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CVS & IBL - Parasitology 🪱 > L1: Malaria > Flashcards

L1: Malaria Flashcards

1
Q

What is the definition of malaria?

A

Malaria is a life-threatening mosquito-borne blood disease caused by a plasmodium parasite.

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2
Q

What are the species of Plasmodium parasite?

A

Plasmodium vivax: Benign tertian malaria or vivax malaria

Plasmodium ovale: Benign tertian malaria or oval malaria

Plasmodium malariae: Benign quartan malaria or malariae malaria.

Plasmodium falciparum: Tertian or subtertian malignant malaria or falciparum

“Plasmodium malarie causes nephrotic syndrome”

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3
Q

What is a definitive host in the lifecycle of plasmodium?

A

♀ Anopheles

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4
Q

What is intermediate host and the reservoir host in the lifecycle of plasmodium?

A
  • IH: man

- RH: non except P.malaraie monkey

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5
Q

What is the infective stage for both humans and female anopheles mosquito?

A
  • Sporozoites inoculated with mosquito’s saliva at the site of bite.
  • Gametocytes which are present in blood
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6
Q

Where does schizogony occur?

A
  • In I.H (man) asexual multiplication in Liver (exoerythrocytic cycle),& Red cells (erythrocytic cycle).
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7
Q

What are the steps of Exoerythrocytic Schizogony?

A
  • hepatocyte invasion in 30 min, 6-15 days, 1000-40,000 merozoites, no overt pathology
  • The released merozoites, some are histiotropic and infect new liver cells initiating secondary exo-erythrocytic tissue phase (never in mammals, only in bird & lizard), and other merozoites are erythrotropic which invade and infect red blood cells initiating erythrocytic cycle.
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8
Q

Which type of malaria has Hypnozoits?

A
  • Hypnozoite Forms only P. vivax and P. ovale
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9
Q

What are the steps of Erythrocytic phase (asexual erythrocytic schizogony)?

A
  • young trophozoite called ‘ring form’, ingests host hemoglobin by cytostome forming hemozoin (malarial pigment), nuclear division, begin schizont stage (6-40 nuclei)
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10
Q

What are the characteristics of Gametocytogenesis?

A
  • ring but with no vacuolation, increase in size → gametocyte, no pathology, infective stage for mosquito
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11
Q

What is the relation between the merozoites of exo-erythrocytic cycle in liver and merozoites of erythrocytic cycle?

A
  • The merozoites of exo-erythrocytic cycle in liver can invade red cells initiating erythrocytic cycle, but the merozoites of the erythrocytic cycle can’t invade the liver cells.
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12
Q

Where does sorogony cycle occur?

A
  • In female Anopheline mosquito vector
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13
Q

what happens in sorogony cycle?

A
  • occurs in mosquito gut, ‘exflagellation’ 8 microgametes formed,
  • Fertilization →rounded zygote, elongates →ookinete →penetrates between the basement membrane & the elastic layer of the stomach →oocyst →sporocyst
  • The sporocysts ruptures and the released sporozoites (infective stages) migrate to the salivary gland
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14
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to RBCs affected

A

Reticulocytes - mature cells - old & mature - all types” that’s why its dangerous”

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15
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to Cell stippling

A
  • Schuffner’s dots, fine pigments
  • Schuffner’s dots, fine pigments
  • Ziemann’s dots, fine pigments
  • Maurer’s clefts, course pigments
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16
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to ring numbers

A

one - one - one - multiple

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17
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to old trophozoites

A

Amoeboid - compact - band form - compact

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18
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to schizont

A
  • Contains 18 merozoites ,Mature in 2 days
  • 8 merozoites ,Mature in 3 days
  • 8 merozoites ,Mature in 2 days
  • 18 merozoites ,Mature in 2 days
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19
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to gametocytes

A

Rounded - rounded - rounded - crescentic

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20
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to stages seen in a blood film

A
  • Ring, trophozoites, schizont, gametocyte
  • Ring, trophozoites, schizont, gametocyte
  • Ring, trophozoites, schizont, gametocyte
  • Ring, Gametocytes only
21
Q

How is malaria transmitted?

A
  • By the bite of an infected female Anopheles mosquito with sporozoites in its saliva (here there is liver affection).
  • Blood-borne: Blood transfusion, Intravenous injection, Congenital transmission, After organ transplantation. “Merozoites”
22
Q

What is the immune response against malaria?

A
  • Protective immunity develops after repeated exposure: Fewer parasites in blood stream & Less fever and clinical signs of disease, No strong immunity to malaria due to Ag variation.
  • Immunologic response of the host to parasite Ag & malaria pigments → +++ TNFa and IL-1 release from host cells → clinical picture
23
Q

Which type of malaria causes fatalities?

A
  • P. falciparum malaria is the cause of virtually all fatalities due to Cytoadherence
24
Q

What activates the reticuloendothelial system in case of malaria?

A
  • The reticuloendothelial system is activated by the rupture of infected red cells and intravascular release of parasites, malarial pigment, and cellular debris.
25
Q

What does anoxia stimulate in case of malaria?

A
  • Anoxia stimulate the erythroblastic activity of bone marrow to produce reticulocytes, which are attached principally by P. vivax, so anaemia is marked in this infection.
26
Q

What causes enlargement of the liver and spleen in case of malaria?

A
  • Enlargement of liver and spleen a result of enhanced phagocytosis of red cell remnants & other debris produced by schizogony.
27
Q

What is the pathogenesis of malaria?

A
  • Rupture of RBCs are main cause of pathology → Release of merozoites → Reinvasion &↑parasitemia → Release of malarial pigment → Release of HB → Jaundice & Black water fever → Destruction of RBCs → Anemia, Anoxia, & Fatty degeneration of organ → Activation of RES → hepato-spleno-megally
28
Q

What are the causes of anemia in malaria?

A

1) Obligatory destruction of RBCs in merogeny
2) Complement mediated & autoimmune hemolysis “AB Vs RBCs”
3) Hypersplensim “Affect normal RBCs”
4) Bone marrow suppression by TNF
5) Short RBCs survival
6) Failure to recycle iron in haemozoin

29
Q

What is cytoadherence?

A
  • RBCs has knobs on surface covered by adhesive protein Lead to adherence to each other “thrombosis” & endothelial cells “infarction”
30
Q

What are of the clinical pictures of malarial infection?

A
  • Uncomplicated malaria
  • In all 4 species of malaria, human infection is followed by incubation period, then malaria paroxysms include 3 stages: Cold stage “due to VC” , Hot stage & Sweating Stage
  • Hepatosplenomegaly (liver & spenic enlargement), Dysenteric symptoms
  • Hemolytic anemia
31
Q

What are the symptoms of uncomplicated malarial infection?

A
  • Fever (paroxysm), Anaemia, & splenomegaly

“FAS”

32
Q

What causes the dysenteric symptoms in malarial infection?

A
  • due to infarctions in large intestine, may occur in P. falciparum
33
Q

Why is hemolytic anemia more severe in plasmodium falciparum infection?

A

 RBCs of all ages can be invaded by parasites

 Unparasitized RBCs undergo haemolysis

 Parasitaemia is higher than in other malarias → destruction of more red blood cells.

“Affects all RBCs in every way”

34
Q

What are diseases of complicated falciparum malaria?

A
  • Cerebral malaria: ↓consciousness, convulsions, paralysis. “DUE TO THROMBUS IN CAPPILARIES THAT SUPPLY THE BRAIN”
  • Algid malaria “‏صاعقة”: ↓ Bl. P, peripheral circulatory failure, Acute renal failure & Black water fever
  • Severe malaria: HB <5g/dL, Pulmonary edema,Metabolic acidosis and shock. “PMS”
35
Q

Why are falciparum infections dangerous?

“They are numerous, furious and fast”

A
  • Highest number of merozoites → ↑parasitemia, Shorest IP, Cytoadherence→ pernicious syndrome, Prediction to all RBCs types
36
Q

What is relapse in malaria?

A
  • Means recurrence of clinical attacks in patients due to reactivation of hypnozoites in the liver (occurs in P. vivax & P. oval infection) only
37
Q

What causes recrudescence in malaria?

A
  • is due to persistence of blood forms between attacks
38
Q

What is recrudescence in malaria?

A
  • recurrence of clinical attacks in patients having low grade parasitaemia when they become debilitated, in all types
39
Q

How is malaria diagnosed?

A
  1. Clinical findings, History of travel (Imported malaria)
  2. Blood film
  3. Therapeutic test
  4. Serodiagnostic methods
  5. Dipstick test
  6. Polymerase chain reaction (PCR): can be used to detect parasite DNA.
40
Q

what is the therapeutic test used to diagnose malaria?

A
  • antimalarial, drug if result in disappearance of fever within 6 days
41
Q

What is serodiagnosis of malaria?

A
  • indirect fluorescent antibody test
42
Q

What is the dipstick test used for detection of malaria?

A
  • by which parasite antigens are detected by placing a drop of blood on a dipstick impregnated with antibody.
43
Q

how is malaria treated?

A
  • Treatment in case of 1st trimester of pregnancy: Quinine + Clindamycin
  • Blood schizonticides: destroying the parasitic stages in the blood, so act as a suppressive line of treatment. Ex Chloroquine, Mefloquine, Artimesinin derivatives.,
  • Tissue schizonticides: that destroy parasitic stages in the liver, so act as a prophylactic measure. Ex. Primaquine
  • Transmission blocking: Primaquine has a gametocidal effect
  • Radical treatment: chloroquine & primaquine
44
Q

How is Uncomplicated falciparum malaria treated?

A
  • Artmesinin combination therapy (ACT) “strongest”
  • Primaquine (gametocidal)
  • Exchange transfusion if parasitemia ≥ 10%.
45
Q

How are other malaria than falciparum treated?

A
  • Chloroquine
  • Primaquin for prevention of relapse
  • Artmesinin combination therapy (ACT) in case of chloroquine resistance.
46
Q

How is chemoprophylaxis against malaria done?

A
  • Causal prophylaxis: primaquine

- Suppressive prophylaxis: chloroquine or mefloquine

47
Q

How is malaria prevented and controlled?

A

Man:- Early diagnosis & treatment

Parasite:- Drugs (prophylactic vs therapeutic use)

Mosquitoes:- Indoor residual spraying & Environmental interventions & Larvicides

Vector-human contact:- Insecticide treated bed nets

48
Q

Why is malaria such a difficult disease to eliminate?

A

a) Resistance to Drugs “By parasite”
b) Resistance to Insecticides “by insect”
c) Global warming. “inc reproduction”
d) No Malaria Vaccine. “Due to antigen variation”
e) Sustaining funds

CVS & IBL - Parasitology 🪱 (3 decks)

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