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Nagasaki Flashcard Extravaganza > Parasites - Malaria > Flashcards

Parasites - Malaria Flashcards

1
Q

What makes Aedes aegypti a good vector?

A

Day biting
Well adapted to urban environments
Multiple meals from multiple hosts

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2
Q

What is HMBPP

A

malaria metabolite which modulates vector blood seeking and susceptibility to infection

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3
Q

When do different species of mosquitos bite?

A

Anopheles bite overnight, Aedes bite during day

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4
Q

What is the gold standard for malaria testing, and the pros and cons of different types?

A

Microscopy

Microscopy
Considered gold standard
Requires technician and a laboratory
Sensitivity and specificity may vary depending on quality of the slides, reagents and operator skills
Can assess severity

Rapid diagnostic tests
Simple to use
Sensitivity/specificity depends on antigen, parasite density

PCR
Highly sensitive and specific
Require (expensive) equipment and trained staff
Not suitable for point-of-care testing

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5
Q

What is the ecology of aedes?

A

Likes clean water
Day biter

Ae. aegypti and Ae. albopictus are distributed worldwide and overlapping (aegypti mostly tropical + urban + inside, originated from Africa, albopictus tropical and temperate + rural + outside, originated from Asia)

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6
Q

What is the global burden of malaria?

A

250million cases per year
500 000- 1m deaths per year
8% of childhood deaths in LMICs
2.4 million people at risk
87 countries are endemic

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7
Q

Which mosquito transmits malaria?

A

Female anopheles at night

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8
Q

What animal reservoir is associated with P. Knowlesi?

A

Macaques

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9
Q

What is the epidemiology of P. Falciparum

A

Sub-Saharan Africa, India, Sri Lanka
A little smattering In South America
90% of severe falciparum occurs in children in Sub-Saharan Africa

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10
Q

What is the epidemiology of P. Vivax?

A

Temperate zones and the sub-tropics
Notably ABSENT from West-Africa
70-80 million cases per year
Most common cause of malaria

To re: There are Anti-Vaxers in West Africa

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11
Q

What is the epidemiology of P. Ovale?

A

West Africa
Philippines
Papua New Guinea
Indonesia
SE Asia

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12
Q

What is the epidemiology of P. Malariae?

A

Sub-Saharan Africa
Amazon basin and south america
South East Asia
Western Pacific islands

Probably under-reported and under diagnosed (unlike all other malaria) as the presentation can be ‘subclinical’

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13
Q

What is the epidemiology of P. Knowlesi?

A

Borneo and malaysia
Absent in Africa

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14
Q

What ‘diseases’ are associated with conferring protection against severe malaria?

A

G6PD deficiency
Duffy Blood Group
Thalassaemia
Sickle Cell Disease

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15
Q

What is the epidemiology of P. Vivax?

A

Temperate zones and the sub-tropics
Notably ABSENT from West-Africa
70-80 million cases per year
Most common cause of malaria

To re: There are Anti-Vaxers in West Africa

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16
Q

What are the factors described in the Ross-McDonald model which determine the risk of malaria occurring in an area?

A
  1. Mosquito factors
    - Number of female mozzies
    - life span of mozzies
    - biting potential of mozzies (need to bite at least to keep up the transmission of malaria)
  2. Human factors
    - duration of infection within humans
  3. Mosquito/human interactions

** Does not account for immunity or super infections

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17
Q

In terms of epidemiology, what is Ro?

A

Ro is number of secondary infections produced by a single infection introduced into a fully susceptible host (i.e. human) population
* If Ro>1 then the infection will spread.
* The goal of eradication efforts is to get Ro<1

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18
Q

In terms of epidemiology, what is aEIR?

A

(annual) Entomological inoculation rate

  • The number of infectious bites per person (invariably per year)
  • Gold standard is ‘human bite catches’ –> i.e. catching mozzies, testing them for sporozoites, then estimating how many bites you think a mozzie can give in its lifetime, compared against the population of the area
  • Other ways e.g. spray huts, count number of infectious mosquitos, divide by number of people in the hut.
  • Infectious mosquitoes defined as those with malaria parasites (sporozoites) detected in the head
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19
Q

In terms of epidemiology, what is the difference between stable and unstable malaria?

A
  • stable malaria: insensitive to natural and man-made perturbations.
    People living in highly endemic areas usually exhibit a high level of immunity and tolerate the infection well.
  • unstable malaria (very sensitive to climate and very amenable to control

Unstable (epidemic) malaria refers to a seasonal type of transmission seen in areas of low endemicity, or to outbreaks in areas previously without malaria, or among non-immune persons. Epidemics can be due to changes in human behaviour, environmental and climate factors. For example, human migration and resettlement can introduce malaria into an area that did not have it previously, and this can expose a population to the disease that was not immune to malaria. Malaria epidemics generally occur when the population in an area has weak immunity to the disease, because so many people in the population will be vulnerable to malaria, not just children under five years of age and pregnant women.

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20
Q

What is the main parasite associated with:
- Stable Malaria?
- Unstable malaria?

A
  • P. Falciparum

-p Vivax

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21
Q

Which population group(s) are most at risk in:
- Stable malaria
- Unstable malaria

A

Stable: Pregnant women and children (the rest of the population have developed immunity to malaria over time

Unstable: Everyone; increased risk of local epidemics

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22
Q

What is the life cycle of Malaria?

A

The malaria parasite life cycle involves two hosts.
1. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host
2. Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver (if untreated) and cause relapses by invading the bloodstream weeks, or even years later.)
3. After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony)
4. Merozoites infect red blood cells forming trophozoites.
5. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites OR Some parasites differentiate into sexual erythrocytic stages (gametocytes)
6. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal
7. The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes.
8. The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts.
9. The oocysts grow, rupture, and release sporozoites, which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle.

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23
Q

What are the characteristic pathophysiological features of P. Falciparum infection?

A

The most characteristic biological features:
1. It infects mature and young erythrocytes
2. The surface of erythrocytes infected with late stage trophozoites or schizonts is altered so they stick to endothelial cells in various tissues (cytoadherence)
3. The pre-erythrocytic cycle starts immediately after injection of the sporozoites by the mosquito
4. Schizogony is particularly prolific in all stages (pre-erythrocytic, erythrocytic and sporogony) that may be the cause of its success as a species and its virulence
5. Infection in the peripheral blood is characterized by the presence of ring forms and gametocytes, whereas late trophozopites and schizonts are only seen exceptionally
6. The level of parasitaemia may be high and multiple infection in a single erythrocyte is
common
7. The gametocytes are characteristically crescent-shaped and, unlike the gametocytes of other species, are very slow to reach maturity (up to 10 days) and early forms of
gametocytes are sequestered

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24
Q

What is sequestration? Why is it important?

A

In P. falciparum only the early trophozoites (ring forms) are present in the peripheral blood and later developmental stages are sequestered in the capillaries of various organs. This sequestration is caused by the adherence of infected erythrocytes to capillary endothelial cells

Sequestration has important consequences for the diagnosis of falciparum malaria, because it means that parasites may not be found on a blood film at a time when the clinical picture is most suggestive of malaria.

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25
Q

Do gametocytes get sequestered?

A

Yes - they can be found sequestered in spleens and bone marrow while they are maturing.

They also can sequester in peripheral surface capillaries, likely so that they are most accessible to mosquitos during a blood meal

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26
Q

What are the characteristic pathphysiological features of P. Vivax infection?

A
  1. Restriction of erythrocyte invasion to reticulocytes bearing Duffy blood group determinants (explains why RBCs infected with trophozoites of P. vivax are sometimes described as larger than normal
  2. The presence of caveolar structures on the surface of the infected erythrocyte membrane
    take up stain, and are described as Schüffner’s dots
  3. After invading the hepatocyte some, or all, of the sporozoites may transform into
    hypnozoites, then remain latent for months or years and be responsible for subsequent
    relapses.
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27
Q

What are the characteristic pathohysiological features of P. Malariae infection?

A
  1. An apparent preference for old erythrocytes, explaining why infected cells are often described as ‘smaller’ by microscopists
  2. The presence of ‘knobs’ at the surface of infected erythrocytes, which are similar to P.
    falciparum, but the cells do not exhibit any cytoadherence (and so no sequestration)
  3. The surface of infected erythrocytes does not exhibit any caveolar/vesicle complexes and, consequently, Schüffner’s dots are absent
  4. Sporozoites of P. malariae do not transform into hypnozoites, and so there are no relapses. However P. malariae can survive for a very long time in the peripheral blood (10 years or more) at a very low level of parasitaemia occasionally producing detectable peaks with a recrudescence of clinical symptoms.
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28
Q

What is the clinical presentation of uncomplicated malaria?

A

Fever
Headache
Malaise
Anorexia
Nausea + Vomiting
Thirst
Abdo pain
Altered sleep
Anaemia

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29
Q

What is the clinical presentation of P. Vivax and P Ovale?

A

‘Benign’ tertian malaria
Relapsing Malaria

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30
Q

Which two species of plasmodium cause relapsing malaria?

A

P. Vivax
P. Ovale

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31
Q

What is the clinical presentation of P. malariae?

A

Quartien Malaria
‘Low parasitaemia’ with the ability to cause chronic infections with few clinical symptoms

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32
Q

What are the clinical presentations associated with P. Falciparum (or severe malaria caused by Vivax/Knowlesi)

A

Severe Malaria, and rapid progression to severe malaria from initial infection
Cerebral Malaria
Shock
Lactic Acidosis
Hypoglycaemia
Anaemia
Renal Failure
Pulmonary Oedema
Tropical Splenomegaly
Sepsis and concurrent underlying bacterial infection
Death
Pregnancy Complications
- Stillbirth
- Preterm birth
- low birth weight

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33
Q

What is the parasitaemia percentage in peripheral blood in severe malaria in:
- Adults
- Children

A

2% is significant

Some debate - in endemic settings may be 5-10%, usually 2% in non-endemic, 2% in knowlesi. Refer to WHO and local guidelines.

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34
Q

How does Cerebral malaria present in children?

A

Low Blantyre coma score
Seizures
Retinal changes
Abnormal posturing (opisthotonus)

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35
Q

What is the pathophysiology of cerebral malaria?

A
  1. Increased cytokine activity leading to large inflammatory processes
  2. Sequestration within the cerebral blood vessels
  3. Coagulopathy at sites of cell adherence and sequestration
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36
Q

What clinical complications are assocaited with P. Vivax/p Ovale?

A

Splenic rupture
Malaria recurrence
Anaemia
Debilitating fevers

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37
Q

What clinical complications are associated with P. Malariae?

A

Glomerulonephritis and Nephrotic syndrome

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38
Q

Name 5 malaria species which infect humans

A

Falciparum, vivax, ovale, malariae, knowlesi

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39
Q

What is the vector of malaria?

A

Female anopheles mosquito

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40
Q

How many malaria cases + fatalities / year?

A

Incidence = 300 million
Deaths = ~0.5 - 1 million

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41
Q

Name 6 ways to measure endemicity of malaria

A
  1. parasitaemia
  2. spleen rate
  3. oocyst rate
  4. sporozoite rate
  5. immunity rate
  6. ecological approach
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42
Q

What is the “parasitaemia” approach to measuring malaria endemicity?

A

Age specific prevalence of parasitaemia, usually measured in 2-10 year olds

hypoendemic = <10%
mesoendemic = 10-50%
hyperendemic = 50-75%
holoendemic = >75%

hypoendemic + mesoendemic = unstable transmission
hyperendemic + holoendemic = stable transmission

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43
Q

What is the “spleen rate” approach to measuring malaria endemicity?

A

Age specific prevalence of splenomegaly in endemic area

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44
Q

What is the “oocyst rate” approach to measuring malaria endemicity?

A

Frequency of mosquitos found with oocysts in stomach in endemic area

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45
Q

What is the “sporozoite rate” approach to measuring malaria endemicity?

A

Frequency of mosquitos found with oocysts in salivary glands in endemic area

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46
Q

What is the “immunity rate” approach to measuring malaria endemicity?

A

Age specific prevalence of serological evidence of past / present infection (eg antibodies against sporozoites)

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47
Q

What is the “ecological” approach to measuring malaria endemicity?

A

Defining epidemiology by environment, eg Savannah, agriculture, urban slums etc

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48
Q

Name 4 ways malaria can be transmitted

A
  1. Bite by infected female anopheles mosquito
  2. Receipt of blood / organ transfusion from infected donor
  3. Transplacental, although rare. Usually seen in areas of unstable tx / children born to non immune mothers
  4. “Airport malaria”, bite outside of endemic area by a mosquito imported in luggage / aeroplane
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49
Q

What is the infective stage of the plasmodium life cycle?

A

Sporozoite

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50
Q

What is the diagnostic stage of the plasmodium life cycle?

A

Trophozoites ( / schizont / gametocyte)

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51
Q

What stage of plasmodium replication occurs in the human hepatocytes?

A

Asexual pre-erythrocytic schizogony

(development from sporozoite –> schizont)

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52
Q

What stage of plasmodium replication occurs in human erythrocytes?

A

Asexual erythrocytic schizogony

(development from trophozoite –> gametocyte)

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53
Q

What stage of the plasmodium lifecycle invades erythrocytes?

A

Merozoites

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54
Q

What stage of the plasmodium lifecycle is taken up by mosquitos to continue the cycle?

A

Gametocytes (distinct male and female)

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55
Q

By what type of reproduction does the plasmodium parasite replicate by

A

Both sexual and asexual
It is apicomplexia parasite
Sexual replication occurs in mosquito gut
Asexual replication occurs in humans (both in hepatocytes and erythrocytes, replication by schizogony)

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56
Q

What is the clinical syndrome of malaria?

A

Fever, splenomegaly, anaemia

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57
Q

What is the fever pattern of falciparum malaria?

A

Quotidian, though often random / constant

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58
Q

What is the fever pattern of vivax / ovale malaria?

A

Tertian (every 3rd day)

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59
Q

What is the fever pattern of p. malariae malaria?

A

Quartan (every 4th day)

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60
Q

What is the fever pattern of p. knowlesi malaria?

A

Quotidian (daily)

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61
Q

What are some of the systemic features of malaria?

A

FEVER –> cyclical with parasite development

HYPOGLYCAEMIA –> more common in children, mimics CNS malaria

NEUTROPAENIA –> +/- secondary bacterial infection

ANAEMIA –> severe in 0.5 to 2 year olds & pregnancy. Associated w retinal haemhorrage and hepatorenal dysfunction

ACIDOSIS –> 2ndary to impaired tissue perfusoin from parasite burden / anaemia / hypotension

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62
Q

What organ systems can be implicated in malaria?

A

CNS, respiratory, renal, spleen, retina

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63
Q

What are the features of CNS malaria?

A

Altered consciousness, coma, seizures. Meningitic signs rare. Occurs due to parasite sequestration in cerebral blood supply. Beware hypoglycaemia mimic

64
Q

What are the features of respiratory complications in malaria?

A

SOB (fever, acidosis), ARDS (more common in non immune adults), pulmonary oedema, secondary bacterial pneumonia

65
Q

What are the features of renal complications in malaria?

A

AKI caused by acute tubular necrosis.

Nephrotic syndrome seen in p. malariae

Blackwater fever

66
Q

What are the outcomes seen in cerebral malaria?

A

20% treated mortality. 10% neurological sequelae eg cortical blindness, hemiparesis, ataxia

67
Q

What is blackwater fever?

A

Massive haemoglobinuria –> “coca cola urine”

More common in G6PD deficiency

Cr >265, pre-renal and renal AKI

45% untreated mortality, low mortality if dialysis available

68
Q

What is the mechanism of jaundice in malaria?

A

All of haemolysis, hepatocellular damage, and cholestasis.

–> therefore conjugated and unconjugated bilirubin seen

Jaundice more common in adults

69
Q

What are the complications for the neonate of malaria in pregnancy?

A

Placental sequestration of RBC –> low birth weight –> increased neonatal mortality and morbidity

Congenital malaria with infant parasitaemia incidence ~50% in areas of stable transmission. Symptomatic neonatal illness is rare

70
Q

What are the complications for the mother in malaria in pregnancy?

A

More likely to get severe malaria, anaemia, hypoglycaemia, acute pulmonary oedema. Worse in G1P0. Premature labour common

71
Q

What are the 6 clinical features of severe malaria?

A
  1. Low GCS / seizures
  2. Prostration
  3. Respiratory distress
  4. Shock (SBP <80 or <50 in kids)
  5. Jaundice
  6. Bleeding
72
Q

What are the 7 laboratory features of severe malaria?

A
  1. Hypoglycaemia <2.2
  2. Metabolic acidosis bicarb <15
  3. Anaemia <70 (or <50 in kids)
  4. Haemaglobinuria
  5. Hyperparasitaemia
  6. Lactate >5
  7. AKI Cr >265
73
Q

Name 5 examples of innate immunity against malaria

A

4 haemaglobinopathies:
1. Sickle cell
2. G6PD deficiency
3. Thalassaemia
4. Ovalocytosis

and 5. Duffy antigen deficiency (duffy antigen used by p. vivax to enter RBC. Duffy antigen deficiency common in Africa hence P. Vivax rare in Africa)

74
Q

Describe acquired immunity in malaria

A

Repeated exposure to parasites, more so from parasites with genetic variation –> acquired immunity. Children remain susceptible to non life threatening febrile illness, which is rare by adulthood

75
Q

Describe neonatal immunity in malaria

A

Common in areas of stable transmission. Maternal antibodies provide protection for first 6.12 of life. Most susceptible aged 0.5 to 5 years once congenital immunity disappears and before acquired immunity starts

76
Q

List one negative and one positive of thick films in malaria

A

Positive: highly sensitive
Negative: requires expertise / platelet debris easily mistaken for parasites

77
Q

List one negative and one positive of thin films in malaria

A

Positive: highly sensitive / allows species diagnosis / allows parasitaemia calculation
Negatives: not as sensitive as thick film

78
Q

What are the features of falciparum trophozoites on a thin film?

A

RBC: any size and shape
Dots: Maurer’s clefts (irregularly spaced, sparce)
Parasite: neat rings, accolé, multiple per RBC

79
Q

What are the features of vivax trophozoites on a thin film?

A

RBC: large reticulocytes, hyperplastic
Dots: Schuffner’s dots (lots of them, regularly spaced)
Parasite: vivacious, large, messy, one per RBC

80
Q

What are the features of ovale trophozoites on a thin film?

A

RBC: oval, fimbriated
Dots: James’ dots (like Schuffner’s dots but larger)
Parasite: neat but chunky ring

81
Q

What are the features of malariae trophozoites on a thin film?

A

RBC: small, old RBCs
Dots: usually absent
Parasite: band form, ‘owl eye’ ring form (rare)

82
Q

What are the features of knowlesi trophozoites on a thin film?

A

RBC: normal size and shape
Dots: usually absent
Parasite: early trophozoites look like falciparum, later ones look like malariae with band forms

83
Q

What are the features of falciparum schizonts on a thin film?

A

Does not fill RBC
Rarely seen unless severe malaria
18-20 merozoites / schizont
Dark staining haemazoin

84
Q

What are the features of vivax schizonts on a thin film?

A

Fills RBC
RBC large
18-20 merozoites / schizont
2 patches of dark staining haemozoin usually seen

85
Q

What are the features of ovale schizonts on a thin film?

A

RBC not always fimbriated or oval shaped
Does not fill RBC
8-10 prominent dark merozoites / schizont

86
Q

What are the features of malariae schizonts on a thin film?

A

Fills RBC
Rosetting
8-10 merozoites / schizont

87
Q

What are the features of knowlesi schizonts on a thin film?

A

RBC not filled, of normal size and shape
16 merozoites / schizont

88
Q

What are the features of falciparum gametocytes on a thin film?

A

Banana shaped whoo
Dark granules of pigment seen around the nucleus
Remain in blood up to 4/52 after successful treatment

89
Q

What are the features of vivax gametocytes on a thin film?

A

Large and round with even distribution of colour
Lighter staining than lymphocyte, otherwise v similar

90
Q

What are the features of ovale gametocytes on a thin film?

A

RBC oval and fimbriated
Does not fill cell
Coarse James’ dots present
Pretty similar looking to trophozoite stage

91
Q

What are the features of malariae gametocytes on a thin film?

A

Fills RBC
Really looks like lymphocyte
Keep your eye out for stained haem - this is main distinguishing factor from lymphocyte

92
Q

What are the features of knowlesi gametocytes on a thin film?

A

Large, pale staining, round in shape. Looks a lot like vivax. Nil distinguishing

93
Q

What is the management of non falciparum malaria?

A

CHLORAQUINE + PRIMAQUINE

Chloraquine:
- P. vivax resistance common in Peru + Oceania –> use ACT
- Some p. vivax resistance to chloraquine in PNG / Indonesia

Primaquine:
- Needed in vivax + ovale to kill liver stage hypnozoite
- Beware haemolysis in G6PD, give lower doses over longer course
- Not for use in pregnancy

94
Q

What is the management of uncomplicated falciparum malaria?

A

ACT
3/7 Malarone = atovaquone + proguanil

3/7 Riamet = artemether + lumefantrine

7/7 Quinine + doxy / clindamycin if pregnant or <8 yrs old

95
Q

What is the management of complicated falciparum malaria?

A

IV rx for any complication / parasitaemia >2% followed by full course oral ACT once well enough

1st line =Artesunate
–> given IV to all, incl children, pregnant / breast feeding women

2nd line = IM artemether

3rd line = IV quinine (beware hypoglycaemia + arrythmia)

96
Q

Management of malaria in pregnancy

A

Can use ACT in all trimesters now

97
Q

Management of malaria in breastfeeding women

A

Follow standard procedure

Avoid: dapsone, primaquine, doxy / tetracyclines

98
Q

Chemoprophylaxis of malaria in travellers to endemic areas

A

Malarone (atovaquone + proguanil)
- start 1/7 before exposure
- stop 7/7 after exposure

Primaquine
- start 1/7 before exposure
- stop 7/7 after exposure

Mefloquine (beware psychiatric effects):
- start 2/52 before exposure
- stop 4/52 after exposure
- good in pregnancy

All other chemoprophylaxis:
- start 1/52 before exposure
- stop 4/52 after exposure

99
Q

Briefly describe IPTP

A

IPTP = intermittent preventative treatment in pregnancy

Start from 2nd trimester

Recommended at least 3 doses of SP (sulphadoxine pyrimethamine) before delivery one month apart

Recommended for all pregnant women in endemic areas in Africa

100
Q

Name 6 practical measures to reduce malaria

A
  1. Insecticide impregnated bednets
  2. Long sleeve clothing
  3. DEET + other repellants
  4. Indoor residual spraying
  5. Mosquito habitat destruction
  6. Test and treat!
101
Q

What are the SDG goals for malaria?

A

Comparing 2015 to 2030:
- Reduce cases of malaria by 90%
- Reduce deaths from malaria by 90%

102
Q

What is the name of the magic equation that tells us how to eradicate malaria? (And what is the difference between eradiation and elimination?)

A

Equation = Ross MacDonald

Elimination = ridding one area of malaria

Eradication = ridding the world of malaria

103
Q

With regards to malaria control + the Ross MacDonald equation, how can we reduce the number of moquitos / person?

A
  • Chemical larva control
  • Destruction of breeding sites (think of different breeding sites for different vectors)
  • Release sterile male mosquitos
    or… increase the number of people (hence why malaria transmission is lower in urban areas than rural areas)
104
Q

With regards to malaria control + the Ross MacDonald equation, how can we reduce the biting rate of mosquitos?

A
  • Bed nets, particularly with insecticide
  • Long sleeve clothing
  • DEET and other repellents
105
Q

With regards to malaria control + the Ross MacDonald equation, how can we reduce susceptibility of mosquitos?

A
  • Genetic modification CRISPR / CAS 9
  • Breed mosquitos at warmer temperatures to strengthen their immune system so they can fight off their own malaria
  • Vaccinate against gametocytes (doesn’t prevent infection of vaccinee but does prevent them from transmitting)
106
Q

With regards to malaria control + the Ross MacDonald equation, how can we reduce susceptibility of humans?

A

Vaccines!
Mosquirix recommended, R21 in trials

107
Q

With regards to malaria control + the Ross MacDonald equation, how can we reduce mosquitos surviving long enough for the malaria incubation cycle to complete and for the mosquito to become infective?

A
  • Shorten their life with insecticide, IRS
  • Lengthen the incubation time of the malaria parasite inside the mosquito by lowering global temperatures (boo to global warming)
108
Q

With regards to malaria control + the Ross MacDonald equation, how can we increase the human recovery rate?

A

Early diagnosis
Effective treatments

109
Q

What are the three potential targets for malaria vaccination?

A
  1. Pre-erythrocytic vaccine
    - Mosquirix (WHO recommended) / R21
    - Targets sporozoite
    - Prevents infection
  2. Asexual blood stage
    - Targets merozoites
    - Anti disease
  3. Gametocytes / ookinetes / oocytes
    - Does not prevent infection but does prevent transmission
    - Effect happens inside the mosquito –> blocking fusion of gametes –> break lifecycle –> reduce transmission
110
Q

Briefly explain the WHO recommended malaria vaccine

A

Recommended vaccine = mosquirix/RTS’S
(R21 still in trials)

Pre erythrocidal

Targets sporozoites –> prevents infection

Adjuvant vaccine, 3 doses required

Fused to Hep B proteins

32% effective at reducing severe malaria
9% effective at reducing death
(R21 ~ 75% effective)

111
Q

What are the habits of anopheles gambiae?

A

Feeding = humans, night time biter

Resting site = indoors, ceiling / walls

Larvae = small, open, sunlit pools of fresh water (eg animal footprints, tyres). Develop quickly 2/52 as their habitats dry out

112
Q

What are the habits of anopheles arabiensis?

A

Feeding = livestock

Resting site = outdoors

Larvae = small, open, sunlit, clean water eg animal footprints and tyres. Develop quickly 2/52 to avoid habitat drying out before they are developed

113
Q

What are the habits of anopheles futensus?

A

Feeding = humans, night time biter

Resting site = indoors, especially in rainy season

Larvae = swampy, like shrek. Develop slowly over 4/52 as their habitat doesn’t dry out, but need to be small and hide in the vegetation to avoid being eaten up by the fishies. Dry season –> less malaria by futensus as their habitat is smaller

114
Q

Which mosquitos are affected by indoor residual spraying?

A

Anopheles gambiae + futensus

Arabiensis gets away with it because it lives outside with livestock boo

115
Q

Which mosquitos are affected by habitat destruction such as removing discarded tyres and plantpots, filling in tyre tracks and animal footprints?

A

Anopheles gambiae and arabiensis

They like small sunlit pools (don’t we all)

Futensus gets away with it living in its fetid swamp like shrek

116
Q
A

P.falciparum
Trophozoite

Neat parasite with Maurer’ clefts in normal sized RBC

117
Q
A

P.falciparum
Trophozoites

Neat rings with Maurer’s clefts in normal sized RBC
& an accole form

118
Q
A

P.vivax
Trophozoite

Enlarged RBC with untidy parasite, Schuffners dots & some pigment

119
Q
A

P.vivax
Trophozoite

Enlarged RBC with irregular ring & Schuffners dots

120
Q
A

P.vivax
Gametocyte

Filling the whole enlarged RBC

121
Q
A

P.vivax

Gametocyte on the left
Schizont on the right

Both are enlarged RBC’s

122
Q
A

P.falciparum
Trophozoites

See double chromatin (headphones) & accole forms in normal sized RBC

123
Q
A

P.falciparum
Trophozoite

Neat parasite with Maurer’ clefts in normal sized RBC

124
Q
A

P.vivax
Trophozoite

Enlarged RBC with untidy parasite, Schuffners dots & some pigment

125
Q
A

P.malariae
Gametocyte

Smaller RBC completely filled

126
Q
A

P.vivax
Schizont

Enlarged RBC with Schuffners dots & pigment

127
Q
A

P.ovale
Gametocyte

Oval, fimbriated cell with coarse James’ dots & parasite does not fill the cell

128
Q
A

P.ovale
Gametocyte

Slightly fimbriated cell with coarse James’ dots & parasite does not fill the slightly enlarged cell

129
Q
A

P.vivax
Early schizont

Enlarged, plastic cell with untidy parasite with 2 nuclei & schuffners dots

130
Q
A

P.falciparum
Schizont

Normal sized RBC containing maurer’s clefts, neat parasite with multiple nuclei that does not fill the cell & a clump of black pigment

131
Q
A

P.vivax
Trophozoite

Enlarged RBC, Schuffners dots, irregular/untidy parasite

132
Q

How do you calculate parasitaemia percentage?

A
  1. Count the number of parasitised cells (not number of parasites) in a field of view
  2. Count the number of parasitised cells (X) in 8 consecutive fields, either in an upwards or downwards direction.
  3. Calc %=(X÷2)/10

ALWAYS calculate percentage parasitaemia for P.falciparum infections

There are ~250 RBC’s per field of view

133
Q

What does this show?

A

Plasmodium spp. on Thick Blood Film

The WBC’s are purple and the background is pale. The RBC’s are lysed, releasing the parasites

134
Q
A

P.falciparum
Gametocyte
on Thick Blood Film

There is a neat banana shaped parasite, on a pale background where the RBC has lysed, releasing the parasite.

Difficult to speciate on thick films due to loss of RBC features

135
Q
A

P.malariae
Schizont

Classic ‘Daisy head’ schizont with 8-10 merozoites, central pigment, filling the whole RBC which is slightly smaller in size.

136
Q
A

P.malariae
Gametocyte

See nucleus with scattered yellow/gold pigment in smaller RBC.
Usually they fill the whole cell but there are no dots/stippling in cytoplasm which indicates P.malariae

137
Q
A

P.ovale
Trophozoite

Neat parasite with thick loop of cytoplasm in normal sized RBC with fimbriations an coarse James’ dots.

138
Q
A

P.ovale
Schizont

Oval shaped RBC containing perfectly round parasite with merozoites and pigment, that does not fill the whole cell.
May also see fimbriations

139
Q

How long does malaria incubate for after the bite?

A

10-15 days

140
Q

What is the basic treatment of malaria?

A

Severe? IV artesunate for at least 24 hours (not available? quinine)

Non severe:
ACT - artemisinin + mefloquine, lumefantrine, or sulfadoxine/pyrimethamine
(Riamet best) for three days

If no artemisinin then quinine plus doxycycline

If vivax or oval chloroquine then need to use primaquine unless G6PD or pregnant or child to target hynozoites/gametocytes (blood stage)

141
Q

Where is artemisinin resistance emerging?

A

Southeast Asia

142
Q

Why is falciparum more severe?

A
  • Higher number of merozoite per hepatocyte and schizont
  • Quicker multiplication * RBC age preference
  • P. falciparum: young and mature RBC
  • P. vivax and P. ovale: very young RBC (reticulocyte)
  • P. malariae: mature RBC
  • Sequestration
143
Q

What are TACTs in malaria?

A

Triple ACT (TACTs)
* Add one more drug with long half-life to ACTs
* AL + amodiaquine
*Dihydroartemisinin/ piperaquine + mefloquine
* To prevent emergence and spread of artemisinin and ACT partner-drug resistance in southeast Asia to India and sub-Saharan Africa

144
Q

Define the two types of treatment failure - early and late - in malaria?

A
  • Early treatment failure: parasite count on day 3 higher than that on day 1, fever
    >=37.5°C more than day 4 of treatment
  • Late treatment failure
  • Late clinical failure:fever >=37.5°C more than five days after treatment initiation
  • Late parasitological failure:Fever and parasitemia more than 8 days after parasite clearance
  • Recrudescence: results from remaining blood stage parasites (all species but mostly P. falciparum)
  • Relapse: results from maturation of persistent hypnozoite in liver (P. vivax and P. ovale)
145
Q

What are the usual CSF results for cerebral malaria?

A

Usually normal
Sometimes mildly high WBC, low glucose, high protein

146
Q

Why might there is a false negative on a malaria RDT?

A

Operator issues
Badly stored (temp)
Low parasitaemia
Certain types of p.falciparum (histidine- rich protein 2/3 (pfhrp2/pfhrp3) gene deletions - esp S America/Amazon)

147
Q

How is a parasitaemia counted?

A

Manually
Count where RBCs touching but not overlapping
Ideally count 2000 RBCs i.e 8 fields
Then divide by 20 = %
>2 significant
Can gauge clinical response

148
Q

What must you advise people with taking Riamet?

A

Do not take on empty stomach, otherwise won’t absorb and may recrudesce

149
Q

What is best prophylaxis for malaria?

A

Malarone = targets lover stage

Otherwise doxy or mefloquine (latter good for pregnant pts)

150
Q

What is the alternative to primaquine if G6PD?

A

Can use at lower intervals e.g. weekly for eight weeks or reduce dose by 75%
OR weekly chloroquine for a year
OR just monitor patient for relapse

151
Q

Where is chloroquine resistance found?

A

SE Asia esp Thailand, PNG

152
Q

What are some patient-related risk factors for mortality in malaria?

A

VFR
No ppx
Pregnant
Old

153
Q

How quickly should patients respond to treatment?

A

Should be afebrile by day 4, with the parasitaemia reducing by day 3

154
Q

Why is P. falciparum so much more dangerous?

A
  • The parasite replicates more quickly than other species (except P.knowlesi) achieving high parasite counts
  • Antigens expressed by P. falciparum infected Red Cells adhere to receptors on endothelial cells in vital organs: brain, kidneys, liver, muscle beds
  • This process is called Sequestration and leads to organ dysfunction
  • Sequestration also prevents clearance by spleen of infected red cells
155
Q

What is blackwater fever, what causes it and how is it managed?

A
  • Intravascular haemolysis with haematuria
  • May lead to acute kidney injury
  • Rare complication of malaria, most commonly P falciparum, but
    also P vivax
  • May be direct consequence of high parasite burden and cell rupture
  • Or may be complication of anti-malarial treatment – Artesunate,
    Quinine implicated
  • Or Primaquine induced G6PD Haemolysis
  • Transfuse and maintain urine output
  • Mortality 2%
156
Q

How many merozoites does each malarial schizont have?

A

Falciparum - 18-20 in grape life cluster (cell not filled). Small

Ovale - 6-12 irregular or clock face (doesn’t fill cell)

Vivax - 12-24, Irregular

Malariae - Up to 12, rosette or daisy pattern. Small

157
Q

What is the Blantyre Coma Score?

A

Assess cerebral malaria in children
5= normal
<5 = abnormal

Not specific

Nagasaki Flashcard Extravaganza (34 decks)

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