Patient fact sheet. Please use browser translation settings.
Also see statewide
Malaria Clinical Practice Guideline.
Background
Malaria is caused by infection with protozoan parasites of the genus Plasmodium, transmitted by female mosquitos of the genus Anopheles. Five species infect humans: P. falciparum, P. vivax, P. ovale, P. malariae and P. knowlesi. Microbiological and clinical features
vary between species (Table 1). In the mid 2000s, the prevalence of malaria in African refugees arriving in Australia was between 5-15%1-3 and as high as 25% in children from sub-Saharan Africa3. This reduced with the introduction of pre-departure screening in 2005 (known as the Departure Health Check (DHC) since 2012). This is a voluntary health check for humanitarian entrants in the week prior to departure for Australia. The DHC includes a rapid
diagnostic test (RDT) for malaria and treatment if positive,4 however screening is voluntary, and uptake is incomplete.
More recent Australian surveillance data (2012-22) recorded 3204 imported malaria cases (45% acquired in sub-Saharan Africa, 18% acquired in Oceania (predominantly Papua New Guinea), 12% acquired in South/Central Asia), with 58% cases P. falciparum and 32% P. vivax.5 A 2023 systematic review (23 studies, 4203 people) found the prevalence of malaria in migrant populations was 8.3% in people from sub-Saharan Africa (highest in migrants from Central Africa), 0% in people from Asia and 0.4% in people from Latin America.6 In 2017-2018, refugee health clinicians reported presentations of African children with P. falciparum malaria in South Australia and Victoria, and cases of P. vivax have been seen in arrivals from Afghanistan.7 From 2025 we have seen more arrivals from highly endemic areas such as Democratic Republic of the Congo.
2016 ASID guidelines recommend malaria screening in people travelling from/through endemic areas (Bangladesh, Bhutan, Burma, India, Pakistan, Sri Lanka, African source countries. Note: not Middle East or Egypt - Egypt declared WHO Malaria free from 2024).
- People living in endemic
areas develop anti-disease immunity followed by anti-parasite
immunity. They may have asymptomatic infection, however they are at
increased risk of symptomatic infection after migration as immunity
wanes.
- The highest burden of
disease occurs in young children (<5 years) prior to the
development of adequate immunity. This age group is at increased
risk of rapid deterioration, severe malaria, and death.
- Severe
malaria is malaria with signs of vital organ dysfunction (including hypoglycaemia) or
hyperparasitaemia (2% or greater). In general, only P. falciparum and (rarely) P. knowlesi causes severe disease.
- Cerebral
malaria is defined as a patient
with P. falciparum parasitaemia who does not respond to a
painful stimulus and has no other identified cause of
encephalopathy.8
- 98% of symptomatic
P. falciparum infections present within 3 months post
arrival, 57% of symptomatic non
falciparum infection present within 3 months post arrival and 96%
within 12 months.9
- Infections can occur with
multiple species, which affects treatment.
- Hypnozoites (dormant
liver forms) only occur in P. vivax and P. ovale - these may cause a relapse of disease, and they require additional treatment.
- Malaria is a nationally notifiable disease in Australia - see Australian Centre for Disease Control: Malaria.
Assessment
History
- Countries of origin and transit, time since arrival. Be aware of areas of documented partial artemisinin resistance: the Greater Mekong subregion (Thailand, Vietnam, Cambodia, Laos, Myanmar), East/Central Africa (Uganda, Rwanda, South Sudan, Tanzania, Ethiopia, Eritrea, Democratic Republic of the Congo) and Papua New Guinea. Several of these are common refugee-source or transit countries. The incubation period for P. falciparum is ~14 days (range 7-30)
- Previous malaria
history and type if known.
- Recent screening and/or
treatment (including prophylaxis).
- Current symptoms,
including fever pattern (a classic fever paroxysm consists of 3 stages (in order) cold, hot, sweat, lasting 6-10 hours total, usually late in the day). Symptoms of malaria may be non-specific, such as fever, cough, headache, abdominal pain or vomiting.
- Capacity to access health
care in Australia (language skills, time since arrival, independent
transport).
- Others in family (who
will also need screening).
Exam
- Assess conscious state, signs of respiratory distress, shock, neurological symptoms
- Other findings on examination may include pallor (anaemia), bruising (thrombocytopenia) or jaundice (haemolysis). Splenomegaly is found in
25-40% of symptomatic cases.
Screening
- Malaria should be
excluded as a priority in all febrile recently arrived refugees
from endemic areas (<3 months in Australia) with thick/thin
film(s) and a RDT. Malaria should also be considered in anyone with a febrile illness within 12 months of arrival from an endemic area, and in refugees settled for longer if there is a compatible travel/relapse history.
- All children aged <5 years
from endemic areas who have been in Australia <3 months should have malaria
screening (thick/thin film and RDT) if not
already performed, regardless of their pre-departure screening/treatment OR the reason for
presentation to ED, inpatient or outpatient care.
- All refugees from endemic
areas in Australia <3 months should be screened for malaria as
part of their initial post-arrival health screening.
- Refugee entrants in Australia for
longer than 3 months warrant screening if there is a history of
recurrent febrile illnesses or a history of non-falciparum
malaria.
Investigations
Note: specify
countries of origin and transit and recent treatment on pathology
request forms.
Thick and thin
films
- Thick films are used for diagnosis of malaria and parasite counts, thin films for morphology (species and stage)
- If the initial film is
negative in patients suspected of having malaria, films should be
repeated daily with fever spikes until either a positive result or confirmation of 3 negative results. Parasite counts are highest 4 hours after the fever has
peaked. Fingerprick specimens are adequate.
- May not be sensitive if
parasite counts are low (<20-50/mcl, possibly <100/mcl)
- P. knowlesi is indistinguishable from P. malariae on microscopy - P. malariae cases with a history of travel to South East Asia are treated as P. knowlesi - hence is it essential to document countries of origin/transit.
Malaria antigen detection
- Uses an immunochromatographic (ICT) lateral flow RDT, and gives information on the presence of Plasmodium species (by detecting parasite LDH) and whether the species is P. falciparum (by detecting HRP2)
- Test sensitivity of the
local RDT is 84-97% (>90% for P. falciparum if
parasite count >100/mcl), and specificity is
81-100%. Insensitive for other species or low density infections.
- False-negative HRP2-based RDT results can occur where the infecting parasite carries a pfhrp2/pfhrp3 gene deletion. This has been documented in isolates from the Horn of Africa (Eritrea, Ethiopia, Sudan) and in cases imported to Australia - low threshold to repeat testing and/or request PCR if RDT is negative but clinical/epidemiological suspicion is high.
- RDT may remain positive
for up to 4 weeks after successful treatment (important to consider if people have been treated before arrival).
Nucleic acid amplification testing
- PCR and loop-mediated isothermal amplification (LAMP) offer improved sensitivity for low-density and mixed infections, which are common in partially immune, recently arrived populations. Laboratory availability may be limited to reference laboratories — discuss with local Infectious Diseases service. Consider requesting PCR where clinical suspicion is high, but film and RDT are negative, or to confirm species/mixed infection
Other tests in symptomatic
patients
- FBE and film
- VBG,
lactate, BSL
- UEC and LFT
- Coagulation
- G6PD screen if
primaquine will be used - order quantitative G6PD testing, particularly in females, as qualitative assays can misclassify heterozygous individuals with intermediate G6PD activity
- Screen for pregnancy if
indicated
- Consider group and hold if transfusion may be required
- Blood cultures, CXR and further septic screen if unwell.
Management
- All patients with malaria
should be managed in conjunction with an Infectious Diseases
Specialist, see statewide Malaria CPG.
- All patients with malaria
require assessment in hospital. If there is any suggestion of
symptoms (i.e. in a patient who has had outpatient refugee
screening) the patient should be recalled to hospital
immediately.
- All patients will require
a period of observation in hospital while treatment is commenced
and/or admission.
- Patients with severe
malaria should be managed as for any severely unwell patient,
including checking BSL and monitoring for anaemia and for seizure
activity.
- Uncomplicated malaria - Artemisinin-combination therapy (artemether-lumefantrine - Riamet) is now first-line for uncomplicated malaria of all species, plus primaquine for P. vivax, P. ovale or unknown species (after G6PD testing) for hypnozoite eradication. See Malaria CPG. Dosing/timing need clear explanation.
- If timed Riamet dosing is not achievable, consider atovoquone proguanil (Malarone, daily dosing) as an alternative - discuss with infectious diseases. Both Riamet and Malarone are PBS-listed (so healthcare card costs).
- Treatment in malaria receptive areas (north of 19°S - from just below Broome (WA), through Tennant Creek (NT), to just above Townsville (Qld) - for P. falciparum treated in these regions, add a single dose of primaquine 0.25 mg/kg (max 15 mg), after G6PD testing, to reduce transmission risk to local mosquitoes (avoid in infants <6 months)
- Tafenoquine (Kozenis) was TGA-approved in 2018 (expanded paediatric approval in 2022) as a single-dose alternative for radical cure of P. vivax, but only in patients aged ≥16 years, after mandatory quantitative G6PD testing (contraindicated G6PD activity <70% of normal). Tafenquine may be relevant for adolescent/adult family members - refer to an adult ID service.
- Severe malaria is treated with IV artesunate (via Special Access Scheme) and may sometimes require combination treatment with IV quinine, severe malaria is generally managed in ICU, with concurrent use of paracetamol (renal protection), broad antibiotic cover, strict fluid balance, and cardiac monitoring - see Malaria CPG.
- Family members should
also be screened for malaria.
- Malaria is a
notifiable disease in Victoria and nationally.
Outpatient management
Outpatient management may
be considered if all the following criteria are met (adapted from10)
- Age >5
years
- Clinically
well
- (Not pregnant)
- Reviewed by a senior
doctor and Infectious Diseases Unit consulted
- No clinical or laboratory
features of severe malaria
- Has resided in endemic
area for most of the previous year
- Tolerated first dose of
oral medication
- Family has sufficient
understanding to ensure compliance and follow-up
- Family has sufficient
understanding and ability to return to hospital (by ambulance) if
child becomes more unwell
- Family have a discharge
letter stating child has malaria (including type of malaria), with
contact numbers and treatment details
- No other co-morbidity
requiring admission
Even if all criteria are
met, home-based nursing/Hospital in the Home should be considered for medication and
clinical supervision.
Follow-up
Patients should be seen in
Infectious Diseases outpatients at 28 days with repeat thick/thin
films and RDT, or immediately if symptoms recur.
Resources
- Malaria prevention and prophylaxis
Severe malaria: WHO definition8
- Prostration
- Impaired
consciousness/coma
- Respiratory distress
(acidotic breathing)
- Multiple
convulsions
- Circulatory
shock
- Pulmonary oedema or Acute
Respiratory Distress Syndrome
- Abnormal
bleeding
- Jaundice
- Haemaglobinuria
- Severe
anaemia
- Hypoglycaemia (<2.2
mmol/L)
- Acidosis (HCO3 <15
mmol/L or base deficit >10 mmol/L)
- High lactate (>5
mmol/L)
- Hyperparasitaemia (>4% if non-immune
child in area unstable endemicity, > 20% in stable endemic
areas)
Table 1: Malaria species
| Species |
P. falciparum |
P. vivax |
P. ovale |
P. malariae |
P. knowlesi
|
|
| Predominant species |
Sub Saharan Africa, PNG, Haiti |
South and North Asia, Eastern Europe, Central America parts South America
|
West Africa, occasional South East Asia, PNG |
Patchy worldwide, less common outside Africa |
Only SE Asia, especially Malaysia |
| |
Equal prevalence: Oceania, East Asia, other parts South America |
| Incubation |
7 - 14 days |
12 - 17 days |
15 - 18 days |
18 - 40 days |
8 - 12 days, up to 27 days |
| Fever Paroxysm |
May be absent or subtertian |
Tertian (48 hours) |
Tertian (48 hours) |
Quartan (72 hours) |
Daily (24 hours) |
| % Cells affected |
May be high |
< 2 - 3% |
< 2 - 3% |
< 1% |
May be high |
| Cerebral malaria |
Yes |
No |
No |
No |
No |
| Severe disease |
Yes |
Rare reports |
Rare reports |
No |
Yes |
| Resistance reported |
Yes |
Yes |
No |
No |
No |
| Natural history (without treatment) |
12 months |
3 years |
3 years |
Many years |
Variable, asymptomatic infections have been reported. |
| Hypnozoite form (can relapse) |
No |
Yes |
Yes |
No |
No |
References and resources
Immigrant health clinic resources. Author: Georgie Paxton, reviewed Aug 2026.