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erica's id 3 > Parasitic Protozoa II > Flashcards

Parasitic Protozoa II Flashcards

1
Q

Toxoplasmosis

A
  • Caused by toxoplasma gondii
  • Widespread infection causing flu-like symptoms
  • Reactivated in immunocompromised
  • Transplacental transmission leads to serious problems
  • Intracellular parasite that can infect any cell
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2
Q

Transmission of toxo among animals

A
  • Transmission from contaminating oocysts (cats) - come from birds or rats getting eaten by cats who get the tissue cysts, and then comes out as a fecal oocyst
  • Eating improperly cooked meat, transfusions, etc.

Essentially you can either get the tissue cysts or fecal oocysts

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3
Q

If someone is seropositive for toxo long before getting pregnant, is the baby at risk for toxo?

A

No you should have immunity against toxo, and so the baby should be protected.

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4
Q

If the maternal infection of toxo is

A

Probably not, the risk is pretty high

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5
Q

If maternal infection of toxo occurs during the first trimester, what disease of the neonate is possible?

A
  • miscarriage
  • stillborn
  • chorioretinitis, hydrocephalus, intracranial calcifications, hepatosplenomegaly, jaundice, fever, anemia
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6
Q

If maternal infection of toxo occurs during 3rd trimester, what might happen?

A
  • baby will be asymptomatic at birth but may have more learning disabilities and neurological sequelae
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7
Q

Can you directly identify toxo?

A

No, it’s pretty difficult. Do serology and PCR

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8
Q

Prevention of toxo

A
  • No vaccine
  • Change litter daily if you own a cat
  • Keep cat indoors
  • Dont eat undercooked meat
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9
Q

Tachyzoites vs. Bradyyzoites

A
  • Tachy = dividing forms in a cell

- Brady = dormant forms in a cell

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10
Q

Chagas disease

A
  • Infection that causes an acute and chronic phase
  • Caused by trypanosoma cruzi
  • There is a blood and tissue form
  • Transmission = via kissing bug bite, congenital, blood transfusion, organ transplant
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11
Q

Life cycle of Chcagas

A
  • You or dog is infected
  • Bloodstream form gets transmitted to kissing bug
  • Kissing bug feeds on human - bites you and then poops so that when it itches and you scratch, you scratch the parasites into the open wound (almost all other vectors use saliva)
  • Gets into blood - travels to muscle cells (heart and intestine are its favorites)
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12
Q

Acute Chagas presentation

A

Initially mild symptoms at site of inoculation and in blood phase (often asymptomatic)

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13
Q

Chronic Chagas presentation

A

Asymptomatic tissue phase in most, but 20-30% will develop heart abnormalities and dilated esophagus or colon (die of heart attack)

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14
Q

Triatomine

A

Kissing bug

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15
Q

What’s the problem with a serological test for Chagas?

A

Doesn’t tell you if you are actively infected, or if you have any of the muscle form.

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16
Q

Why is chronic Chagas harder to diagnose?

A

Trypomastigotes are not found in blood and so you have to do a biopsy or some faulty serology

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17
Q

How to prevent Chagas

A

Don’t get bitten and pooped on.

  • Feed at night
  • Bugs breed in the cracks of poorly constructed homes
  • Spray the houses
18
Q

Leishmaniasis

A

3 types = cutaneous, mucocutaneous, visceral

  • caused by Leishmania
  • Intracellular parasite of macrophages (phagolysosome is a happy living place for them)
  • Transmission: bite from sand flies or cutaneous contact
19
Q

Life cycle of Leishmaniasis

A

Sand flies bite someone infected –> macrophage bursts and amastigotes transform into promastigotes, and then sand fly bites you and gives you the promastigotes. These go visceral to the spleen or cutaneous

20
Q

Clincal presentation of the forms of Leishmaniasis

A
  1. Cutaneous - skin lesions/ulcers
  2. Mucocutaneous - partial or total destruction of mucous membranes of the nose, mouth and throat
  3. Visceral - irregular bouts of fever, weight loss, enlargement of spleen and liver
21
Q

Diagnosis of Leishmaniasis

A

ID of parasites within cells in a biopsy

- rRNA its PCR

22
Q

Best way to prevent leishmaniasis

A

People should sleep under bed nets, and the bed nets should be impregnated with an insectiscide

23
Q

African sleeping sickness

A

Trypanosomiasis (tsetse fly vector)

  • Hemoflagellate parasites
  • Daylight biters, and can fly long ways
  • Multiply in blood stream and can eventually enter CNS
24
Q

Presentation of trypanosomiasis

A
  • Wasting with fever, severe headaches, irritability, fatigue, lymph nodes, aching muscles and joints
25
Q

Control of trypanosomiasis

A
  • Reduce the disease reservoir controlling the tsetse fly vector
  • Treatment
26
Q

Why can’t the immune system take out trypanosomiasis?

A

Because it undergoes antigenic variation - keeps changing its colors.

You wipe yourself out trying to chase it, and you end up getting wasting, neurological involvement and eventually coma.

27
Q

Malaria

A
  • Plasmodium infects RBCs

- Most serious parasitic disease (50% of deaths are in children

28
Q

Incubation of malaria

A

9-14 days

29
Q

Life cycle of malaria

A

Mosquito has it, goes through the sporogenic cycle

  • bites a hooman and injects sporozoites
  • sporozoites go to the liver first – eventually ruptured schizont gets into human blood and goes through erythrocytic cycle
30
Q

Control of malaria

A
  • bed nets!

- Prophylactic drugs

31
Q

How long does a classical malaria attack last?

A

6-10 hours

  • cold stage
  • hot stage
  • sweating stage

Tertian parasites have attacks every 2nd day
Quartan parasites have attacks every 3rd day

32
Q

Malaria pathogenesis

A
  1. Infection and destruction of RBCs
  2. Anemia
  3. Blockage of blood vessels, particularly in the brain
  4. Cytoadherence in P. falciparum - sticky adherence to endothelial cells. Leads to rosetting of RBCs and clumping
  5. Rosettes cause clogging and hemorrhaging
  6. Cytokine response leads to endothelia getting stickier
33
Q

Malaria diagnosis

A
  1. Symptoms
  2. Blood smear (thick or thin)
  3. Antigen detection, molecular diagnosis, serology
34
Q

What is sterile immunity?

A

Once you get infected, you can completely clear the bug

35
Q

Malaria immunity

A
  • No sterile immunity known
  • Variants and antigenic variation
  • Ineffective malaria vaccine for now…
36
Q

Control and prevention of malaria

A
  • Mosquito control
  • Reduce mosquito bites
  • Prophylactic treatment – leads to resistance
  • Treatment – need new drugs but we’re overly reliant on drug treatment
37
Q

What genetic mutation provides resistance for malaria?

A

Sickle cell trait (heterozygous for abnormal HbS)
G6P deficiency
Thalassemia

38
Q

What does the duffy blood group have to do with RBC resistance to infection by P. Vivax?

A

If you are negative for the duffy blood group, then you are protected.

39
Q

Babesiosis

A
  • Infected RBCs by Babesia microti

- Spread by deer ticks or blood transfusion

40
Q

Clinical presentation of babesiosis

A
  • asymptomatic to life threatening
  • worse in immunocompromised
    Diagnosis via blood specimens and RBCs

erica's id 3 (13 decks)

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