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MMI 426 > Malaria & Babesia > Flashcards

Malaria & Babesia Flashcards

1
Q

apicomplexa

A

type of protozoan
Plasmodium
has micronemes that make proteins that manipulate RBCs = infection

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2
Q

four species of Plasmodium that cause malaria in humans

A

P. vivax
P. ovale
P. falciparum (most severe; most deaths)
P. malariae

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3
Q

P. knowlesi

A

emerging pathogen
aka Monkey Malaria (from long-tailed Maques)
clinically similar to P. malariae
overtaking in Malaysia and Philippines

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4
Q

T or F. The anopheles mosquito is a mechanical vector of Plasmodium

A

F! biological vector bc part of its life cycle takes place inside mosquito (not all external; mechanical)

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5
Q

incubation of malaria

A

10-15 days

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6
Q

general symptoms of malaria

A

headache
nausea
chills
diarrhea
fever (41C)
- due to rupture of RBCs as parasites released
- fragments of RBCs = antigenic components that act as inflammatory response

anemia
splenomegaly
- risk of splenic rupture esp. in ovale and vivax

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7
Q

gold standard for diagnosing malaria

A

microscopy
but need good equipment and experienced person

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8
Q

rapid diagnostic tests for malaria

A
  • some detect only one species, other several species
  • practical; don’t need experienced personnel
  • detect antigen so not reliant on good immune functioning
  • only need small amt blood
  • all detect one or more of: HRP2/histidine-rich protein 2 (only P. falciparum), subtypes of pLDH (plasmodium lactate dehydrogenase) and aldolase (ALL species)
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9
Q

most widespread species of plasmodium

A

P. vivax and P. falciparum (over 95% mortality)

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10
Q

hypnozoites

A

P. vivax and P. ovale can remain latent in liver
treatment must eradicate these and treatment is different

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11
Q

this malaria can sometimes be known as benign

A

P. malariae
can remain infected for up to 40 yrs

same with P. knowlesi

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12
Q

the most deadly form of malaria

A

P. falciparum
- infects all ages of RBCs
- high % of infected RBC in blood (parasitemia)

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13
Q

complications that arise in P. falciparum malaria

A

cerebral malaria
blackwater fever
severe anemia

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14
Q

cerebral malaria

A
  • P. falciparum- cerebral anoxia
  • increased glucose breakdown
  • increased lactate production
    = sticky RBC clumps = block vessels
    SEQUESTRATION
  • hard to treat
  • altered states of consciousness, confusion, hallucinations, seizures, motor abnormalities, coma
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15
Q

blackwater fever

A
  • P. falciparum
  • hemoglobinuria secondary to massive hemolysis (idiopathic?? may be due to hypersensitivity to drugs)
  • hepatic, renal, pulmonary complications also seen with severe infection
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16
Q

purpose of gametocyte form?

A

parasite can communicate with other parasites to let them know they need to differentiate!! want to stay alive

  • extracellular vesicles = exosomes formed by endocytosis of segments of plasma membrane
  • exosomes secreted by P. falciparum infected RBC act as intracell communication mediators = ring forms release exosomes containing plasmids with genes for antimicrobial resistance or genes for differentiation to gametocytes
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17
Q

what is different about P. falciparum’s pathogenesis?

A
  • ability to sequester in deep vasculature
  • sticky, RBCs stiff = rosetting
  • blocks blood flow
  • accumulation of parasites in organs
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18
Q

what is schizogony?

A

refers to a replicative process in which the parasite undergoes multiple rounds of nuclear division without cytoplasmic division followed by a budding, or segmentation, to form progeny (merozoites)

19
Q

define ‘rosetting’

A

where an infected RBC binds to non-infected RBCs and platelet induced clumping of RBCs

20
Q

major determinants of pathogenicity of P. falciparum

A

PfEMP1
- P. falciparum erythrocyte membrane protein 1
- surface of mature RBCs infected with P. falciparum = clonal antigenic variation = bind several different cell receptors
- sequestration for evading spleen-dependent killing
- antigenic variation for evading antibody-dependent killing

21
Q

PfEMP1

A
  • binds to complement receptor CR1 + blood group antigen A
  • binds to CD36 on endothelial cells, monocytes, platelets
  • binds to ICAM-1 in brain
  • binds to chondroitin sulfate A (CSA) on syncytiotrophoblasts (placenta ,,, different kind of PfEMP1?)
  • may bind to downregulate dendritic cell function
22
Q

lack of glucose and oxygen can lead to this

A

cerebral malaria

23
Q

how do we get sick from Plasmodium?

A

after binding, rosetting and antigen accumulation = increased production of inflammatory cytokines like TNF-alpha = upregulation of ICAM-1 = more sequestration (CYCLE!)
- decreased glucose and O2 = hypoglycemia, also depletion of glycogen and also cerebral malaria

24
Q

anemia from malaria is due to

A

lysis of RBC

25
Q

in malaria, release of TNF-alpha from immune cells is associated with…

A

decreased EPO = decreased production of new RBCs

26
Q

earliest antimalarial drug

A

quinine
- bark of cinchona tree

27
Q

chloroquine

A

synthetic antimalarial
- forms complexes ith heme = toxic for Plasmodium

28
Q

due to resistance, what is now used to treat malaria?

A

artemisinin based combo therapy or ACT
- artemisinin = old chinese herbal remedy
- combine this w newer versions of antimalarials

29
Q

only vaccine we have for malaria

A

RTS.S/A01 vaccine for children

  • induces Ab production to cicumsporozoite protein found on sporozoites
  • reduces infectivity of sporo but no effect on other life forms
  • no reduction in transmission
30
Q

the most effective preventative method for malaria

A

bed nets impregnated with insecticide

31
Q

Babesia

A

apicomplexan similar to Plasmodium

32
Q

vector for Babesia

A

Ixodes scapularis (tick)

33
Q

who is most susceptible to Babesia?

A
  • > 50 yrs
  • diabetics, immunocompromised
  • location where ticks are prevalent
  • can be transmitted by blood transfusions and to fetus transplacentally
34
Q

symptoms of Babesia

A
  • fever (>40C)
  • headache
  • myalgia (muscle pain)
  • anorexia
  • abdominal pain (if splenic rupture)
35
Q

when do symptoms of Babesia appear?

A

1-4 wks after tick bite
nymph staged tick must be attached for at least 36 hrs

36
Q

how long until Babesia sporozoites are transmitted in body

A

after 72 hrs

37
Q

mixed infections with tickborne agents

A

Babesia and lyme disease = more severe!

38
Q

how does Babesia cause disease?

A
  • sporozoites injected by nymph ticks = attach RBC
  • AMA1 or apical membrane 1 on sporos attach to glycosylphosphatidy… anchored proteins in RBC
    = once inside RBC = trophozoites = binary fission to make 2-4 merozoites
  • release of meros = hemolysis
    no exoerythrocytic stage
39
Q

how to diagnose Babesia?

A

blood smears with Giemsa like Plasmodium

PCR

serology test (antibodies to Babesia); not ass good if no IgM found (ongoing infection)

40
Q

treatment for Babesia

A

combination of an antimalarial and an antibiotic like clindamycin or azithromycin

41
Q

T or F. There is a vaccine available for Babesia

A

F!

42
Q

how to control Babesia?

A

control tick vectors
testing blood products

43
Q
A

MMI 426 (20 decks)

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