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Biomedical Parasitology > Malaria > Flashcards

Malaria Flashcards

1
Q

kills one child in 20

before the age of 5

A

Malaria

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2
Q

how many people are affected with Malaria every year?

A

Every year, more than 225 million people become

severely ill with malaria

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3
Q

How many people die from malaria?

A

800,000 people die each year.

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4
Q

Based on
epidemiological
considerations Alphonse
Laveran concluded what?

A

“Swamp fevers are due

to a germ”

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5
Q

He discovered Malaria’s life cycle

A

Alphonse Laveran, 1880

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6
Q

Who is Giovanni Maria Lancisi?

A

He first described a characteristic black pigmentation of the brain and
spleen in the victims of malaria. Lancisi linked malaria with poisonous
vapours of swamps or stagnant water on the ground

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7
Q

Who is Camillo Golgi?

A 
an Italian
neurophysiologist, established that
there were at least two forms of
the disease, one with tertian
periodicity (fever every other day)
and one with quartan periodicity
(fever every third day).
• He prepared high quality
micrographs and described the
asexual replication of the parasite
within the red blood cell
• He observed that fever coincided
with the rupture and release of
merozoites into the blood stream.
• He was awarded a Nobel Prize in
Medicine for his discoveries in
neurophysiology in 1906.
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8
Q

Who is Patrick Manson?

A

Discovered the transmission of Wucheria

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9
Q

He demonstrated that mosquitos are also involved in the transmission of human malaria

A

battista Grassi

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10
Q

He identified the major vectors of plasmodium

A

Battista Grassi

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11
Q

He shows how plasmodium enters an orgnism

A

Ronald Ross, 1902

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12
Q

The first one to notice parasites in the blood of a patient suffering from malaria

A

Alphonse Laveran, 1907

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13
Q

Use plasmodium as a treatment for dementia

A

Junius Wagner-Jauregg. 1927

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14
Q

Discovered the high efficiency of DDT as a contact poison against several arthropods

A

Paul Muller

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15
Q

Discovered the structure of the nervous system - Malaria.

A

Camilo Golgi

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16
Q 
The parasite
spends part of
its life cycle
inside the red
blood cells
A

Plasmodium

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17
Q 
Humans act as
intermediate
hosts where
sexual and
asexual forms of
the parasite are
found.
A

Plasmodium

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18
Q

The parasite is transmitted by the
bite of the female anopheline
mosquito which acts as the
definitive host

A

Plasmodium

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19
Q

malignant tertian malaria. Tropics.

Accounts for 50% of all malaria cases. Most pathogenic.

A

Plasmodium falciparum:

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20
Q

causes benign tertian malaria. Tropics,
subtropics, and some temperate regions. Mostly found in Asia. About 43%
of all malaria cases. Some Africans are refractory to infection because
they lack the red cell receptor that the parasite use to enter.

A

Plasmodium vivax:

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21
Q

quartan malaria. Subtropics. About 7% of

malaria cases

A

Plasmodium malariae:

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22
Q

mild tertian malaria. West Africa,

occasionally East Africa. Rare. It was used to treat syphilis

A

Plasmodium ovale

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23
Q

Invades erythrocytes

A

Merozoite

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24
Q

invades mosquito salivary gland and liver cells

A

sporozites

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25
Q

invades mosquito’s gut epithelial cells

A

ookinete

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26
Q

blood forms what when infected with plasmodium?

A 
merozoites
rings
trophozoite
schizonts
"MRTS"
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27
Q

Mosquito forms what when infected with plasmodium?

A 
gametocytes
oocyst
ookinete
sporozoite
"GOOS"
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28
Q

Describe Malaria’s life cycle

A 
zygote
ookinete
oocyst
sporozoite
mosquito's salivary gland
female mosquito injects sporozoites 
sporozoites invade liver cells
sporozoites turn to merozoite
schizont ruptures and mezoroites are released into the blood
merozoite transform into ring stage trophozoite and some become gametocytes.
mosquito bites you and sucks blood with gametocytes.
Release eggs infected with plasmodium.
CYCLE GOES ON
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29
Q

How many days does it take for sporozoite development in mosquitoes?

A

10-14 days

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30
Q

made up of thousands of merozoites

A

schizont

31
Q

What is a sporozoite?

A

• 10-15 μm long
• 2 sporozoite surface proteins contain hepatocyte
adhesive domains (CSP circumsporozoite protein and
TRAP thrombospondin related anonymous protein)
• Both proteins bind to glycosoaminoglycans on the surface
of hepatocytes and this binding is important for entry

32
Q

schionts take how many days to develop?

A

5-7 days

33
Q 
the parasite
undergoes
multiple rounds
of mitosis to
generate nuclei
that are
assembled into
the daughter
merozoites.
At 48 hours, the
infected
erythrocyte
ruptures to
release
merozoites.What is this structure?
A

schizogony

34
Q

What is the ring stage?

A 
1st 14-16 hours
spent as ring
stage, or young
trophozoite
• little to no Hb
degradation
• only form seen in
blood films of P.
falciparum
35
Q

What is a trophozoite?

A

It forms inside the RBC after 10-18 hours post infection.

It takes up Hg and digest it in a food vacuole

36
Q

SCHIZOGONY

A 
form of asexual
reproduction in which multiple
mitoses take place, followed by
cytokinesis resulting in multiple
daughter cells
• multiple mitoses produce 20-24 nuclei
• once nuclei & organelles replicated
cytokinesis occurs
• rupture of RBC membrane releases
merozoites
37
Q

What is gamogony?

A

Formation of gametocytes

38
Q 
form of asexual
reproduction in which multiple
mitoses take place, followed by
cytokinesis resulting in multiple
daughter cells
• multiple mitoses produce 20-24 nuclei
• once nuclei & organelles replicated
cytokinesis occurs
• rupture of RBC membrane releases
merozoites
A

Ookinete

39
Q

These invade the mosquito’s salivary gland

A

sporozoites

40
Q

Clinical Symptoms of Malaria

A

patient’s symptoms and physical examination.
The first symptoms (fever, chills, sweats, headaches, muscle pains, nausea
and vomiting) are not specific.
In severe malaria, clinical findings are more striking (confusion, coma,
neurologic focal signs, severe anemia, respiratory difficulties.

41
Q

Transmission of Malaria

A

Female anopheles mosquitoes, and blood transfusion (ei, organ transplant, sharing of needles)
** Transmission is greater in warmer areas

42
Q

Species of anopheles present in the area influence the intensity of transmission. Might be resistant to insecticides

A

anopheles mosquitoes

43
Q

Malaria and sickle cell, Malaria and negative duffy blood group

A

People with sickle cell are resistant to plasmodium

44
Q

Prevention of Malaria

A

use of bed nets, getting rid of stagnant water, cleanliness, insecticides

45
Q

Malaria and pregnancy

A

severe maternal anemia
delivery of low infant
fetal loss

46
Q

Malaria and HIV

A 
HIV-associated immunosuppression
contributes to more and worse malaria
and its consequences in adults, pregnant
women, and children.
• Malaria contributes to stimulus of HIV
replication and possibly(?) to its
consequences: disease progression,
transmission in adults, and mother to
child transmission.
• Co-infection with Malaria and HIV in
pregnant women contributes to anemia,
low birth weight, and their risk for poor
infant survival.
• Malarial anemia in children too frequently
requires blood transfusion and may still
lead to HIV
transmission
47
Q

President’s Malaria Initiative (PMI)

A

represents an
historic five-year expansion of U.S. Government resources
to fight malaria in the region most affected by the disease.
• $30m (2006) - $500m (2010) in malaria funding to this
Initiative with the goal of reducing malaria-related deaths by
50% in 15 focus countries.

48
Q

Human Malaria is what?

A

a blood disease but can causes pathology in a variety of most organs and tissues

49
Q

What causes malaria?

A

It is due to the parasite’s development within the RBC

50
Q

Incubation period

A

9-14 days

51
Q

What is cerebral malaria?

A

is
characterized by multiple brain
hemorrhages (vessel rupture
and bleeding)

52
Q

What is the pathogenesis of falciparum malaria?

A

Parasite infected RBC’s become ‘sticky’ and
adhere to endothelial cells
• Unique to falciparum malaria
• This phenomenon takes about 10-12 hours to
develop after parasite invasion
• Under high flow this first results in rolling and
then in attachment.

53
Q

seems to be
the main culprit for
pathogenesis

A 
Cytoadherance.
Infected RBCs will adhere to
the endothelium as well as to
each other and cause
clogging and hemorrhaging
54
Q

The wonder drug

A

Chloroquine

55
Q 
a synthetic
quinine analog developed
by German and American
chemists during WWII, was
a very potent drug that was
cheap to make, stable, and
had no serious side effects
A

Chloroquine

56
Q

Antifolates as malaria drugs

A 
The synthesis of certain
building blocks of DNA
requires reduced folate (more
specifically the synthesis of
dTMP)
• No reduced folate -- no DNA
• The malaria drug Fansidar
uses a drug combination to
hit the same target pathway
twice
• Combinations that are more
effective than the sum of their
individual activities are called
synergistic.
57
Q

Human Malaria is what?

A

a blood disease but can causes pathology in a variety of most organs and tissues

57
Q

Human Malaria is what?

A

a blood disease but can causes pathology in a variety of most organs and tissues

58
Q

What causes malaria?

A

It is due to the parasite’s development within the RBC

58
Q

What causes malaria?

A

It is due to the parasite’s development within the RBC

59
Q

Incubation period

A

9-14 days

59
Q

Incubation period

A

9-14 days

60
Q

What is cerebral malaria?

A

is
characterized by multiple brain
hemorrhages (vessel rupture
and bleeding)

60
Q

What is cerebral malaria?

A

is
characterized by multiple brain
hemorrhages (vessel rupture
and bleeding)

61
Q

What is the pathogenesis of falciparum malaria?

A

Parasite infected RBC’s become ‘sticky’ and
adhere to endothelial cells
• Unique to falciparum malaria
• This phenomenon takes about 10-12 hours to
develop after parasite invasion
• Under high flow this first results in rolling and
then in attachment.

61
Q

What is the pathogenesis of falciparum malaria?

A

Parasite infected RBC’s become ‘sticky’ and
adhere to endothelial cells
• Unique to falciparum malaria
• This phenomenon takes about 10-12 hours to
develop after parasite invasion
• Under high flow this first results in rolling and
then in attachment.

62
Q

seems to be
the main culprit for
pathogenesis

A 
Cytoadherance.
Infected RBCs will adhere to
the endothelium as well as to
each other and cause
clogging and hemorrhaging
62
Q

seems to be
the main culprit for
pathogenesis

A 
Cytoadherance.
Infected RBCs will adhere to
the endothelium as well as to
each other and cause
clogging and hemorrhaging
63
Q

The wonder drug

A

Chloroquine

63
Q

The wonder drug

A

Chloroquine

64
Q 
a synthetic
quinine analog developed
by German and American
chemists during WWII, was
a very potent drug that was
cheap to make, stable, and
had no serious side effects
A

Chloroquine

64
Q 
a synthetic
quinine analog developed
by German and American
chemists during WWII, was
a very potent drug that was
cheap to make, stable, and
had no serious side effects
A

Chloroquine

65
Q

Antifolates as malaria drugs

A 
The synthesis of certain
building blocks of DNA
requires reduced folate (more
specifically the synthesis of
dTMP)
• No reduced folate -- no DNA
• The malaria drug Fansidar
uses a drug combination to
hit the same target pathway
twice
• Combinations that are more
effective than the sum of their
individual activities are called
synergistic.
65
Q

Antifolates as malaria drugs

A 
The synthesis of certain
building blocks of DNA
requires reduced folate (more
specifically the synthesis of
dTMP)
• No reduced folate -- no DNA
• The malaria drug Fansidar
uses a drug combination to
hit the same target pathway
twice
• Combinations that are more
effective than the sum of their
individual activities are called
synergistic.

Biomedical Parasitology (6 decks)

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