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MMI 426 > Trypanosomiasis > Flashcards

Trypanosomiasis Flashcards

1
Q

What are the 2 subspecies of African Trypanosomiasis? What disease does this cause?

A

T. brucei rhodesiense
T. brucei gambiense

African sleeping sickness

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2
Q

What is the subspecies of American trypanosomiasis? What what disease does this cause?

A

T. cruzi and Chagas Disease

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3
Q

Describe the different Human Trypanosomiasis infections?

A

African Trypanosomiasis (African sleeping sickness)
- East African Trypanosomiasis is an acute infection caused by T. brucei rhodesiense
- West African Trypanosomiasis is a slow prgressing and chronic infection caused by T. brucei gambiense

American Trypanosomiasis (Chagas disease)
- caused by T. cruzi

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4
Q

What subspecies of Trypanosomiasis only affects animals? and what disease does this cause?

A

T. brucei brucei and Nagana

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5
Q

Nagana

A

Caused by T. brucei brucei and infects wild/ domestic animals (not humans)

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6
Q

Describe the physical properties of African trypanosomes.

A
  • Protozoan hemoflagellates
  • unicellular
  • does not have an intracellular form
  • T. brucei gambiense and T. brucei rhodesience are not morphologically distinguishable
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7
Q

What does African trypanosomasis replicate as in a host?

A

multiply as trypamastagotes that circulate mammilian blood stream and other extracellular spaces

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8
Q

What is the African trypanosome vector? How are they distinguishable?

A

Tse Tse fly (blood sucking fly)

They fold their wings completly so that 1 wing rests directly on top of the other and they have a long probosis which is attached by a distint bulb to the bottom of its head

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9
Q

Where does Human African trypanosomiasis occur?

A

Only in sub-Saharan Africa

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10
Q

How is African trypanosomiasis transmitted?

A
  • mostly via vector (Tse tse fly)
  • rarely via: transfusion, mother to child, mechanical transmission via other blood sucking insects, lab accidents, and sexual transmission
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11
Q

Describe the lifecycle of African Tryanosomiasis.

A
  1. Tsetse fly takes a blood meal and injects metacyclic trypomastigotes (infectious stage) into host
  2. Injected metacyclic trypamastagotes transform into bloodstream trypomastigotes which are carried to other sites
  3. Trypomastigotes multiply by binary fission and circulate (diagnosic phase)
  4. Tsetse fly takes a blood meal and injests the bloodstream trypomastigotes
  5. Bloodstream trypomastigotes transform into procyclic trypamastigotes in the tsetse fly midgut where they also mutiply by binary fission
    6.Procyclic trypamastigotes leave the midgut and transorm into epimastigotes
  6. epimastigotes multiply in the salivary glands and transform into metacyclic trypamastigotes and the cycle repeats with other blood meal
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12
Q

What is the incubation period for T. brucei rhodesiense?

A

3-21 days (usually 5-14)

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13
Q

What is the incubation period for T. brucei gambiense?

A

longer than the rhodensiense but not well defined

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14
Q

Describe the pathogenisis of T. brucei.

A

A bite from an infected tsetse fly causes a chancre where interstitial multiplication of trypanosomes occurs. Here there is an intense mononuclear cell rxn to the parasite causing the parasite to move to the lymph nodes causing an inflammatory response and they move through the bloodstream and lymphatic system (continuing to replicate). The parasite can alos egress from vessels into intersticial spaces and increase vessel impermeability.
The parasite can also reach the brain and menegies causing meningoencephalitis.

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15
Q

What are self-protecting machanisms of the parasite in the host?

A
  • they change the surface coat of the outermembrane of the trypamastogotes to help them evade the host’s immune system
  • Antigenic Variation: the trypomastigote surface is covered in a dense coast of vsg’s (variant surface proteins) which is changed about every 5-7 days and causes a wave of parasitemia every 1-2 weeks and allows the parasite to evade host immune responses
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16
Q

What are the 2 stages of African trypanosomiasis?

A
  1. hemolymphatic stage: from bite to brain, parasite is found in circulation but has not invaded the CNS
  2. Meningoencephalitis stage: infection of the CNS
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17
Q

What are the clinical manifestations of T. brucei gambiense?

A
  • a cutaneous nodule (chancre) at the site of tsetse fly bite
  • chronic illness occuring minths to years later and characterized by intermittent fever, posterier cervical lymphadenopathy (winterbottom sign; essencilly inflammed lymph nodes)
18
Q

What are the clinical manifestations of T. brucei rhodesiense?

A

Generalized illness developed days to weeks after parasite inoculation. Acute illness characterized by high fever, thrombocytopenia, hepatitis, myocarditis, cutaneou chnacre, and anemia

19
Q

What are the important differences between the rhodesiense and gambiense subspecies?

A

Rhodesiense:
- primary resovior’s are cattle, antelope, domestic pigs and dogs
- acute early CNS disease
- progresses rapidly
- a large sore at the site of tsetse fly bite
- severe symptomes at first: high fever, headache, muscle pain, enlarged lymph nodes
- death within months if not treated

Gambiense:
- Primary resovoir is humans
- Chronic late CNS disease
- progresses slowly
- mild symptoms at first: intermediate fever, headache, muscle and joint pain
- Death within years (6-7) if not treated
- Parasites in blood= low

20
Q

How is African Trypanosomiasis diagnosed?

A
  • microscopy of blood, lymph fluid, chancre biopsy/ aspirate, and CSF (must to do this): this is good for both subtypes
  • Serology (not FDA approved)
21
Q

Epimastigotes

A
  • Nucleus and kinetoplast are close to each other
22
Q

Trypomastigote

A
  • Blood stream form
  • Has a undulating membrane
  • kinetoplast and kinetosome at the posterior end behind the nucleus
23
Q

What are the labratory morphological features of T. cruzei and T. brucei?

A

T cruzei:
- trypomastigote form has a large posterior kinetoplast and undulating membrane with anteriorly directed flagellum
- exhibists a C-shaped form
- dividing form does not exist

T. brucei:
- flagellum that begins as an undulating membrane originating posterior to the kinetoplast
- have small kinetoplats
- dividing forms can be seen

24
Q

Treatment for both subspecies of T. brucei for clinical stage 1 and 2?

A

Stage 1: Suramin and Pentamidine (only for gambiense)

Stage 2: Melarsoprol and Eflornithine (only for gambiense)

All thse drugs are very toxic and cause terrible side effects in paitents!!

25
Q

When should blood and CSF specimens be examined?

A

before, during and months after therapy

26
Q

How do you prevent African trypanomyosis?

A
  • Eradication of the vector, national vector control programs
  • drug treatment of infected humans and animals
  • decrease indivisual risk by using insect reprellent and wearing bite repelling clothing
27
Q

Where are the most infections of T. cruzi?

A

Latin America

28
Q

What is the Vector of American Trypanosomiasis?

A

Kissing bugs (aka Triatomine bug)

they are very active at night and bites are found around the mouth (they can go weeks without feeding).

29
Q

How is American Trypanosomiasis trasmitted?

A
  • Primarly vis the Kissing bug vector
  • Rarely due to: injestion of contaminated food/drink, mother to child, blood transfusion, organ transplant, lab accidents
30
Q

What is the infectious stage of American Trypanosomiasis? How are they released?

A

metacyclic trypamastigotes, released when the kissing bug poops after a blood meal (sleeping person may accidently scratch or rub the poo into the bite, eyes or mouth)

31
Q

what needs to happen for transmission of American Trypanosomiasis to occur from the vector?

A

transmission occurs when mucous membranes, conjunctivia or breaks in the skin are contaminated with bug feces.

32
Q

Amastigote

A

A protest cell that does not have a visible external flagella or cilia. This is the intracellular stage of the American Trypasomiasis and are found in the cytoplast of a infected human cell.

33
Q

Describe the lifecycle of T. cruzi.

A
  1. Kissing bug takes a blood meal from a host and passes the metacyclic trypamastigotes (infectious stage) to the host through its feces.
  2. Metacyclic trypamastigotes penetrate the cells at the site of the bite and transfom into amastigotes and these multiply by binary fission
  3. Intracellular amastigotes transform into trypamastigotes and burst out of the cell into the blood stream (both diagnostic stages); however, the trypamastigotes can reinfect other cells and retransform into intracellular amastigotes
  4. A kissing bug takes a blood meal from the host and injests trypamastigotes
  5. The trypamastigotes multiply in the midgut and then turn into metacyclic trypamastigotes in the hindgut. The cycle repreats with another bloodmeal.
34
Q

Describe the acute phase of American Trypasomiasis.

A
  • Lasts about 8-12 weeks after transmission
  • characterized by a chagoma (inflammatory leison caused by T. cruzi at the site of parasitic entry (Romona sign)
  • Symptoms include fever/chills, anorexia, malaise, edema of the face and lower extremities, lymphadenopathy, and hepatosplenomegaly
35
Q

Describe the chronic phase of American Trypasomiasis.

A
  • Happens when the host immune system decreases parasitemia and makes it so we cannot detect the parasite via microscopy and it goes untreated.
  • infection stays for years-decades after inicial presentation
  • affects heart (heart rythym disturbances and heart failure) and GI tract (esophogus and gut)
36
Q

Describe GI Chagas Disease.

A
  • Digestive Chagas disease is throught to be caused by damage to the intramural neurons by the parasite
  • Symptoms include weight losee, dysphagia, odynophagia, regurgitation, and aspiration
  • Antitrypanosomal therapy has not been proven to affect the progression of GI disease
37
Q

How do you diagnose American Trypanosomiasis?

A

-Serology for IgG (2 serologic assays are recommended), tests include Enzyme immunoassay (EIA) and immunoblot (TESA)
- Microscopy of circulating parasites (from blood and lymph fluid)
- Tissue biopsys
- PCR

38
Q

How do you diagnose congenital Chagas?

A

Microscopic examination of cord blood by PCR, serology is not indicated as maternal antibodies will be present in the new born blood.

39
Q

How do you treat American Trypanosomiasis?

A

Antitrypanosomals (Benznidazole or Nifurtimox)

In adult patients chronic T. cruzi infections can be treated with advanced cardiomyopathy but there is no evidence

40
Q

How do you prevent and control the spread of American Trypanosomiasis?

A
  • avoid habitation in buildings vulnerable to infestations
  • insecticide soaked bed nets
  • dont camp/ sleep out doors
  • inspect homes for vectors
  • screen blood donars in endemic areas
41
Q

What type of percaustions have to be in place for patients hospitalized with Chagas Disease?

A

tandard percautions

MMI 426 (10 decks)

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