Congenital falciparum malaria in New Zealand: Symptoms, Causes & Treatment

Congenital falciparum malaria in New Zealand: Symptoms, Causes & Treatment | aihealz

§ 02

How you might notice it

01Fever rising to 39-41 °C, classically cyclical every 48 hours in P. vivax, P. ovale, and P. falciparum (tertian) and every 72 hours in P. malariae (quartan), although in clinical practice fever is often irregular in the first week.

02Shaking chills and rigors that precede the fever spike by 1-2 hours, followed by a sweating phase as the temperature falls — the classic paroxysm pattern.

03Severe headache, often frontal or generalised, that worsens during the febrile phase and partially responds to paracetamol.

04Muscle and joint aches with profound back pain, often described by travellers as flu-like at onset and easily mistaken for influenza or dengue.

05Nausea, vomiting, abdominal pain, and diarrhoea, which can dominate the picture in children and lead to misdiagnosis as gastroenteritis.

06Marked fatigue, malaise, and reduced exercise tolerance that persists between paroxysms and worsens with each cycle.

07Pallor and breathlessness from progressive haemolytic anaemia, especially in children with falciparum infection and in pregnant women.

08Jaundice with yellowing of the sclerae and dark cola-coloured urine from haemolysis and bilirubin release.

09Splenomegaly that develops over days to weeks of untreated infection; a tender, palpable spleen is a useful physical sign in endemic settings.

10Confusion, drowsiness, or seizures in cerebral malaria — a medical emergency requiring parenteral artesunate within the hour.

11Cough and shortness of breath from pulmonary involvement, particularly in falciparum and knowlesi malaria with adult respiratory distress syndrome.

early warning signs

•Any fever beginning 7 days to 3 months after travel to a malaria-endemic country — treat as malaria until proven otherwise with a rapid diagnostic test and blood film
•Recurring fever spikes every 48 or 72 hours in a returning traveller or resident of an endemic area
•Unexplained falling haemoglobin or low platelet count in a febrile patient from an endemic region
•A child under five from an endemic area becoming lethargic, refusing food, or sleeping more than usual during a febrile illness
•Persistent low-grade fever after stopping malaria prophylaxis — sub-therapeutic chemoprophylaxis can delay but not prevent infection

● emergency signs

•Reduced consciousness, confusion, or coma — cerebral malaria with Glasgow Coma Scale below 11 carries 15-20% mortality even with treatment
•Repeated or prolonged seizures in a febrile patient from an endemic area — needs immediate parenteral artesunate, glucose check, and supportive care
•Respiratory distress with deep acidotic breathing (Kussmaul respiration), oxygen saturation below 92%, or bilateral lung crackles suggesting acute pulmonary oedema or ARDS
•Severe anaemia with haemoglobin below 5 g/dL in a child or below 7 g/dL in an adult, especially with pallor, breathlessness, or circulatory collapse

§ 03

How it’s diagnosed

Giemsa-stained thin blood smear showing Plasmodium falciparum ring-form trophozoites inside red blood cells — the diagnostic microscopy finding — Plasmodium falciparum ring forms inside red blood cells on a Giemsa-stained thin smear. · Credit: Steven Glenn, CDC Public Health Image Library / Wikimedia Commons · Public Domain (CDC PHIL)

diagnosis

Diagnosis of malaria starts with a low threshold for testing: any fever in a returning traveller from an endemic area, or any febrile illness in a resident of an endemic region, warrants malaria testing the same day. The 2023 WHO guidelines and the CDC Yellow Book recommend parasitological confirmation in every suspected case before starting antimalarials, except when severe malaria is suspected and treatment cannot be delayed. Microscopy of Giemsa-stained thick and thin blood films remains the diagnostic gold standard — the thick film concentrates parasites for detection at low parasitaemia, while the thin film allows species identification and quantification of percent parasitised red cells, which is required to define hyperparasitaemia (>10%). Rapid diagnostic tests (RDTs) detect Plasmodium-specific antigens (histidine-rich protein 2 for P. falciparum and lactate dehydrogenase for non-falciparum species) from a finger-prick blood sample, with results in 15-20 minutes; sensitivity exceeds 95% for P. falciparum at parasitaemia above 200 parasites/µL and they have largely replaced microscopy in primary care settings. Increasing reports of HRP2/3 gene deletions in the Horn of Africa cause false-negative falciparum RDTs and have prompted WHO to recommend dual-antigen tests in affected regions. Polymerase chain reaction (PCR) detects very low parasitaemia, identifies species in mixed infections, and is used for confirmation in atypical cases and in research; loop-mediated isothermal amplification (LAMP) is increasingly used in surveillance. A single negative test does not exclude malaria — guidelines recommend repeating microscopy or RDT every 12-24 hours for up to 72 hours if clinical suspicion persists. Severity is assessed clinically and with laboratory markers including haemoglobin, platelet count, blood glucose, renal function, lactate, and arterial blood gas. Differential testing for dengue, typhoid, leptospirosis, viral haemorrhagic fevers, and bacterial bloodstream infection runs in parallel because co-infection is common.

Key tests

Thick and thin blood film microscopy (Giemsa stain)Diagnostic gold standard. The thick film concentrates parasites for detection at low parasitaemia; the thin film allows species identification (ring forms, gametocytes, schizonts) and quantification of percent parasitised red blood cells. Both inform severity classification.

Rapid diagnostic test (RDT) — HRP2 and pLDH antigen detectionFirst-line bedside test detecting P. falciparum HRP2 and/or pan-Plasmodium or species-specific pLDH antigens. Sensitivity exceeds 95% for P. falciparum at parasitaemia above 200 parasites/µL. Used at the point of care worldwide.

Polymerase chain reaction (PCR) or LAMP for Plasmodium speciesDetects parasitaemia below 1 parasite/µL, identifies mixed-species infections, and confirms species when microscopy is equivocal. Used in returning travellers with suspected low-grade infection, in pregnancy, and in surveillance.

Complete blood count, blood glucose, and renal function panelIdentifies severity markers: anaemia (haemoglobin <5 g/dL in children, <7 g/dL in adults), thrombocytopenia (often <100 x 10^9/L), hypoglycaemia, and acute kidney injury. A baseline before treatment is the standard of care.

Arterial blood gas with lactateSevere falciparum malaria produces lactic acidosis (lactate >5 mmol/L) and respiratory failure; metabolic acidosis is the strongest predictor of mortality. Used to triage severity and guide fluid management.

G6PD activity assay before primaquine or tafenoquineMandatory before radical-cure 8-aminoquinoline therapy for P. vivax or P. ovale. G6PD-deficient patients given standard-dose primaquine or tafenoquine can develop severe acute intravascular haemolysis.

Outlook

Uncomplicated malaria, when diagnosed early and treated with a quality-assured artemisinin-based combination, has a cure rate above 95% at 28 days and a near-zero mortality. Most patients are afebrile within 48 hours and back to baseline function within 1-2 weeks. Severe falciparum malaria carries a case-fatality of 8-15% in adults and 5-10% in African children even with parenteral artesunate and intensive care, rising to 20-30% in cerebral malaria and over 50% in adults with multi-organ failure. Pregnancy doubles maternal mortality risk and increases stillbirth, preterm delivery, and low-birth-weight rates. P. vivax has historically been considered benign but causes substantial morbidity through repeated relapses and chronic anaemia; severe vivax malaria with respiratory or renal involvement is increasingly recognised. P. knowlesi can progress from uncomplicated to severe disease within 24-48 hours because of its short erythrocytic cycle. Long-term outcomes after severe paediatric malaria include neurocognitive sequelae in roughly 25% of cerebral malaria survivors. Strict adherence to a full ACT course, vector control, chemoprevention in high-risk groups, and now vaccination in children are the strongest determinants of outcome at the population level.

§ 05

Causes & risk factors

known causes

Bite of an infected female Anopheles mosquito: Malaria is transmitted almost exclusively through the bite of a female Anopheles mosquito that has previously fed on an infected human. Sporozoites injected into the skin reach the liver within hours. Anopheles gambiae, A. funestus, and A. arabiensis dominate transmission in sub-Saharan Africa; A. stephensi has recently spread into the Horn of Africa and is adapted to urban breeding sites.
Plasmodium falciparum infection: The most virulent of the five human-infecting species and the cause of nearly all malaria deaths. P. falciparum invades red cells of any age, can produce parasitaemia exceeding 10%, and triggers sequestration in cerebral, renal, and placental microvasculature, generating the cerebral, renal, and obstetric complications that define severe disease.
Plasmodium vivax and Plasmodium ovale infection with relapsing hypnozoites: P. vivax and P. ovale form dormant liver-stage parasites called hypnozoites that reactivate weeks to years after the original infection, producing relapses. Curing the blood stage with an ACT does not eliminate hypnozoites — radical cure with primaquine or single-dose tafenoquine is required after testing for glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Plasmodium malariae and Plasmodium knowlesi infection: P. malariae causes a chronic, low-grade quartan infection that can persist asymptomatically for decades, occasionally producing immune-complex glomerulonephritis. P. knowlesi is a zoonotic simian parasite of long-tailed and pig-tailed macaques in Southeast Asia; its 24-hour erythrocytic cycle drives rapid rises in parasitaemia and severe disease can develop within days.
Mother-to-child (congenital) transmission: Plasmodium parasites can cross the placenta, especially in non-immune mothers infected late in pregnancy, producing congenital malaria within the first 30 days of life. Placental sequestration of P. falciparum also contributes to maternal anaemia, low birth weight, and stillbirth.
Transfusion, transplant, and needle-stick transmission: Plasmodium remains viable in stored blood for weeks and has been transmitted by transfusion, organ transplantation, and contaminated needles. Most national blood services screen donors from endemic areas with travel history questions and, where available, antibody tests.

risk factors

Travel to or residence in a malaria-endemic countryenvironmental: 85 countries report ongoing malaria transmission. Sub-Saharan Africa, the Indian subcontinent, Southeast Asia, the Amazon basin, and parts of the Horn of Africa carry the highest risk. WHO and CDC publish country-by-country maps and prophylaxis recommendations updated annually.
Age under 5 years in endemic areasnon-modifiable: Children under 5 carry roughly 76% of malaria deaths in Africa. They lack the partial immunity that develops after repeated exposures and are particularly vulnerable to severe anaemia and cerebral malaria. Seasonal malaria chemoprevention now protects ~50 million children annually.
Pregnancy, especially first and second pregnanciesnon-modifiable: Pregnant women are at ~3-fold higher risk of severe falciparum malaria; placental sequestration causes maternal anaemia, preterm birth, low birth weight, and stillbirth. Intermittent preventive treatment in pregnancy (IPTp) with sulfadoxine-pyrimethamine is recommended from the second trimester in endemic Africa.
HIV infection and other immunosuppressionmodifiable: HIV-positive adults have higher parasite densities, more frequent clinical episodes, and worse treatment outcomes. Co-trimoxazole prophylaxis taken for HIV provides some incidental protection but is not a substitute for antimalarial measures.
Absence of malaria chemoprophylaxis when travellingmodifiable: Non-immune travellers who do not take appropriate chemoprophylaxis have a 1-3% per month risk of malaria in West Africa. Atovaquone-proguanil, doxycycline, mefloquine, and tafenoquine are first-line options depending on destination and resistance patterns.

§ 06

Living with it

01Sleep under a long-lasting insecticidal net every night in endemic areas — reduces all-cause child mortality by ~17% and clinical malaria episodes by ~50%

02Take destination-appropriate chemoprophylaxis when travelling to an endemic country (atovaquone-proguanil, doxycycline, mefloquine, or tafenoquine) starting before travel and continuing after return as directed

03Apply N,N-diethyl-meta-toluamide (DEET 20-50%) or picaridin insect repellent to exposed skin from dusk to dawn and wear long sleeves and trousers in transmission zones

04Use indoor residual spraying or window screens, especially in rooms used during the evening and night

05Vaccinate children with RTS,S/AS01 or R21/Matrix-M in moderate-to-high transmission settings as part of national immunisation programmes

06Offer intermittent preventive treatment in pregnancy (IPTp) with sulfadoxine-pyrimethamine from the second trimester in endemic Africa, plus seasonal malaria chemoprevention for children 3-59 months in the Sahel

recommended foods

•Frequent small meals during the acute febrile phase to maintain calorie intake despite anorexia
•Fatty foods or milk taken with artemether-lumefantrine doses to maximise lumefantrine absorption
•Iron-rich foods (lean red meat, lentils, leafy greens) and folate during recovery from haemolytic anaemia
•Oral rehydration salts or balanced electrolyte solutions during diarrhoea or vomiting
•Vitamin A, zinc, and protein-adequate diet for paediatric recovery, particularly after severe disease
•Plenty of water — at least 2 litres in adults unless restricted for severe anaemia or pulmonary oedema

foods to avoid

•Alcohol during antimalarial treatment due to additive hepatotoxicity and neurotoxicity
•Unwashed raw produce in endemic areas where co-infection with enteric pathogens is common
•Untreated tap water and ice in regions with poor water sanitation
•Grapefruit and grapefruit juice with quinine, mefloquine, or lumefantrine — CYP3A4 interactions raise drug levels
•Fasting or prolonged poor intake during acute illness, which precipitates hypoglycaemia, particularly with quinine

§ 07

When to seek help

why see a neonatology

Refer to an infectious-disease or tropical-medicine specialist for any patient with severe malaria, P. falciparum infection in pregnancy, suspected drug resistance, treatment failure, complicated P. vivax or P. knowlesi infection, returning travellers with persistent symptoms after treatment, or G6PD deficiency requiring an alternative radical-cure strategy. National malaria reference centres and travel clinics also provide pre-travel chemoprophylaxis advice tailored to destination-specific resistance patterns.

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01Cerebral malaria with coma, seizures, and Glasgow Coma Scale <11 — mortality 15-25% even with treatment, neurocognitive sequelae in ~25% of paediatric survivors

02Severe haemolytic anaemia with haemoglobin <5 g/dL in children or <7 g/dL in adults, often requiring transfusion and iron repletion

03Acute kidney injury and blackwater fever from massive intravascular haemolysis, dark urine, and renal failure requiring dialysis

04Acute respiratory distress syndrome and pulmonary oedema, particularly in pregnancy and in older adults with falciparum or knowlesi infection

05Hypoglycaemia from impaired gluconeogenesis and parasite glucose consumption — most common in children, pregnant women, and patients on quinine

06Placental malaria with maternal anaemia, preterm delivery, low birth weight, and stillbirth in non-immune or first-pregnancy women

07Splenic rupture, especially in P. vivax infection with marked splenomegaly — a rare but life-threatening surgical emergency

08Quartan nephropathy with immune-complex glomerulonephritis after chronic P. malariae infection

09Post-malaria neurological syndrome (PMNS) presenting days to weeks after recovery from severe falciparum disease, especially after mefloquine exposure

choosing the right hospital

01Access to parenteral artesunate 24/7 and ability to give the first dose within 1 hour of severity recognition
02Laboratory capable of urgent thick and thin film microscopy and RDT, with quantification of parasitaemia
03Point-of-care G6PD testing before radical-cure 8-aminoquinoline therapy
04Paediatric and adult intensive care capacity with mechanical ventilation, renal replacement, and blood-product availability for severe disease
05Trained team familiar with WHO severe-malaria protocols and pregnancy-specific management

Types and stages

Plasmodium falciparum malariaThe deadliest species and the cause of nearly all severe malaria. Dominant in sub-Saharan Africa, accounting for ~99% of African cases. Infected red blood cells sequester in the cerebral, renal, and placental microvasculature, producing cerebral malaria, severe anaemia, and acute kidney injury. No dormant liver stage, but parasitaemia can rise tenfold every 48 hours if untreated.

Plasmodium vivax malariaThe most geographically widespread species and the leading cause of malaria outside Africa, dominant in South and Southeast Asia, Latin America, and the Horn of Africa. Forms dormant liver-stage hypnozoites that reactivate weeks to years later as relapses. Severe disease is less common than with P. falciparum but well documented. Duffy-negative individuals in West Africa are mostly resistant.

Plasmodium ovale malariaBiologically similar to P. vivax with relapsing hypnozoites; largely confined to West and Central Africa and parts of Southeast Asia. Two subspecies (P. ovale curtisi and P. ovale wallikeri) are recognised. Often milder than P. vivax, but radical cure with an 8-aminoquinoline is still required to prevent relapse.

Plasmodium malariae malariaCauses a chronic, low-grade quartan fever every 72 hours and can persist asymptomatically in the bloodstream for decades. Distributed worldwide but at low intensity. Long-standing infection occasionally produces immune-complex glomerulonephritis (quartan nephropathy).

Plasmodium knowlesi malariaA simian malaria of long-tailed and pig-tailed macaques that is transmitted to humans in the forested regions of Borneo, Malaysia, Indonesia, and parts of mainland Southeast Asia. The 24-hour erythrocytic cycle means parasitaemia rises faster than any other species, and severe disease develops quickly without recognition.

Uncomplicated malariaSymptomatic infection with detectable parasitaemia in a patient who is alert, able to tolerate oral medication, and free of any WHO severity criterion. Treated with a 3-day artemisinin-based combination therapy (ACT) regimen.

Severe malariaWHO-defined as infection with one or more of impaired consciousness (Glasgow Coma Scale <11), prostration, multiple convulsions, respiratory distress with acidotic breathing, circulatory collapse, abnormal bleeding, jaundice with parasitaemia, severe anaemia (haemoglobin <5 g/dL in children or <7 g/dL in adults), hypoglycaemia, acute kidney injury, pulmonary oedema, or hyperparasitaemia (>10%). Requires parenteral artesunate and intensive care.

Living with Congenital falciparum malaria

Timeline

Fever and chills typically settle within 48-72 hours of starting artemether-lumefantrine or another ACT; parasitaemia clears from peripheral blood by day 3 in over 90% of patients. Fatigue and post-malaria asthenia can persist for 2-4 weeks. Anaemia recovers over 4-8 weeks with iron repletion. Severe malaria with multi-organ involvement requires 1-3 weeks of inpatient care followed by a 6-12 week structured recovery, including renal follow-up if acute kidney injury occurred and neurocognitive review for cerebral malaria survivors. P. vivax and P. ovale relapses, when they occur, are seen weeks to months after the initial episode and require radical cure to prevent further cycles.

Lifestyle

01Maintain consistent prophylaxis adherence throughout travel and for the full post-travel period; missed doses are the leading reason for breakthrough infection in non-immune travellers
02Recognise the malaria red flags (fever, chills, headache, fatigue) for at least 3 months after returning from an endemic area and seek same-day testing
03Eliminate standing water around homes and workplaces — discarded tyres, water containers, blocked gutters, and tree holes are major Anopheles breeding sites
04Hydrate generously and rest during fever; oral rehydration salts in children prevent the dehydration that often dominates the early illness
05Avoid alcohol during antimalarial treatment, especially with mefloquine, atovaquone-proguanil, or quinine, because of hepatotoxicity and central nervous system side effects
06Take iron and folate supplementation as recommended in pregnancy and after severe haemolytic episodes to support red-cell recovery
07Inform any new clinician about recent malaria history — relapse from P. vivax or P. ovale can present months to years later

Daily management

01Take every dose of the ACT or chemoprophylaxis on time and complete the full course — partial treatment is the main driver of recrudescence and resistance
02Track temperature 3-4 times daily during the first week and seek same-day review if fever persists beyond 72 hours of ACT therapy
03Watch for the danger signs taught at discharge (drowsiness, breathlessness, dark urine, no urine, repeated vomiting, bleeding) and return immediately if any appear
04Continue insecticide-treated net use during recovery and for the rest of the season — recovered patients can be reinfected within weeks
05Take primaquine or tafenoquine exactly as prescribed after G6PD testing if you had P. vivax or P. ovale — radical cure prevents relapse months later
06Attend the day-28 follow-up appointment for repeat film or RDT to confirm cure

Exercise

Rest and supportive care dominate the first week of treatment, especially during fever and post-paroxysm exhaustion. Most patients with uncomplicated malaria feel substantially better after 48-72 hours of ACT and can resume light walking within a week. Avoid strenuous exercise for 2-4 weeks after severe malaria, particularly if anaemia, renal injury, or ARDS occurred. Children who had cerebral malaria benefit from structured neurodevelopmental rehabilitation in the months that follow.

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Frequently asked

How long after a mosquito bite do malaria symptoms appear?

Symptoms typically appear 7 to 30 days after an infected Anopheles mosquito bite, though Plasmodium vivax and P. ovale can present months or even years later because of dormant liver-stage hypnozoites. P. falciparum is usually the fastest, with most cases presenting within 2-4 weeks. Anyone with a fever within 3 months of travel to an endemic area should be tested immediately.

What are the classic symptoms of malaria?

The classic symptoms are fever, chills with shaking rigors, severe headache, muscle and joint aches, fatigue, nausea, and sometimes vomiting and diarrhoea. Many patients describe cyclical fever spikes every 48 or 72 hours. Severe malaria adds confusion, seizures, breathlessness, jaundice, and very dark urine and is a medical emergency.

Which countries have the highest malaria risk?

Sub-Saharan Africa carries 94% of global malaria cases and 95% of deaths. Nigeria, the Democratic Republic of Congo, Uganda, Mozambique, and Niger together account for roughly half of all cases. Parts of South Asia, Southeast Asia, the Amazon basin, and the Horn of Africa also have significant transmission. The WHO and CDC publish updated country-specific maps.

How is malaria diagnosed?

Diagnosis requires parasitological confirmation, usually with a rapid diagnostic test detecting Plasmodium antigens from a finger-prick sample, microscopy of Giemsa-stained thick and thin blood films, or PCR. WHO recommends testing every suspected case before treatment, except where severe malaria requires immediate parenteral artesunate. A single negative test does not exclude malaria, and repeat testing over 72 hours is standard if suspicion persists.

Is malaria curable?

Yes. Uncomplicated malaria is cured in over 95% of patients with a 3-day artemisinin-based combination therapy course. Plasmodium vivax and P. ovale also require radical cure with primaquine or single-dose tafenoquine to clear dormant liver-stage hypnozoites and prevent relapse. Severe malaria is treated with parenteral artesunate followed by a full oral ACT course.

Can malaria come back after treatment?

Yes. Plasmodium vivax and Plasmodium ovale form dormant liver-stage hypnozoites that can reactivate weeks to years later, producing relapses. Plasmodium falciparum and P. malariae do not relapse but can recrudesce if the original blood-stage infection was incompletely cleared. Radical cure with primaquine or tafenoquine prevents vivax and ovale relapse.

What is severe malaria?

The WHO defines severe malaria as Plasmodium infection with any of impaired consciousness, repeated seizures, prostration, respiratory distress with acidotic breathing, circulatory collapse, abnormal bleeding, jaundice with parasitaemia, severe anaemia, hypoglycaemia, acute kidney injury, pulmonary oedema, or parasitaemia over 10%. It is a medical emergency requiring parenteral artesunate and intensive care.

What is the best treatment for malaria?

Artemisinin-based combination therapy (ACT) is the WHO-recommended first-line treatment for uncomplicated falciparum malaria worldwide. Artemether-lumefantrine and dihydroartemisinin-piperaquine are the most widely used. Severe malaria is treated with intravenous or intramuscular artesunate, followed by a full 3-day oral ACT course once the patient can take oral medication.

Is there a malaria vaccine?

Yes. Two vaccines, RTS,S/AS01 (Mosquirix) and R21/Matrix-M, are WHO-recommended for children in moderate-to-high transmission areas. RTS,S/AS01 reduced clinical malaria episodes by ~36% over 4 years in phase 3 trials. R21/Matrix-M reduced clinical malaria by 75% in seasonal settings over 12 months. Both target the Plasmodium falciparum circumsporozoite protein.

Can malaria be prevented?

Yes. Key prevention measures include sleeping under insecticide-treated nets, indoor residual spraying, mosquito repellents containing DEET or picaridin, chemoprophylaxis for travellers, intermittent preventive treatment in pregnancy, seasonal malaria chemoprevention for children in the Sahel, and now WHO-recommended vaccination with RTS,S/AS01 or R21/Matrix-M in moderate-to-high transmission areas.

Which malaria pills should I take when travelling?

Common chemoprophylaxis options include atovaquone-proguanil, doxycycline, mefloquine, and tafenoquine. Choice depends on the destination, length of stay, drug-resistance patterns, pregnancy, and individual tolerance. Start before travel, continue throughout the trip, and complete the post-travel course as directed. A travel-medicine clinician should tailor the regimen to your itinerary.

Can children get malaria?

Yes. Children under five carry roughly three-quarters of malaria deaths in Africa because they lack the partial immunity that develops with repeated exposure. They are especially vulnerable to severe anaemia, cerebral malaria, and hypoglycaemia. Seasonal malaria chemoprevention, insecticide-treated nets, and the new RTS,S/AS01 and R21/Matrix-M vaccines are central to protecting this age group.

Is malaria dangerous in pregnancy?

Yes. Pregnancy roughly triples the risk of severe malaria and increases maternal anaemia, miscarriage, preterm delivery, low birth weight, and stillbirth. Placental sequestration of Plasmodium falciparum is the underlying mechanism. WHO recommends intermittent preventive treatment in pregnancy with sulfadoxine-pyrimethamine from the second trimester and use of insecticide-treated nets in endemic areas.

How many species of malaria parasite infect humans?

Five Plasmodium species infect humans. Plasmodium falciparum causes nearly all severe disease and most deaths. Plasmodium vivax is the most widespread, especially outside Africa, and forms relapsing liver-stage hypnozoites. Plasmodium ovale is similar to vivax and largely confined to West Africa. Plasmodium malariae causes chronic low-grade infection. Plasmodium knowlesi is a zoonotic simian malaria found in Southeast Asia.

What is artemisinin resistance?

Artemisinin partial resistance is defined as delayed clearance of Plasmodium falciparum from the blood after artesunate or another artemisinin derivative. It is associated with kelch13 gene mutations and was first detected in the Greater Mekong subregion; cases have now been reported in East Africa and the Horn of Africa. WHO surveillance guides regional ACT choice to preserve efficacy.

What is the difference between malaria and dengue?

Malaria is a parasitic infection transmitted by Anopheles mosquitoes; dengue is a viral infection transmitted by Aedes mosquitoes. Malaria produces cyclical fever, parasites on a blood smear, and responds to artemisinin-based combination therapy. Dengue causes a single febrile illness with retro-orbital pain, a rash, low platelets, and is diagnosed by NS1 antigen or IgM. Co-infection occurs in shared endemic regions.

Why is G6PD testing required before primaquine?

Primaquine and tafenoquine cause severe acute haemolysis in people with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Because G6PD deficiency is common in populations historically exposed to malaria, the WHO recommends quantitative or qualitative G6PD testing before standard-dose radical cure of P. vivax or P. ovale. Reduced-dose primaquine regimens exist for partial deficiency but should be supervised.

How much does malaria treatment cost?

In endemic countries, artemether-lumefantrine and other quality-assured ACTs are typically provided free or at heavily subsidised cost through national malaria programmes and the Global Fund. A private 3-day ACT course costs roughly USD 1-5 in Africa and USD 30-60 in the United States. Parenteral artesunate for severe malaria is more expensive but procured through WHO-prequalified suppliers.

Can you get malaria more than once?

Yes. People living in endemic areas often have multiple episodes a year, especially children. Adults gradually develop partial immunity with repeated exposure that reduces disease severity but does not prevent infection. This partial immunity wanes within 1-2 years of leaving an endemic area, which is why returning expatriates and second-generation migrants are at higher risk of severe imported disease.

How long does recovery from malaria take?

Most patients with uncomplicated malaria are afebrile within 48-72 hours of starting an ACT and back to baseline within 1-2 weeks. Anaemia and fatigue can persist for 4-8 weeks. Severe malaria with multi-organ involvement requires 1-3 weeks of inpatient care followed by a 6-12 week structured recovery. Cerebral malaria survivors may need neurocognitive rehabilitation lasting months.

Can malaria spread from person to person?

No. Malaria does not spread directly from person to person through casual contact, coughing, or sharing food. It is transmitted by the bite of an infected female Anopheles mosquito. Rare exceptions include transmission through blood transfusion, organ transplantation, contaminated needles, and from mother to baby during pregnancy or delivery (congenital malaria).

When should I see a doctor after returning from a malaria-endemic country?

See a doctor the same day for any fever, chills, headache, or flu-like illness within three months of returning from a malaria-endemic country, even if you took chemoprophylaxis. Mention the travel history at the first encounter. Plasmodium falciparum infection can progress to severe disease within 24 hours, so emergency assessment is appropriate if you feel unwell.

Congenital falciparum malaria.Care & specialists in New Zealand

What it is

How you might notice it

How it’s diagnosed

Treatment & cost

Causes & risk factors

Living with it

When to seek help

Related conditions

Easily confused with

Often appears alongside

Types and stages

Living with Congenital falciparum malaria

Complementary approaches

Patient support resources

Frequently asked

Sources & references

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