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Diagnostic Parasitology > (M) Plasmodium (lecture-based) > Flashcards

(M) Plasmodium (lecture-based) Flashcards

Dr. Jasper Pablo coverage

1
Q

Phylum

A

Sporozoa (formerly known as Apicomplexa)

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2
Q

Class

A

Sporozea

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3
Q

Subclass

A

Coccidia

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4
Q

Superorder

A

Eucoccidea

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5
Q

Order, Suborder and Family of Plasmodium

A

Haemosporida, Aconoidna, Haemospiridae

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6
Q

The malaria antigen was detected in? dates back from 3200-1304 BC

A

Egyptian remains

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7
Q

Indian writings of the Vedic period (1500 - 800 BC) called malaria the?

A

King of diseases

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8
Q

In 270 BC, who linked tertian and quartan fevers with splenomegaly and blamed malaria’s headaches, chills, and fevers on demons in Chinese literature

A

Nei Chin

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9
Q

According to Nei Chin, what are the 3 demons?

A

one carrying a hammer (headaches), another carrying a pail of water (chills), and the third a stove (fever),

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10
Q

He mentions Malaria in The Iliad, as foes Aristophanes in The Wasps, and Aristotle, Plato, and Sophocles

A

Homer

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11
Q

He described the disease in a medical text in the 4th or 5th century BC

A

Hippocrates

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12
Q

This person may have died of a Malaria infection at age 30

A

Alexander the great

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13
Q

TOF. The greek physician, Torti, coined the term Malaria in 1718.

A

F (italian)

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14
Q

Italian word Malaria which means?

A

Bad air

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15
Q

Roman physicians believed that the disease was caused by?

A

malignancies in the swamp air

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16
Q
  • Definitively showed that Malaria is caused by another type of single-celled organism, a protozoan of the Plasmodium family, which attacks RBC’s
  • 1907 Nobel Prize Winner in Physiology or Medicine
A

CHARLES LOUIS ALPHONSE LAVERAN

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17
Q

What did Laveran discovered?

A

protozoan plasmodium

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18
Q

He found out that the plasmodium is the causative agent of Malaria

A

CHARLES LOUIS ALPHONSE LAVERAN

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19
Q

Over how many species of plasmodium have been described?

A

200

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20
Q

Plasmodium species are limited to five

A

Plasmodium falciparum
P. ovale
P. vivax
P. malariae
P. knowlesi

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21
Q

still considered a zoonotic plasmodium, i.e. it is a disease of animals such as Macaque monkeys

A

Plasmodium knowlesi

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22
Q

In the 2022 CDC update, Malaria has remained to be endemic in the ff regions:

A
  1. Central and South America
  2. Africa
  3. Middle East
  4. Asia

CA SA A A M E

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23
Q

TOF. In 2023, the Department of Health (DOH) reported a decrease in the cases of Malaria

A

F (increase)

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24
Q

only province in the Philippines where Malaria is endemic

A

Palawan

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25
Q

there are more regions where Malaria has become endemic, other than palawan

A

Occidental mindoro and Sultan kudarat

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26
Q

Species

  • most widespread
  • can be life threatening
A

P. vivax

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27
Q

primary Malaria species of public health importance in the Philippines are?

A

P. falciparum and P. vivax

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28
Q

This species comprise 88% and 9% of the total indigenous Malaria cases

A

P. falciparum and P. vivax

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29
Q

The vectors (6)

A
  • Anopheles minimus
  • A. flavirostris
  • A. litoralis
  • A. maculatus
  • A. mangyanus
  • A. balabacensis
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30
Q

P. vivax

A. Malignant Tertian Malaria
B. Benign Tertian Malaria
C. Ovale Tertian Malaria
D. Quartan Malaria
E. Quotidian Malaria

A

B. Benign Tertian Malaria

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31
Q

P. vivax

TOF. Widespread location is in Sub-Saharan Africa, Southeast Asia, South America.

A

F (Southeast Asia and Latin America; for P. ovale ‘yan)

isipin mo nalang na may viva max sa asia at latin america

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32
Q

For one to be infected with P. vivax, one must possess?

A

Duffy antigens

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33
Q

p. vivax

produces what color?

A

Yellow-brown colored pigment

Schuffner dots

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34
Q
  • Last of the malaria parasites of humans to be described
  • Rarely causes severe illness or death
  • Relatively unusual to acquire infections outside Africa
A

P. ovale

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35
Q

P. ovale

AKA
A. Malignant Tertian Malaria
B. Benign Tertian Malaria
C. Ovale Tertian Malaria
D. Quartan Malaria
E. Quotidian Malaria

A

C

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36
Q

PLASMODIUM OVALE

Endemic

A

West africa & South africa

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37
Q

PLASMODIUM OVALE

TOF. There have been rare cases of P. ovale infection in the Philippines, other Asian countries, and in Papua New Guinea.

A

T

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38
Q

PLASMODIUM OVALE

Colored pigment

A

Dark brown called James’ pigment

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39
Q
  • this species has the lowest incidence rate out of all the plasmodium
  • Maximum parasite count is low
A

PLASMODIUM MALARIAE

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40
Q

Most immunogenic when the infection produces an immune complex deposition in the kidneys, which is associated with nephrotic syndrome

A

PLASMODIUM MALARIAE

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41
Q

PLASMODIUM MALARIAE

A. Malignant Tertian Malaria
B. Benign Tertian Malaria
C. Ovale Tertian Malaria
D. Quartan Malaria
E. Quotidian Malaria

A

D

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42
Q

PLASMODIUM MALARIAE

it’s growth and development are suppressed by

A

P. falciparum and P. vivax

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43
Q

PLASMODIUM MALARIAE

Colored Pigment

A

Brown black called Ziemann’s pigment

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44
Q

PLASMODIUM MALARIAE

Widepsread in?

A

Sub-Saharan Africa, Southeast Asia

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45
Q
  • Predominant species in the world
  • Can be life-threatening
A

P. falciparum

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46
Q

PLASMODIUM FALCIPARUM

AKA
A. Malignant Tertian Malaria
B. Benign Tertian Malaria
C. Ovale Tertian Malaria
D. Quartan Malaria
E. Quotidian Malaria

A

A. Malignant Tertian Malaria

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47
Q

PLASMODIUM FALCIPARUM

Pigment

A

Black (maurer’s pigment)

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48
Q

Life cycle

Agent

A

Plasmodium

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49
Q

Life cycle

Intermediate host

A

Human

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50
Q

Life cycle

Definitive host

A

Anopheles minimus

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51
Q

Life cycle

Clinical illness

A

Malaria

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52
Q

Life cycle

Vector

A

Infected Female Anopheles mosquito

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53
Q

Life cycle

Infective form

A

Sporozoites

however, trophozoites may also be infective

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54
Q

Life cycle

Reservoir

A

Infected Humans

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55
Q

Life cycle

Source of Infection

A
  • mainly, saliva of infected female anopheles mosquito containing sporozoites
  • infected blood of man containing trophozoites
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56
Q

Enumerate the mosquito spp.

A
  1. Aedes/albopictus
  2. Culex tarsalis
  3. Anopheles
  4. Female anopheles mosquitos
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57
Q

MOSQUITO SPP.

  • Characterized by its sharp abdomen and striped legs
  • bites during daytime
  • breeds on stagnant water
A

Aedes/Albopictus

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58
Q

AEDES / ALBOPICTUS

Carries what diseases?

A
  • Dengue
  • Chikungunya
  • Yellow fever
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59
Q

MOSQUITO SPP.

  • blunt abdomen and striped legs
  • bites during the night
  • breeds on polluted water
A

Culex tarsalis

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60
Q

Culex tarsalis

Diseases

A

West nile virus

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61
Q

MOSQUITO SPP.

  • dark blunt abdomen and dark legs
  • bites before dawn and right after darkness
  • breeds in clean, slow-moving water
  • Holds the record for the deadliest animal, killing around 1 million people per year
A

Anopheles

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62
Q

Anopheles

Most common form

A
  • A. minimus
  • A. flavirostris
  • A. maculatus
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63
Q

MOSQUITO SPP.

  • Accounts for >95% of transmission globally
  • body is dark brown to black in color
  • When resting, the stomach of the mosquito points upward, rather than being even with the surrounding surface like most mosquitoes
  • Most active before dawn and after dusk sets
  • Clean, slow-moving water is considered prime
    breeding grounds
A

Female Anopheles mosquitos

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64
Q

Female anopheles mosquitos

3 sections of the body

A
  • head
  • thorax
  • abdomen
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65
Q

TOF. ASEXUAL reproduction occurs in the INTERMEDIATE host while SEXUAL reproduction occurs in the DEFINITIVE host.

A

T

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66
Q

HOST

TOF.
Asexual reproduction = humans
Sexual = the vector

A

T

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67
Q

HOST

  • Asexual multiplication occurs
  • Sexual differentiation occurs
A

INTERMEDIATE HOST

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68
Q

INTERMEDIATE HOST

When asexual multiplication occurs, this process is called schizogony which forms?

A

schizonts

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69
Q

INTERMEDIATE HOST

Sexual differentiation is also a process called?

A

gametogony

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70
Q

INTERMEDIATE HOST

In sexual differentiation, there’s a production of?

A

microgametocytes and
macrogametocytes

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71
Q

microgametocytes (male or female)

A

male

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72
Q

macrogametocytes (male or female)

A

female

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73
Q

INTERMEDIATE HOST

In sexual differentiation, there’s a presence of this which are infective to the definitive host

A

immature sex cells

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74
Q

DEFINITIVE HOST

TOF. Asexual multiplication and sexual differentiation occurs.

A

F (sexual multiplication only)

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75
Q

DEFINITIVE HOST

The sexual multiplication is also called?

A

Sporogony

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76
Q

DEFINITIVE HOST

There’s a production of what that is infective to the intermediate host

A

Sporozoites

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77
Q

SOURCE OF INFECTION

  • Transfusion of infected blood
  • transplacental
  • infected needles
A

Trophozoites

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78
Q

SOURCE OF INFECTION

  • Bite of infected female Anopheles mosquito
  • Most common form of transmission
A

Sporozoites

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79
Q

INCUBATION PERIOD

P. falciparum

A

10-14 days

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80
Q

INCUBATION PERIOD

P. malariae

A

18 days - 6 weeks

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81
Q

INCUBATION PERIOD

P. vivax

A

10-14 days

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82
Q

INCUBATION PERIOD

P. ovale

A

10-14 days

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83
Q

pls study the life cycle of plasmodium

A

thx

i suggest yung module basahinniyo, mas detailed

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84
Q

MOSQUITO STAGE - SEXUAL STAGE

End product:

A

sporozoite

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85
Q

Summarize the development of sporogony

A

Zygote > Ookinete > Oocyst > Sporozoite

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86
Q

MOSQUITO STAGE - SEXUAL STAGE

  • The mosquito will bite an infected human
  • As it sucks the human’s blood, it will ingest the male and female gametocytes
  • The gametocytes travel to the mosquito’s gut, where the male gametocyte will fertilize the female gametocyte
  • Once the female gametocyte has been fertilized, it will now become a?
A

Zygote

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87
Q

MOSQUITO STAGE - SEXUAL STAGE

  • After 6-8 hours, the zygote will mature into an invasive motile?
  • From the gut of the mosquito, it will penetrate the epithelium of the gut and travel to the circulatory and lymphatic system of the mosquito
A

Ookinete

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88
Q

MOSQUITO STAGE - SEXUAL STAGE

  • Once outside the gut, ookinete, it will transform into the?
  • This will travel from the blood and lymph fluid into the salivary glands
  • It will mature into a sporozoite
A

oocyst

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89
Q

MOSQUITO STAGE - SEXUAL STAGE

  • End product of sporogony
  • Once they are released from the mosquito, they are ready to infect humans
A

Sporozoite

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90
Q

MOSQUITO STAGE - SEXUAL STAGE

The whole sexual cycle usually takes?

A

8-30 days

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91
Q

TOF. After 6 days of being bitten with anopheles mosquito, it will develop into malaria.

A

F (Plasmodium has not yet reached 7 days of development)

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92
Q

HUMAN STAGE - ASEXUAL STAGE

4 stages

A
  • Primary Exoerythrocytic / Pre-Erythrocytic / Hepatic
  • Erythrocytic
  • Gametogony
  • Secondary Exoerythrocytic / Dormant
  • Schizogony
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93
Q

HUMAN STAGE - ASEXUAL STAGE

Once the sporozoites reach the liver, it will transform to?

A

Sporozoite > Schizont > Merozoite

94
Q

HUMAN STAGE - ASEXUAL STAGE

pls study the hepatic stage in detail

A

ok thanks

95
Q

Primary Exoerythrocytic / Pre-Erythrocytic / Hepatic

how will the sporozoites enter the blood vessels once its embedded in the dermis?

A

traverse the epithelial cells and fibroblasts and enter the blood vessels

96
Q

Primary Exoerythrocytic / Pre-Erythrocytic / Hepatic

Why do sporozoites prefer the liver?

A

Due to the interaction of the Plasmodium Circumsporozoite protein and Heparan Sulfate Proteoglycan of the liver

97
Q

Primary Exoerythrocytic / Pre-Erythrocytic / Hepatic

The plasmodium will not immediately infect the parasite, they will first become?

A

transient vacuoles until they find a suitable cell to infect

98
Q

Primary Exoerythrocytic / Pre-Erythrocytic / Hepatic

Once the suitable cell has been found they will transform into a?

A

parasitophorous vacuole and begin its maturation

99
Q

Primary Exoerythrocytic / Pre-Erythrocytic / Hepatic

Once it fully matures, it will be released from the liver into the blood as?

A

hepatic merozoites

marks the end

100
Q

ERYTHROCYTIC STAGE

STUDY IN DETS PLS

A

jfkjdckdfc

101
Q

ERYTHROCYTIC STAGE

How does this begin?

A

Begins once the hepatic merozoites reach the blood

because only RBC has the receptor sites for merozoites

102
Q

ERYTHROCYTIC STAGE

The erythrocytic merozoites remain and continue to mature in the?

A

RBC

103
Q

ERYTHROCYTIC STAGE

what (2) occur in this stage

A

Schizogony and Gametogony

104
Q

ERYTHROCYTIC STAGE

How does the stage develop?

step by step

A

Ring form > Young Trophozoite > Mature Trophozoite > Schizont > Merozoites

105
Q

ERYTHROCYTIC STAGE

the primary morphological form that is found in RBC’s

A

ring form

106
Q

ERYTHROCYTIC STAGE

  • The presence of a cytoplasmic ring with a single chromatin dot
  • At this point there is no visible cytoplasm
A

ring form

107
Q

ERYTHROCYTIC STAGE

  • Cytoplasmic ring with single chromatin dot
  • There is the presence of a bluish cytoplasm, but it is barely conspicuous
A

Young Trophozoite

108
Q

ERYTHROCYTIC STAGE

  • Cytoplasmic ring with single chromatin dot, may become ameboid in shape
  • Cytoplasm has become greater and more conspicuous
  • Malarial pigments may begin to become
    apparent at this stage
  • Changes in shape and size may also become apparent at this stage
A

Growing trophozoite

109
Q

ERYTHROCYTIC STAGE

  • Cytoplasmic ring with a single chromatin dot
  • Cytoplasm is very conspicuous
A

Mature Trophozoite

110
Q

ERYTHROCYTIC STAGE

  • Once the nucleus begins to divide
  • A mature form of this will contain merozoites which will be released into the bloodstream
A

Schizont

111
Q

ERYTHROCYTIC STAGE

  • Will lyse the RBC and be released into the bloodstream which can go into one of two directions
  • Reinfect other RBCs or Differentiate into gametocytes (Gametogony)
A

Erythrocytic merozoite

112
Q

GAMETOGONY

When does the life cycle restart?

A

once ingested by the anopheles mosquito

113
Q
  • Secondary Exoerythrocytic /Dormant schizogony
  • Only occurs in P. vivax and P. ovale
  • Sporozoites may remain dormant in the liver and may become active even after years of initial infection
  • Once activated it will become a merozoite
  • Responsible for relapse
A

HYPNOZOITE

114
Q

Sporozoite or Trophozoite

Route of entry: Mosquito bite

A

Spo

115
Q

Sporozoite or Trophozoite

Pre-erythrocytic schizogony: Absent

A

Tro (skips to erythrocytic stage)

116
Q

Sporozoite or Trophozoite

Pre-erythrocytic schizogony: present

A

spo

117
Q

Sporozoite or Trophozoite

Hepatomegaly: Occurs

A

Spo

sa tropho walay

118
Q

Sporozoite or Trophozoite

Incubation period is long

A

Sporo

119
Q

Sporozoite or Trophozoite

Incubation period is short

A

Tro

120
Q

Sporozoite or Trophozoite

Exoerythrocytic schizogony: Absent

A

Tro (present kapag sporo)

121
Q

Sporozoite or Trophozoite

Relapse may occur

A

Spo (does not occur sa tro)

122
Q

Sporozoite or Trophozoite

Can be radically cured, no EE* forms

A

Tro (Schizonticidal drugs: in sporo, there’s no radical cure because of the presence of EE* forms)

123
Q

○ No pre erythrocytic stage
○ No exoerythrocytic schizogony
○ Incubation period will be shorter

A

Trophozoite

124
Q

Majority of the symptoms we can see in malaria
infections are due to (2)?

A

○ Erythrocyte changes
○ Host response

125
Q

TOF. Both infected and uninfected RBCs can cause symptoms.

A

T

126
Q

Familiarize the pathophysiology

A

thx uli

127
Q

Pathophysiology

Infected RBCs result to?

4

purple

A

Toxic mediators
Phagocytosis
Anemia
Adhere to blood vessels

128
Q

Uninfected RBC results to?

2

A
  • Loss of deformability
  • Clearance and destruction of uninfected RBCs
129
Q

Erythrocytic stage of malarial infection

A

Uninfected and Infected RBCs

130
Q

What stage invades the RBC?

A

merozoites

hepatic

131
Q

TOF. Heme is toxic to RBC.

A

T

132
Q

Heme degradation

What happens to the RBC when there’s a presence of heme?

2

A

○ RBC may die
○ Plasmodium will die alongside the RBC

133
Q

HEME DEGRADATION

The plasmodium will convert heme to a non-toxic material called?

A

hemozoin pigment

134
Q

enumrate the hemozoin pigments

A

○ Maurer’s
○ Schuffner’s
○ Ziemann’s
○ James’s

135
Q

When RBC’s become prone to sticking to each other it will lead to?

A

blockage of capillaries and
venules

136
Q

ALTER RBC MEMBRANE

RBC will be more
A. antigenic
B. less deformable
C. more irregular in shape.
D. AOTA

A

D

137
Q

ALTER RBC MEMBRANE

When infected RBCs compact with uninfected RBCs

A

Rosette formation

138
Q

ALTER RBC MEMBRANE

When infected RBCs compact with other infected RBCs

A

Agglutination

139
Q

HOST RESPONSE

Which does not belong:
A. Activation of non-specific defense mechanism of the Spleen
B. Removal infected RBCs
C. Removes damaged ring form parasites
D. RBCs return to the circulation with shortened survival
E. Escaped RBCs are destroyed when Schizont ruptures

A

B (Removal of parasitized and uninfected RBCs)

the following are actual host response

140
Q
  • Non-specific immunity
A

ACQUIRED IMMUNITY

141
Q

TOF. Multiple infections of Malaria do not confer lifelong immunity.

A

T

142
Q

CLINICAL PRESENTATION

densities of parasitic blood for symptomatic stage of infection to begin

A

more than 50/uL

143
Q

FEBRILE ATTACK

Periodic attacks of fever due to release of toxic metabolites of the parasite formed during each?

A

erythrocytic schizogony

release of merozoites = fever

144
Q

FEBRILE ATTACK

Malarial fever maintains a specific pattern except in?

A

Falciparum

145
Q

Febrile attack

Stages of malaria (3)

A

Cold, hot and sweating stage

146
Q

Stages of malaria

■ Lasts from 15 mins to 1 hr
■ Corresponds to the release of
merozoites
■ Dividing generation of parasites
rupture their host RBCs and escape
into the blood

A

Cold stage

147
Q

Stages of malaria

■ Lasting 1 to 4 hrs
■ Spiking fever that frequently
reaches 40 deg celsius or more
■ Parasites invade new RBCs

A

Hot stage

148
Q

Stages of malaria

Fever spontaneously comes down
over several hours and the patient sweats profusely

A

Sweating stage

149
Q

PATTERN OF FEVER

Subtertian/Malignant tertian, Benign tertian, Ovale tertian

A

48hrs

150
Q

PATTERN OF FEVER

Quotidian malaria

A

24 hrs

151
Q

PATTERN OF FEVER

Quartan Malaria

A

72 hours

152
Q

Can be normocytic, hypochromic, or microcytic hypochromic type

A

ANEMIA

153
Q

ANEMIA

○ Shortened RBC life span
○ Erythrophagocytosis by macrophages
○ Complement-mediated hemolysis
○ Loss of complement regulatory proteins from the RBC surface

A

increased destruction

154
Q

ANEMIA

○ Morphological abnormalities in red cell precursors
○ Dyserythropoiesis
○ Inadequate reticulocyte production
○ Effect of parasite factors (hemozoin, malaria toxins)
○ Effects of inflammatory cytokines
○ Inadequate EPO production

A

DECREASED PRODUCTION

155
Q

DECREASED PRODUCTION or INCREASED DESTRUCTION

○ Morphological abnormalities in red cell precursors
○ Dyserythropoiesis
○ Inadequate reticulocyte production

A

DECREASED PRODUCTION

156
Q

DECREASED PRODUCTION or INCREASED DESTRUCTION

○ Complement-mediated hemolysis
○ Loss of complement regulatory proteins from the RBC surface

A

increased

157
Q

DECREASED PRODUCTION or INCREASED DESTRUCTION

○ Shortened RBC life span
○ Erythrophagocytosis by macrophages

A

Increased

158
Q

DECREASED PRODUCTION or INCREASED DESTRUCTION

○ Inadequate reticulocyte production
○ Effect of parasite factors (hemozoin, malaria toxins)
○ Effects of inflammatory cytokines
○ Inadequate EPO production

A

decreased

159
Q

Clinical presentation

  • Due to enhanced immune response to the plasmodium
  • Aberrant immune response to antigenic stimulation
A

HYPERREACTIVE MALARIAL SPLENOMEGALY

160
Q

Associated with macroglobulinemia, the production of cytotoxic IgM antibodies to CD8+ lymphocytes, antibodies to CD5+ lymphocytes, and an increase in
the ratio of CD4+ to CD8+ cells

A

HYPERREACTIVE MALARIAL SPLENOMEGALY

161
Q

Stimulated lymphoid hyperplasia and clearance
activity

A

HYPERREACTIVE MALARIAL SPLENOMEGALY

162
Q

Enumerate complications

A
  • CEREBRAL MALARIA
  • BLACKWATER FEVER
  • QUARTAN MALARIAL NEPHROPATHY
163
Q

➢ Most common cause of coma and death in falciparum malaria
➢ Many parasitized cells can be found in the capillaries of the brain and in the late stages, hemorrhaging from small blood vessels can occur

A

CEREBRAL MALARIA

164
Q

The formation of this could be the cause of cerebral malaria, as there could be a blockage to the blood flow of the brain, mimicking a stroke

A

rosette formations and agglutination

165
Q
  • Patients may present with impaired consciousness, delirium, and/or seizures
  • Usual presentation is diffuse, symmetric encephalopathy, focal neurological signs are present
A

CEREBRAL MALARIA

166
Q

➢ Rare but acute condition in which there is a rapid and massive intravascular hemolysis of both parasitized and non-parasitized RBCs
➢ Results in hemoglobinemia and hemoglobinuria
➢ Urine appears dark-red to brown-black due to the presence of free hemoglobin
➢ Can occur in non-immune adults with severe falciparum malaria
➢ Previously thought to be a complication of quinine treatment

A

BLACKWATER FEVER

167
Q

➢ Nephrotic syndrome
➢ Chronic or repeated infections with P. malariae may
cause insoluble immune complex injury to glomerular basement membrane, resulting in nephrotic syndrome
➢ Characterized by albuminuria, low blood protein, generalized edema, asymptomatic proteinuria, renal failure, anemia, hepatomegaly, and hepatosplenomegaly
➢ Usually there is no treatment, as it responds poorly to antimalarial agents or glucocorticoids and cytotoxic drugs

A

QUARTAN MALARIAL NEPHROPATHY

168
Q

Which is correctly paired.
QMN = Hemoglobinemia
Cerebral = Rosette formations
Black water fever = Coma

A

Cerebral = = Rosette formations

169
Q

Diagnosis

  • Demonstration of malarial antigen, antibody, or nucleic acid sequence
  • Parasite itself is not demonstrated
A

Indirect

170
Q

Diagnosis

  • Demonstration of malarial parasite
  • Through this method identification is possible
A

Direct

171
Q

Enumarate direct diagnosis

A

PBS (Thick and Thin film)

172
Q

Gold standard in diagnosis of malarial infection

A

Peripheral blood smear (PBS)

173
Q

PBS

stain

A

Giemsa

174
Q

PBS

Best TIME for specimen collection

A

Prior to fever

175
Q

TOF. No parasites will be demonstrated if the timing in collecting specimen is during the peak of fever.

A

T

kaka-release lang raw kasi sa RBC

176
Q

Thick or Thin

  • dehemoglobinized* (lysed) RBCs
  • used in low parasitemia
  • More efficient detection of parasites (increased sensitivity)
  • Species can not be diagnosed
A

Thick

177
Q

Thick or thin

  • Consists of blood spread in a layer such that the thickness decreases progressively toward the feathered edge
  • Fixed in anhydrous methanol
  • Can not be used in low parasitemia
  • Species can be diagnosed
A

Thin

178
Q

➢ Dried thoroughly and stained without fixing
➢ Multiple layers of erythrocytes lay on top of one another and are lysed during the staining procedure, the thick film has the advantage of concentrating the
parasites
➢ Both parasites and WBCs are counted
➢ Minimum of 200 WBCs should be counted under oil immersion
➢ Before thick smear is judged negative, 100-200 fields should be examined

A

Thick blood smer

179
Q

TOF. Clinically, if there is presence of >50,000/uL parasites in the blood, the patient is at increased risk of severe malaria

A

F (>100,000/uL)

180
Q

Find the incorrect finding

vivax = Enlarged infected RBCs
malariae = band form
ovale = polymorphism
falciparum = multiple infection

A

Ovale (should be fimbriated or ragged RBCs)

181
Q

Enumerate the PCR used (4)

A
  1. Conventional
  2. Nested
  3. Real-time
  4. Multiplex
182
Q

○ Amplifies specific regions of the malaria parasite DNA, allowing for the detection of different plasmodium spp.
○ Requires gel electrophoresis to visualize the amplified DNA

A

Conventional PCR

183
Q

there is visible pigment in >20 of parasites or of phagocytosed pigment in >5 of PMNs (WBC)

A. average prognosis
B. good prognosis
C. acute prognosis
D. worse prognosis

A

D

184
Q

RAPID DIAGNOSTIC TEST

TARGET ANTIGEN: Plasmodium falciparum HRP2
PURPOSE: Detecting P. falciparum

A

HISTIDINE-RICH PROTEIN 2 (HRP2)

185
Q

TARGET ANTIGEN: Aldolase enzyme, present in all malaria species
PURPOSE: Typically used as a pan-malaria test to detect all malaria species, often combined with HRP2 of pLDH to differentiate species

A

ALDOLASE-BASED TEST

186
Q

ADVANTAGE: Can detect all species of malaria, providing a broad diagnostic tool
LIMIT:
* Generally lower sensitivity compared to HRP2 and pLDH tests
* Not commonly used as a standalone test due to its lower sensitivity specificity

A

ALDOLASE-BASED TEST

187
Q

RAPID DIAGNOSTIC TEST

ADVANTAGES:
* High sensitivity for P. falciparum, especially in high-transmission areas
* Long-lasting positive results, which can help track ongoing infections
LIMITATION:
* Can not detect non-falciparum species
* Persistence of HRP2 antigen in the blood can lead to false-positive results even after successful treatment
* HRP2 gene deletions in some P. falciparum strains can lead to false-negative results

A

HISTIDINE-RICH PROTEIN 2 (HRP2)

188
Q

RAPID DIAGNOSTIC TEST

TARGET ANTIGEN: Plasmodium lactate dehydrogenase (pLDH), which is produced by all malaria species
PURPOSE: Can be designed to detect all malaria species (pan-specific) or to differentiate between P. falciparum and non-falciparum species

A

PLASMODIUM LACTATE DEHYDROGENASE(PLDH)

189
Q

ADVANTAGE:
* Can distinguish between different species of malaria (e.g. falciparum vs non-falciparum)
* pLDH levels decrease rapidly after successful treatment, making it useful for monitoring treatment efficacy
LIMITATION:
* Generally less sensitive than HRP2-based tests for detecting P. falciparum
* pLDH levels drop quickly, which can result in false negatives if blood samples are taken too soon after treatment

A

PLASMODIUM LACTATE DEHYDROGENASE(PLDH)

190
Q

TARGET ANTIGEN: Detect multiple antigens, usually a combination of HRP2 and pLDH or HRP2 and Aldolase
PURPOSE: Designed to provide more comprehensive testing by detecting both P. falciparum and non-falciparum species

A

COMBINATION RDTS (MULTI-ANTIGEN TEST)

191
Q

ADVANTAGE:
* Improved diagnostic accuracy by combining multiple antigens
* can differentiate between falciparum and other species while detecting mixed infections
* useful in areas where multiple malaria species are prevalent
LIMIT:
* Higher cost compared to single-antigen RDTs
* Increased complexity may require more training for health workers

A

COMBINATION RDTS (MULTI-ANTIGEN TEST)

192
Q

PCR

○ Involves using two rounds of PCR to increase sensitivity and specificity
○ Especially used for detecting low parasitemia levels or mixed infections

A

Nested

193
Q

PCR

○ Quantifies the parasite DNA in real-time
using fluorescent dyes or probes
○ Provides both qualitative and quantitative results, offering high sensitivity and rapid
results

A

Real time PCR

194
Q

PCR

○ Allows for the simultaneous detection of multiple malaria species in a single reaction by amplifying different target DNA sequences using multiple sets of primers

A

Multiplex

195
Q

PCR

➢ Amplifies DNA at a constant temperature, avoiding the need for thermal cycling as in PCR
➢ It is designed to be simpler and faster, with results typically obtained in less than an hour

A

LOOP-MEDIATED ISOTHERMAL AMPLIFICATION

196
Q

➢ Amplifies RNA rather than DNA
○ RNA unstable so it is converted to DNA
➢ Useful for detecting the presence of viable parasites, as RNA is less stable than DNA and is only present in metabolically active parasites

A

QT NASBA

197
Q

➢ Variant of PCR that first converts parasite RNA into
a complementary DNA (cDNA) using reverse
transcription, followed by PCR amplification
➢ Often used to detect the presence of RNA transcripts, indicating active infections

A

RT-PCR

198
Q

➢ Post-PCR analysis method used to identify genetic variations in DNA of malaria parasites
➢ Detects differences in the melting temperature of DNA, which can indicate different species or genotypes

A

HIGH-RESOLUTION MELTING (HRM) ANALYSIS

199
Q

➢ Involves sequencing the entire genome or specific regions of the malaria parasite DNA
➢ Provides detailed information about the genetic makeup, drug resistance mutations, and transmission dynamics of malaria parasites

A

NEXT-GENERATION SEQUENCING (NGS)

200
Q

ADVANTAGE:
High sensitivity and specificity
Faster results (within an hour) and easier to perform -
does not sophisticated infrastructure or highly trained personnel require laboratory

DISADVANTAGE
Less versatile in differentiating between all malaria species
The colorimetric detection method used in some LAMP assays may be prone to subjective interpretation

A

LOOP-MEDIATED ISOTHERMAL AMPLIFICATION

201
Q

Advantage (A): High sensitivity, especially for detecting low levels of parasites
Can differentiate between active infections (as it detects RNA) and past infections (where DNA may still be present)
- Useful for monitoring treatment efficacy and detecting recrudescence or relapse
Disadvantage (D): Requires specialized equipment and reagents, making it less suitable for routing use in resource-limited settings
- RNA degradation can be a challenge, requiring careful sample handling and storage

A

QT-NASBA

202
Q

A: High sensitivity for detecting low parasite loads - Provides information about the viability and stage of the parasite, which can be useful in research and monitoring treatment efficacy
D: Requires more complex protocols and equipment compared to conventional PCR
- RNA handling and stability can be a limiting factor

A

RT PCR

203
Q

A: Rapid and cost-effective for species identification and genotyping after initial PCR amplification
Can identify mutations associated with drug resistance
D: Requires specialized equipment for melting analysis
Less sensitive than some other molecular methods for detecting very low parasite densities

A

HIGH-RESOLUTION MELTING (HRM) ANALYSIS

204
Q

A: Extremely high resolution for detecting subspecies, diversity, and resistance mutations
Valuable for research, epidemiological studies, and understanding transmission patterns
D: High cost, complex data analysis, and the need for advanced bioinformatics tools
Not practical for routine diagnostics in most clinical settings

A

NEXT-GENERATION SEQUENCING (NGS)

205
Q

SEROLOGIC METHODS

  • Detects specific antibodies (IgM, IgG) or antigens associated with malaria infection in blood sample
  • Antibody detection: measures the presence of antibodies (IgM, IgG) against malaria antigens to indicate current or past infection
A

ELISA

206
Q

SEROLOGIC METHODS

A: High sensitivity and specificity, especially for detecting antibodies; Useful for epidemiological studies to assess exposure and transmission rates
D: Cannot distinguish between active and past infections when detecting antibodies; Requires specialized laboratory equipment and trained personnel; Antigen detecting ELISA may not be sensitive enough to detect low-level parasitemia

A

ELISA

207
Q

SEROLOGIC METHODS

  • Detects antibodies against malaria parasites in a patient’s serum
  • Involves placing parasite antigens on a slide, adding patient serum, and then adding a fluorescent-labeled secondary antibody that binds to any antibodies in the patient serum
  • If antibodies are present, they will bind to the parasite antigens, and the fluorescent marker will be visible under a fluorescent microscope
    *
A

INDIRECT FLUORESCENT ANTIBODY TEST (IFA)

208
Q

SEROLOGIC METHODS

A: High sensitivity for detecting antibodies against all plasmodium species; Useful in epidemiological surveys to determine past exposure to malaria
D: Cannot distinguish between current and past infections; Requires a fluorescent microscope, skilled personnel, and is time-consuming; Less commonly used in routine diagnostics due to complexity and cost

A

INDIRECT FLUORESCENT ANTIBODY TEST (IFA)

209
Q

SEROLOGIC METHODS

➢ Highly sensitive technique that uses radioactively labeled antigens or antibodies to detect specific antibodies in a blood sample
➢ Involves mixing the patient’s serum with radio-labeled malaria antigens and then measuring the radioactivity to determine the presence and quantity of antibodies

A

RADIOIMMUNOASSAY (RIA)

210
Q

SEROLOGIC METHODS

A: High sensitivity and specificity for detecting antibodies against malaria
B: Requires equipment, materials, personnel
specialized radioactive and trained; Not commonly used due to safety concerns related to radioactivity and the need for specialized disposal of radioactive waste

A

RADIOIMMUNOASSAY (RIA)

211
Q

SEROLOGIC METHODS

➢ Detects antibodies by observing whether the complement system is activated when patient serum is mixed with specific malaria antigens
➢ Based on the principle that if specific antibodies are present, they will bind to the antigen and fix the complement, preventing lysis of RBCs added to the mixture

A

COMPLEMENT FIXATION TEST

212
Q

SEROLOGIC METHODS

A: Can provide evidence of past exposure to malaria
D: Less sensitive and specific compared to more modern techniques like ELISA and IFA; Time-consuming and requires careful handling and precise interpretation

A

COMPLEMENT FIXATION TEST

213
Q

SEROLOGIC METHODS

Enumerate Primary Prophlaxis

A
  • CHLOROQUINE
  • ATOVAQUONE
  • DOXYCYCLINE
  • MEFLOQUINE
214
Q

PRIMARY PROPHYLAXIS

1-2 weeks before leaving, take weekly while away, and then take once weekly for 4 weeks after returning home

A

CHLOROQUINE

215
Q

PRIMARY PROPHYLAXIS

Once daily started 1-2 days before travel, for duration of stay, and then for 1 week after returning home

A

ATOVAQUONE

216
Q

PRIMARY PROPHYLAXIS

Taken 1-2 days before travel, daily while away, and then up to 4 weeks after returning

A

DOXYCYCLINE

217
Q

PRIMARY PROPHYLAXIS

Given once weekly

A

MEFLOQUINE

218
Q

SECONDARY PROPHYLAXIS

Primaquine for (what plasmodia sp.)

A

P. vivax or P. ovale

219
Q

SECONDARY PROPHYLAXIS

Primaquine daily for how many days after departure from the malarious area

A

14 days

220
Q

TOF. A good malaria treatment should be able to cover all the stages of the parasite.

A

T

221
Q

TREATMENT

Hepatic stage

A

Tissue schizonticides

222
Q

TREATMENT

Erythrocytic stage

A

Blood schizonticides

223
Q

TREATMENT

Gametogony

A

gametocides

224
Q

only drug that covers all stages

A

primaquine

225
Q

first pre-erythrocytic RTS vaccine was created in

A

1987 and by 2019

226
Q

was the first malaria vaccine approved for widespread use

A

In 2021, RTS vaccine

227
Q

TOF. Patients with sickle cell TRAIT are conferred protection from severe malaria due to the presence of the gene. While, patients with sickle cell DISEASE are not conferred protection from malaria, they are still vulnerable to malaria.

A

T

228
Q

➢ First line of treatment for uncomplicated and severe P. falciparum malaria
➢ Cannot be bought in any drugstore ➢ 3-7 days, to cover 2 asexual cycles ➢ Can only be acquired from DOH
○ This is to control the resistance of the parasite to the drug
➢ Ensures that only a small fraction of parasites remain for clearance by the partner drug
➢ Monitor clinical response and check parasite density every 12-24 hours

A

ARTEMETHER-LUMEFANTRINE (AL)

229
Q

➢ Second line of treatment if AL is not available ➢ Or if the patient is allergic to AL

A

QUININE + TETRACYCLINE / CLINDAMYCIN

230
Q

➢ To prevent relapse in P.vivax or P.ovale infection ➢ 14 days of treatment to target hypnozoite

A

PRIMAQUINE

231
Q

➢ Called Mosquirix
➢ Prevents only around 50-60% of infections
➢ First malaria vaccine approved for public use in 2021
➢ Recombinant vaccine, consisting of the P. falciparum circumsporozoite protein (CSP) from the pre-erythrocytic stage
○ Different from other vaccines that elicit immune responses
○ Targets the proteins in sporozoites
➢ Delivered intramuscularly
➢ First dose is given at 5 months of age
➢ The first 3 doses are administered monthly, and the
third should be completed by 9 months of age
➢ Reduces hospital admission from severe malaria by
around 30%

A

RTS.S / AS01

232
Q

➢ Most effective malaria vaccine with 77% efficacy shown in initial trials
➢ Novel pre-erythrocytic malaria vaccine with a similar mechanism of action to RTS.S, but designed to induce increased Anti-Circumsporozoite Protein antibody and lower Anti-Hepatitis B surface antigen antibody responses
➢ Given intramuscularly at 3 doses, 4 weeks apart
➢ Malaria vaccine can be used for the prevention of P. falciparum malaria in children living in regions with
moderate to high transmission

A

R21 / MATRIX-M

Diagnostic Parasitology (37 decks)

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