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Biol 305 > Chapter 5 — Trypanosomes > Flashcards

Chapter 5 — Trypanosomes Flashcards

1
Q

Who are people that have great history with trypanosome-related diseases & which disease (3)?

A
  1. Carlos Chagas — chagas’ disease
  2. David Bruce — Africa sleeping sickness
  3. David Livingston — arsenic (it killed the trypanosome organism, but the side affects would eventually kill them after a couple weeks —> year) and African sleeping sickness
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2
Q

What kingdom and phyla is trypanosomes in?

A
  1. Kingdom Excavata
  2. Phylum Kinetoplastida
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3
Q

What is a kinetoplast?

A

disc shaped, large mass of circular, mitochondrial DNA, visible with the light microscope
- contains many copies of the mitochondrial genome

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4
Q

What are the 4 morphological stages in different life cycles?

A
  1. Trypomastigote
  2. Epimastigote (insect stage)
  3. Promastigote (insect stage — has simple flagella)
  4. amastigote stage
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5
Q

What is the agent of chagas’ disease?

A

Trypanosoma cruzi — can get anywhere, common in texas and is expanding range each year (has been found in roanoke)

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6
Q

Which 2 genera have insect intermediate hosts?

A
  1. trypanosoma (the trypanosomes)
  2. Leishmania
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7
Q

What are some characteristics of the family trypanosomatidae?

A
  • about 95-98% parasitic
  • heterogenous life cycle (requiring at least 2 kinds of host
  • Morphological changes during life cycle
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8
Q

What are characteristics of the promastigote stage?

A
  • vertebrate blood form
  • free flagellum
  • undulating membrane
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9
Q

What are characteristics of the epimastigote form?

A
  • insect form
  • trypanosoma brucei (african form)
  • trypanosoma cruzi
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10
Q

What’s are some characteristics about the trypomastigote stage?

A
  • vertebrate blood form
  • trypanasoma cruzi
  • trypanasoma brucei
  • free flowing flagellum
  • undulating membrane
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11
Q

What is the amastigote stage?

A
  • vertebrae tissue form
  • typanosoma cruzi
    -no flagellum
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12
Q

What is the reason for the trypomastigote - epimastigoate change in trypanosoma brucei?

A
  • adaptation to low (O2), glucose in blood
  • in vertebrate blood —> high O2, glucose
  • Insect gut —> low O2, glucose
    (LOOK AT SLIDE 5)
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13
Q

What is the anterior station development?

A
  • transmitted by bite
  • Trypanosoma brucei
  • develops in insect
    (look at diagram on slide 6)
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14
Q

What is the posterior station development?

A
  • transmitted by feces
  • trypanosoma cruzi
    (look at diagram on slide 6)
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15
Q

How does the feces of posterior station get in the blood?

A

they lay their feces on your skin, which is itchy. you then itch your skin allowing the feces to get into the blood stream

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16
Q

What are the 3 species of trypanosoma brucei? How can we distinguish between these?

A
  1. trypanosoma brucei brucei (nagana-only in animals)
  2. Trypanosoma brucei gambiense (west africa)
  3. Trypanosoma brucei rhodesiense
    - can only distinguish using PCR, looks same under microscope
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17
Q

What transmits trypanosoma?

A
  • tsetse fly
  • the bite hurts —> you will know if you get bight
  • only occurs in africa
  • highly pathogenic
  • in both sexes
  • flies are aggressive
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18
Q

Can trypanosoma brucei brucei affect grazing animals?

A

yes!
- the native ruminants (bushbuck — no effect)
- domestic cattle — fatal

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19
Q

Look at slide 11 for life cycle in the cattle to fly

A

draw out on paper!!!!

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20
Q

Do all subspecies of trypanosoma brucei have multiple hosts?

A

no!

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21
Q

Know infected and diagnostic stages

A
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22
Q

What are the disease mechanisms of Trypanosoma brucei?

A
  • invasion of CNS by trypomastigotes
  • antibody mediated damage to blood vessels
  • body responds but has proliferation of antibodies
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23
Q

??

A
  • antibody + complement —> parasite lysis
  • Fragments stick to endothelium —> lysis of endothelial cells
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24
Q

What is perivascular cuffing?

A

inflammation around the brian —- causes seepage of fluid into brain (cerebral edema)

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25
Q

What does cerebral edema lead to?

A

a coma —> death (results in disruption of brain function)

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26
Q

What does the severity of the disease depend on? What are some examples of these?

A

the host species
- antelope —> no disease
- domestic cattle —> death in several days
- dogs & horses —> death in 15 days

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27
Q

What is nagana? What species does it affect?

A
  • causes by trypanasomes in animals
  • characterized by fever, lethargy, edema
  • affects animals
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28
Q

How do you control Naga?

A
  • intermediate host (what is it??)
  • DDT (chemicals)
  • remove brush
  • destruction of reservoir hosts
  • breed resistant cattle
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29
Q

How does the body respond to trypanasomes?

A
  • body can respond well at first
  • then the VSG can change its protein outer coat (DNA) and the body can no longer respond
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30
Q

What does VSG stand for?

A

Variable surface glycoprotein

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31
Q

How does the parasite avoid host immune response?

A
  1. VSG coat trypomastigote plasma membrane
  2. Tsetse fly injects clone (all with same VSG)
  3. trypomastigote changes to expression of new VSG when attacked by host antibodies
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32
Q

Look at graph on slide 16

A

getting successive clones with different VSGs

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33
Q

What is the bait and switch strategy?

A

(like putting cheese out to catch a mouse on a trap)
- the organism that enters the body enters the bloodstream in a different form
- it gets the body to go after one form & not the other to distract it
- then the body can not respond
(coaddaptation going on between host and parasite)

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34
Q

Is trypanosomiasis increasing or decreasing in Africa?

A
  • increasing in central africa (not multiple hosts though)
35
Q

What is prevalence of a disease?

A

the number of cases at any given time

36
Q

What is the incidence of a disease?

A

fresh/new cases —> acute

37
Q

What is the prevalence of trypanosomiasis in Africa?

A

> 300,000

38
Q

What is the incidence of trypanosomiasis in Africa?

A

30,000 and increasing

39
Q

What is the pathogenicity of T.b. gambiense (West Africa — riverine)?

A

CNS involvement in months/years (“sleeping sickness”)

40
Q

What is the resevoir host of T. b. gambiense?

A

None

41
Q

What is the immediate host of T. b. gambiense?

A
  • Glossina palpalis
  • Glossina tachinoides
42
Q

What is the pathogenicity of T.b. rhodesiense (east africa — savannah)?

A

death in several months (before CNS involvement)

43
Q

What is the resevoir host of T.Bl. rhodesiense?

A

impala, warthog, domestic animals (pig)

44
Q

What are the immediate hosts of T.b. rhodesiense?

A
  • glossina pallipides
  • glossina swvnnertoni
45
Q

Look at slide 20 and know the CDC life cycle in entirely extracellular in human

A

(both mammalian stages and tsetse fly stages)
- look at slender/thick forms?? (idk mentioned in class)

46
Q

What are symptoms of T.b.gambiense?

A
  • headache
  • diarrhea
  • nausea
  • fever
  • chancre (very large — bigger then lyme)
  • rash
  • lymphadenopathy (Winterbottom’s sign — pic on slide 22)
  • progressive wasting
  • neurological symptoms: insomnia, depression, mood disorders, mental deterioration, coma
    ***feeds off of glucose, which is why you are tired and sleepy
47
Q

How is T. b. gambinese diagnosed?

A
  • puncture cerebral spinal fluid
  • trypomastigotes in blood, lymph node, aspirate, SDP, new card test
48
Q

What are treatments of T. b. gambinese?

A
  • supra in (can have negative side affects, no longer drug of choice)
  • melarsoprol — now drug of choice, affective in areas without resistance. if resistance then eflornithine is used
  • drug needs to be administered within 48 hours or the patient will die
    (drugs are outdated, toxic, and expensive to use)
49
Q

How to prevent T.b.gambinese?

A

no chemoprophylaxis or vaccine

50
Q

What is the prevalence of trypanosoma cruzi?

A
  • 16-18+ million cases
  • 45,000 deaths per year
51
Q

What causes Chagas’ disease? Where is it?

A

trypanosoma cruzi
(in central and south america, NOT Africa — starting to increase in the state of texas)

52
Q

What transmits trypanosoma cruzi?

A

kissing bug (family reduviidae, subfamily triatominae)
- called kissing bug because bites peoples faces
- also called reduviidae bug
- also called triatominae bug

53
Q

How does an infective metacyclic trypomastigotes passed into human through kissing bug?

A

deposited through posterior station development through feces (enters human in trypomastigote stage)
- look where the different parts of the bacteria is in the kissing bug

54
Q

Where are the different parts of bacteria in kissing bug and in which form?

A
  1. trypomastigote in anterior station
  2. epimastigote in mid-gut
  3. metacyclic trymastigote in posterior station (sent to human)
55
Q

What is the epidemiology of trypanasoma cruzi?

A
  • victims often live in mud-walled, thatched roofed houses (bugs can come in at night)
  • feces deposited on skin by bug (or rains) from roof — traps rubbed into wound or eye
  • other (blood, transplacental (enters bloodstream), eating bugs)
  • resevoir hosts (dogs, cats, cattle, raccoons, rodents)
    *** can help people by giving good roof, education, teaching to not eat bugs
56
Q

What are some resevoir hosts of trypanasoma cruzi?

A
  1. dogs (common in texas)
  2. cats
  3. cattle
  4. raccoons
  5. rodents
57
Q

look at lifecycle on slide 28 (more important then other life cycle because its in our country and is spreading — chagas’ disease)(in texas, closest case to us in roanoke)

A

look at it on power point, weird on goodnotes
- Know infective and diagnostic stages

58
Q

What is the diagnostic stage of trypanasoma cruzi?

A

the amastigotes in muscle tissue

59
Q

What is a pathological mechanism of amastigotes? (more acute response)

A
  • heart disease
  • destroy cells —> esp. cardiac myofibers, motor neurons, etc.
60
Q

Slide 31 — evasion of immune response

A
61
Q

What is chagoma?

A

swelling at infection site, called Romana’s sign if at eye

61
Q

How long is the acute stage of Chagas’ disease? What are its symptoms?

A
  • 2-4 months
  • Chagoma
  • lymphadenopathy (swollen lymph notes)
  • hepatosplenomegaly
  • fever
  • 5% fatality in children’s (most vulnerable)
62
Q

What is the best way to diagnose?

A

DNA PCR — can look similar to other organisms (cousin) under microscope)

63
Q

What characterizes chronic disease of chaga’s?

A
  • can be 2ish years (acute symptoms can disappear, then chronic stage pops up)
  • ## Immunodiagnosis though Elisa can be used (but trypomastigotes are rare in blood)
64
Q

How can a parasite be diagnosed if it is not shown well in blood? What is it called?

A
  • Xenodiagnosis
  • take a germ free bug and allow it to bite a person
  • if the person has the bacteria, then the big will get it
65
Q

What is the best way to treat Chaga’s?

A
  • Acute: 2 nearly 100% effective drugs given but most acute infections are not detected (only take when necessary because toxic)
  • Chronic: no fully effective treatment
  • Control: eliminate intermediate hosts, screen the blood
66
Q

What is Leishmania?W

A
  • “white leprosy”
  • 3 types (have to use PCR to tell them apart)
  • have indistinguishable morphology
  • transmitted by sand fly (small)
  • have many mammal reservoirs (dogs, rodents)
  • Prevalence: 12 million, incidence 2 million/yr
67
Q

What are the three types of Leishmania?

A
  • cutaneous (L. tropics, L.major, L. mexicana)
  • mucocutaneous (L. braziliansis — from first chapter ruining septum)
  • Visceral (L. donovan i — enters spleen, liver, etc)
68
Q

What is the old/new world sand fly?

A
  • old: Phlebotomus
  • new: lutzomyia
69
Q

What is the pathological mechanism?

A

destruction of macrophages (mf) resultin in tissue damage

70
Q

How does Leishmania evade immune responses?

A
  1. privileged site
  2. suppression of intracellular killing by ROI
  3. manipulation of TH2 immune response
    - if TH2 (antibody) response —> amastigotes survive
    - if TH1 response —> mf activation—> amastigotes killed
71
Q

What does the type of disease stand for?

A

depend on whether amastigotes spread from bite site

72
Q

What is Cutaneous Leishmaniasis?

A
  • stay at bite site
  • old world
  • Jereco buttons: in Mediterranean, middle east, Africa, India
  • Phlebotomus spp. vector
73
Q

What is Leishmaniannis mexicana?

A
  • White Leprosy
  • Rising in numbers
  • in N, C, and S America
  • Vector = Lutzomyia spp.
  • Ulcer forms at bite site a few days to several months after, heals spontaneously, leaving a scar
74
Q

What is diffuse cutaneous leishmaniasis?

A
  1. due to defective T cell immunity
  2. Responds very poorly to drugs
75
Q

What is Mucocutaneous leishmaniasis (espundia)?

A
  • Amastigotes spread to mouth/nose
  • ulcer at initial bite site
  • secondary lesions months to years later
  • untreated —> massive tissue loss
  • grows at cooler temps
76
Q

What is visceral leishmaniasis (kala azar)?

A
  • amastigotes disseminate to internal organs
  • advanced forms
  • organs targeted: spleen & liver (also bone marrow???)
  • mf all over body become infected
77
Q

What are symptoms of visceral leishmaniasis (kala azar)?

A
  • fever
  • hepatosplenomegaly
  • examine smear for amastigotes
78
Q

What drug can treat leishmaniasis?

A
  • Pentavalent Antimony (periodic element)
    1. is very toxic — only for L. brazilians is and L. donovani
    2. possible complications: post kalaazar dermal lesions, treatable (unlike DCL)
79
Q

How to control for

A

New Normal Microbiota Enhancement
1. best method is insecticide spraying
2. end of malaria eradication program in Mediterranean —> resurgence of Leishmaniasis

80
Q

What is an endemic?

A

The constant amount of a specific disease that is usually present in a geographic location, like a state or county

81
Q

What is an epidemic?

A

similar to an outbreak, but with a larger number of cases or occurring over a greater area or both

82
Q

What is a pandemic?

A

disease on multiple continents, or global

83
Q
A

Biol 305 (5 decks)

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