Microbiology-Trypanosomes Flashcards

1
Q

Why are trypanosomes also called kinetoplastidae?

A

They have an organelle called the kinetoplast which has its own DNA and is in close association with the basal body of the flagella.

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2
Q

Causative agent of west African trypanosomiasis? How does it present? What is the vector?

A

T.b. gambiense. This is the more subacute form of HAT and can cause changes in cognition, behavior and psychosis. It is transmitted by the glossina palpalis tsetse fly near water.

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3
Q

Causative agent of east African trypanosomiasis? How does it present? What is the vector?

A

T.b. rhodesiense. This is the more acute and severe form that results in death within a year. It is transmitted by the glossina mortisans tsetse fly in savannah areas and feeds on wild game.

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4
Q

What is the life cycle of trypanosoma brucei gambiense and trypanosoma rhodesiense?

A

Tsetse fly takes blood meal & injects metacyclic trypomastigote -> Trypomastigotes multiply by binary fission in blood, lymph, CSF -> Tsetse fly takes blood meal and bloodstream trypomastigotes are ingested -> Bloodstream trypomastigotes transform into pro cyclic trypomastigotes in tsetse fly gut and multiply -> Procyclic masticates transform to epimastigotes -> epimastigotes multiply in salivary gland and become metacyclic trypomastigotes.

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5
Q

Identifying the tsetse fly

A

Male & female mate 1x. Cleaver cell in wing.

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6
Q

Presence of tsetse fly means absence of what?

A

Cattle. They carry nagana which causes lots of livestock death.

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7
Q

Stages of Human African Trypanosomiasis (HAT) infection?

A

1) Hemo-lymphatic stage: chancre at inoculation site, fever, headaches, muscle pain and Winterbottom’s sign (enlarged posterior cervical lymph nodes) 2) Meningo-encephalitic stage: elevated ICP, Mott cells (plasma cells containing lots of IgM), elevated protein in the CSF and polysomnography (discombobulation of REM cycles throughout day)

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8
Q

Why is there not a vaccine for HAT?

A

Antigenic variation of the variant surface glycoprotein (VSG) is continually rearranged by the var gene.

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9
Q

Diagnosing HAT?

A

Giemsa-stained blood smears. LP must be done for stage 2. Card agglutination trypanosomiasis test for T. b. gambiense (CATT test).

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10
Q

Tx for HAT

A

Stage I) Pentamidine and suramin. Stage II) Melarsoprol (both gambiense and rhodesiense) or eflornithine (gambiense)

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11
Q

Side effects of melarsoprol

A

Local site and vein sclerosis, it is basically arsenic. It also causes encephalopathy and peripheral neuropathy.

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12
Q

Vector controls for HAT

A

The tsetse fly (glossina) like the color blue, so make the traps blue.

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13
Q

Life cycle of American trypanosomiasis

A

Triatomine bug takes blood meal -> Metacyclic trypomastigote passed in feces and enters bite wound -> Transform into amastigotes and multiply by binary fission -> Infect other cells -> Intracellular amastigotes transform to trypomastigotes and lyse cells to enter blood stream -> Triatomine bug takes blood meal -> Epimastigotes in midgut -> Multiply and become metacyclic trypomastigotes in hindgut

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14
Q

Important reservoirs of T. cruzi? Important vectors?

A

Reservoirs: Possums, armadillos and tree sloths. Vectors: reduviidae: triatoma (infestans is most notorious), rhodnius and panstrongylus.

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15
Q

How does the kinetoplast differ in Chagas from HAT?

A

It is much larger in T. cruzi.

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16
Q

Where do the triatomes like to live?

A

In cracks of poorly constructed housing

17
Q

2 pathogens involved in Chagas disease?

A

T. cruzi I: less pathogenic, more commonly seen in animal reservoirs. T. cruzi II: more commonly seen in human reservoirs

18
Q

Non-vector transmission of Chagas disease

A

Blood transfusions, organ transplants, vertical transmission (pregnancy)

19
Q

Common presentations of Chagas disease

A

Romania’s sign: unilateral painless periorbital edema. Chagoma: indurated lesion at site of parasite entry.

20
Q

Progression of disease with Chagas

A

60% remain indeterminate (asymptomatic). The parasites nest in the heart, cause bundle branch block, apical aneurism and chronic cardiomyopathy. It also causes mega-esophagus and mega-colon.

21
Q

Diagnosing Chagas disease

A

Serology, PCR, peripheral blood smear and xenodiagnosis (lab raised bugs are sacrifices and you look for parasites in them)

22
Q

Treating Chagas? What is the cure rate?

A

Benznidazole and nifurtimox. If disease has been presented longer cure rates go lower, but if tx happens < 1 year after infection, resolution is 100%.