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PARASITOLOGY 1 > MALARIA > Flashcards

MALARIA Flashcards

1
Q

List the causative agents of human malaria

A
  • Plasmodium vivax: Benign Tertian Malaria
  • Plasmodium falciparum: Malignant Tertian Malaria
  • Plasmodium malariae: Benign Quartan Malaria
  • Plasmodium ovale: Benign Tertian Malaria
  • Plasmodium knowlesi (monkey-derived malaria)
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2
Q

Frequency of fever in tertian and quartan malaria

A

=”Tertian Malaria” (P. falciparum, P. ovale and P. vivax)
*fever occurs every third day.

=“Quartan Malaria” (P. malariae)
*fever occurs every fourth day.

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3
Q

Where is P. vivax distributed?

A

=Asia
=North Africa
=Central and South America

*Nearly Worldwide, 16 Degrees North -20 degrees South. P. vivax
rare in West Africa

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4
Q

Where is P. falciparum distributed?

A

Predominant species in:
=Africa
=Papua New Guinea
=Haiti

Rapidly spreading in:
=South-east Asia and India

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5
Q

Where is P. malariae distributed?

A

=Present in most places but is rare, except in Africa

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6
Q

Which plasmodium parasite is endemic to West Africa

A

=P. ovale

  • Tropics, esp W.Africa, Burma, China, S.E.Asia, Ethiopia
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7
Q

How is malaria transmitted?

A

=Female Anopheles mosquito bite; dusk until dawn
=blood transfusion
=congenitally acquired disease
=organ transplantation
=sharing of contaminated needles

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8
Q

What is meant by “Airport Malaria”?

A

→ infected mosquitoes can enter a country via airplane thereby transmitting infection

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9
Q

Explain how Malaria can both be endemic and epidemic?

A

–Endemic, when it occurs constantly in
an area over a period of several successive years and

–Epidemic, when periodic or occasional sharp rises occur in its incidence

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10
Q

Hypoendemic (Transmission pattern)

A
  • Transmission is low
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11
Q

Mesoendemic (Transmission pattern)

A
  • Transmission is moderate
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12
Q

Hyperendemic (Transmission pattern)

A
  • Transmission is intense but seasonal
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13
Q

Holoendemic (Transmission pattern)

A
  • Transmission of high intensity
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14
Q

What is the habitat of P. falciparum?

A

=RBCs of all ages

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15
Q

Describe the Morphology of P. falciparum

A
  1. Trophozoite, ring stage. multiple infections, High parasitaemia.
  2. Schizont infected cell ruptures to release up to 32 merozoites.
  3. Gametocytes: enclosed in rbc membrane Banana shaped, called crescents
  4. Zygote, Ookinete, Oocyst, Sporozoites
  5. Infected rbc show stippling on the surface (Maurer’s clefts)
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16
Q

What is the habitat of P. vivax?

A

=Young RBCs

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17
Q

Describe the Morphology of P. vivax

A

1.Trophozoites- large, fragmented amoeboid cytoplasm.
* infected rbcs enlarged and pale,
* Schuffner’s dots in infected rbc cytoplasm

  1. Schizonts 8-24 merozoites,
    * schizogony 48hourly
  2. Gametocytes compact and round,
    * fill rbc without sign of schizogony
  3. Hypnozoites: Latency for several years
    * Dormant sporozoites in hepatocytes
    * Uninucleate, Explains clinical malaria relapses.
  4. No Knobs,no sequestration, all stages seen in blood smears.
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18
Q

What is the habitat of P. ovale?

A

Young RBCs

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19
Q

Describe the morphology of P. ovale

A
  1. Trophozoites: compact cytoplasm, not amoeboid, large prominent nuclei
  2. Schuffner’s dots, infected rbc slightly enlarged
  3. 20-30% parasitised rbcs oval, show fimbria, ragged end, artifact
  4. Low merozoite numbers 8-10, central darker pigment
  5. Gametocytes: oval, rbcs fimbriated, show Schuffner’s dots.
  6. Hypnozoites present
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20
Q

What is the habitat of P. malariae?

A

Old RBCs

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21
Q

Describe the morphology of P. malariae

A
  1. Trophozoites form bands around rbc, invades mature cells
  2. Schizogony 72 hourly
  3. No Schuffner’s dots, Zieman’s
    stippling
  4. Schizonts: 6 - 12 merozoites,
    with malaria pigment at the
    center forming Daisy heads or marguerites
  5. Gametocytes oval
  6. No Hypnozoites: 40 year recrudescence
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22
Q

Summarise the malaria parasite life cycle

A
  • Malaria parasite passes its life cycle in 2 hosts.
    – Definitive host: Female Anopheles mosquito
    – Intermediate host: Man
  • an asexual phase occurring in humans, which act as the
    intermediate host and= SCHIZOGONY
  • a sexual phase occurring in mosquito, which serves as a
    definitive host for the parasite= SPOROGONY
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23
Q

What is the other name for the Plasmodium asexual phase in man?

A

vertebrate, intrinsic, or endogenous phase

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24
Q

In humans, schizogony occurs in 2 locations, these are?

A

– In the red blood cell (erythrocytic schizogony) and

– In the liver cells (exoerythrocytic schizogony or the
tissue phase)

  • Products of schizogony, whether erythrocytic or exoerythrocytic, are called MEROZOITES (meros: a part,
    zoon: animal)
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25
Q

What is the other name for sporogony?

A

=invertebrate, extrinsic, or exogenous phase

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26
Q

Where does sporogony occur?

A

=Takes place in female Anopheles mosquitoes

  • Maturation and fertilization give rise to a large number of
    SPOROZOITES (from sporos: seed)
  • Usually, 10–15 sporozoites are injected at a time
27
Q

What is the infective form of Plasmodium?

A

=Sporozoite

28
Q

Describe the pre-erythrocytic/Exoerythrocytic schizogony

A

Sporozoites=> Schizonts=> Merozoites

  • Mature liver stage schizonts contain 2000–50,000 merozoites
  • Mature schizonts rupture in 6–15 days and release thousands of merozoites into the blood stream
  • The merozoites infect the erythrocytes
29
Q

Describe the Erythrocytic schizogony

A

=> Merozoites from liver enter RBCs=> Ring form/ Young Trophozoites=> Late Trophozoites=> Schizonts/ Meronts=> Mature Schizonts with 8-32 merozoites and hemozoin=> The mature schizont bursts releasing the merozoites into
the circulation=> Merozoites infect RBCs===> REPEATS ++PARASITEMIA UNTIL ARREST BY HOST IMMUNITY

  • Rupture of mature schizont= large quantities of pyrogens.
  • This is responsible for the febrile paroxysms
  • In P. falciparum, erythrocytic schizogony always takes place inside the capillaries and vascular beds of internal organs.
  • The parasite feeds on the haemoglobin of the erythrocyte
  • It does not metabolize haemoglobin completely and
    – therefore, leaves behind a haematin-globin pigment called the malaria pigment or haemozoin pigment as residue
30
Q

After a few erythrocytic cycles, gametogony starts, describe the human sporogony cycle

A

Merozoites=> Gametocytes
* Development of gametocytes takes place within the internal organs and only the mature forms appear in circulation

  • The gametocytes do not cause any clinical illness in the host, but are essential for transmission of the infection
31
Q

When do Gametocyte appear in circulation in P. vivax?

A

– 4–5 days after the first appearance of asexual form

32
Q

When do Gametocyte appear in circulation in P. falciparum?

A

– and 10–12 days

33
Q

Describe the mosquito phase of plasmodium sporogony

A
  • Female Anopheles mosquito ingests parasitized erythrocytes with its blood meal:
    – the asexual forms of malaria parasite are digested
    – but the gametocytes are set free in the midgut (stomach) of mosquito and undergo further
    development
  • The nuclear material and cytoplasm of the male
    gametocytes divides to produce 8 microgametes with long, actively motile, whip-like filaments (exflagellating male gametocytes)
  • The female gametocyte does not divide but:
    – undergoes a process of maturation to become the female gamete or macrogamete
    – It is fertilized by one of the microgametes to produce the zygote
  • The zygote, which is initially a motionless round body, gradually elongates and:
    – within 18–24 hours, becomes a vermicular motile form called the ookinete (travelling vermicule)
  • The ookinete develops into oocyst:
    – which is yet another multiplicatory phase, within which numerous sporozoites are formed
  • The mature oocyst ruptures releasing sporozoites which find their way to the salivary glands
  • The mosquito is now infective and when it feeds on humans:
    – the sporozoites are injected into skin capillaries to initiate human infection
  • The time taken for completion of sporogony in the mosquito is about 1–4 weeks (extrinsic incubation period)
34
Q

What’s the average incubation period of P. vivax?

A

—14 (8–31) days

35
Q

What’s the average incubation period of P. falciparum?

A

—12 (8–14) days

36
Q

What’s the average incubation period of P. ovale?

A

—14 (8–31) days

37
Q

What’s the average incubation period of P. malariae?

A
  • P. malariae —28 (18–40) days
38
Q

What is meant by incubation period?

A
  • This is the interval between the entry of sporozoites into the host and the earliest manifestation of clinical illness.
39
Q

What is meant by pre-patent period?

A
  • This is the interval between the entry of the parasites into the host and the time when they first become detectable in blood
40
Q

What is meant by Recrudescence?

A

=Recurrence of malaria from ineffective treatment that did not CLEAR the infection.
*common in places with high anti-malarial resistance

  • Recrudescence may be due to
    – waning immunity of the host, or possibly due to antigenic variation, drug resistance or under-dosage
  • In P. falciparum infections=> 1–2 years
  • In P. malariae infection=> up to 50 years
41
Q

What happens in malarial relapse?

A

Blood is cleared of merozoites but hypnozoites persist in the liver
* occurs in P. vivax and P. ovale
=24 weeks to 5 years

42
Q

list the stages in the Pathogenesis of Malaria

A
  1. Erythrocytic infection
  2. Cytoadherence, rosetting and sequestration - P. f
  3. Host defense mechanism -immunopathology
43
Q

What are the consequences of erythrocytic infection?

A

Anaemia: Normocytic, hemolytic

a. Parasite multiplication and survival=> Hb digestion

b. Destruction of parasitized rbcs at end of schizogony

c. Auto-antibodies specific for unparasitized cells: - autoimmune, nonspecific sensitization, rbcs bind
Ab/Ag complexes that fix complement.

44
Q

What are the consequences of Cytoadherence, sequestration and rosetting in Pf?

A
  • altered deformability and fragility of parasitized erythrocytes;
  • endothelial activation,
45
Q

what leads to sequestration of RBCS?

A

Cytoadherance=> Sequestration

  • Sequestration of the growing P. falciparum parasites in these deeper tissues provides them the microaerophilic venous environment
  • that is better suited for their maturation and the adhesion to endothelium allows them to escape clearance by the spleen and to hide from the immune
    system.
46
Q

which proteins help P. falciparum erythrocyte bind to endothelial membrane?

A

=P. falciparum erythrocyte membrane protein 1(PfEMP1) =Histidine rich protein II (HRP II)

47
Q

which proteins help P. falciparum erythrocyte bind to placenta?

A

– chondroitin sulfate A (CSA) protein (placenta)

48
Q

Which ligands are involved in sequestration?

A

=CD36
=thrombospondin
=vascular cell adhesion molecule1 (VCAM 1)
=intercellular adhesion molecule II (ICAM II)
=E-selectin

49
Q

Describe rosetting

A

=The infected red cells also adhere to the uninfected red cells resulting in the formation of red cell rosettes

  • Rosetting is mediated by binding of:
  • PfEMP1-DBLα on the surface of infected red cells to
    complement receptor 1
  • CD31, and heparin sulfate-like glycosaminoglycans of
    uninfected RBCs
50
Q

=only the ring-stage trophozoites of P. falciparum are seen circulating in the peripheral blood, Why?

A

Due to the sequestration

51
Q

Describe the immunopathology in malaria?

A
  1. Anemia
    = autolysis of unparasitized rbcs, increases splenic clearance, drug induced hemolysis, dyserythropoeisis in BM

2a. Nephropathies
= Ab/Ag complexes cause lesions
in Kidney glomerular walls
* In P. falciparum: Acute nephropathy, reversible, oliguria,
renal failure due to IgM,
* Malaria antigen and Complement
* Clears after treatment

2b. Nephropathies
= In P. malariae: Nephropathy is
Chronic
* - progressive, severe
* - Deposits of IgG, IgM, complement
* and Pm antigen in glomerular walls
* - Auto immune response to damaged tissue
* - Quartan Malaria nephrosis with persistent heavy proteinuria, hypoalbinemia, edema,
* - Deterioration of renal functions
* - Hypertension.
* - Treatment - little effect

  1. Splenomegaly:
    * Oedema of the pulp, RES hyperplasia, increased phagocytic fxn
    * Tropical Splenomegaly Syndrome (TSS) in young and adults
  2. Immunodepression:
    . Bone marrow depression (iron sequestration- dyserythropoeisis; dysthrombopoeisis)
    . Auto antibodies
    . Pregnancy
    . Burkitt’s lymphoma; endemicity correlating with malaria endemicity
52
Q

What are the clinical presentations of Uncomplicated (Benign) Malaria?

A
  • Prodromal phase:
    – Severe headache, nausea, and vomiting are common &
    intermittent fever or paroxysms of chills
  • Paroxysms of chills (intermittent fever)= Sudden attack of fever 104- 105 F (40-40.6 C).
    =Release of schizogony products
  • Paroxysm comprises of 3 successive stages i.e. cold stage, hot stage and sweating stage
53
Q

What are the most nottsble complictions of severe malaria?

A

cerebral, algid, and
septicemic varieties

54
Q

more complications

A

D. Gastrointestinal: vomiting, coughing, diarrhoea, or acute dysentery
E. Pulmonary oedema:
* Malaria Shock syndrome
* Fluid overload during treatment Induce diuresis and haemodialysis. Often fatal
* DIC

F. Respiratory distress (metabolic acidosis bicarbonate less
than 15 meq/l
G. Hepatorenal syndrome/Haemolytic jaundice =
jaundice and renal failure
=Liver failure,
however, occurs only in individuals in whom a concurrent viral hepatitis is present.

Malarial anaemia: is multifactorial
important cause of death in children under two years of age.

H. Jaundice and kidney failure

I. Blackwater fever:
=in repeated infections with Pf with inadequate quinine treatment Haemolysins formed against quininized and
unparasitised cells – autoimmine
Haemoglobinuria, bilirubinaemia, haemoglobinaemia
Fever, jaundice, nausea, vomiting, anuria,
=Haemoglobinuria can also
be drug induced in patients deficient in the enzyme glucose 6-phosphate dehydrogenase (G-6-PD).

J. Severe anaemia (haemoglobin less than 5g/dl or haematocrit less than 15%)

K. Renal failure-presenting as oliguria or anuria

L. Confusion or drowsiness with extreme weakness

55
Q

Malaria complications in children

A
  1. Pf common
  2. Symptoms atypical
  3. Drowsiness, vomiting, diarrhoea, unproductive
    cough, fever without periodicity.
  4. Cerebral manifestations- convulsions and coma twitching
  5. High body temperature
  6. Spleen enlargement, jaundice
  7. Severe anaemia fatal in babies
    Malarial anaemia: malarial anaemia is an important cause of death in children under 5 years
    Malaria in children
  8. Hyperpyrexia
  9. medical shock, renal involvement
  10. splenic enlargement, jaundice
  11. severe normocytic anemia
  12. Pv and Po - milder in children.
  13. Pm - Nephrotic syndrome, glomerulonephritis leads
    to gross edema, proteinuria and hypoprotinemia
56
Q

Malaria complications in pregnancy

A
  1. high prevalence: highly susceptible
  2. haemolytic anemia- jaundice, ,splenomegaly, death
  3. acute renal insufficiency
  4. abortions, stillbirths, awaken latent malaria
  5. low birth weight
  6. Treatment must not be withheld, Intermittent Preventive
    Treatment (IPTp) or chemophylaxis for at least 3 months
57
Q

How is malaria diagnosed?

A
  1. Clinical diagnosis – based on S/S being presented
    by a patient
  2. LAB diagnosis of malaria is confirmed by blood tests
    i.e. microscopic and non-microscopic tests
58
Q

Which microscopic methods are used in malaria diagnosis?

A

=Demonstration of malarial parasites in Thick and Thin blood smear Light Microscopy
* Giemsa-staining of thick and/or thin blood smears →conventional method of diagnosing malaria
– combination is gold standard

  • smears allow species identification
  • can calculate the parasite density (prognosis)
59
Q

Advantages of rapid simple dipstick?

A

▪ Rapid immunochromatographic test (ICT/RDTs) for detection of malaria antigen (PfHRP2 and PLDH)
* A rapid simple dipstick test → results in 10-15 minutes
* useful in situations where diagnostic expertise or microscopic facilities are limited

60
Q

List the Limitations rapid dipstick malarial testing

A

– cannot determine degree of parasitemia
– false positives
– not fully reliable for accurate species diagnosis

61
Q
  • 3 assays currently used for testing: these are?
A

=HRP-2
=aldolase
=pLDH

62
Q

Polymerase Chain Reaction (PCR) in malarial diagnosis

A
  • Has the ability to detect parasitemia at very low levels
  • Is helpful in species identification when microscopy is
    equivocal
  • Disadvantages are high cost, labor intensive
63
Q

Treatment of malaria depends on the following factors: (4)

A
  • Type of infection
  • Severity of infection
  • Status of the host
  • Associated conditions/ diseases
64
Q

What is the prognosis of Malaria?

A
  • Mortality of untreated falciparum is almost 100% and 10-40% for treated
  • Poor prognostic factors:
    – Age<3
    – Seizures
    – Acidosis
    – Respiratory distress

PARASITOLOGY 1 (8 decks)

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