Parasitology I (Amebiasis, Balantidium, Leishmania, & Malaria) Flashcards

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1
Q

What parasite causes amebiasis?

A

Entamoeba histolytica

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2
Q

Which Entamoeba is pathogenic?

A

histolytica

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3
Q

Which entamoeba is nonpathogenic?

A

dispar

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4
Q

What is the infective stage of amebiasis?

A

cyst

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5
Q

What is the pathology stage of amebiasis?

A

trophozoite

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6
Q

How is amebiasis transmitted?

A

fecal contaminated food and water; anal-oral sex

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7
Q

Where does amebiasis act?

A

large intestine, liver, CNS

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8
Q

What are the GI symptoms of amebiasis?

A

bloody diarrhea, watery diarrhea, constipation and then diarrhea

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9
Q

What is the GI pathology of amebiasis?

A

ulcers

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10
Q

What are the liver symptoms of amebiasis?

A

pain in the right quadrant; takes months or years to develop into an abscess

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11
Q

Why are the liver symptoms a time bomb?

A

because 60% of people with liver involvement never remember having any GI problems

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12
Q

What common organelles are missing in Entamoeba histolytica?

A

mitochondira, endoplasmic reticulum (ER), golgi apparatus, microtubules

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13
Q

What is the main host of Balantidium Coli?

A

pig

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14
Q

What two stages does Balantidium coli have?

A

trophozoite and cyst

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15
Q

What is special about the trophozoite stage?

A

it has cilia

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16
Q

What is the infective stage of Leishmania?

A

from the Sandfly

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17
Q

What is the pathology stage of Leishmania?

A

the amastigote

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18
Q

Where does Leishmania affect the human body?

A

depends on the type

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19
Q

How is Leishmania transmitted?

A

bite of sandfly

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20
Q

How is Leishmania diagnosed?

A

dipstick, biopsy, and culture

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21
Q

How is Leishmania treated?

A

toxic drugs

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22
Q

What is the vector for Leishmania?

A

the sandfly

23
Q

What is cutaneous leishmaniasis?

A
  • A simple skin lesion in skin where infected sandfly had previously bit the person
  • 1 infected bite = 1 lesion
24
Q

What is diffuse cutaneous leishmaniasis?

A

when a person has a defect in their cell mediated immune system the lesions can develop all over the skin of the body

25
Q

What is mucocutaneous leishmaniasis?

A

lesions in the mucocutaneous tissues of the mouth, nose, and genital areas

26
Q

What is visceral leishmaniasis?

A

lesions in the spleen, liver, and bone marrow

27
Q

What are the symptoms of visceral leishmaniasis?

A
  • fever
  • hepatosplenomegaly
  • anemia
  • hypergaminaglobulinemia (polyclonal B cell activation) - cause of anemia - antibodies coat normal RBC’s that are lysed
28
Q

Is leishmania zoonotic?

A

yes, many different wild animals are infected including rodents, sloths, and domestic dogs

29
Q

What is the the relationship between HIV & leishmania?

A

visceral leishmaniasis is more pathogenic in HIV-infected people

30
Q

What is the original theory of transmission for malaria?

A

inhaling bad (mal) air (aira) from swamps

31
Q

What are some of the malaria species?

A
  • Plasmodium falciparum
  • P. vivax
  • P. malariae
  • P. ovale (rare and like vivax)
  • P. knowlesi (normally in monkeys but now find a problem in humans)
32
Q

What is the vector for malaria?

A

Anopheles sp. of mosquitoes

33
Q

What are the stages of malaria in the liver?

A
  • sporozoite
  • exoerythrocytic schizont (EE stage) - in all 5 species of malaria w/ developing merozoites
  • hypnozoite (only P. vivax and P. ovale) - a slow growing EE stage
34
Q

How is malaria treated?

A
  • Prophylaxis = ACT drugs - a combination of Artemisinin and another drug
  • Primaquine
35
Q

What do ACT drugs target?

A

they only kill blood stages

36
Q

What does Primaquine target?

A

it kills hypnozoites

37
Q

What is the problem with primaquine?

A

it’s toxic, so it can’t be given before travel, only for treatment when you return with P. vivax to kill hidden hypnozoites

38
Q

What organelle is used for entry into RBC’s?

A

merozoite

39
Q

What are the stages of malaria in RBC’s?

A
  • merozoites
  • rings (young trophozoites)
  • trophozoites (mature)
  • schizonts (once nucleus divides)
  • gametocytes (sexual stages)
    ~ microgametocytes - male
    ~ macrogametocytes - female
40
Q

What are the symptoms of malaria?

A
  • fever
  • anemia
  • splenomegaly
41
Q

What are the complications of P. falciparum?

A
  • anemia
  • severe anemia
  • hyperparasitemia
  • hyperthermia diarrhea
  • hypoglycemia acidosis
  • death
  • cerebral malaria
  • renal failure
  • pulmonary edema
42
Q

Who dies from malaria?

A
  • children
43
Q

Who lacks immunity?

A
  • young children

- people that have never been infected

44
Q

What is premunition immunity?

A
  • people are immune as long as they have a low grade infection
  • when you lose your parasites you lose your immunity
45
Q

What RBC variants confer resistance?

A
  • hemoglobinopathies
  • RBC enzyme variants
  • RBC membrane variants
46
Q

How is sickle cell anemia related to malaria?

A
  • children w/ SS die
  • children w/ AS have a 70-fold less risk of severe malaria
  • children w/ AA have normal Hb
47
Q

What is normal oxygen tension?

A

parasite grows well in AA, AS, and SS, but when parasites get sequestered in capillaries the oxygen tension drops and lowers pH which causes sickling and parasitized cells die

48
Q

What is the new mechanism of sickle cell protection against malaria?

A

parasitized AS & AC RBC’s show similar reduction in surface PfEMP-1 expression & in adherence to endothelial cells lining blood vessels

49
Q

How does malaria affect pregnancy?

A
  • increased risk of severe pathology during 1st pregnancy in infected mother
  • cerebral malaria risk is increased
  • low birth weight is common (these children often don’t develop normally)
50
Q

How is malaria diagnosed?

A

blood films and dipsticks

51
Q

How are different blood films used in diagnosing malaria?

A
  • thick is to find parasites

- thin is to speciate for proper treatment

52
Q

What dipsticks are used to diagnose malaria?

A
  • antigen capture tests
  • OptiMAL - follow drug treatment
  • determine
53
Q

How does malaria affect those with HIV?

A
  • increase in viral load in macrophages in HIV patients that have an active malaria infection
  • the viral load goes down after treatment for malaria
  • increased viral genotypic heterogeneity & CD4 lymphocyte loss leading to accelerated decline in immune function
54
Q

What is malariotherapy for human HIV?

A
  • infect patients with P. vivax
  • induce high levels of cytokine activities & change T-lymphocyte subsets & phenotypes in HIV patients
  • may help HIV-infected patients whose CD4 baselines are in the range of 200-500
  • need much larger studies to confirm findings