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Host Defense & Microbiology > Arbo-Parasites > Flashcards

Arbo-Parasites Flashcards

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Biology 101 flashcards
2
Q

Leishmaniases are what type of parasite?

A

protozoa

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3
Q

where do leishmania parasites reside within the host?

A

intracellularly inside macrophages

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4
Q

what is the vector for leishmaniasis?

A

sand flies

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5
Q

life cycle of leishmania parasite between humans and sand flies

A

sandfly injects promastigote into human, phagocyt by macrophage, turns into amastigote (pathogenic), amastigotes multiply in cells, ingested when a sand fly bites, transform into promastigotes in midgut of sandfly

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6
Q

in what ways can leishmania be transmitted other than through sand fly vectors?

A

parenteral, congenital, occupational (needle stick), sexual

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7
Q

New World leishmania species cause ______ leishmaniasis.

A

cutaneous, mucocutaneous

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8
Q

cutaneous leishmaniasis

A

self-healing, slowly enlarging nodule at bite site that turns into ulcer and leaves hypo-pigmented scar

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9
Q

mucocutanous leishmaniasis

A

nodular and ulcerative lesions of the oral-nasal-pharyngeal mucosal surfaces, nasal septum lesion or hoarseness is first indication, Brazilian strain

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10
Q

CL and ML are generally confined to?

A

Central America, tropical South America, Middle East and Northern Africa

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11
Q

visceral leishmaniasis

A

much more severe disease with classic pentad: fever, cachexia, splenomegaly, pancytopenia, high levels of IgG

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12
Q

90% of VL is in what 5 countries?

A

Bangladesh, India, Nepal, Sudan, & Brazil

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13
Q

Leishmaniasis is exacerbated by?

A

primary immune disease (AIDS), immunosuppressive drugs, organ transplantations

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14
Q

Diagnosis of leishmaniasis in the US

A

find the parasites (invasive procedure: scrapes, aspirates, biopsies) – can visualize/stain amastigotes inside macrophages (promastigotes in culture) or do PCR; histo not very sensitive

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15
Q

parasite burden is highest in what type of lesihmaniasis?

A

visceral

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16
Q

other countries have this diagnostic test, which is similar to a PPD test and very helpful at detecting organism at low burden

A

DTH (delayed type hypersensitivity test)

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17
Q

there are specific drugs to treat certain strains of CL, but this drug covers everyone

A

antimony

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18
Q

Treatment for VL

A

Amphotericin B (resistance, esp. in India), pentavalent antimony

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19
Q

How to prevent leishmaniasis

A

sandflies are terrible fliers, windy areas are safer, bed nets, rodent control

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20
Q

What is schistosomiasis?

A

waterborne parasitic fluke infection (flat worms) – 97% of cases in poor regions of Africa

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21
Q

Schistosomiasis life cycle.

A

Cercariae released by snails into water, penetrate humans, enter circulation, migrate to portal vein and mature into adults, paired worms lay eggs that are shed in stool or urine, hatch releasing miracidia which penetrate snail and develop into sporocysts, then released as cercariae

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22
Q

Age distribution of schistosomiasis

A

frequently affects young teen boys, called “male menarchy” because boys pee red in their teens

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23
Q

risk factors for urinary schisto

A

male, close to water source, previous infection, 8-13 yo

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24
Q

the majority of schisto infections are?

A

urinary/urogenital

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25
Q

Diagnosis of schisto

A

none, serology is negative for months

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26
Q

What determines whether schisto is urinary vs. intestinal/hepatic?

A

depends on where the worms migrate to lay their eggs (haematobium to venous plexus of bladder, mansoli to mesenteric vessels)

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27
Q

how to schisto evade host immune response?

A

accretion of host molecules on their surface!

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28
Q

what do schisto eggs do once they are laid?

A

100/day; spikes on outer shell + dissolving enzymes = bore their way through blood vessel to enter bladder or intestine (leads to mechanical damage of vessels, blood loss, granulomas, inflammation)

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29
Q

symptoms of urinary schisto lead to what long-term problems?

A

growth retardation, undernutrition, cognitive delays, poor performance, renal failure, infertility in women, increased transmission of HIV

30
Q

symptoms of intestinal schisto leads to?

A

liver enlargement, diarrhea, loss of appetite, liver disease

31
Q

diagnose schisto by?

A

detecting s. haematobium eggs in urine, s. mansoni eggs in stool

32
Q

treatment and control of schisto

A

praziquantel

33
Q

African trypanosomiasis is transmitted by _________.

A

tsetse fly

34
Q

African sleeping sickness life cycle.

A

metacyclic trypomastigote injected by fly, enters bloodstream, multiplies, blood meal of tsetse fly, turn into procyclic trypomastigotes, leave gut and turn into epimastigotes, multiply in saliva, turn into metacyclic trypomastigotes

35
Q

West African sleeping sickness has a ____ reservoir, likes ____ climate, and causes _____ disease.

A

human reservoir, humid climate, chronic disease

36
Q

East African sleeping sickness has a _____ reservoir, likes _____ climate, and causes _____ disease.

A

wild animal reservoir, savannah, acute disease

37
Q

primary symptoms of African Sleeping Sickness

A

chancre, posterior lymphadenopathy

38
Q

secondary African Sleeping Sickness

A

system disease (fever, wasting)

39
Q

advanced African Sleeping Sickness

A

CNS disease (lethargy, insomnia, seizures, coma) – starve while seizing

40
Q

trypanosoma’s main virulence factor is?

A

antigenic variation (periodically switch their variable surface antigen – leads to waves of parasitemia)

41
Q

Treatment for african sleeping sickness

A

pentamidine or suramin (doesn’t work for late stage CNS)

42
Q

Chagas Disease life cycle.

A

triatomine bug bites, poops, rubbed into wound, once inside cells metacyclic trypomastigote turns into amastigote that multiplies in tissue, transforms into trypomastigote to reinfect other cells or be ingested by triatomine bug (turns into epimastigote briefly inside bug)

43
Q

Geographic distribution of Chagas.

A

South America, central america, USA

44
Q

signs of acute Chagas disease

A

Romano’s sign (periorbital swelling), acute febrile illness, severe disease in 1%

45
Q

Chagas Heart Disease develops ______ years after initial infection.

A

10-20 years later!

46
Q

Chagas can also cause?

A

toxic mega colon (loss of neurons in the gut)

47
Q

Diagnosis of chronic chagas disease

A

xenodiagnosis (put bugs on them?), indirect fluorescent antibody

48
Q

Treat acute Chagas disease with?

A

Benznidazole, Nifurtimox (neither FDA approved, must ask CDC)

49
Q

Treat chronic Chagas disease with?

A

No Rx :(, only management

50
Q

Malaria

A

obligate intracellular eukaryotic parasite that infects liver cells and red blood cells

51
Q

Malaria rates are currently _____.

A

decreasing!

52
Q

Malaria infections in pregnant women cause?

A

low birth weight babies

53
Q

Malaria is transmitted by the _______ mosquito

A

female anopheles

54
Q

Malaria life cycle

A

mosquito bites human, injects sporozoites that are in circ for only 30 min, enter liver (asymptomatic stage), merozoites rupture from liver to infect RBCs (symptomatic stage), turn into trophozoites, then schizonts that rupture and become gametocytes that have sex inside mosquito

55
Q

The agent in 98% of malaria infections is…

A

plasmodium falciparum

56
Q

Why is malaria falciparum so vicious?

A

invades all RBCs (not just certain types)

57
Q

Clinical course of uncomplicated malaria

A

prepatent period (asymptomatic while parasite multiplies in liver), paroxysm (shaking chills, high fever as merozoites are released from RBCs), HA, nausea, vomiting, malaise, etc.

58
Q

Severe malaria

A

cerebral (coma, seizures), severe anemia due to RBC lysis, multi organ failure (iCAM, parasite proteins on RBC surface cause them to stick to organ walls)

59
Q

In areas with lots of infected anopheles, adults are ______.

A

semi-immune

60
Q

first time mothers infected with malaria have low birth weight children because?

A

falciparum parasite turns on specific genes to promote placental cytoadherence, which decreases nutrients crossing the placenta

61
Q

Vivax malaria is different from falciparum in that it is?

A

chronic (dormant liver stage

62
Q

Liver stages of malaria can be treated with ______ except in ______ patients.

A

primaquine, causes hemolyic anemia in G6PD deficient patients

63
Q

______ remains prevalent because it is protective against malaria.

A

sickle cell trait (heterozygote), thalassemia

64
Q

Diagnosis of malaria

A

Giemsa blood smears, rapid antigen tests, PCR (species specific)

65
Q

immunochromatography to diagnose malaria

A

distinquishes between both major strains, but big variation in quality and can breakdown in areas with poor transportation

66
Q

this kills female anopheles mosquitos and is non-toxic to humans

A

indoor residual spray (insecticide)

67
Q

the mainstay therapy for malaria is?

A

quinine-related antiobiotics with increasing resitance (newest is Artemisinin Combination Therapy)

68
Q

Artemisinin is derived from?

A

chinese herbal remedy

69
Q

Is there any resistance to artermisinin?

A

looks more like tolerance, starting to see prolonged clearance time, don’t know what this means

70
Q

Is there a future for malaria vaccines?

A

Probably not? (not in the blood long enough)

Host Defense & Microbiology (19 decks)

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