Plasmodium II Flashcards

1
Q

[2] Phase

A
  1. Invertebrate phase
  2. Vertebrate phase
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2
Q

4-15 days after ingestion of gametocyte.

[phase]

A

Invertebrate phase

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3
Q

Mosquito takes a blood meal containing gametocytes from infected person.

A

Female Anopheles

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4
Q

[2] gametocytes

A
  1. Microgametocytes
  2. Macrogametocytes
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5
Q

male

[gametocytes]

A

Microogametocytes

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6
Q

Nuclear division and exflagellation.

[gametocytes]

A

Microgametocytes

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7
Q

female

[gametocytes]

A

Macrogametocytes

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8
Q

Shifting of nucleus to the surface to form a
projection.

[gametocytes]

A

Macrogametocytes

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9
Q

Microgamete penetrates macrogametes producing an ookinete.

[gametocytes]

A

Macrogametocytes

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10
Q

Mosquito injects sporozoites to man.

[phase]

A

Vertebrate phase

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11
Q

Sporozoites disappear from the blood.

[phase]

A

Vertebrate phase

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12
Q

– Some are destroyed by the host immune system.

– Enters liver parenchymal cells (hypnozoites in P. vivax and P. ovale)

A

Vertebrate phase

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13
Q

[9] Insect Vector in the Philippines

A
  1. Anopheles Flavirostris
  2. Anopheles Balabacensis
  3. Anopheles Lesteri
  4. Anopheles Philippinensis
  5. Anopheles Umbrosus
  6. Anopheles Leucosphyrus
  7. Anopheles Litoralis
  8. Anopheles Maculates
  9. Anopheles Mangyanu
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14
Q

Primary vector in the Philippines, night biter, breeds in slow-flowing clean water mountain streams.

[anopheles]

A

Anopheles Flavirostris

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15
Q

Rest either indoors or outdoors, in puddles, pools, ponds, and in shades.

[anopheles]

A

Anopheles Balabacensis

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16
Q

rest either indoors or outdoors, in pools, ponds, lakes, and in ricefields.

A

Anopheles lesteri

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17
Q

rest either indoors or outdoors, in pools ponds or lakes.

A

Anopheles philippinensis

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18
Q

rest out of doors, in pools, ponds, lakes, running streams and canals in shades.

A

Anopheles umbrosus

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19
Q

Vector of Plasmodium knowlesi, typically found in forest areas in South East Asia but with a greater clearing of forest areas for farmland.

A

Anopheles leucosphyrus

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20
Q

can occur over months or years.

[malaria transmission]

A

recrudescences and relapses

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21
Q

Can develop severe complications (especially P. falciparum).

A

Malaria transmission

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22
Q

Periodic episodes of fever alternating with symptom-free periods.

A

Malaria transmission

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23
Q

[3] Clinical features of Malaria transmission

A
  1. Cold stage
  2. Hot stage
  3. Sweating stage
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24
Q

Chilly sensations that progresses to a teeth chattering, frankly shaking chill. The peripheral blood vessels are constricted and the lips and nails are cyanotic.

[clinical features of MT]

A

Cold stage

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25
The body temperature begins to mount rapidly as the blood vessels dilate. [clinical features of MT]
Hot stage
26
Temperature peaks at 39-41 C, skin is hot and the face flushed. [clinical features of MT]
Hot stage
27
Sign and symptoms includes nausea, vomiting headache and rapid pulse. [clinical features of MT]
Hot stage
28
High fever may produce convulsion in children. [clinical features of MT]
Hot stage
29
The patient perspires profusely, temperature falls and the headache disappears. [clinical features of MT]
Sweating stage
30
The patient is exhausted but symptomless. And the next day the patient can feel quite well, before the next paroxysm occurs. [clinical features of MT]
Sweating stage
31
feeling of intense cold. [clinical features of MT]
Cold stage
32
vigorous shivering, rigor. [clinical features of MT]
Cold stage
33
lasts 15-60 min. [clinical features of MT]
Cold stage
34
intense heat and dry burning skin. [clinical features of MT]
Hot stage
35
throbbing headache. [clinical features of MT]
Hot stage
36
lasts 2-6 hours. [clinical features of MT]
Hot stage
37
profuse sweating and declining temperature. [clinical features of MT]
Sweating stage
38
exhausted, weak — sleep. [clinical features of MT]
Sweating stage
39
lasts 2-4 hours. [clinical features of MT]
Sweating stage
40
Periodicity varies according to species.
Malarial paroxysms
41
Depends on the length of the asexual cycle.
Malarial paroxysyms
42
[3] Malarial Paroxysms
1. Plasmodium falciparum 2. Plasmodium vivax and P. Ovale 3. Plasmodium malariae
43
Malignant tertian malaria (36 hours or less).
Plasmodium falciparum
44
Benign tertian malaria (48 hours).
Plasmodium vivax and P. ovale
45
Quartan malaria (72 hours).
Plasmodium malariae
46
In P. falciparum infections, as the parasite begins to grow, the red cell membrane becomes sticky and cells adhere to the endothelial lining of the capillaries of the internal organs.
Pathogenicity of Malaria
47
thus, only ring forms and gametocytes appear in the peripheral blood.
Pathogenicity of Malaria
48
More pronounced in P. falciparum.
Anemia
49
[3] Anemia
1. Hemolytic 2. Normochromic 3. Normocytic
50
Decrease Oxygen carrying capacity leading to what? [anemia]
Anoxia
51
Caused by an increase in splenic activity.
Splenomegaly
52
Parasitized red cells pass through the spleen, loss their deformability, thus destroyed in the process.
Splenomegaly
53
Normal RBC’s are destroyed due to increase activity of macrophages.
Splenomegaly
54
Parasitized red cells pass through the spleen, loss their deformability, thus destroyed in the process.
Splenomegaly
55
Seen in Plasmodium Malariae infection.
Nephrotic Syndrome
56
Antibody complexes causes thickening of the capillary walls of the basement membrane. [nephrotic syndrome]
Deposition of antigen
57
Presence of focal hyalinizing lesions of the tuft of the glomerulus and segmental endothelial cell proliferation progressing to glomerular sclerosis.
Nephrotic Syndrome
58
Syndrome of acute intravascular hemolysis, accompanied by hemoglobinemia and hemoglobinuria.
Black water fever
59
Abrupt onset, passage of dark red or almost black urine, vomiting of bile stained fluid, jaundice.
Black water fever
60
High mortality.
Black water fever
61
Rapid and severe hemolysis of both parasitized and non parasitized red cells.
Black water fever
62
Presence of the parasite changes the antigenic structure of individual erythrocytes and stimulates the production of antibodies.
Black water fever
63
Most serious hematologic complication.
Disseminated Intravascular Coagulation (DIC)
64
Activation of the clotting system resulting to thrombin generation and intravascular coagulation.
Disseminated Intravascular Coagulation (DIC)
65
Present in P. ovale and P. vivax.
Relapse
66
Activation of hypnozoites (liver stages) resulting to renewal of malarial infection.
Relapse
67
Renewal of parasitemia or clinical features arising from persistent undetectable asexual parasitemia in the absence of an exo erythrocytic cycle.
Recrudescense
68
P. falciparum: Due to infected RBC sequestered by the spleen.
Recrudescense
69
screening for positivity and parasite count. [blood smear]
Thick film
70
species identification easier. [blood smear]
Thin film
71
[4] Diagnosis of Malaria
1. Quantitative Buffy Coat (QBC) 2. Rapid Diagnostic Test (RDT) 3. Serological Test 4. Polymerase Chain Reaction (PCR)
72
Usually prepared capillary tube coated with acridine orange. [diagnosis of malaria]
Quantitative Buffy Coat (QBC)
73
Malaria parasites take up the stain and appear bright green and yellow under a fluorescent microscope. [diagnosis of malaria]
Quantitative Buffy Coat (QBC)
74
Detects parasitic antigens: - Pan malaria: p-LDH (Diamed Optimal IT) - Falciparum malaria: HRP-II (Paracheck Pf Test, ParaHIT f Test)– [diagnosis of malaria]
Rapid Diagnostic Test (RDT)
75
Makes use of immunochromatographic methods in order to detect Plasmodium specific antigens in a finger-prick blood sample. [diagnosis of malaria]
Rapid Diagnostic Test (RDT)
76
Cannot differentiate current and past infections. [diagnosis of malaria]
Serological tests
77
Most helpful in epidemiological studies. [diagnosis of malaria]
Serological test
78
To significantly enhance the microscopic diagnosis of malaria especially in cases of low parasitemia and in cases of mixed infection. [diagnosis of malaria]
Polymerase Chain Reaction (PCR)
79
IHA means
Indirect Hemagglutination
80
IFAT means
Indirect Fluorescent Antibody Test
81
ELISA
Enzyme-linked Immunosorbent Assay