (Tbr) to 3 years (Tbg)

47
Q

What if the rate of disease progression in Tbr

A

death within a few months

Rapidly invades the parasite and invades the CNS

48
Q

What is a chancre?

A

sore at bite site

49
Q

What is the rate of disease progression in Tbg?

A

death within 3 yrs

more slow

50
Q

What symptoms can occur in each stage of human African trypanosomiasis?

A

Mild symptoms occur early on - fever, headaches, muscle & joint aches
In later stages (1-2 yrs), there is an evidence of CNS involvement (personality change, tend to suffer from daytime sleepiness, nighttime sleep disturbance, paralysis, and problems with balance/walking)

51
Q

What is Winterbottom’s sign?

A

swollen lymph nodes at base of neck

52
Q

In which subspecies is the parasite load in the blood higher?

A

Tbr

53
Q

Why is serological testing used only to detect Tbg infections?

A

Lower parasite load means that one would need to use the antibodies to detect the parasite

54
Q

Why must cerebrospinal fluid be examined in all sleeping sickness infections?

A

to see involvement in CNS in infection

55
Q

Who should receive treatment for sleeping sickness?

A

everyone

56
Q

What factors will determine which drug should be used?

A
  1. type of infection (Tbr or Tbg)

2. disease stage

57
Q

What are the 4 drugs which can be used to treat sleeping sickness?

A
  1. pentamidine
  2. suramin
  3. melarsopral - Mel B
  4. eflorinithine
58
Q

Does pentamidine cross the BBB?

A

no

59
Q

Against which stage is pentamidine effective?

A

1st stage of Tbg

inhibits DNA & RNA synthesis

60
Q

Is pentamidine used to treat Tbg, Tbr, or both?

A

Tbg

61
Q

Does surmain cross the BBB?

A

no

62
Q

Against which stage is surmain effective?

A

1st stage of Tbg & Tbr
inhibits oxidation of NADH
too much is toxic = kidney failure

63
Q

Is surmain used to treat Tbg, Tbr, or both?

A

both

64
Q

Does melarsopral cross the BBB?

A

yes

65
Q

Against which stage is melarsopral effective?

A 
late stage Tbr & Tbg
inactivates tyrp pyruvate kinase = inhibits ATP synthesis
arsenis based = high toxicity
seizures
1/20 die of treatment
66
Q

Is melarsopral used to treat Tbg, Tbr, or both?

A

both

67
Q

Does eflorinithine cross the BBB?

A

yes

68
Q

Against which stage is eflorinithine effective?

A

late stage - “resurrection drug”
inhibits ornithine decarboxylase
cell division & differentiation

69
Q

Is eflorinithine used to treat Tbg, Tbr, or both?

A

Tbg

70
Q

What is a drawback to using melarsoprol?

A

high toxicity

1/20 die of treatment

71
Q

Why is eflornithine known as the “resurrection drug”?

A

used on late stage comotose patients

72
Q

Why & for how long do patients require follow up examinations?

A

serial examination of cerebrospinal fluid for 2 yrs

73
Q

What is the main method of prevention and control of sleeping sickness?

A

minimized testse fly exposure

74
Q

What type of clothing should be worn to minimize testes fly bites?

A

neutral colors

75
Q

Why are tsetse flies often found inside vehicles?

A

motion & dust

76
Q

What is sterile insect technique?

A

SIT - sterilize tsetse flies and release

3-4 generations w/ insecticides will eliminate local populations

77
Q

What is antigenic variation?

A

altering surface proteins in order to avoid a host immune response

78
Q

The surface coat of T.brucei blood typromastigotes consists primarily of a single protein which is know as the

A

VSG (variant surface glycorprotein)

79
Q

Does the immune system recognize VSG?

A

yes

80
Q

Does the immune response to VSG remove all of the parasite?

A

yes: <1% of tryps survive b they posses variant VSG

81
Q

How are the waves of T.brucei infection produced?

A

variant forms next wave of infection after multiplying

82
Q

What is a variant antigenic type?

A

Maintains chronic infection as a result of this antigenic variation of the surface coat and can last for years

83
Q

How many genes are involved in antigenic variation?

A

~1000 VSG genes

84
Q

Trypanosoma cruzi is found in which section?

A

Stercoraria

85
Q

What is the vector for T.cruzi?

A

reduviid bugs

86
Q

What stage of the T.cruzi parasite is infective tohumans?

A

Metacyclic tryps

87
Q

How does T.cruzi enter the human?

A

enter blood when vector takes bloodmeal and vector defecates on skin letting in metacyclic tryps

88
Q

What is the intracellular stage of T.cruzi?

A

amastigotes

89
Q

What stage of T.cruzi is infective to the vector?

A

amastigotes

90
Q

What is distinctive about the posterior end & kinetoplast of T.cruzi tryps?

A

very pointed posterior end

very large kinetoplast

91
Q

Is T.cruzi capable of antigenic variation?

A

no

92
Q

How does the lack of antigenic variation affect the # of T.cruzi tryps in the blood?

A

very low #s of tryps in blood

93
Q

What is a chagoma?

A

local inflammation at bit site

entry of metacyclic tryps

94
Q

What is Romana’s sign?

A

enters eye

edema of eyelid & conjective

95
Q

What is a pseudocyst?

A

cluster of amastigotes

96
Q

What symptoms are associated with the acute stages of T.cruzi infection?

A

fatigue, fever, swollen lymph nodes
if parasite spreads: muscle,intestine, blood marrow
anemia, nervous disorders, weakness, muscle pain

97
Q

What is the common outcome of infection in children?

A

death in 3-4 wks

98
Q

What organs are most commonly affected in chronic T.cruzi infections?

A

heart, intestinal tract, muscles

99
Q

The amastigotes in T.cruzi produce ___ which results in loss of muscle function

A

neurotoxins

100
Q

What happens in the intestinal tract during chronic T.cruzi infection?

A

smooth muscle peritalsis
esophagus & colon lose tone
megaesophagus & megacolon

101
Q

What are the megaesophagus and megacolon

A

muscle in esophagus & colon is streched out bc of smooth muscle peritalsis

102
Q

What happens in the heart during T.cruzi infection?

A

muscle contraction affected
enlarged & flabby
decreased pumping efficiency
heart failure

103
Q

How is T.cruzi diagnosed?

A
  1. examine tissue fluid for asmastigotes

2. Xenodiagnosis

104
Q

What is xenodiagnosis?

A 
lab raised vectors in suspected patient
~40 lab raised bugs feed on patient
3-4 wks: squeeze bugs to see fecal droplet
dissect hindgut
examine for parasite
105
Q

How is T.cruzi infection controlled?

A
  1. hemotherapy - Nifurtimax

2. vector control

106
Q

How can T.cruzi vector be controlled?

A 
plaster wells
concrete floors
metal roofs
screen doors &amp; windows
insecticides
bed netting
107
Q

What is the distribution fo T.cruzi?

A

Mexico, C.America, S.America: ~10 million cases
urban areas - blood transfusion
US - mainly SW

Human Parasitology (22 decks)

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