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Amy Somerville > INF2 - E. PLASMODIUM AND MALARIA DIAGNOSIS-COVERED > Flashcards

INF2 - E. PLASMODIUM AND MALARIA DIAGNOSIS-COVERED Flashcards

1
Q

what are the 5 causative agents of malaria in humans

A

Plasmodium falciparum
Plasmodium ovale
Plasmodium vivax
Plasmodium malariae

Plasmodium knowlesi (infects primates: apes which infect us - zoonotic infection)

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2
Q

how is malaria spread

A
  • plasmodium spread by mosquitos of genus Anopheles (vector)
  • Anopheles deposit eggs in stagnating water ie: rice paddies, swamps, marshes, rain = higher risk
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3
Q

where are Anopheles spp.

A
  • worldwide including cold countries like Scandinavia, UK
  • plasmodium development slows down between 20-27 degrees Celcius and stops below 16 degrees Celsius
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4
Q

how does malaria infection begin

A
  • bite of an infected female anopheles mosquito
  • injects saliva and anticoagulants into blood vessel
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5
Q

life cycle of a malaria parasite

A

2 hosts:
us - 2 phases, liver and erythrocyte phase
vector

  1. infected female anopheles inoculates sporozoites into human host during blood meal
  2. sporozoites infect liver cells and mature into schizonts which rupture and release merozoites
  3. merozoites infect RBCs (plasmodium parasite undergoes stages of development inside RBC)
  4. ring-form trophozoites mature into schizonts which rupture and release merozoites, continues to infect more healthy RBCs
  5. some differentiate into gametocytes (male and female - infective part, taken up by mosquito)
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6
Q

P. falciparum development in human host

A
  • 10 days in liver
  • merozoite infects RBC at 0 hours
  • trophozoite (ring form) at 0-24 hours
  • trophozoite stage at 24-36 hours
  • schizont stage at 36-48 hours
  • rupture and release of merozoites which infect more RBCs at 48 hours
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7
Q

symptoms of malaria

A
  • none with liver stage
  • RBC stage when cells rupture and release toxins an pyrogens
  • fever caused by host cytokines in response to pyrogens
  • anaemia due to decreased RBC count
  • splenomegaly
  • jaundice due to liver damage
  • diarrhoea
  • vomiting

initial few weeks = no regular fever pattern
particularly with P. vivax
- cold stage: shivers or shows rigorous (15-60 mins)
- hot stage: flushed, rapid pulse, high temp (2-6 hours)
- sweating stage: sweats abruptly, temp drops (2-4 hours)

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8
Q

long-term effects of P. falciparum and P. malariae

A
  • develop severe malaria and die from complications
  • others, fever attacks may recur over next year then die out
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9
Q

long-term effects of P. vivax and P. ovale

A
  • weaker symptoms and less mortality
  • some, hypnozoites (dormant parasite in liver) can survive in liver cells fro years or decades and relapse
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10
Q

what is the most dangerous parasite

A

P. falciparum
- altered consciousness and coma caused by hypoglycaemia, acidosis, seizures
- cerebral malaria: death, many parasitised RBCs in capillaries/venules of brain

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11
Q

pregnancy

A
  • may have a miscarriage, stillbirth, premature birth
  • can cause anaemia and hence LBW baby as depletion of RBCs carrying nutrients and oxygen around bloodstream
  • risk of vertical transmission or during delivery (blood contamination)
  • not all anti-malarial can be used
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12
Q

immunity in endemic areas

A
  • produce parasite-specific IgG
  • this require frequent re-exposure and is lost when living in non-endemic areas for a few years
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13
Q

morphological diagnosis off malaria

A
  • take blood sample from patient
  • spread on thin glass slide
  • look at it under microscope
  • diagnose parasites in thin blood films using light microscope
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14
Q

rapid diagnostic tests (lateral flow)

A
  • detection of antigens in blood sample
  • might get a false negative if not enough antigens
  • might get false positive if parasite is killed but bits of protein and breakdown products are in bloodstream
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15
Q

serodiagnosis

A
  • detection of anti-malarial antibodies
  • those in endemic countries likely to have IgG in blood
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16
Q

PCR

A
  • detection of DNA
  • parasite DNA can persist in blood after cure for up to a month
17
Q

thin blood films

A
  • RBCs not lysed and spread over large surface
  • can determine size/shape and characteristic features in infected cells
  • need RBCs to be spread evenly
  • reduced sensitivity as only looking at a small amount of cells
  • SPECIFICITY: specify and diagnose specifically what parasite
18
Q

thick blood films

A
  • more blood spread on smaller surface so higher sensitivity
  • thicker, darker, denser
  • as RBCs are lysed, shape and size can’t be observed
  • SENSITIVITY: can defo see if have malaria, not what parasite
19
Q

reliability of blood films

A
  • represents infection at time of blood taking
  • might contain various developmental stages
  • P. falciparum is usually only ring stages (trophozoites) and rarer gametocytes seen
  • gametocytes sequestered by blood vessels (attached to endothelium)
  • other stages may be seen if blood has sat for hours
  • delays in preparation may cause changes in parasite morphology - misidentification
20
Q

P. falciparum: trophozoites (ring-form)

A
  • ring-form are thin and delicate (beats heaphones/haribos)
  • rings may possess 1 or 2 chromatin dots
  • may be found on periphery of RBC
  • no enlargement of infected RBCs
  • early developmental stage
21
Q

P. falciparum: trophozoites and Maurer’s clefts

A
  • stippling seen: irregular spaced dots in cytoplasm
  • ring is thicker
  • yellow pigment (haemozoinb) produced by parasite to avoid toxicity of free haem from digestion of haemoglobin
22
Q

P. falciparum: schizonts

A
  • about to rupture and release merozoites into blood
  • dark pigment
  • contain 8-24 merozoites
  • rarely seen in peripheral blood and hence blood films
23
Q

P. vivax: trophozoites (ring-form)

A
  • large chromatic dot and amoeboid in shape
  • enlarged and distorted RBCs
  • look wrapped around non-infected RBCs (plasticity of RBC membrane, non-circular now)
24
Q

P. vivax: trophozoites and schuffner’s dots

A
  • large amoeboid shape with shufflers dots
  • stippling evenly spaced
  • giemsa stain only
  • RBCs enlarged and distorted
  • band-form
25
Q

P. vivax: schizonts

A
  • contain 12-24 merozoites
  • dot of chromatin and mass of cytoplasm
  • infected ones alerted than uninfected
  • pigment organised in 1 or 2 clumps
26
Q

P. malariae: trophozoites (ring-form)

A
  • looks like a birds eye
  • single large chromatin dot
  • thick cytoplasm ring
  • no enlargement
  • infects older abcs which are smaller
27
Q

P. malariae: trophozoites (band-form and basket-form)

A
  • cytoplasm may elongate across RBC forming a band-form
  • cytoplasm may be oval with vacuole forming a basket form
  • large chromatin dot
  • pigment granules larger
28
Q

P. malariae: schizonts

A
  • large yellow-brown chromatin in centre
  • merozoites in Rosette pattern (8-10)
29
Q

P. ovale: trophozoites (ring-form)

A
  • large chromatin dot (single)
  • stippling - James dot
  • oval shaped
  • not enlarged
30
Q

P. ovale: trophozoites and James’s dots

A
  • deforms RBC with finger like spikes (fimbriae)
  • slightly enlarged
  • James’s dots
31
Q

P. ovale: shizonts

A
  • 4-16 merozoites
  • elongation to an oval shape
  • fimbriation
32
Q

rapid diagnostic tests

A
  1. blood mixed with lysing agent in test strip of well
  2. blood and buffer mix with labelled antibody and drawn up strip
  3. antigen present: labelled antibody-antigen complex trapped at test line
  4. excess labelled antibody accumulates at control line
33
Q

parts of a rapid diagnostic test

A
  • labelled antibody (target antigen specific) on lower end of nitrocellulose strip
  • antibody (target antigen specific) bound at 1st line
  • antibody specific for labelled antibody bound at control line
34
Q

specificity

A
  • true negative rate
  • proportion of negative which were correctly identified
35
Q

sensitivity

A
  • true positive rate
  • how many correct positives

Amy Somerville (70 decks)

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