Trypanosomes Flashcards

1
Q

What stain can ID trypanosomes ?

A

Wright-Giemsa

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2
Q

2 subspecies of African trypanosomiasis. Causes what disease ?

A

T. Brucei rhodesiense
Trypanosoma brucei gambiense
- African sleeping sickness

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3
Q

Species of American trypanosomiasis. Causes what disease ?

A

T. cruzi
- Chagas disease

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4
Q

Species of Trypanosomes that infects animals. Causes what disease ?

A

T. brucei brucei
- Nagana disease

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5
Q

T or F: subspecies of African trypanosomes can be morphologically differentiated

A

FALSE; subspecies of African trypanosomes ARE NOT morphologically differentiated

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6
Q

Are African trypanosomes flagellated ?

A

Yes, they are protozoan hemoflagelletes

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7
Q

Vector for African trypanosomes

A

Tsetse flies, belongs to Glossina genus

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8
Q

Where does sleeping sickness ONLY occur ?

A

In Sub-Saharan Africa

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9
Q

Two anatomical characteristics that distinguish Tse-tse flies

A
  1. Rested wings fold directly over another
  2. Long proboscis extends directly forward, attached by distinct bulb to bottom of head
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10
Q

Life cycle of African trypanosomes

A

Mammalian:
1. Tse-tse takes blood meal
2. Injected metacyclic from transforms into bloodstream trypomastigotes = multiple by binary fission in various body fluids (blood, lymph, spinal)
3. Detectable trypomastigotes in blood during acute phase

Tse-tse:
1. Tse-tse takes blood meal
2. Bloodstream trypomastigotes transform into procylic form in midgut
3. Leaves midgut and transform into epimastigotes
4. Epimastigotes multiply in salivary gland = transform into metacyclic form

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11
Q

Incubation period of T. brucei rhodesiense

A

5-20 days*

NOTE: 3-21 days (usually 5-14)

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12
Q

Describe pathogenesis of T. brucei

A
  1. Bite = proliferation of trypanosomes within chancre
    - parasites invade lymph nodes; continue proliferation
    - enters bloodstream from lymphatics; proliferation
    - invade interstitial spaces = vessel impeermeability and mott cells
  2. Invades brains = meningoencephalitis
    - CNS infiltrated with plasma cells/ lymphs, mott cells
    - CSF = increased pressure, total protein, mono, eos

NOTE: complex/ poorly understood

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13
Q

Self-protecting mechanism of African trypanosomes

A
  • antigenic variation = trypomastigote changes surface glycoproteins on outer membrane = evade’s host immune response
  • by the time host can respond, trypomastigote has already switched its coat
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14
Q

Differentiate disease states between T. brucei rhodesiense (East) and T. brucei gambiense (West)

A

T. b rhodesiense:
- animals
- early CNS disease
- acute; rapid
- sore at tse-tse bite
- enlarged lymph nodes
- death within months

T. b gambiense:
- humans
- late CNS disease
- chronic; slow
- low parasitemia
- death within years

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15
Q

Diagnosis of T. brucei rhodensiense vs T. brucei gambiense

A

T. brucei rhodensiense:
- blood smear (HIGH %parasitemia)
- LYMPH NODE fluid
- chancre biopsy/ aspirate
- CSF

T. brucei gambiense:
- blood smear (low %parasitemia)
- LYMPH NODE fluid
- chancre biopsy/ aspirate
- CSF
-CATT
-ELISA
-**IFA*

CATT - card agglutination test for trypanosomes

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16
Q

Blood and CSF specimens should be examined __ therapy and __ months post-therapy

A

Blood and CSF specimens should be examined DURING therapy and 1-2 months post-therapy

17
Q

T or F: African trypanosomes do not have intracellular forms and multiple as trypomastigotes that circulate the blood/ intracellular spaces

A

TRUE; African trypanosomes do not have intracellular forms and multiple as trypomastigotes that circulate the blood/ intracellular spaces

18
Q

Diagnosis of African Trypanosomiasis

A
  • history (travel)
  • physical exam (chancre)
  • laboratory (blood smear, CSF lumbar puncture staining,
19
Q

Diagnosis of African Trypanosomiasis

A
  • history (travel)
  • physical exam (chancre)
  • ## laboratory (blood smear, CSF lumbar puncture staining,
20
Q

When should %parasitemia be measured ? Why ?

A

Blood during febrile period; HIGHEST %PARASITEMIA

21
Q

Describe structural stages of Trypanosomes

A

Vector (trypomastigote/ epimastigote):
- anterior (sharp); flagella
- posterior (blunt); kinetoplast
- undulating membrane reduced over stages

Human (promastigote/ amastigote):
- anterior (flagella AND kinetoplast) and posterior
- no undulating membrane
- becomes more circular (intracellular), loses flagella

22
Q

Transmission of T. Cruzi

A
  • Triatomine insects/ “kissing bugs” (vector)
  • ingestion of triatomine poop
  • pregnant women to child
  • blood transfusion/ organ transplant
23
Q

Structure Stages of American Trypanosomes

A

Vector:
1. Trypomastigotes
- (anterior) flagella runs entire length from posterior
- undulating membrane
- kinetoplast (posterior)
2. Epimastigotes
- loses undulating membrane
3. Promastigotes
- kinetoplast AND flagella (anterior)

Human:
4. Amastigote (intracellular, human stage)
- round
- no flagella or cilia

24
Q

WIP Life cycle of Trypanosoma cruzi

A

Triatomine insect:
1. Takes blood meal

25
Q

Symptoms of Acute Chagas Disease

A
  • Romana sign = Chagoma (inflamed lesion on face)
  • fever/ chills
  • anorexia
  • malaise
  • edema
  • lymphadenopathy
  • hepatosplenomegaly
26
Q

Symptoms of Chronic Chagas’ disease

A
27
Q

Disease states of T. Cruzi

A
  1. Acute
    - Romana sign (inflamed lesion)
    - fever
  2. Chronic
    - persists for years
    - host response lowers %parasitemia
    - myocarditis
28
Q

Diagnosis of T. Cruzi

A
  • IgG serology (ELISA, IFA)
  • wet prep of blood (T. Cruzi is motile)
  • buffy coat
  • tissue biopsies
  • xenodiagnosis
  • PCR

Newborn:
- microscopy or PCR of cord blood
- serology 6-9 months POST-BIRTH (maternal Ab present at birth)

NOTE: IgG = released later, detects chronic disease

29
Q

T or F: Both American and African Trypanosoma are intracellular

A

FALSE; only American (T. cruzi) Trypanosoma

30
Q

What is the goal of antitrypanosomal therapy in T. Cruzi ?

A
  • treat early Chagas’ disease
  • prevent Chagas cardiomyopathy
  • anti-trypanosomal therapy cannot reverse established Chagas cardiac disease