American Trypanosomiasis Flashcards

1
Q

T. cruzi

A

Chagas disease

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2
Q

T. cruzi and T. brucei have little in common

A
  • epidemiologically different
  • differences in transmission (both vectors but different vectors)
  • pathogenesis
  • clinical course
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3
Q

transmission of T. cruzi

A
  • triatomine insects or kissing bugs
  • ingestion of food or drink contaminated with T.c. excreta (RARE)
  • mother to child
  • blood transfusion
  • organ transplantation
  • lab accidents
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4
Q

Triatomine insects

A
  • insect becomes infected by sucking blood from humans or other animals that have circulated trypomastigotes
  • ingested parasites multiply in midgut of insects as epimastigotes => infective metacyclic trypomastigotes = discharged in feces
  • transmission to humans occurs when mucus membranes, conjunctiva or breaks in the skin are contaminated w bug feces
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5
Q

T or F. T. c. enters a variety of host cells and multiplies in cytoplasm

A

T

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6
Q

T or F. Triatomine bugs are active in the day

A

F! Active at night
- typically live in the wall or roof cracks of poorly constructed homes in rural areas

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7
Q

what is an amastigote?

A

protest cell that does not have visible external flagella or cilia
intracellular phase in life-cycle of trypanosomes that replicates
T.c. has this stage

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8
Q

T. cruzi is characterized by two phases…

A

acute and chronic
- acute = 8 to 12 weeks after transmission
- chronic = host immune response decreases parasite replication so parasitemia falls below levels detectable by microscopy, acute symptoms resolve

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9
Q

what happens if no successful therapy

A

8-12 acute symptoms and chronic phase lasts for life

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10
Q

inflammation lesion caused by T. c. at site of entry is called

A

chagoma
- if periocular tissue and painless edema = Romana sign

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11
Q

Romana sign

A

T. c. enters periocular site and painless edema appear

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12
Q

disease presentation of Chagas

A

fever, chills, anorexia, malaise, edema of face and lower extremities, lymphadenopathy and hepatosplenomegaly

** sometimes CNS involvement and acute myocarditis w arrhythmias

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13
Q

~ ___ to ___% will develop cardiac and/or GI forms of T.c. disease

A

20 to 30%

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14
Q

diagnosis of T. c.

A
  • serology (ELISA, IFA) = IgG!; chronic = low level parasitemia
  • circulating parasites (motile); wet preps of anticoag blood, buffy coat
  • tissue biopsies (amastigotes -> Giemsa, H&E)
  • xenodiagnosis (OLD method; uninfected bug - let them eat from pt suspected w Chagas = then look for trypanosomes in GI of bug)
  • PCR
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15
Q

congenital Chagas

A

microscopic examination of cord blood or PCR or serology is not indicated as maternal Abs will be present in newborn
if microscopy and/or PCR negative = serology (IgG should be done 6-9 mos later)

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16
Q

why do we have to do 2 serologic assays to diagnose T. c.

A

to rule out FP with
- malaria
- Leishmania
- syphilis
- some other parasitic and non-parasitic infections

17
Q

two first-line serological tetss for T.c.

A

EIA (enzyme immunoassay) on recombinant T. c. antigens and immunoblot (ESA)

  • if discordant, IFA as tie-breaker
18
Q

T or F. There is no clinical evidence that antitryp therapy can reverse established Chagas cardiac disease

A

T! so prevention is key to avoid chronic Chagas cardiomyopathy (CCC)

19
Q

what is the focus for treatment on patients w advanced heart disease

A

supportive care for heart failure, arrhythmia, and thromboembolism

20
Q

T or F. Antitrypanosomal therapy has not been proven to affect progression of GI disease

A

T! management focuses on symptom amelioration

21
Q

T or F. Risk of Chagas disease to travelers is low

A

T!

22
Q
A