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Microbiology > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

What is the species and vecor of malaria?

A
  • Plasmodium spp
  • Mosquitoes
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2
Q

What disease does plasmodium spp cause

A

malaria

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3
Q

What is the vector of plasmodium spp

A

mosquitoes

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4
Q

What is the species and vector of sleeping sickness

A
  • Trypanosoma brucei
  • Tsetse Fly
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5
Q

What does trypanosoma brucei cause?

A

Sleeping sickness

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6
Q

What is the species and vector of chagas’ disease

A
  • Trypanosoma cruzi
  • Triatomine bugs
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7
Q

What does trypanosoma cruzi cause

A

Chagas’ disease

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8
Q

What is the species and vector of leishmaniasis

A
  • Leishmania spp
  • Sandflies
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9
Q

What does lesihmania spp cause?

A

lesishmaniasis

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10
Q

What is the species and transmission of Toxoplasmosis

A
  • Toxoplasma gondii
  • Oral, fecal-oral infection
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11
Q

What are the main divisions of protozoa?

A
  • Sporozoa
  • Flagellates
  • Amoebae
  • Cilliates
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12
Q

What genus (+disease) is in sporaoza division

A

Plasmodium (malaria)

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13
Q

What genus (+disease) is in Flagellates division

A

Trypanosomes (sleeping sickness and chagas disease)

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14
Q

What genus (+disease) is in amoebae division

A

Entameba (amebiasis)

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15
Q

What genus (+disease) is in ciliates division

A

free living not parasitic

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16
Q

What is the parasite and transmission of malaria

A

Plasmodium spec. and mosquito insect vector

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17
Q

When are the mosquitos that transmit malaria the most active?

A

Nighttime

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18
Q

Where is malaria (location) restricted to?

A

tropical and subtropical areas and altitues BELOW 1,500 meters

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19
Q

Explain the lifecycle of plasmodium spec

A
  • The mosquite bites then sporozoties enter the bloodstream
  • Sporozoites go to liver to be changed to schizont
  • Released from the liver as merozoties which go and infect RBC
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20
Q

What infects RBC in malaria

A

merozoites

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21
Q

There are two pathways that the merozoties to trophozonite go through

A
  • The trophozote can go through an asexual blood stage (make more merozoties)

OR

  • become gametocytes to be taken up by the mosquito
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22
Q

What are the different ways that the immune system can target the different phases of the phasmodium spec.

A
  • Every stage can use antibodies except the liver stage
  • Liver uses cytotoxic T cells
  • The asexual stage can use antibodys and ROI
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23
Q

Who does malaria affect most?

A
  • infants and young children below age 5
  • Pregnant mothers
  • Non-immune (tourists)
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24
Q

what does malaria cause? (disease)

A
  • Anemia
  • Cerebral malaria
  • Maternal malaria
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25
Q

What is anemia from malaria

A

severe malarial anemia when hemoglobin <5g/dL; short supply of blood/unsafe blood supply

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26
Q

What is cerebral malaria

A

infected RBCs that stick to capillary walls in CNS

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27
Q

What is maternal malaria ?

A

Infected RBCs stick to placenta
* Caused by P. falciparum cytoadherence

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28
Q

What are the two subspecies that cause malaria

A

plasmodium falciparium and plasmodium vivax

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29
Q

What are the characteristics of P. falciparum

A
  • banana shaped gametocytes
  • most severe and deadly form of malaria
    • high parasitemia of all (young and adult) RBCs
    • Severe cerebral malaria
    • Prolonged fever
30
Q

What is the characteristics of P. vivax

A
  • Schuffner’s dots of infected RBCs
    * Infects only young RBCs
  • Causes most sporadic outbreaks of malaria in southern california and florida
31
Q

What are the clinical outcomes (what protects people from malaria)

A
  • Sickle cell trait
  • Thalassemia
  • G6PDeficiency
32
Q

Sickle cell Trait and malaria

A

AFRICA
* sickle cell hemoglobin (Hbs) mutation–> sickling of HbS RBC’s under low oxygen tension–> increased destruction by spleen
* Infected hbS RBCs=destroyed by spleen, elimination parasite as well

33
Q

Where is the sickle cell trait to protect from malaria

A

Africa

34
Q

Thalassemia and malaria

A

Mediterranean and south-east asia
* Less hemoglobin per cell–> lower oxygen carrying capacity compensatory increase in RBC production
* More RBC’s=increased ability to cope with infection

35
Q

Where is thalassemia that protects against malaria

A

mediterranean, south east asia

36
Q

G6PD deficiency and malaria

A

Mediterranean and middle east
* Decrease production of NADPH–> increase oxidative stress in cell so it is deadly for parasite

37
Q

what do we do to protect ourselves from malaria?

A

mosquito nets with insecticides

38
Q

What are the antimalarial drugs?

A
  • melfoquine (once a week)
  • Chloroquine (once a week; frequent resistance)
  • Doxycycline (daily; travel prophylaxis)
  • Malarone (daily; travel prophylaxis)
    * active against liver stages
39
Q

What are the two medication used for travel prophylaxis against Malaria

A

Doxycycline
Malarone

40
Q

What is the parasite and transmission of sleeping sickness?

A
  • Trypanosoma brucei
  • Tsetse fly
41
Q

What does the t. brucei do to survive better?

A

variant surfact glycoprotein (VSG) coat protects trypanosomes through antigenic variation

42
Q

When is the tsetse fly active?

A

daytime

43
Q

Where is the tsetse fly found

A

savanna forests

44
Q

What is the life cycle T. brucei

A
  • enters as trypomastigotes and remains that throughout cycle
  • Remains on the outside of RBCs (e.g. blood lymph and spinal fluid
45
Q

Where is the chronic form and acute form of sleeping sickness located?

A
  • Chronic: West-African
  • Acute: East-Aftican
    * More severe and deadly
46
Q

What are the early stages of sleeping disease

A
  • swollen lymph noeds
  • Known as Winterbottom’s sign
47
Q

What is the late stages of sleeping disease?

A
  • initated by invasion of CNS
  • Fatal if untreated
48
Q

What is the protection against sleeping sickness

A

Fly traps (optical and chemical attraction)

49
Q

The 2nd stage requires hospitalization. there are severe side effects and toxicity of what two drugs to treat sleeping sickness

A
  • Melarsoprol: arsenic-based drug against second/CNS stage
  • Eflornithine: less toxic BUT depresses bone marrow and immune system; causes anemia
50
Q

What is the parasite and transmission fo chagas’s disease?

A

Trypanosoma cruzi
Triatomine bug (kissing bug or chinche picuda)

51
Q

Where do chinche picuda hide and when do they bite?

A

hide in adobe walls during the day (rural homes with natutal substances)

52
Q

What is the area the chagas’ disease occurs?

A

Latin america and southern US

53
Q

What is the life cycle of T. cruzi including the tissue type

A

Enters as trypomastigotes then when it goes into the tissues (heart muscle and GI smooth muscle) they turn to amastigotes. Released back as trypomastigotes

54
Q

What is teh early sign of infection of chaga’s disease then the subsequent deveelipment of the disease

A
  • Romana’s sign (edema of the eyelid)
  • acute myocarditis and megacolon
55
Q

What is the protection and treatment of chagas disease

A

Protection:Regional initiative to eredicate and reduce triatomine buds
Treatment Nifurtinox and benzinidazole

56
Q

what is leishmanisis also known as?

A

Oriental sore, kala-azar

57
Q

What is the parasite and transmission of leishmanisis

A

leishmania species
sandfly (phelbotome)

58
Q

Where does leishmanisis infection located?

A

Infection worldwide
Endemic in the US

59
Q

Zoonosis of leishmanisis

A

dogs and rodents are imporant animal hosts

60
Q

What is the life cycle of leishmania

A

Enter as promasitgotes then phagocytied by macrophages then transform into amastigotes inside macrophages. Can also be in dentritic cells!

61
Q

What are three diseases that leishmania can cause

A
  • Cutaneous leishmaniasis (oriental sore)
  • Mucocutaneous leishmaniasis
  • Visceral leishmaniasis (kala-Azar)
62
Q

What is cutaneous leishmaniasis?

A

Oriental sore
* Self-healing within 2-12 month
* T cell mediated immune response through Th1 cells/INFy
* Type 4 reaction and leads to lesions

63
Q

What is mucocutaneous leishmaniasis

A

Espundia
* Inital cutaneous infection spreads to mucosa and cartilage
* Espundia is caused by a specific Lesishmania RNA virus

64
Q

What is visceral leishmaniais

A

Kala-Azar
* Splenomegaly (typical symptom)
* Hepatomegaly
* Retardation
* Fetal if untreated

65
Q

What is the txt of leishmanisis

A

Pentostam (i.m. for one month )
* Pentavalent antimonial;very toxic

Amphotericin B (antigungal)
* less toxic if applied as lipsomal formulation

Miltefosine (impavido)
* Phosphocholine analogue, new promissing drug for both visceral and cutaneous leishmanisis

66
Q

What is the parasite and transmission of Toxoplasmosis

A

Parasite: Toxoplasma gondii
Transmission:
* fecal oral (oocysts in cat litter)
* Oral (consumption of undercooked meat
* Highest risk in immunocompromised

67
Q

What is the zoonosis of toxoplamosis

A
  • Felines are a definitive host which produce infective oocysts
  • Any warm blood mammal or bird can serve as an intermediate host
68
Q

What is the life cycle of toxoplasma gondii

A
  • sporulated oocysts in feed, water, or soil which infects the tissue (cysts) intermediate host (pig, cow, etc) then the human can eat uncooked mean and ingest cysts. Becomes tachyzoites in human then transmitted through placenta
  • sporulated oocysts can be ingested through contaminated food and water to enter human then become tachyzoites to be transmitted through placenta
69
Q

What are some characteratics of toxoplasma oocysts?

A
  • can survive in the enviroments for several months
  • Remarkable resistant to disinfectants , freezing and drying
  • killed by heating to 70 C for 10mins
70
Q

What are the diseases caused by Toxoplasmosis

A
  • Cerebral toxoplamosis
  • Congenital toxoplamosis
71
Q

What is cerebral toxoplasmosis

A

primarily affects immunocompromised patients (i.e. AIDS patients)

72
Q

What is congenital toxoplasmosis?

A

Infected fetus with severe cerebral complication (hydrocephalus neonatal encephalitis)

Microbiology (18 decks)

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