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Skin/MSk > Exam 4 parasites > Flashcards

Exam 4 parasites Flashcards

1
Q

What is the vector for Chagas’ disease

A

Kissing bug (traitomine insect)

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2
Q

What is the vector for African Sleeping Sickness

A

TseTse fly

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3
Q

How does toxoplasmosis infect someone?

A

through ingestion of cysts

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4
Q

What is the vector for river blindness (onchocerciasis)

A

Black fly

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5
Q

What is the vector for babesiosis?

A

Deer tick (I. scapularis)

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6
Q

What is the vector of leishmaniasis?

A

Sand fly

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7
Q

What is the vector for lymphatic filariasis (elephantiasis)?

A

Mosquito

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8
Q

What is the treatment of Onchocerciasis?

A

invermectin

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9
Q

What is the larval stage of onchocerciasis that infects humans?

A

L3 larvae

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10
Q

Where does onchocerciasis mature and sexually reproduce?

A

Under the skin of the human host

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11
Q

What is the target of ivermectin? What’s it used for?

A

unsheathed microfilariae which are the offspring of adult sexual reproduction, onchocerciasis

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12
Q

Where is onchocerciasis endemic to?

A

Sub-saharan Africa

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13
Q

What is the species that causes onchocerciasis?

A

Onchocerca volvulus

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14
Q

What are the symptoms of onchocerciasis?

A

Nodules under the skin, hyper pigmented skin (post inflammatory response), severe itching, eye lesions, skin lesions, keratitis

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15
Q

How is onchocerciasis positively diagnosed

A

skin snip method

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16
Q

What is one way that has proved useful to eliminate onchocerciasis as a public health problem?

A

Mass drug administration

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17
Q

What is the mechanism of action of ivermectin? What’s it used for?

A

binds to and blocks glutamate-gated chloride channels that are present in invertebrate muscle and nerve cells; onchocerciasis

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18
Q

What are the classic signs of leishmaniasis?

A

Ulcerative skin lesions with raised outer border, mucocutaneous lesions, marked splenomegaly

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19
Q

What stage of leishmania infects humans?

A

promastigote

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20
Q

What is required by leishmania promastigotes to achieve mammalian life cycle stage?

A

phagocytosis by macrophage to replicate in phagolysosome, evades immune system

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21
Q

What are the three kinds of leishmania?

A

Cutaneous leishmaniasis (old world, new world), mucocutaneous leishmaniasis, visceral leishmaniasis

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22
Q

What causes mucocutaneous leishmaniasis?

A

metastasis of an untreated cutaneous leishmaniasis

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23
Q

What’s the worst kind of leishmania?

A

visceral leishmaniasis

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24
Q

What are symptoms of visceral leishmaniasis?

A

weight loss, enlarged spleen and liver, low blood counts

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25
Q

How do you definitively diagnose leishmaniasis?

A

microscopic detection in blood or tissue sample, serological tests for visceral leishmania

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26
Q

What are the treatments of leishmania?

A

Sodium stibogluconate, meglumine antimoniate, Miltefosine, Liposomal amphotericin B

27
Q

What are the actions of sodium stibogluconate and meglumine antimoniate, what are they used for?

A

Leishmaniasis, organic antimonials

28
Q

What is the mechanism of miltefosine? What’s it used for?

A

misunderstood mechanism; leishmaniasis?

29
Q

What is the mechanism amphotericin B? What’s it used for?

A

Binds ergosterol to form pores in membranes; VISCERAL leishmaniasis

30
Q

What does leishmaniasis look like under the microscope?

A

Depends on the life stage, but its intracellular when in the macrophages (looks like 2 dots for the HE stain)

31
Q

What are the effects of a chronic Chagas’ disease infection?

A

cardiomyopathy, megacolonic segment, megaesophagus

32
Q

What are the acute symptoms of Chagas’ disease

A

often asymptomatic, but can be mild typical immune response to infection

33
Q

What causes Chagas’ disease?

A

T. cruzi

34
Q

Where does T. cruz replicate?

A

intracellularly

35
Q

How is Chagas’ disease (T. cruzi) definitively diagnosed?

A

ID of parasites in blood, chronic infection is usually diagnosed with more than one serological test

36
Q

What is the treatment of Chagas’ disease (T. cruzi)

A

Nifurtimox and Benznidazole

37
Q

What is the mechanisms of action for nifurtimox? What does it treat?

A

Induces oxidative stress due to inhibition of NAD(P)H-dependent dehydrogenases; Chagas’ disease (T. cruzi)

38
Q

What is the mechanism of action for benznidazole?

A

Induces oxidative stress due to inhibition of NAD(P)H-dependent dehydrogenases; Chagas’ disease (T. cruzi)

39
Q

What is required for nifurtimox and benznidazole to work?

A

Type-I nitroreductase to turn it from prodrug to active form

40
Q

What does T. cruzi look like under the microscope

A

depends on what point it is in the life cycle; looks like T. brucei extracellularly, can be intracellular

41
Q

What point in its life cycle does T. brucei infect humans at?

A

metacyclic trypomastigotes

42
Q

What is a dead giveaway for T. brucei over T. cruzi

A

T. brucei reproduces asexually out of cells; they will be connected extracellularly

43
Q

Where does T. brucei reproduce/live?

A

Extracellular. ALWAYS.

44
Q

What two forms of T. brucei; where are they found?

A

T. brucei gambiense (West Africa, less severe), T. brucei rhodesiense (East Africa, acute)

45
Q

What causes African sleeping sickness?

A

Trypanosoma brucei

46
Q

What are side effects of African Sleeping sickness?

A

First stage: Chancre at bite site, fever, headache, swollen lymph nodes, muscle and joint aches.
Second stage: CNS development, somnolence (extreme sleepiness), altered gait, tremors, cranial neuropathies

47
Q

What are the time scales for symptoms of T. brucei gambiense and rhodesiense?

A

Gambiense: CNS involvement after 1-2 years, death in 3 if not treated.
Rhodesiense: CNS involvement after a few weeks, death in months if untreated

48
Q

What makes T. brucei gambiense so difficult to treat?

A

“Waves” of parasitemia where the parasite changes its active surface glycoproteins

49
Q

What are treatments of African sleeping sickness?

A

Suramin, Pentamidine, Eflornithine, Melarsoprol

50
Q

Whats the mechanism of action for suramin? What does it treat?

A

inhibits enzymes of pentose phosphate and glycolytic pathway; African sleeping sickness

51
Q

What is the mechanism of action of pentamidine? What does it treat?

A

Interferes with DNA replication of mt genome; african sleeping sickness

52
Q

What is the mechanism of action of eflornithine? What does it treat?

A

inhibits ornithine decarboxylase; african sleeping sickness

53
Q

What is the mechanism of action of melarsoprol? What does it treat?

A

may relate to metabolism; african sleeping sickness

54
Q

What does lymphatic filariasis cause?

A

elephantitis

55
Q

What species causes lymphatic filariasis?

A

Wucheria bancrofti

56
Q

What stage of Wucheria bancrofti is injected into humans?

A

L3 larvae

57
Q

What stage of Wucheria bancrofti causes elephantitis?

A

Unsheathed microfilariae migrating to blood and lymph channels

58
Q

What is the treatment of lymphatic filariasis?

A

Diethylcarbamazine

59
Q

What is the mechanism of action of diethylcarbamazine? What does it treat?

A

arachidonic acid metabolic pathway of microfilariae; lymphatic filariasis

60
Q

What causes toxoplasmosis?

A

Toxoplasma gondii

61
Q

How is toxoplasmosis transmitted?

A

Via ingestion of oocyst from uncooked meat or cleaning a cat’s litter box

62
Q

What are symptoms of toxoplasmosis?

A

In immunocompromised: fever, confusion, headaches, seizures, nausea, poor coordination
Ocular toxoplasmosis: red, painful photophobic eye
“headlight in the fog”
Can cause abnormal head size in fetus

63
Q

Do you treat toxoplasmosis?

A

Not always, unless pregnant or immunocompromised

64
Q

What are the treatments of toxoplasmosis?

A

Sulfadiazine and pyrimethamine, spiramycin in pregnant women, Atovaquone

Skin/MSk (31 decks)

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