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haematology > Malaria > Flashcards

Malaria Flashcards

1
Q

What could be making the incidence fall?

A

Prevention (*Gates foundation)

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2
Q

What could be making the incidence rise?

A

resistance of parasite to antimalarials/mosquitoes to insecticides

increased travel to endemic areas

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3
Q

what are the 4 species of plasmodia that cause human malarial disease?

A 
P (plasmodium)
P. falciparum
P. ovale
P. vivax
P. malariae
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4
Q

Features of infection with P. vivax

A

incubation 10-17 days

fever spikes every 48hrs

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5
Q

Features of infection with P. ovale

A

similar to P.vivax

except untreated infection does not last long

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6
Q

Which 2 species are referred to as benign tertian malaria?

A

P.vivax + p.ovale

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7
Q

what may both of the benign tertian malarias produce?

A

relapses = invasion of blood by latent hypnozites in liver, up to a few years after complete clearance of parasites from blood

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8
Q

Features of P.malariae

A

incubation 18-40 days
recurs 72-hrly

can lie low in blood and reappear between 1-52yrs

rarely fatal

may cause glomerulonephritis

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9
Q

Features of p.falciparum

A

incubation 7-10 days

recurs 36-48hourly

fulminating disease (occurs suddenly)

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10
Q

what are the vectors in malaria?

A

female anopheles mosquitos

parasite undergoes temp dependent cycle of development in gut of insect

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11
Q

what does the mosquito inject into the human host?

A

plasmodium protozoa

it multiplies in human RBCs

  • -> haemolysis
  • -> cytokine release
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12
Q

Human liver stages

-exo-erythrocytic cycle

A

Mosquito takes blood meal = human bite = injects sporozites (immature parasite)
Protozoa is filtered into liver  infected hepatocyte
In the liver sporozites mature  exoerythrocytic schizonts
Schizonts escape by rupturing the hepatocyte they matured in

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13
Q

How do p.ovale and p.vixav cause relapse months later?

A

they lie dormant as hypnozoites in hepatocytes

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14
Q

Human blood stage pathway#1 (leading to ruptured schizont)

  • erythrocytic cycle
A
  • forms immature trophozoite (ring stage)
  • -> mature trophozoite in RBC
  • -> mature into Schizont
  • -> rupture RBC it matured in

–> infect more RBCs and erythrocytic cycle continues

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15
Q

Human blood stage pathway#2
(producing gametocytes)

  • erythrocytic cycle
A
  • forms immature trophozoite (ring stage)
  • -> gametocytes
  • -> replicate DNA and produce strains of parasite
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16
Q

Mosquito stage (sporogonic cycle)

A

mosquito takes a blood meal = bites human = uptaking gametocytes

fertilization + development of sporozites in mosquito gut occurs

–> infective stage –> cycle continues

17
Q

detail of the fertilization of spopzites in mosquito gut

A

Flagellated microgametocyte received joins the macrogametocyte → ookinete → oocyte

Oocyte rupture = release of sporozoites

Migration of new sporozoites to mosquito salivary gland

18
Q

Severe P.falciparum malaria can result in what?

A

cerebral malaria, fatal infection!!

sequestration of parasitized erythrocytes in microvasculature of vital organs = tissue hypoxia and widespread organ damage

19
Q

Complications of cerebral malaria

A 
shock 
metabolic acidosis
hypoglycaemia
renal failure
ARDS
20
Q

Rx for cerebral malaria

A

anti-malarials in full dose ASAP
parenteral artesunate > quinine
IV then oral

21
Q

what are merozoites?

A

1.any protozoan cell produced by the fission of a schizont, e.g. that of the malaria protozoan

22
Q

when does the pt become symptomatic?

A

merozoites/schizonts are released into the bloodstream

fever and haemolysis

23
Q

Presentation

A

fever paroxysms (sudden attack) = synchronous release of flocks merozoites from mature schizonts

  1. shivering
  2. hot stage (T>41); flushed, dry skin, nausea/vom, headache
  3. sweats (3hrs) as temp falls
24
Q

Symptoms

A

Fever in a recent traveller!!
90% present within 1 month of mosquito bite
- prodromal headache (prodrome = early symptom)
- chills/sweats, rigors
- malaise, fatigue
- myalgia, anorexia
- vom, nausea, diarrhoea
–> may be no pattern to fever spikes initially

25
Q

Signs

A

ANAEMIA, JAUNDICE, HEPATOSPLENOMEGALY,

NO RASH OR LYMPADENOPATHY

26
Q

Serious signs e.g. p.falciparum

A
  1. declining consciousness/coma
  2. convulsions/shock
  3. co-existing chronic illness
  4. acidosis
  5. renal failure
  6. ARDS
  7. hypoglycaemia
27
Q

Diagnosis - history

A

fever in returning traveller
mosquitos

more common areas: SE Asia, Sub-Saharan Africa

28
Q

Diagnosis - investigations

A

serial thin + thick blood films - (trophozoites)
FBC (anaemia, thrombocytopenia)
Mildly elevated transaminases e.g. ALT, AST
Clotting (disseminated intravascular coagulation)
glucose (hypoglycaemia)
ABG/lactate: (lactic acidosis)
U&E: (renal failure)

29
Q

What is the RDT?

A

rapid diagnostic (antigen) test = lateral flow assay = detects plasmodium antigens in blood

30
Q

Management

A

IV artesunate or IV quinine + supportive therapy

- if taken prophylaxis, dont use same drug for Tx

31
Q

If species unknown or mixed infection, treat as ________?

A

P.falciparum

32
Q

what is nearly all p.falciparum resistant to?

A

chloroquine

33
Q

what is chloroquine 1st choice for?

A

treating uncomplicated p.ovale, p.vivax and p.malariae

the 2 benign ones (p.vivax + p.ovale) are also treated with primaquine after chloroquine to prevent relapse

34
Q

treating uncomplicated p.falciparum

A

multidrug resistance common

WHO recommends combination therapy containing artemisinin derivatives (oral route if can swallow)

35
Q

Other treatments

A

monitor vital signs

tepid sponging and paracetamol for fever

transfuse for severe anaemia

36
Q

prophylaxis

A

e.g. doxycycline or malarone

doesn’t give full protection!

also need to take preventative measures: avoid mosquitoes

37
Q

protective traits

A

lack of G6PD
sickle-cell carrier (Ss)
Melanesian ovalocytosis

haematology (10 decks)

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