L28: Malaria Flashcards

1
Q

Malaria vector

A

Female anopheles mosquito

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2
Q

2 most common malaria species that account for 95% of cases

A

Plasmodium vivax

Plasmodium falciparum

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3
Q

What stage of malaria does the mosquito transmit to humans via saliva?

A

sporozoites (motile forms) which migrate to the liver

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4
Q

Asexual division of sporozoites in the liver

A

Schizogony cycle

releases Merozoites

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5
Q

What can merozoites released from the liver infect?

A

Other liver cells or RBCs

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6
Q

Merozoite infection of RBCs

A

Erythrocytic cycle

enlarges, differentiates into uninucleate cell called a Ring Trophozoite
OR
Multinucleated form called a schizont

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7
Q

Trophozoites age and develop into

A

Amoeboid trophozoites

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8
Q

What does the mosquito ingest out of human blood?

A

Gametocytes which reproduce to produce sporozoites which then travel to their salivary glands
(gametocytes don’t rupture RBC)

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9
Q

Malaria eats

A

Hemoglobin

this is why sickle cell anemia is protective against P vivax: altered hemoglobin

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10
Q

What do RBC release when they rupture?

A

Pyrogen: changes hypothalmic set point: fever

Tumor necrosis factor (TNF)

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11
Q

Malaria symptoms

A

Fever
Anemia
Vasodilation causing hypotension
N/V/D, constitutional symptoms

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12
Q

Describe a method of host resistance (besides sickle cell)

A

Don’t express the Duffy antigen (glycoprotein) which is a receptor for P vivax
without it P vivax can’t enter RBC

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13
Q

Malaria reservoir

A

Humans

Simians

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14
Q

What’s gonna make malaria more prevalent

A

Climate change bringing mosquitos to areas where hosts aren’t exposed/no immunity

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15
Q

Play a role in spread of malaria

A

Tolerant carrier

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16
Q

Incubation of P vivax

A

9-15 days

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17
Q

P vivax likes to infect

A

young erythrocytes

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18
Q

How often do fever paroxysm occur with P vivax, and how long do they last?

A

every 48 hours
last 2-5 hours
Chills and shaking last 10-15 mins, with other symptoms

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19
Q

What causes a fever paroxysm?

A

Rupture of RBC schizonts

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20
Q

Does P vivax have relapses?

A

Yes
Due to liver hypnozoites
3-5 years after initial infection

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21
Q

P vivax is most prevalent in ______ and has a reservoir _____

A

Caribbean, Latin America

ONLY humans

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22
Q

Sickle cell anemia offers resistance to

A

P vivax

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23
Q

Enlarged infected RBCs with Schuffner’s dots (surface invaginations and stipling)

A

P vivax

taken from venous blood + Giemsa stain

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24
Q

P vivax aka

A

Benign tertian malaria

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25
P falicparum incubation period
8-17 days
26
P falicparum causes
High grade parasitemia: infects many RBC, of any age, and multiplies rapidly. Very high fever
27
Blackwater fever
P falicparum with very high parasite levels | Causes autoimmune destruction of kidney tissue, free hemoglobin in urine (black)
28
Dark to black urine
``` Blackwater fever (P falicparum) due to hemoglobin ```
29
Cereberal malaria
P falicparum occlusion of capillaries with infected RBCs necrosis, hemorrhages, mania, convulsions, death
30
Gastric falciparum malaria
just a bunch of vomiting
31
Algid malaria
P falicparum | Skin is cold but internal temperature is high
32
Does P falicparum relapse?
NO | no hypnozoite stage
33
Maurer's clefts
P falicparum identification
34
Double or multiple ring stages
P falicparum identification
35
Many infected cells with young trophozoites and gametocytes in periphery
P falicparum identification
36
Is P falicparum fatal?
Left untreated, yes
37
P malariae aka
Quartan malaria
38
P falicparum aka
Malignant tertian malaria
39
P malariae infects ____ and paroxysms occur ____
Older RBCs | Every 4th day
40
Basket and band shaped trophozoites | rosette shaped schizonts
P malariae
41
P ovale
Similar to vivax Relapses West coast Africa
42
P knowlesi
Zoonotic Southeast Asia High parasite burden can be fatal
43
What's a target for new chemotherapy against malaria?
Duffy antigen antibodies to block P vivax from binding
44
Main method of Malaria drug resistance
Efflux pumps
45
Babesia microti causes
Babesiosis/Nantucket Island Fever
46
Babesia infects ____ and is prevalent in ____
RBCs | New England warm months
47
Babesia vector
Deer tick--> coinfection with Lyme disease --> Severe | also blood transfusions
48
Babesiosis symptoms
Malaria-like fever, chills, HA, anemia No rash, small pinpoint lesions
49
Babsesiosis prognosis
asymptomatic to life threatening (10%) | worse: immunocompromised, asplenic, in Europe
50
Maltese cross morphology in RBCs
Babesiosis
51
Babesisosis morphology
Similar to P falciparum
52
Trypanosoma brucei aka
African sleeping sickness
53
Trypanosoma cruzi aka
Chagas disease
54
Leishmania
Visceral, mucocutaneous, or cutanous Leishmaniasis
55
Trypanosomatids are
flagellate protozoa
56
3 trypanosomatoids
Leishmania Trypanosoma brucei Trypanosoma cruzi
57
Chaga's disease is prevalent in
Mexico, Central and South America
58
Chaga's disease vector
``` Triatomine bugs (kissing bugs) Passes trypanosoma cruzi through: feces, blood/organ transplant, congenital ```
59
Can you be immune to Chaga's disease for life?
No, difficult
60
Trypomastigotes
what the tiatomine bug passes in feces differentiate into amastigotes in host, which replicate by binary fission and are released as trypomastigotes into circulation and eaten by bugs
61
Acute Chaga's disease
Asymptomatic, mild non-specific constitutional symptoms +/-chagoma Romaña's sign
62
Romaña's sign
Acute Chaga's disease | swelling of eyelid near parasite entry site
63
How do you get Chronic Chaga's disease?
When acute symptoms wane, the organism persists you can be asymptomatic for years lifetime risk of complications from Chronic disease: 30%
64
Chronic Chaga's disease
Pseudocysts of amastigotes in cells Preference: muscle and nerves Crazy organomegaly, degeneration, lots of problems
65
Blood smear Chaga's disease
Trypomastigotes
66
Biopsy Chaga's disease
Amastigotes
67
Is there a Chaga's disease vaccine?
No