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PARASIT > Malarial Parasite > Flashcards

Malarial Parasite Flashcards

1
Q

PLASMODIUM
● Normally transmitted by the bite of Plasmodium infected

A

female mosquito

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2
Q

Vertebrates: asexual or sexual

A

asexual cycle (Schizogony)

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3
Q

Invertebrate: asexual or sexual?

A

: sexual cylce (Sporogony)

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4
Q

Stage:
● Feeding or growing stages in the asexual cycle
● Lives within the tissue cells

A
  1. TROPHOZOITE
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5
Q

Stage:
Sporozoan body during schizogony

A

SCHIZONT

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6
Q

stage: ● Released from the infected cell
● Some will infect other tissue cells going back to the
trophozoite stage
● Others will be differentiated into male and female forms
(gametocytes)

A
  1. MEROZOITES/ LATE SEGMENTERS
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7
Q

IMMATURE SEXUAL FORM

A

. GAMETOCYTES -

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8
Q

stage:
● Fertilized ovum/ova before cell division
● Union of macrogamete and microgamete

A
  1. ZYGOTE
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9
Q

○ Female gametocyte
○ Produce a macrogamete
○ Mature only to be fit for fertilization

A

MACROGAMETOCYTES

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10
Q

○ Male gametocyte
○ Produce a group of microgametes

A

MICROGAMETOCYTES

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11
Q

Mature sexual form of plasmodium

A
  1. GAMETES
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12
Q

○ Female gametocyte
○ Produce a macrogamete
○ Mature only to be fit for fertilization

A

A. MICROGAMETOCYTES

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13
Q

○ Male gametocyte
○ Produce a group of microgametes

A

B. MICROGAMETOCYTES

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14
Q

Male sex cells in sporozoa

A

MICROGAMETES

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15
Q

○ Female sex cells in sporozoa

A

MACROGAMETES

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16
Q

stage:
● Encysted zygote

A
  1. OOCYST
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17
Q

stage:
● end product of sexual multiplication of malarial parasites in
mosquito

A
  1. SPOROZOITE
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18
Q

stage: ● one of a number of bodies in many sporozoa into which the
zygotes divide and from which sporozoites are formed

A
  1. SPOROBLAST
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19
Q

stage:
● the separated membrane that surrounds a sporoblast and
subsequently the group of sporozoites formed from this
sporoblast

A
  1. SPOROCYST
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20
Q

● Fertilized ovum/ova before cell division
● Union of macrogamete and microgamete

A

ZYGOTE

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21
Q

– rapidly multiplying stage in the development of the tissue phase of
certain organisms such as Toxoplasma gondii

A

Tachyzoites

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22
Q

P.vivax cause what disease?

A

Benign Tertian Malaria

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23
Q

Incubation Period of p.vivax

A

12-20 days

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24
Q

Incubation Period:PLASMODIUM OVALE

A

11-16 days

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25
Q

prepatent period of p.vivax

A

11-15 days

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26
Q

PLASMODIUM OVALE Has recently been shown by genetic methods to consist of two
species

A

1) Plasmodium ovale curtisi
(2) Plasmodium ovale wallikeri

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27
Q

Intermittent fever every 72 hours

A

PLASMODIUM MALARIAE

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28
Q

Prepatent period: PLASMODIUM OVALE

A

14-26 days

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29
Q

Intermittent fever every 48 hours

A

PLASMODIUM OVALE and p.vivax

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30
Q

The ____ can lead to severe disease and death due
to splenomegaly

A

vivax malaria

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31
Q

P.ova causes what disease

A

Ovale Tertian Malaria

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32
Q

Incubation Period: PLASMODIUM MALARIAE

A

18-40 days

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33
Q

Prepatent period:PLASMODIUM MALARIAE

A

3-4 weeks

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34
Q

p.mala cause what disease

A

Quartan Malaria

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35
Q

MALARIAL PAROXYSM
 3 STAGES:Symptoms would usually diminish at this stage

A

SWEATING STAGE

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36
Q

Causative agent PLASMODIUM FALCIPARUM

A

Malignant Tertian Malaria

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37
Q

MALARIAL PAROXYSM
 3 STAGES:
● There is a sudden feeling of cold or a feeling of inappropriate
convulsion
● characterized by mild shivering, violent teeth chattering
● Vomiting and febrile convulsions

A
  1. COLD STAGE
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38
Q

Intermittent fever every 36-48 hours

A

PLASMODIUM FALCIPARUM

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39
Q

incubation Period PLASMODIUM FALCIPARUM

A

8-15 days

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40
Q

Prepatent period: PLASMODIUM FALCIPARUM

A

11-14 days

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41
Q

MALARIAL PAROXYSM
 3 STAGES: Rigors last for 14-60 minutes

A

COLD STAGE

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42
Q

MALARIAL PAROXYSM
 3 STAGES:
● Characterized by very high temperature of 40-41C

A

. HOT STAGE OR FLUSH PHASE

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43
Q

ERYTHROCYTIC CYCLE: 48 hours

A

P. FALCIPARUM:

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44
Q

MALARIAL PAROXYSM
 3 STAGES:
Manifests with headache
● palpitations , tachypnea, epigastric discomfort
● Because of the high temperature, thirst, nausea and vomiting
● Last for 2-6 hours

A
  1. HOT STAGE OR FLUSH PHASE
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45
Q

MALARIAL PAROXYSM
 3 STAGES: Temperature lowers over the next 2 to 4 hours because of the
sweating

A
  1. SWEATING STAGE:
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46
Q

MALARIAL PAROXYSM
 3 STAGES: In this stage, there is also convulsion and the patient can
become delirious because of the very high temperature and
the skin is usually flushed and very hot

A

HOT STAGE OR FLUSH PHASE

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47
Q

ERYTHROCYTIC CYCLE: paroxysms occur on alternate days hence causing Tertian
malaria

A

P. OVALE AND P VIVAX

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48
Q

MALARIAL PAROXYSM
 3 STAGES: Total Duration: 8-12 hours

A

SWEATING STAGE:

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49
Q

ERYTHROCYTIC CYCLE: paroxysms 72 hours (on 1 and 4 days)
❖ Quartan malaria
PICTURE: DISSEMINATED INTRAVAS

A

P. MALARIAE:

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50
Q

DIAGNOSIS: ❖ In P. falciparum only the____can be found which would
usually be done 10 days after symptoms begin, gametocytes
may be found.

A

ring form ; THICK AND THIN BLOOD FILM EXAMINATION

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51
Q

s Disseminated Intravascular Coagulation
that can be seen in

A

P. falciparum

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52
Q

DIAGNOSIS: Malarial parasites: bright green and yellow under fluorescent
microscope

A

QUANTITATIVE BUFFY COAT (QBC)

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53
Q

DIAGNOSIS:
❖❖ Special capillary tube coated with Acridine orange

A

QUANTITATIVE BUFFY COAT (QBC)

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54
Q

DIAGNOSIS:❖ Giemsa and Wright’s stain
❖ Specimen collection which can be done anytime every 6-8
hrs is appropriate)

A

THICK AND THIN BLOOD FILM EXAMINATIO

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55
Q

DIAGNOSIS: ❖ Only used for screening and needs thick, thin films

A

QUANTITATIVE BUFFY COAT (QBC)

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56
Q

DIAGNOSIS:Antigen capture test

A

PARASIGHT F TEST

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57
Q

DIAGNOSIS: High sensitivity and good specificity

A

PARASIGHT F TEST

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58
Q

DIAGNOSIS: This is a dip stick test for simple and rapid diagnosis of P.
falciparum

A

PARASIGHT F TEST

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59
Q

DIAGNOSIS:
PARASIGHT F TEST antigen

A

Ag: trophozoite-derived histidine-rich protein II
(HRP-II)

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60
Q

TREATMENT To prevent establishment of the parasite in the liver

A

CAUSAL PROPHYLACTIC DRUGS

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61
Q

TREATMENT destroy the sexual form of parasite in the blood

A

GAMETOCYTOCIDAL DRUGS

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62
Q

MORPHOLOGY:
 Ovoidal, pyriform or cresentic

A

TOXOPLASMA GONDII

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63
Q

TREATMENT attacks the parasite in red blood cells

A

BLOOD SCHIZONTICIDAL DRUGS

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64
Q

TREATMENT prevents the occurrence of the disease

A

HYPNOZOITICIDAL OR ANTI-RELAPSE

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65
Q

MODE OF TRANSMISSIONTOXOPLASMA GONDII

A

Ingestion of uncooked meat, fecal contamination, nasal route,
transplacental

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66
Q

Drug of choice for malaria

A

CHLOROQUINE

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67
Q

TREATMENT it inhibits the development of the oocysts in the gut of the
mosquitoes.

A

SPORONTICIDAL DRUGS:

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68
Q

MAIN USES OF ANTIMALARIAL DRUGS: MAIN USES OF ANTIMALARIAL DRUGS:

A

Curative-

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69
Q

MAIN USES OF ANTIMALARIAL DRUGS: prophylactic

A

Protective-

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70
Q

CHLOROQUINE combination

A

Pyrimethamine/sulfadoxine

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71
Q

So there is an exogenous asexual phase in the mosquito
called the

A

sporogony

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72
Q
A
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73
Q

MODE OF REPRODUCTION TOXOPLASMA GONDII

A

longitudinal binary fission

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74
Q

drug for severe falciparum malaria

A

Quinine or quinidine:

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75
Q

TOXOPLASMA GONdii HOST:

A

cats

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76
Q

OPPORTUNISTIC SPOROZOANS:

A
  1. Toxoplasma gondii
  2. Cryptosporidium specie
  3. Pneumocystis carinii
  4. Isospora belli
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77
Q

TOXOPLASMA GONDII DISEASE:

A

Toxoplasmosis

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78
Q

T,gon infective stage

A

oocyst

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79
Q

ONE OF THE MOST
COMMON HUMAN INFECTIONS THROUGHOUT THE WORLD

A

TOXOPLASMOSIS

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80
Q

IS A PROTOZOAN PARASITE THAT
INFECTS MOST SPECIES OF WARM BLOODED ANIMALS
INCLUDING MAN AND CAN CAUSE THE DISEASE

A

TOXOPLASMA GONDI

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81
Q

a high prevalence of infection in ___ has been related to a
prevalence for eating raw or undercooked meat

A

France; t,gondi

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82
Q

high prevalence in ____ has been related to the
frequency of stray cats in a climate favoring survival of
OOCYST and soil exposure

A

central America; t.gondii

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83
Q

TISSUE STAGES IN MAN of T.gondi; fast rapid, multiplication, acute phase

A

TACHYZOITEs

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84
Q

TISSUE STAGES IN MAN of T.gondi ; slow proliferation during this stage, chronic phase

A

BADYZOITES

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85
Q

TISSUE STAGES IN MAN of T.gondi; Female who first to acquire the infection
during pregnancy may transmit the
infection to embryo resulting in fetal
death, or mental retardation on newborn,
or blindness in later life

A

TACHYZOITES

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86
Q

TISSUE STAGES IN MAN of T.gondi ; Major cause of encephalitis in AIDS
patients

A

TACHYZOITES

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87
Q

congenital or acquires toxoplasmosis? Regional lymph node invasion
o Intracellular multiplication in various organ

A

ACQUIRED TOXOPLASMOSIS

88
Q

TISSUE STAGES IN MAN of T.gondi  Toxoplasma divide in tissues of man as
tachyzoites
 Associated with RES, or endothelium of
the circulatory system
 Serous fluids in body cavities
 Necrosis of the invaded area
 Pseudocysts (group of bradyzoites) are
also formed

A

TACHYZOITES

89
Q

congenital or acquires toxoplasmosis? o Occurs in 1-2% per 1000 pregnancies
o Severe and fatal

A

CONGENITAL TOXOPLASMOSI

90
Q

congenital or acquires toxoplasmosis? Hydrocephaly, choiretinitis, microcephaly,
psychomotor disturbances and convulsions

A

CONGENITAL TOXOPLASMOSIS

91
Q

 Appears after the infection and
regional lymph node invasion
 Parasite is blood borne to
many organs where
intracellular multiplication
takes place

A

Acquired toxoplasmosis:

92
Q

congenital or acquired toxoplasmosis? Clinical course: Usually benign and self-limited
o Symptoms usually resolve in a few weeks to
months

A

ACQUIRED TOXOPLASMOSIS

93
Q

congenital or acquires toxoplasmosis? , 10-20% of patients with acute infection
may develop cervical lymphadenopathy and flu-like
illness

A

ACQUIRED TOXOPLASMOSIS

94
Q

congenital or acquired toxoplasmosis? o Rare cases: ocular infection with visual loss can
occur
o Immunodeficient patients often have central
nervous system disease that may have
retinochoroiditis pneumonitis or other systemic
disease

A

acquired toxoplasmosis

95
Q

In patients with AIDS,____ is
the most common cause of intracerebral mass
lesions and is thought to usually because by the
activation of chronic infection

A

toxoplasmic encephalitis

96
Q

Toxoplasmosis in patients being treated with
immunosuppressive drugs may be due to either

A

newly acquired or reactivated latent infection

97
Q

CRYPTOSPORIDIUM SPECIES
DIAGNOSTIC STAGE:

A

oocyst with 4 naked sporozoites

98
Q

CRYPTOSPORIDIUM SPECIES INFECTIVE STAGE:

A

sporozoites

99
Q

PATHOGENESIS
● acute , self-limiting diarrhea of 1-2 weeks duration
● Intense abdominal pain and bloating, anorexia, weakness

A

CRYPTOSPORIDIUM SPECIES

100
Q

CRYPTOSPORIDIUM SPECIES DIAGNOSIS \● observe for mucosal changes and partial villous atrophy
● Trophozoites, schizonts, and merozoites can be found in
the microvilli

A

. BIOPSIES OF ILEUM AND JEJUNUM:

101
Q

CRYPTOSPORIDIUM SPECIES DIAGNOSIS; ● Perform DFS and concentration techniques

A
  1. CRYPTOSPORIDIUM OOCYSTS IN STOOL
102
Q

PNEUMOCYSTIS JEROVECI (CARINII) / PNEUMOCYSTIS
JEROVECI PNEUMONIA
DISEASE

A

● Interstitial plasmacellular pneumonia or pneumocytosi

103
Q

Most common opportunistic infection in patients with HIV
infection

A

pNEUMOCYSTIS JEROVECI (CARINII) /

104
Q

Organism is a rare cause of infection in the general population

A

PNEUMOCYSTIS JEROVECI (CARINII)

105
Q

Frequent cause of morbidity and mortality in persons who are
immunocompromised especially patients with acquired
immunodeficiency syndrome (AIDS)

A

PNEUMOCYSTIS JEROVECI (CARINII)

106
Q

is classified as a fungal pneumonia but does not respond to
antifungal therapy

A

PCP (PNEUMOCYSTIS JEROVECI PNEUMONIA)

107
Q

Incidence has decreased as a result of a highly active
antiretroviral drugs

A

PCP (PNEUMOCYSTIS JEROVECI PNEUMONIA

108
Q

PNEUMOCYSTIS JEROVECI HABITAT:

A

lungs

109
Q

P.jiro MOT

A

airborne

110
Q

○ small, round, with 8 uninucleated bodies

A

P.jiro cyst

111
Q

crescent, sickle or pear-shaped with amoeboid
movement

A

P.jiro troph

112
Q

Alveolar septal infiltration with plasma cells

A

P.jiro

113
Q

● In the lungs: honeycombed masses of parasites within the
alveoli

A

P.jiro

114
Q

P.jiro death due to

A

Asphyxia

115
Q

a condition where the body does not get enough
oxygen, if left untreated it can cause coma or death

A

ASPHYXIA; p.jiro

116
Q

treatment for P.jiro

A

Trimethoprim- sulfamethoxazole is the drug of choice.

117
Q

Recognized as a opportunistic small bowel pathogen in
patients with HIV infection

A

ISOSPORA BELLI

118
Q

P.jiro: The samples that we get will be stained
___ to demonstrate cyst and
trophozoites

A

methenamine silver

119
Q

diagnosis P.jiro

A

Percutaneous needle biopsy of the lungs and lung aspirates

120
Q

I.bel disease

A

human coccidiosis

121
Q

ISOSPORA BELLI
INFECTIVE STAGE:

A

sporulated oocyst

122
Q

Acute diarrhea with abdominal pain, it can be severe in
immunocompromised patients and children, eosinophilia has
also been reported

A

I.belli

123
Q

Most commonly found in tropical and subtropical climates
● Can be diagnosed by identification of the oocyst in the stool
or biopsy, stools through DFS

A

I.belli

124
Q

MORPHOLOGY:
● Immature oocyst:
○ Elongate ovoidal

● Mature oocyst:
○ Contains 2 sporocyst, each containing 4
sporozoites

A

ISOSPORA BELLI

125
Q

ISOSPORA BELLI habitat

A

small intestine of man

126
Q

Infects epithelial cells in the small intestines
● Symptoms which can last for weeks and results in
malabsorption and weight loss

A

I.belli

127
Q

● Mild cases - mild abdominal pain and mucoid diarrhea

A

I.belli

128
Q

Principal vector of plasmodium spp

A

Anopheles minismus var. flavirostris

129
Q

what parasite: ➢ Single large compact ring or band forms

A

Plasmodium malariae

130
Q

what parasite?Invades old RBCs

A

Plasmodium malariae

131
Q

Schizont with merozoites arranges around central pigment
(resembles fruit pie)

A

p.malariae

132
Q

ovoid gametocyte

A

p.malar

133
Q

Small ring forms (1/6 diameter red cell), applique forms, double
nuclear dots

A

Plasmodium falciparum

133
Q

Organisms invades all ages of red blood cells (most severe)

A

Plasmodium falciparum

134
Q

arge pale red cells with Schuffner’s dots which may be oval
and fimbriated

A

Plasmodium ovale

134
Q

Single compact ring

A

Plasmodium ovale

134
Q

Only reticulocytes are invaded

A

. Plasmodium vivax

135
Q

remains the gold standard
method for plasmodium spp identification

A

. Microscopic identification of the malarial parasites in thick and thin
blood smears stained with Giemsa or Wright’s stain is still important in
making the definitive diagnosis

135
Q

produced by both sexual and asexual stages
and can distinguish between P. falciparum and non-P.
falciparum specie

A

Plasmodium LDH

135
Q

Crescent/banana-shaped gametocytes

A

Plasmodium falciparum

136
Q

Single large ring succeeded by amoeboid form in pale large
red cel

A

Plasmodium vivax

137
Q

Round gametocyte

A

. Plasmodium vivax

137
Q

disease? sudden massive intravascular hemolysis
resulting to hemoglobinuria

A

o Blackwater fever:

137
Q

– detects Plasmodium-specific
antigens; these target antigens are called HRP II (Histidine-rich
protein

A

Immunochromatography

137
Q

disease? red cells, organisms and pigment can block
the brain vessels

A

Cerebral malaria

138
Q

Plasmodium____ infection is most likely fatal

A

Plasmodium falciparum

139
Q

36- 48 hours Paroxysm
cycle

A

p.falci

140
Q

72 hours

A

P.malariae

141
Q

48 hours

A

p.ovale and p.vivax

142
Q

appearance of
RBC size: Normal

A

lasmodium
malariae

142
Q

infected rbc: Sometimes
enlarged;
frequently oval
with ragged
margins

A

p.ovale

142
Q

Appearance of
RBC size:
Normal;
multiply
infected red
blood cells are
common

A

p.falci

142
Q

infected rbc not enlarged

A

p.falci, malar, vivac

142
Q

Appearance of
RBC size; Enrlaged;
maximum size
may be 1 – 2
times normal
RBC diameter

A

Plasmodium

142
Q

Appearance of
RBC size; Enlarged;
approximately
20% or more of
infected RBCs
are oval
and/or
fimbriated
(border has
irregular
projections)

A

Plasmodium
ovale

143
Q

Number of
merozoites; 6 – 14; average
is 8

A

p.oval

143
Q

Number of
merozoites; 12 – 24;
average is 16

A

p.vivax

143
Q

Number of
merozoites; 6 – 32
(average is
20 – 24)

A

p. fal

143
Q

Schuffner’s
stippling
(precipitated
Hb): Maurer’s dots
occasionally
seen)

A

p. fal

143
Q

Number of
merozoites; 6 – 12
(average is 8);
“rosette”
schizonts

A

p,mal

143
Q

Schuffner’s
stippling
(precipitated
Hb): +
(James’ dots;
present in all
stages except
early ring
forms)

A

P.oval

143
Q

Parasite
cytoplasm; Young rings are
small, delicate,
often with
double
chromatin
dots;
gametocytes
are crescentshaped or
elongated

A

p.fal

143
Q

Schuffner’s
stippling
(precipitated
Hb): (Ziemann’s
dots rarely
seen

A

P,mal

143
Q

Schuffner’s
stippling
(precipitated
Hb): +
(Schuffner’s
dots; present
with all stages
except in early
ring forms)

A

P.vivax

144
Q

Parasite
cytoplasm Rounded,
compact
trophozoites
with dense
cytoplasm;
band-form
trophozoites

A

P.mal

145
Q

Parasite
cytoplasm Rounded,
compact
trophozoites;
occasionally
slightly
amoeboid;
growing
trophozoites
have large
chromatin
mass

A

P.oval

145
Q

Parasite
cytoplasm Irregular,
ameboid
trophozoites;
has “spread
out”
appearance

A

P. vivax

146
Q

Trophozoite: Amoeboid

A

P.vivax

146
Q

Trophozoite: Accole or
Applique forms
May have
multiple rings

A

p.falc

146
Q

Appearance of
parasite
pigment: Black; coarse
and
conspicuous in
gametocytes

A

P.fal

146
Q

Least common
Rarely fatal
May cause
relapses

A

P, oval

146
Q

Appearance of
parasite
pigment: Dark brown,
coarse,
conspicuous

A

P.malar

146
Q

Trophozoite; Band

A

P.malar

146
Q

Appearance of
parasite
pigment: Golden brown,
inconspicuous

A

P.vivax

146
Q

Trophozoite: Red cell
containing
trophozoite
may have
fimbriated
edges

A

P. oval

146
Q

Appearance of
parasite
pigment: Dark brown,
conspicuous

A

P.oval

146
Q

Shape of
gametocyte: Sausage or
crescentshaped

A

P.falc

146
Q

Stages seen in
circulating
peripheral
blood: Rings and/or
gametocytes;
other stages
develop in
blood vessels
of internal
organs but are
not seen in
peripheral
blood EXCEPT
in severe
infection

A

p.falc

146
Q

Shape of
gametocyte: round

A

P. mal, oval, vivac

146
Q

Stages seen in
circulating
peripheral
blood:All stages

A

P.oval

146
Q

Stages seen in
circulating
peripheral
blood: All stages; wide
range of
stages may be
seen on any
given film

A

p.vivax

146
Q

Stages seen in
circulating
peripheral
blood: All stages; wide
variety of
stages usually
not seen;
relatively few
rings or
gametocytes
generally
present

A

P,malar

146
Q

Highy mortality

A

p,falc

146
Q

Rarely fatal

A

p. malar

146
Q

slowly multiplying trophozoite contained in the cyst of T. gondii

A

Bradyzoites

146
Q

Most common
Rarely fatal
May cause
relapses

A

p,vivax

147
Q

extrusion of rapidly waving flagellum-like mircogametes from
microgametocytes

A

Exflagellation

147
Q

mature sex cell of plasmodia

A

▪ Gamete –

147
Q

– immature sexual form of plasmodia (male microgametocyteor
female microgametocyte) that is present in peripheral blood

A

Gametocyte

147
Q

– development phase in the life cycle of malaria and coccidian
parasites in humans in which male and female gametes are formed

A

Gametogony

147
Q

– exoerythrocytic schizont of P. vivax and P. ovale in the human liver,
characterized by delayed primary development; responsible for true relapse in
malaria

A

Hypnozoite –

147
Q

also known as schizogony; leading to the production of merozoites
in some intestinal coccidians

A

Merogony –

147
Q

– product of schizogonic cycle in malaria; produced in the liver (preerythrocytic cycle) and in the red blood cells (erythrocytic cycle); motile and
infects the red blood cells

A

▪ Merozoite –

147
Q

– encysted form of the ookinete that occurs in the stomach wall of
Anopheles spp.

A

Oocyst

147
Q

motile zygote of Plasmodium spp; formed by microgamete
fertilization of macrogamete

A

▪ Ookinete –

147
Q

ever, chills, sweats syndrome in malaria; spiking fever corresponds to
the release of merozoites and toxic material from the rupturing parasitized red
blood cells, and shaking chills occur during subsequent schizont development

A

Paroxysm

147
Q

– increased severity of a disease after a remission or following
treatment as a result of an inadequate immune response by the host or
inadequate response to treatment

A

▪ Recrudescence –

147
Q

a recurrence of illness/signs and symptoms of a disease after a period
of improvement; In malaria, it is caused by the reactivation of hypnozoites in the
liver that begins a new cycle in red blood cells; occurs only in Plasmodium vivax
and P. ovale infections

A

▪ Relapse -

147
Q

(Asexual cycle) occurs on the epithelial cells of the intestinal
mucosa producing schizonts

A

Schizogony

147
Q

developed stage of asexual division of the sporozoa; ruptures to
produce merozoites

A

Schizont

147
Q
A
147
Q

occurs within the intestinal lumen of the invertebrate
host. End product → sporozoite

A

Sporogony

147
Q

slender, spindle-shaped organism; infective stage of malaria
parasites; inoculated into humans by the bite of an infected female mosquito; It
is the result of the sexual cycle in the Anopheles mosquito

A

Sporozoite

147
Q

– rapidly multiplying stage in the development of the tissue phase of
certain organisms such as Toxoplasma gondii

A

Tachyzoites

147
Q

feeding or growing stage in the asexual cycle

A

Trophozoite

147
Q
A
147
Q

union of the macrogamete and microgamete; fertilized ovum/ova
before cell division

A

Zygote

147
Q
A
147
Q
A
147
Q
A
147
Q
A
147
Q
A
147
Q
A
148
Q
A
148
Q
A

PARASIT (29 decks)

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