{
  "id": "malaria",
  "title": "Malaria",
  "lang": "en",
  "source_lang": "en",
  "summary": "A mosquito-borne parasitic disease caused by Plasmodium, covering its biology, clinical course, treatment, prevention, history, and global burden.",
  "category": "health",
  "subcategory": "diseases",
  "type": "concept",
  "aliases": [
    "paludism",
    "ague (historical term)"
  ],
  "generated_at": "2026-10-08",
  "model": "pro/claude-haiku-5-5",
  "url": "https://aiwiki.page/en/malaria/",
  "translations": {
    "zh-Hans": {
      "url": "https://aiwiki.page/zh/malaria/",
      "json": "https://aiwiki.page/zh/malaria.json"
    }
  },
  "sections": [
    {
      "heading": "",
      "text": "Malaria is a mosquito-borne infectious disease caused by single-celled parasites of the genus Plasmodium, which are eukaryotes rather than bacteria or viruses. Humans are infected when a female Anopheles mosquito injects parasites during a blood meal. The parasites multiply first in the liver and then inside red blood cells, which produces recurrent fever, anemia, and, in severe cases, organ failure and death. Young children and pregnant women in endemic regions carry the greatest risk, and the disease has shaped the development of public health systems, drug discovery, and human genetics.\n\nMalaria remains one of the deadliest infectious diseases. According to the World Health Organization's 2025 report, there were an estimated 282 million cases and 610,000 deaths in 2024, and about 95% of deaths occurred in the WHO African Region, most of them among children under five. Its long history of selection pressure has left visible marks on the human genome, including the sickle-cell and thalassemia variants, and its treatment has produced landmark discoveries, from the quinine of cinchona bark to the artemisinin-based drugs that are now the standard of care.\n\nThis entry first explains the parasite's life cycle and the mosquito vectors that transmit it, then describes clinical features, diagnosis, and treatment, including the growing problem of drug resistance. It next reviews prevention tools, human genetic and immune resistance, and the history of how the disease was understood and controlled. It closes with the current global burden, elimination efforts, and the challenges that remain."
    },
    {
      "heading": "Causative parasites and life cycle",
      "text": "Species that infect humans\n\nMalaria is caused by unicellular eukaryotic parasites of the genus *Plasmodium*. More than 200 species have been described, but only five regularly infect people: P. falciparum, P. vivax, P. ovale, P. malariae and P. knowlesi. The first four are adapted to humans. P. knowlesi is zoonotic, circulating mainly among macaques in Southeast Asia, and it increasingly infects people in forested areas. P. ovale is now usually regarded as two sibling species, which are morphologically similar and distinguished by molecular methods.\n\nThe species differ sharply in virulence and geography. P. falciparum is responsible for most malaria deaths and dominates in sub-Saharan Africa, where it accounts for more than 85% of cases. P. vivax is the most widely distributed species, prevalent across much of Asia, Central and South America, and the Middle East, where it can make up 70–90% of the burden. P. malariae occurs at low levels across Africa, parts of India, the western Pacific and South America, while P. ovale is largely confined to tropical Africa, New Guinea and the Philippines. P. malariae causes chronic, low-grade infections that can persist for years. P. knowlesi can cause severe disease and is a notable diagnostic problem: in Malaysia, when P. falciparum and P. vivax declined, many P. knowlesi cases were initially recorded as P. malariae because microscopy cannot reliably separate the two.\n\nSporozoites, liver stage and hypnozoites\n\nAn infected female Anopheles mosquito injects sporozoites into the skin during a blood meal. The traditional view held that sporozoites reach the liver quickly, but newer work suggests they can persist in the dermis for hours, enter the capillaries slowly and travel partly through the lymphatic system before reaching the liver. In hepatocytes, the parasite undergoes exoerythrocytic schizogony, forming a tissue schizont that releases tens of thousands of merozoites. The number varies by species, with roughly 10,000 in P. vivax and P. ovale and up to 30,000 in P. falciparum. Maturation takes about six days in P. falciparum and up to around 16 days in P. malariae. The schizont then ruptures, releasing merozoites into the bloodstream.\n\nP. vivax and P. ovale differ because some sporozoites form hypnozoites, dormant liver forms that can persist for weeks, months or even years before reactivating. Reactivation seeds relapses, which are distinct from recrudescence, where blood-stage parasites survive treatment. The proportion of relapses varies widely. In Papua New Guinean children, one trial-based model attributed roughly four in five P. vivax infections to relapse. The evidence for hypnozoites in P. ovale is weaker than for P. vivax, and some P. vivax recurrences may not depend on hypnozoites at all. The trigger for hypnozoite activation remains unidentified. Primaquine is the drug that clears hypnozoites, and tafenoquine is an alternative, although both are discussed in the treatment section.\n\nErythrocytic asexual cycle and fever\n\nMerozoites invade red blood cells using an actin-myosin motor. Inside the cell, the parasite passes through ring, trophozoite and schizont stages while consuming host hemoglobin, then ruptures the cell and releases new merozoites that invade fresh cells. The duration of this cycle is characteristic of each species: about 48 hours for P. falciparum, P. vivax and P. ovale, about 72 hours for P. malariae, and about 24 hours for P. knowlesi. P. malariae invades only mature red cells, which helps explain its slow, chronic course.\n\nThe synchronous rupture of infected cells releases parasite debris and toxins that provoke fever spikes. Those spikes give rise to the classic \"tertian\" (about every 48 hours) and \"quartan\" (about every 72 hours) patterns. In P. falciparum, the periodicity is often irregular in practice because many natural infections are not fully synchronous. Why the cycle is synchronized is still debated. Studies of P. falciparum and P. vivax suggest an intrinsic parasite oscillator, while recent work on P. vivax in patients found that the parasite cycle is phase-coupled to the host's circadian rhythm, which may help parasites coordinate their development and evade host defenses. Some researchers have also proposed that fever itself may benefit the host while synchrony benefits the parasite. Erythrocytic stages cause almost all of the clinical disease, and their cytoadherence and immune effects are covered in a later section.\n\nSexual stages, mosquito infection and sporogony\n\nOnly a small fraction of merozoites leave the asexual cycle and develop into sexual forms called gametocytes, which circulate in the peripheral blood. P. falciparum gametocytes take roughly ten days to mature and are largely sequestered in deep tissues, which helps them evade removal. When a mosquito takes a blood meal, male and female gametocytes are released in the midgut. Males produce motile microgametes that fertilize females, forming a zygote that transforms into a motile ookinete. The ookinete crosses the midgut wall and settles beneath the outer lining, where it becomes an oocyst. Within the oocyst, sporogony produces thousands of sporozoites that migrate to the salivary glands, where they await transmission to the next host. The pace of sporogony depends strongly on ambient temperature, typically taking one to two weeks, so warmer conditions shorten the time an infected mosquito needs to become infectious.\n\nGenetic diversity\n\nThe P. falciparum genome was sequenced in 2002, followed by the genomes of P. vivax and P. knowlesi, which allowed comparative work across the genus. Parasite populations are genetically diverse. A single human infection often contains several genetically distinct clones, and sexual recombination in the mosquito midgut reshuffles genes each time parasites pass through a vector. This diversity influences transmission because mixed infections and differing gametocyte densities affect how efficiently parasites are passed on. It also influences drug response: point mutations and copy-number changes in genes such as those for chloroquine transporters, the kelch13 gene linked to artemisinin partial resistance, and enzymes targeted by sulfadoxine-pyrimethamine have been selected under drug pressure, so natural selection can spread resistant lineages. Genome studies in wild African apes have also revealed that the lineage of P. falciparum is more complex than once thought, with related parasites found in gorillas, bonobos and chimpanzees. Diversity of this kind also complicates vaccine design, as covered in the prevention section."
    },
    {
      "heading": "Mosquito vectors and transmission",
      "text": "Anopheles vectors and their competence\n\nOnly female Anopheles mosquitoes transmit human malaria. Of the several hundred Anopheles species described, a few dozen are considered important vectors, and their relative importance differs by region. In sub-Saharan Africa, Anopheles gambiae sensu stricto and Anopheles funestus account for most transmission. Epidemiologists separate two properties. Vector competence is the intrinsic ability of a mosquito to take up gametocytes, let the parasite develop, and deliver sporozoites to its salivary glands. Vectorial capacity is the broader measure of how fast a vector population can transmit a parasite in a community. It combines competence with mosquito density, how often each female bites, whether she prefers human or animal hosts, and how long she survives.\n\nSeveral traits decide whether a species is an efficient vector. Preference for human blood increases the chance that an infectious mosquito bites a person, while feeding on livestock dilutes transmission. Survival matters most of all, because the parasite needs roughly ten days or more to develop inside the mosquito, and only females that live that long can become infectious. The larval habitat also shapes adult traits. Sunny, shallow, algae-rich pools favored by many species produce a larval environment that affects the size, longevity and infection outcome of the adults. In laboratory experiments with a rodent malaria parasite, halving larval food reduced the proportion of mosquitoes that became infected by about a third. Temperature during larval development interacted with food supply: at low food, warming from 21 °C to 29 °C raised competence, whereas at standard food the same warming lowered it.\n\nEnvironmental determinants\n\nRainfall creates the standing water in which Anopheles larvae develop, so rainy seasons often precede malaria peaks, but very heavy rain can flush out breeding sites and drought can concentrate what water remains. Temperature has the strongest effect on the parasite itself. Development of the parasite within the mosquito (the extrinsic incubation period) slows sharply in cool conditions, and the minimum temperature for Plasmodium falciparum and P. vivax development is generally put at about 16 °C. The classic degree-day model, which requires about 111 degree-days above that threshold, dates from the 1930s and has been poorly validated, particularly because it was built on constant temperatures, whereas field temperatures fluctuate daily.\n\nEarly studies placed the optimum for falciparum transmission at roughly 25–27 °C, with efficiency falling below 18 °C or above 32 °C. More recent work shows these limits vary with vector species, parasite species and local ecology. Humidity governs vector survival: monthly relative humidity below about 60% is generally considered too dry for adult mosquitoes to live long enough to transmit. Suitability criteria used in national programs have combined monthly rainfall of at least 80 mm, mean temperatures of 18–32 °C and humidity of at least 60%. Altitude acts as a thermal barrier, and highland fringes above about 2,400 m are often free of transmission, although warming is shifting these boundaries upward.\n\nHuman–mosquito contact patterns\n\nMany Anopheles populations historically bit people indoors and at night, when people were asleep under bed nets or within houses. Where people sleep under treated nets and houses are sprayed, some vector populations shift toward earlier evening biting and outdoor biting, which reduces the protection that indoor tools offer. Outdoor activity in the evening, when people are not sleeping under nets, can therefore expose them to bites that existing measures do not cover. This behavioral plasticity leaves residual transmission even where coverage is high, and it is one reason control programs add complementary measures, such as larval source management and drug-based approaches.\n\nTransmission intensity and reservoirs\n\nEpidemiologists describe malaria transmission as stable or unstable. Stable transmission is high and largely perennial, with many infective bites per person per year. Under these conditions, adults develop partial immunity, and most infections in young children are asymptomatic. Unstable transmission is low or seasonal and can give rise to epidemics. Immunity is weak in such settings, so people of all ages become ill when transmission rises. Seasonal transmission follows rainfall, whereas perennial transmission persists through the year.\n\nAsymptomatic infections are central to transmission in endemic areas. People with low-density parasitemia often feel well, yet they can carry gametocytes that infect mosquitoes, and standard rapid tests may miss them. These infections therefore act as a reservoir that sustains transmission and makes elimination difficult, even when clinical cases fall.\n\nTransmission modeling and the basic reproduction number\n\nRonald Ross's 1911 model described malaria as a two-host system in which humans and mosquitoes infect each other, and it introduced the concept of a threshold mosquito density below which malaria cannot persist. Macdonald refined this model in 1957 and formalized the basic reproduction number \\(R_0\\) as the average number of secondary human cases produced by one infectious case in a fully susceptible population. In the standard form,\n\n\\[R_0 = \\frac{a^2 b c m}{r \\mu}\\]\n\nwhere \\(a\\) is the biting rate per mosquito, \\(b\\) the probability that an infectious bite infects a human, \\(c\\) the probability that a human infects a mosquito, \\(m\\) the number of mosquitoes per person, \\(r\\) the human recovery rate, and \\(\\mu\\) the daily mosquito death rate. Transmission can persist only when \\(R_0 > 1\\), and prevalence rises nonlinearly with \\(R_0\\).\n\nThe formula explains why control tools work. Because biting rate appears squared, reducing contact between people and mosquitoes has a disproportionate effect, while increasing mosquito mortality shortens the window in which parasites can complete development. Lengthening the incubation period, whether in humans or mosquitoes, also reduces \\(R_0\\). Refinements by Smith and McKenzie in 2004 re-derived the entomological parameters, but the core message of the model remains the same."
    },
    {
      "heading": "Clinical course and pathophysiology",
      "text": "Uncomplicated malaria\n\nThe interval between the bite and the first symptoms depends on the species. Plasmodium vivax symptoms can begin 8 days to 12 months after the bite, while Plasmodium malariae symptoms can begin 18 to 40 days or even years later. The typical early picture is nonspecific. Patients commonly present with a combination of fever, chills, sweats, headache, nausea and vomiting, body aches, and general malaise. In countries where malaria is infrequent, these symptoms may be attributed to influenza, a cold, or other common infections.\n\nThe classic paroxysm follows the rupture of infected erythrocytes. Hemolysis of infected red cells releases merozoites and other malaria antigens, and the resulting inflammatory response produces the attack. The fever typically falls after several hours, and heavy sweating and extreme fatigue follow. Fevers are irregular at first but, over time, recur at regular intervals.\n\nSpecies differ in the periodicity and severity of attacks. Fevers tend to recur at 48-hour intervals with P. vivax and P. ovale, and at 72-hour intervals with P. malariae. P. knowlesi has a 24-hour replication cycle and can progress rapidly from uncomplicated to severe infection. Anemia is also species-dependent: it may be severe in P. falciparum or chronic P. vivax infection but tends to be mild in P. malariae infection.\n\nSevere malaria\n\nSevere disease is overwhelmingly associated with P. falciparum, which causes severe malaria through a property not shared by other human malaria species, namely sequestration. Severe presentations include acute respiratory distress, metabolic acidosis, hypoglycaemia, renal failure, anaemia, pulmonary oedema, cerebral malaria, and placental malaria in pregnant women. For many years the severe disease was described mainly as two syndromes: severe anaemia caused by destruction of red blood cells, and cerebral malaria caused by obstruction of small brain vessels by sequestered parasites. Autopsy work has since shown more heterogeneous patterns. In children with cerebral malaria, one group shows sequestration alone, while another shows sequestration together with vascular pathology such as ring hemorrhages, fibrin-platelet thrombi, and monocytes.\n\nSequestration of infected erythrocytes\n\nSequestration is the central virulence mechanism. In the mature asexual stages of the 48-hour cycle, the parasite alters the surface properties of the infected red cell, so that it adheres to blood vessel walls, a process called cytoadherence. The main adhesive ligand is a parasite protein expressed on the infected cell surface. These proteins bind vascular endothelial cells, which lets the infected cells avoid clearance in the spleen. Adhesion is concentrated in the later part of the intraerythrocytic cycle. Sequestration occurs principally during the second half of the intra-erythrocytic asexual growth phase. Accumulated cells obstruct the microcirculation. This obstruction is thought to cause hypoxia and haemorrhage, which are associated with organ-specific syndromes such as cerebral and placental malaria. Post-mortem studies have found greater accumulation of parasitized cells in the brain than in other organs among people who died of cerebral malaria.\n\nHost inflammatory responses and organ damage\n\nSequestration alone does not explain severity, and host inflammation is a second determinant. Two main determinants of severe malaria are sequestration of parasitized red cells and strong pro-inflammatory responses. Tumour necrosis factor is raised in people with severe malaria and has been implicated in the pathogenesis of cerebral malaria. Interferon-γ and interleukin-1β have also been associated with disease severity in human malaria. Inflammatory mediators act on the endothelium. They are thought to increase expression of adhesion molecules such as ICAM-1, which bind infected cells to the vessel wall. Leukocytes are also recruited to the sites of sequestration, potentially exacerbating organ-specific inflammation.\n\nAnti-inflammatory signalling is part of the balance. Interleukin-10 is a key anti-inflammatory cytokine with a regulatory role in malaria models. In experimental work, IL-10 reduced endothelial ICAM-1 expression, with a corresponding decrease in sequestration. Its effects are not uniformly protective, as its potent anti-inflammatory activity may paradoxically favour parasite growth. Overall, a good balance between pro- and anti-inflammatory responses is needed to clear parasites without damaging organs. The damage pathways include mitochondrial dysfunction, in which TNF impairs tissue use of oxygen, and blood lactate in severe malaria has been found to correlate closely with TNF and interleukin-1 levels. Cytokines can also increase blood-brain barrier permeability, compounding the effects of vaso-occlusion.\n\nGroups at higher clinical risk\n\nYoung children bear the largest burden. About 94% of malaria deaths occur in Africa, most commonly in children under five. In African children, severe features include severe anemia, hypoglycemia, and cerebral malaria.\n\nPregnancy increases susceptibility. Pregnant women are more susceptible than non-pregnant women, and the susceptibility is greatest in the first and second pregnancies. This reflects a combination of immunological and hormonal changes, together with the ability of a subset of infected cells to sequester in the placenta. Infection during pregnancy can also cause premature delivery or delivery of a baby with low birth weight.\n\nNonimmune travelers are at risk because they lack protective exposure. Partial immunity from continuous exposure is lost quickly, so people who have left endemic areas should be treated as nonimmune. Diagnosis may be delayed in travelers returning to malaria-free countries, because clinicians may be unfamiliar with the disease and effective drugs may be unavailable.\n\nPeople with HIV also face higher risk. HIV impairs acquired immunity to malaria in older children and in both pregnant and nonpregnant adults in stable endemic areas. In a prospective cohort in an area of unstable transmission, nonimmune adults with HIV had a higher risk of severe P. falciparum malaria, and that risk was associated with CD4 counts below 200 cells per mm³."
    },
    {
      "heading": "Diagnosis",
      "text": "Malaria diagnosis means finding Plasmodium parasites or their products in a patient's blood. Three approaches are in routine use: light microscopy of stained blood films, antigen-based rapid tests, and molecular assays. Light microscopy of Giemsa-stained films has served as the reference standard for more than a century, but its accuracy depends on the reader's skill, training, motivation and laboratory resources. Thick films have also produced false-positive readings, which caused problems in clinical trials.\n\nThe two film types do different jobs. The thick film concentrates blood so that it detects very low parasite densities, and it is far more sensitive for screening than the thin film. The thin film is used to identify species, to recognize mixed infections, to measure parasitaemia, and to see species-specific red-cell changes such as enlargement in P. vivax infections. Density is usually estimated on the thick film by counting parasites against a set number of white blood cells, typically 200, and extending the count when parasites are scarce. National programmes govern the whole chain through standard operating procedures covering finger-prick collection, staining, reading, reporting and independent re-reading of slides, with stain quality treated as critical for species identification.\n\nRapid diagnostic tests (RDTs) are lateral-flow strips that detect parasite proteins in a few microlitres of blood and give a result in about 20 minutes without a laboratory. Most field products detect histidine-rich protein 2 (HRP2), which only P. falciparum makes, so they miss other species unless paired with a test for a pan-Plasmodium antigen such as lactate dehydrogenase. Their limits include false negatives at very high parasite densities, variable quality between manufacturing batches, and persistent positivity after treatment. A growing problem is deletion of the pfhrp2 and pfhrp3 genes, which removes the HRP2 target and produces false-negative results. Such deletions have been documented in South America and in several African countries. A Brazilian case of misdiagnosis led to inappropriate treatment, and the proposed remedy is to use tests that target two distinct antigens. Surveillance for deletions combines antigen assays with genetic analysis, and because PCR failure alone can overstate deletion prevalence, protein-level confirmation is preferred.\n\nPCR amplifies parasite DNA and detects infections far below the density visible on a smear. It is used to identify species reliably, to find low-density and asymptomatic infections in surveys, to confirm gene deletions, and to analyse trial and surveillance samples. Its requirements for equipment, cost and trained staff confine it mainly to reference and research laboratories.\n\nFever is common in endemic areas, and many other illnesses share malaria's symptoms, including typhoid, dengue, pneumonia and common colds. For decades, many sub-Saharan African health programmes promoted presumptive treatment, giving antimalarials to every febrile patient without a test. This led to overdiagnosis, wasted drugs, and neglect of the actual cause of fever. In a Ugandan study, untested patients were treated for malaria they did not have, and those patients were less likely to receive antibiotics and had a higher risk of death. Once artemisinin-based combinations replaced cheaper drugs, presumptive treatment became harder to justify economically. Tanzania piloted a policy restricting treatment to RDT-positive patients, and by 2010, 37 African countries had adopted test-based policies. Retail drug shops, where testing is rarely done, remain a major source of unconfirmed treatment.\n\nQuality assurance covers both laboratory microscopy and point-of-care testing. Its elements include competency assessment of microscopists, blind re-reading of slides, external proficiency panels, lot testing of RDTs, and secure storage and supply, since stock-outs have repeatedly forced presumptive treatment back into routine use."
    },
    {
      "heading": "Treatment and drug resistance",
      "text": "Artemisinin-based combination therapies (ACTs) are the standard first-line treatment for uncomplicated Plasmodium falciparum malaria. Each pairs a fast-acting artemisinin derivative (artesunate, artemether or dihydroartemisinin) with a longer-acting partner drug. The derivative rapidly reduces parasite biomass during the first three days, while the partner drug eliminates the parasites that remain. The combination also protects the artemisinin itself, because using it alone would select resistant parasites much faster. WHO currently recommends six ACTs: artemether–lumefantrine, artesunate–amodiaquine, artesunate–mefloquine, artesunate–sulfadoxine–pyrimethamine, dihydroartemisinin–piperaquine and artesunate–pyronaridine. The choice among them depends on how well each partner drug still works locally, and ACTs are also recommended as second-line treatment and for chloroquine-resistant P. vivax.\n\nSevere falciparum malaria is treated with intravenous artesunate, which has replaced quinine as the preferred parenteral drug. In a large randomized trial in African children, artesunate was associated with lower mortality than quinine. Patients are switched to a full oral ACT course once they can swallow tablets safely. Supportive care is often as important as the drug itself. Clinicians monitor blood glucose, since hypoglycemia is common in severe disease, manage fluid balance and acidosis, transfuse for severe anaemia, treat seizures, and provide renal support when acute kidney injury develops. In remote settings, rectal artesunate may be given before referral to a hospital.\n\nRadical cure of P. vivax and P. ovale requires eliminating the dormant liver-stage hypnozoites, which blood-stage drugs cannot reach. The classic option is primaquine, an 8-aminoquinoline, usually given for 14 days at 0.25 mg/kg per day, although shorter 7-day regimens are used in some countries. Poor adherence to the long course is a recognized weakness, and reduced CYP2D6 activity, which is common in some populations, lowers primaquine's effectiveness. Tafenoquine can be given as a single dose, and in Thai pilot data a 300 mg dose was used for people with normal G6PD activity. Both drugs can cause oxidant haemolysis in people with G6PD deficiency, an X-linked enzyme disorder common in populations long exposed to malaria. Quantitative point-of-care G6PD testing before dosing is therefore essential. In Thailand, the dosing regimen is selected by enzyme activity, with weekly primaquine for intermediate-activity patients, and no drug-induced acute haemolytic anaemia was confirmed in the pilot. In the Brazilian Amazon, 99.7% of adults with single-species infection were treated or not treated appropriately according to their G6PD status.\n\nHistorically, quinine, derived from cinchona bark, was the mainstay for centuries. In the twentieth century, inexpensive monotherapies such as chloroquine and sulfadoxine–pyrimethamine became widespread, but the parasite quickly developed resistance to many of them. These failing drugs were replaced by ACTs, which WHO began recommending as first-line treatment in 2006. The switch has reduced malaria morbidity and mortality substantially, though resistance to other drugs remains a constant concern.\n\nPartial artemisinin resistance is now the most serious threat to ACTs. It is linked to mutations in the Plasmodium falciparum kelch13 gene that slow the clearance of young ring-stage parasites. Because a fully effective partner drug can still cure most infections, treatment failure usually occurs only when resistance to the partner drug also emerges. In western Cambodia, the efficacy of dihydroartemisinin–piperaquine fell from about 98% to 63% as resistance markers spread. In Africa, validated kelch13 mutations were first identified in Rwanda in 2014, followed by Uganda and Ethiopia–Eritrea in 2016, and by 2024 WHO had recorded confirmed or suspected partial resistance in at least eight African countries. The P441L mutation has recently spread across southern Africa, with prevalence reported at 7.3% in Angola, 33% in Namibia and 47% in Zambia at study sites.\n\nThe response combines several strategies. Multiple first-line therapies, in which health facilities deploy several different ACTs at once, were piloted in Burkina Faso, where most confirmed cases received the appropriate drug. Triple ACTs, which add a second partner drug, are being evaluated for their ability to delay resistance, and molecular surveillance of kelch13 and partner-drug markers is used to guide treatment policy. Some researchers argue for preemptive policy changes before failures become widespread in Africa."
    },
    {
      "heading": "Prevention and control tools",
      "text": "Malaria control combines tools that act on the mosquito vector, on the parasite inside the human host, and on the human's risk of severe disease. Vector control has the largest measured effect. Between 2000 and 2015, long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS) accounted for most of the approximately 1.3 billion fewer cases and 6.8 million fewer deaths recorded over that period.\n\nVector control: nets and indoor residual spraying\n\nLLINs are bed nets impregnated with insecticide, which both kill and deter Anopheles mosquitoes that bite people at night. IRS involves applying a residual insecticide to the interior walls of houses, where mosquitoes rest after feeding; a single application can remain active for at least four months. Until 2018, WHO recognized only pyrethroids for net treatment, and pyrethroids remain the dominant class. Because pyrethroids are cheap, heavy reliance on them has selected for resistance in Anopheles populations across much of Africa. Resistance arises through several routes: metabolic detoxification by enzymes that break down the insecticide, mutations in the insect's nerve-channel target that reduce binding, and behavioral shifts such as biting earlier in the evening or outdoors. These are classic cases of natural-selection acting on a population under chemical pressure.\n\nResistance limits both tools, and the responses are largely strategic. WHO recommends rotating insecticide classes, using mosaics, or deploying mixtures of unrelated active ingredients, including nets that combine a pyrethroid with a second chemical class. WHO's 2025 guidance recommends IRS in areas with ongoing transmission, and its elimination framework holds that IRS should supplement, not compensate for, poor net coverage. Neither tool protects people who are awake and outdoors at dusk, which is why biting behavior limits their reach.\n\nChemoprevention\n\nSeasonal malaria chemoprevention (SMC) is given to children in the Sahel, where transmission is concentrated in a rainy season. It consists of monthly full treatment courses of sulfadoxine-pyrimethamine plus amodiaquine, generally for four to five months a year. Intermittent preventive treatment in pregnancy (IPTp) uses sulfadoxine-pyrimethamine given at scheduled antenatal visits, at least a month apart, from the second trimester onward. Updated WHO guidance extended this to all pregnancies regardless of parity. Uptake remains the main problem: in 2023, only 44% of eligible pregnant women across 34 African countries received three or more doses, well short of the 80% target. Community-based IPTp, delivered through community health workers, is intended to close this gap. Mass drug administration, which treats whole populations in defined areas regardless of individual infection, is used in some settings to reduce the parasite reservoir, though its value depends heavily on local coverage and drug resistance.\n\nLarval source management and environmental measures\n\nAnopheles larvae develop in standing freshwater, so eliminating or treating breeding sites can reduce adult populations. Larval source management uses larvicides, such as Bacillus thuringiensis israelensis, and physical measures including drainage, filling of pools, improved water flow in channels, and removal of containers. It works best where breeding habitats are few, fixed and mappable, as in many urban and peri-urban settings. It is less practical where habitats are numerous and ephemeral, so it is typically combined with other measures rather than used alone.\n\nRTS,S and R21 vaccines\n\nTwo malaria vaccines are now recommended by WHO. RTS,S/AS01, recommended in 2021, fuses a truncated form of the Plasmodium falciparum circumsporozoite protein (CSP) to the hepatitis B surface antigen. R21/Matrix-M, recommended in October 2023, targets the same CSP antigen using a virus-like particle carrying repeats of the NANP sequence and a Matrix-M adjuvant. Both aim to induce antibodies against sporozoites before they reach liver cells, thereby blocking the pre-erythrocytic stage. In phase 3 trials, R21 reduced clinical malaria by 75% at seasonal sites and 68% at sites with perennial transmission over 12 months. Protection wanes over time, and the R21 schedule recommended by WHO is three monthly primary doses starting from five months of age, followed by a fourth dose a year later. Supply of RTS,S has lagged demand, and R21 was recommended in part to fill that gap.\n\nCase management and community health workers\n\nEffective case management depends on diagnosing malaria before treating it, so that antimalarials are not given to febrile patients who have other illnesses. Rapid diagnostic tests and microscopy support this, and the first-line treatment is covered elsewhere in this article. Community health workers extend these services to remote villages by performing tests, providing treatment, distributing nets, and referring severe cases. Their performance depends on training, supervision, and secure supply chains, and they are central to delivering community-based chemoprevention and vaccination in many endemic countries."
    },
    {
      "heading": "Human genetic and immune resistance",
      "text": "Malaria has exerted strong selective pressure on the human genome, and several inherited red blood cell variants are among the best-documented forms of host resistance. The most studied is the sickle-cell mutation, a single amino acid substitution in the beta-globin chain of hemoglobin. People who carry one copy (sickle-cell trait) are substantially protected against severe Plasmodium falciparum malaria, while people with two copies develop sickle-cell disease. The mechanisms are still debated. Proposals include slower parasite growth in cells that partly sickle at low oxygen tension, reduced adhesion of infected cells to blood vessel walls, faster clearance of infected cells by the spleen and macrophages, and an acquired immune component. Alpha- and beta-thalassemia, which reduce the output of globin chains, also appear to confer partial protection. Haldane proposed a heterozygote advantage against malaria for thalassemia in 1949, and the idea was later extended to sickle-cell trait.\n\nOther variants act through different routes. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked defect in an enzyme that supplies reducing power to protect red cells against oxidative stress. Parasites grow less well in deficient cells, and heterozygous females are partly protected. The Duffy-negative phenotype is a different case. The Duffy antigen serves as the receptor used by the P. vivax ligand for red cell entry, and a promoter variant that is common in sub-Saharan Africans and their descendants abolishes its expression on red cells. Duffy-negative people were long regarded as absolutely resistant to P. vivax blood-stage infection, but field studies in Madagascar and the Brazilian Amazon have documented infections in them, suggesting that the protection is strong but not absolute. Duffy negativity offers no protection against P. falciparum. Details of these variants are covered in sickle-cell trait and Duffy blood group.\n\nSuch variants persist in populations because of natural-selection acting on allele frequencies. In heterozygous sickle-cell carriers, the survival benefit against malaria outweighs the harm, and the resulting balancing selection keeps the allele at high frequency where malaria is or was endemic. Homozygotes for the sickle allele bear the cost of disease, which is what stabilizes the frequency. The genotype often matters more than the phenotype for this reason. Duffy negativity follows a different pattern, because a homozygous genotype is needed for full resistance and the selective advantage is largely directional rather than balancing.\n\nNaturally acquired immunity develops slowly, and it does not stop infection. Children in high-transmission areas gain protection against severe disease first and against uncomplicated illness later, while adults in the same settings often carry parasites without symptoms. This immunity wanes when exposure falls, and it rarely achieves sterilizing protection. Much of the explanation lies in antigenic variation. The major surface antigen PfEMP1 is encoded by about 60 var genes per parasite genome, and only one is typically expressed at a time, so the infected cell presents a new antigen as the parasite switches between variants. Antibodies that recognize one variant therefore leave others untouched, and children must encounter many variants before their repertoire is broad. Antibodies against relatively conserved PfEMP1 types are linked to protection from severe disease, and adults recognize a wider range of variant antigens than children. Antibodies against non-variant blood-stage antigens, antibody and T-cell responses against pre-erythrocytic antigens such as the circumsporozoite protein, and cellular responses that support antibody production all contribute, but their individual roles are not fully defined. Some parasite proteins also appear to mask protective IgG epitopes; for example, nonspecific IgM binding has been reported to block specific antibody binding to a placental-malaria PfEMP1 variant. Sterilizing immunity is hard to achieve partly because the parasite's surface repertoire keeps changing.\n\nImmune responses can also cause harm. Severe malaria is accompanied by high levels of pro-inflammatory cytokines, including tumour necrosis factor and interferon-gamma, and inflammation that is poorly controlled is associated with cerebral malaria and severe anemia. Counter-regulatory responses, including interleukin-10 and regulatory T cells, moderate this but can also dampen pathogen clearance. Repeated infection is linked to an expansion of atypical memory B cells that show reduced function, which has been proposed to explain why immunological-memory against malaria is short-lived and why vaccine responses are often weaker in exposed populations. Epidemiological studies also associate malaria with later anemia, impaired growth and cognition in children, and increased susceptibility to other infections, although establishing causation has proved difficult."
    },
    {
      "heading": "Early history and recognition of the disease",
      "text": "Descriptions of recurrent fever that resemble malaria appear in some of the oldest written records. Cuneiform tablets is not used here; instead, Mesopotamian clay tablets from about 2000 BCE describe chills and fevers, and Sumerian and Egyptian texts mention fevers accompanied by enlarged spleens. The Ebers Papyrus, dated to about 1550 BCE, is often cited for the Egyptian record, and malaria antigen has been reported in Egyptian remains. The Chinese Huangdi Neijing is associated with the same symptom pattern, but its date is disputed: some sources place it near 2700 BCE, while others date its compilation to roughly 300 BCE–200 CE. Indian medical texts such as the Charaka Samhita classified fevers by their periodicity, including tertian and quartan forms, and the Susruta Samhita linked some fevers to insect bites. Chinese and Roman popular accounts personified fevers as demons or a fever goddess.\n\nIn ancient Greece, the physician Hippocrates (c. 460–370 BCE) distinguished intermittent fevers by their rhythm: a fever recurring every third day, which the Latin tradition later called tertiana, and one recurring every fourth day, called quartana. Writers in the Roman Empire refined these categories. Celsus separated tertian fevers with a clear fever-free interval from semi-tertian fevers with little remission, and Galen noted the association of malaria with jaundice. The Roman poet Horace recorded the recurring rigors of the illness. The Greek word miasma, meaning pollution or stain, was used by Hippocratic writers for harmful vapours rising from the ground, and this idea became central to explanations of the disease for the next two thousand years.\n\nThe miasma theory held that disease arose from noxious air, particularly the vapours of marshes and decaying matter. Its influence on the name of the disease is direct: \"malaria\" comes from the Italian mal aria, meaning \"bad air,\" a term tied to the marshy lowlands around Rome. The theory was stated most clearly by the Italian physician Giovanni Maria Lancisi in 1717, who linked the illness to swamp effluvia. Because the theory connected disease with wet, stagnant ground, it encouraged drainage of marshes, removal of waste and settlement policies that avoided low-lying land. Some of these measures were effective in reducing mosquito breeding, even though their explanation was wrong. The miasma idea was discarded only after the mosquito transmission of the parasite was established in the late nineteenth century (see germ theory).\n\nThe first effective drug against the disease came from the bark of the cinchona tree of the Andes. Indigenous peoples of the Andean region are generally credited with knowing the bark's properties before European contact, and Spanish Jesuits are credited with introducing it into European medical use around 1640. A popular story about a Spanish viceroy's wife being cured in 1631 is widely regarded as legend. In 1820 the French pharmacists Pierre-Joseph Pelletier and Joseph Bienaimé Caventou isolated the active alkaloid, which they named quinine, and it was then used in purified form. Quinine became a tool of European colonial expansion into tropical regions, and until the 1930s it remained the only effective antimalarial, so the cinchona tree was of major commercial and strategic importance to the British and Dutch empires. For the broader drug history, see cinchona bark and pharmacology.\n\nThe association between malaria and the spread of farming, irrigation and dense settlement is widely discussed by historians and geneticists. Clearing land, building canals and storing water created standing pools, and larger settlements could sustain a parasite population in a way that small, mobile groups could not. The timing of the parasite's adaptation to humans is still debated, and genomic dating estimates differ considerably, with many placing the emergence of Plasmodium falciparum as a human pathogen within the last several thousand to ten thousand years. Ancient DNA is now providing more direct evidence. Genetic analysis of leg bones from a sixth-century Roman skeleton in Lugnano, Italy, showed that P. falciparum had affected that community. Molecular studies have also confirmed a high prevalence of P. falciparum in ancient Egypt, and the earliest Egyptian samples are a reminder that the disease was present in the Nile valley long before classical medicine described it."
    },
    {
      "heading": "Scientific discovery and the transmission chain",
      "text": "The modern account of malaria was assembled over roughly four decades, and several stages were contested. The first step came in Algeria. On 6 November 1880, while working at the military hospital in Constantine, the French army physician Charles Louis Alphonse Laveran examined fresh blood from a patient under the microscope and saw whip-like, moving bodies pushing aside red blood cells. He later identified the organisms in the blood of 148 of 192 patients he examined and concluded that they were a living protozoan, not a by-product of the disease. Earlier, Rudolf Virchow had described the dark malarial pigment in 1849, but no one had tied a microorganism to the illness. Laveran's parasitic hypothesis was not accepted immediately, because the prevailing explanations still centred on marsh air. His 1880–1882 communications to the Paris academies and his 1881 monograph gradually established the claim. Laveran was awarded the Nobel Prize in Physiology or Medicine in 1907 for showing the role of protozoa in disease.\n\nCamillo Golgi's work in 1886 linked the parasite's life cycle to the clinical course. He showed that the forms seen in tertian and quartan fevers differed, and that the timing of the fever coincided with the maturation of the parasite's spores. Patrick Manson, working in London, suspected that mosquitoes transmitted malaria by analogy with filarial worms, and he sent his colleague Ronald Ross to India to test the idea. In Secunderabad, on 16 August 1897, Ross allowed anopheline mosquitoes to feed on a malaria patient. Four days later he found cysts containing the parasite in the mosquito stomach wall. Similar experiments with Culex and Aedes species were negative, which pointed to a specific vector.\n\nRoss could not easily work with human malaria in India, so he turned to avian malaria, which he studied in sparrows and crows. In 1898 he traced the parasite from the mosquito gut to the salivary glands and showed that bites from infected mosquitoes passed the infection to healthy birds. This was the first experimental demonstration that a malaria parasite could complete its development in a mosquito and reach a new vertebrate host. Ross's bird work, however, did not by itself prove transmission of human malaria. In Italy, Giovanni Battista Grassi, with Amico Bignami and Giuseppe Bastianelli, screened mosquito species on the basis of their systematics and local distribution, initially suspecting Anopheles claviger and two Culex species. In November 1898 a healthy volunteer in a non-malarial area contracted tertian malaria after being bitten by A. claviger mosquitoes raised in the laboratory. The Culex suspicions were dropped. Robert Koch, visiting Rome that year, had rejected Anopheles as a vector, citing its presence in malaria-free areas near Berlin, and the Italian result was therefore contested as well.\n\nThe priority dispute between Ross and Grassi grew sharper after 1899, when Ross published on the role of mosquitoes in Annales de l'Institut Pasteur, and it was complicated by the British physician Edmonston Charles, who had visited Grassi's laboratory and reported to Ross. Historians now generally divide the credit. Ross was the first to demonstrate transmission of avian malaria by mosquitoes, while Grassi's group identified the vector of human malaria and proved transmission experimentally. The Nobel Prize in Physiology or Medicine in 1902 went to Ross for his work on malaria, but Grassi felt cheated of recognition, and the quarrel continued until his death in 1925. Medical historians also note that Ross's account, and the Italian account, relied on different species and different hosts, which partly explains why each side claimed the decisive step.\n\nBy the early twentieth century, the main outline of the life cycle was complete: sexual forms in the mosquito, sporozoites in the salivary glands, and asexual multiplication in the blood. Classification of the human parasites followed, and the genus name Plasmodium, introduced by Fritz Schaudinn in 1902, became standard. The discoveries had direct consequences for public health. Once the mosquito was known to be the vector, control could target breeding water and adult mosquitoes rather than marsh air. Ross himself worked on larval control in Egypt, and the same logic was later applied in Panama. Experimental models were central to this progress. Avian parasites provided the first complete transmission chain, and monkey models, such as the species later named Plasmodium knowlesi in rhesus macaques, allowed researchers to study human-infecting species that could not easily be maintained in the laboratory. In 2002 the genome of Plasmodium falciparum was published, and genome sequencing has since revealed parasite genetic diversity and markers associated with drug resistance."
    },
    {
      "heading": "Global burden and distribution",
      "text": "Cases and deaths in 2024\n\nThe WHO estimated 282 million malaria cases and 610,000 deaths in 80 countries in 2024, which is 3% and 2% higher, respectively, than in 2023. Rates are expressed per population at risk, a denominator that the World Health Organization uses in its annual reports. In 2024 the incidence was 64.0 cases per 1000 population at risk, while the mortality rate remained stable at 13.8 deaths per 100 000 population at risk. The mortality rate is more than three times the 2030 target of the global technical strategy, which is 4.5 per 100,000 (see mortality rate). Deaths have fallen far less than cases in the long run: 610,000 people died of malaria in 2024, compared to 578,000 in 2015. Earlier figures are also revised between reports. The 2023 case count, for instance, was first reported as 263 million and later rising from 273 million in 2023 to 282 million in 2024.\n\nConcentration in the African Region\n\nThe burden is heavily concentrated in Africa. The WHO African Region accounted for 94% of global malaria cases and 95% of malaria deaths in 2024, with five countries – Nigeria (24.3%), the Democratic Republic of the Congo (12.5%), Uganda (4.7%), Ethiopia (4.4%) and Mozambique (3.6%) – contributing nearly half of all cases. Deaths are even more concentrated: over half of all deaths in the Region occurred in three countries: Nigeria (31.9%), the Democratic Republic of the Congo (11.7%), and Niger (6.1%). Age is another major axis of inequality. Children under 5 years of age accounted for about 75% of all malaria deaths in the Region. Within sub-Saharan Africa, household socioeconomic status and maternal education are associated with infection risk. In a study of 11 countries, children whose mothers have secondary education have about 56% lower risk (odds ratio = 0.44) of malaria infection and 73% lower (odds ratio = 0.37) among children living in the richest households, compared to children living in the poorest households.\n\nTrends over time and the effect of COVID-19\n\nBetween 2000 and 2024, an estimated 2.3 billion cases and 14 million deaths were averted globally. Those gains have been uneven. Since 2015, reductions in cases and deaths have largely stalled in many countries with moderate or high transmission, and the stall was worsened in sub-Saharan Africa by disruptions during the COVID-19 pandemic (the situation was made worse, especially in sub-Saharan Africa, by disruptions during the COVID-19 pandemic).\n\nThe clearest shock was in 2020. This represents about 14 million more cases in 2020 compared to 2019, and 69 000 more deaths. Approximately two-thirds of these additional deaths (47 000) were linked to disruptions in the provision of malaria prevention, diagnosis and treatment during the pandemic. Early projections had been far more pessimistic. Early in the pandemic, WHO had projected a doubling of malaria deaths in sub-Saharan Africa, as a worst-case scenario. Yet, the analysis found there was an estimated 12 per cent increase in deaths in the region between 2019 and 2020. A separate modelling study estimated that disruptions in access to antimalarial treatment in sub-Saharan Africa likely resulted in approximately 5.9 (4.4–7.2 95% CI) million more malaria cases and 76 (20–132) thousand additional deaths in the 2020–2021 period. In 2025, the WHO warned that the 2025 funding cuts to malaria programmes put millions of additional lives at risk.\n\nRegional patterns\n\nBurden and trends differ sharply between regions. The WHO Region of the Americas carries less than 1% of global cases, yet it recorded a 16% increase from 2023 to 2024, largely driven by an increase in cases in Colombia, Haiti, Peru and the Plurinational State of Bolivia. In Asia, the picture is more mixed. The Eastern Mediterranean Region, which accounts for nearly 4% of global cases in 2024, experienced an estimated 6% decrease in malaria case incidence from 2023 to 2024, the first decline since 2020. In the Western Pacific, malaria is mostly concentrated in Indonesia and Papua New Guinea, incidence remained stable at 2.3 cases per 1000 population at risk in 2024. The South-East Asia Region continued to make progress and remains on track to achieve the GTS 2025 targets of at least a 75% reduction in malaria case incidence and mortality rate since 2015.\n\nConflict, displacement and climate shocks account for several of the recent increases. The rise in 2024 was predominantly in countries affected by conflict (Ethiopia, Yemen) or climatic disruption (Madagascar). Population movement, including displacement from conflict, is likewise a recognized factor in transmission, although the sources consulted for this section do not quantify its contribution.\n\nEconomic costs and poverty\n\nMalaria imposes costs on households, health systems and national economies, although the sources consulted here do not provide reliable continent-wide cost totals. Households bear the cost of treatment and lost working days, and health systems redirect staff and funds toward acute care. The disease is also closely tied to poverty and development. It burdens the communities that are least able to absorb its costs, and it affects child development: among under-five children, malaria has been linked to poor educational outcomes and reduced cognitive function. This two-way relationship between disease and poverty is why malaria control is often discussed alongside social determinants of health, universal health coverage and sustainable development goals."
    },
    {
      "heading": "Elimination efforts and unresolved challenges",
      "text": "The Global Malaria Eradication Programme\n\nIn 1955 the World Health Assembly launched a campaign to end malaria transmission worldwide, chiefly by spraying DDT inside homes. The campaign's four phases (preparation, attack, consolidation and maintenance) rested on house spraying, drug treatment and surveillance. Mosquitoes resistant to DDT were first reported in Greece in 1951, before the programme began, and chloroquine resistance was confirmed in 1960 after treatment failures in Venezuela and Thailand.\n\nThe programme produced large but uneven results. In Sri Lanka, cases fell from a high of two or more million a year in 1958 to just 17 in 1963. In sub-Saharan Africa, by contrast, the effect was small: of about 220 million people living in areas where malaria was originally endemic, only slightly more than 4 million lived where elimination had been achieved by 1969. Problems in some settings were recognized only in the mid-1960s, when mosquitoes in southern Mexico were found to avoid contact with the insecticide. Analysts also cite the dependence on a single, uniform method. Locally adapted environmental control had been largely set aside after DDT became available, so the strategy offered, in one account's words, either complete success or utter failure. When India's malaria declined, USAID withdrew funding, expecting the government to cover the costs, but India could not produce or procure the DDT required. The lack of DDT was likely a key factor in the re-establishment of malaria, which peaked at 6 million cases by 1976.\n\nEradication was dropped in stages. In 1969, the 22nd World Health Assembly, in resolution WHA22.39, accepted that eradication was not feasible in the short term in some countries and that control was an appropriate step, while keeping eradication as the long-term goal. Post-programme lessons emphasize flexible strategies, integration with health systems and community involvement, because no single strategy can be applicable everywhere.\n\nThe Global Technical Strategy, 2016–2030\n\nThe WHO strategy sets targets for incidence and mortality, and the latest assessments show that progress is well behind them. The 2025 World Malaria Report states that the current incidence is 3.5 times higher than the GTS target of 18 per 1000 population at risk, and the mortality rate three times higher than the target of 4.5 per 100 000 population at risk. In 2024, the world recorded 282 million malaria cases and 610,000 deaths, a slight increase from 2023. An estimated 95% of global malaria deaths were in the WHO African Region, with most occurring among children under 5. Since 2000, malaria control efforts have averted 2.3 billion cases and 14 million deaths globally.\n\nRegional trends diverge. The Eastern Mediterranean Region saw a decline in 2024, while the Region of the Americas recorded a 16% increase, driven mainly by Colombia, Haiti, Peru and Bolivia.\n\nCertification of malaria-free countries\n\nCertification requires proof that indigenous malaria transmission has been interrupted nationwide for at least the past three consecutive years and that the country can still detect and respond to new cases. The final decision rests with the WHO Director-General, based on advice from the Technical Advisory Group on Malaria Elimination and Certification. A total of 47 countries and one territory have been certified as malaria-free by WHO. Recent additions include Georgia, certified in January 2025; Suriname, which became the first country in the Amazon region to be certified; and Timor-Leste, which cut cases from a peak of over 223,000 in 2006 to zero indigenous cases from 2021 onwards.\n\nEmerging tools and their concerns\n\nCurrent tools are still expanding. By the end of 2024, malaria vaccines had been introduced in 17 countries, with over 10.5 million doses delivered. Gene drive mosquitoes, which use genome-editing systems to spread modifications through wild populations, could in principle reduce vector competence or population size. Their risks include irreversibility, effects on non-target species, cross-border spread and regulatory oversight under biosafety frameworks, and field releases remain at the research and approval stage. Novel vector control and new diagnostics face similar questions. Diagnostic gaps are already a problem: the 2025 report warns that parasites are evading rapid diagnostic tests and that Anopheles stephensi is spreading into urban areas.\n\nConverging threats\n\nSeveral threats now coincide. The 2025 report notes antimalarial drug resistance, now confirmed or suspected in eight African countries. Resistance to pyrethroid insecticides in mosquitoes is also widespread, and artemisinin partial resistance challenges combination therapies that rely on a limited number of combinations. Climate-related threats, conflict and declining funding for programmes, surveillance and research also slow progress. External funding is dropping sharply at the same time, and the disruptions of 2025 came on top of pre-existing shortfalls. Whether recent gains can be sustained depends on whether these pressures can be managed together."
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      "title": "link.springer.com",
      "url": "https://link.springer.com/article/10.2165/00003495-200059040-00001"
    },
    {
      "title": "WHO Certifies Georgia as Malaria-Free",
      "url": "https://www.aabb.org/news-resources/news/article/2025/01/24/who-certifies-georgia-as-malaria-free"
    },
    {
      "title": "Suriname certified malaria-free by WHO - PAHO/WHO",
      "url": "https://www.paho.org/en/news/30-6-2025-suriname-certified-malaria-free-who"
    },
    {
      "title": "WHO / Karen Reidy",
      "url": "https://www.who.int/news/item/24-07-2025-timor-leste-certified-malaria-free-by-who"
    },
    {
      "title": "Global Malaria Programme",
      "url": "https://www.who.int/teams/global-malaria-programme/elimination"
    }
  ],
  "license": "https://creativecommons.org/licenses/by/4.0/"
}