The disease is widespread in the tropical
regions that exist in a broad band around the equator
This includes much of sub-Saharan Africa
, and Latin America
In 2018 there were 228 million cases of malaria worldwide resulting in an estimated 405,000 deaths.
Approximately 93% of the cases and 94% of deaths occurred in Africa.
Rates of disease have decreased from 2010 to 2014 but increased from 2015 to 2017, during which there were 231 million cases.
Malaria is commonly associated with poverty and has a significant negative effect on economic development
In Africa, it is estimated to result in losses of US$12 billion a year due to increased healthcare costs, lost ability to work, and adverse effects on tourism.
Signs and symptoms
Main symptoms of malaria
The signs and symptoms of malaria typically begin 8–25 days following infection,
but may occur later in those who have taken antimalarial medications as prevention
Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms
and can resemble other conditions such as sepsis
, and viral diseases
The presentation may include headache
, joint pain
, hemolytic anemia
, hemoglobin in the urine
, retinal damage
, and convulsions
The classic symptom of malaria is paroxysm
—a cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occurring every two days (tertian fever
) in P. vivax
and P. ovale
infections, and every three days (quartan fever
) for P. malariae
. P. falciparum
infection can cause recurrent fever every 36–48 hours, or a less pronounced and almost continuous fever.
belong to the genus Plasmodium
). In humans, malaria is caused by P. falciparum
, P. malariae
, P. ovale
, P. vivax
and P. knowlesi
Among those infected, P. falciparum
is the most common species identified (~75%) followed by P. vivax
Although P. falciparum
traditionally accounts for the majority of deaths,
recent evidence suggests that P. vivax
malaria is associated with potentially life-threatening conditions about as often as with a diagnosis of P. falciparum
infection. P. vivax
proportionally is more common outside Africa.
There have been documented human infections with several species of Plasmodium
from higher apes
; however, except for P. knowlesi
species that causes malaria in macaques
—these are mostly of limited public health importance.
The life cycle of malaria parasites. A mosquito causes an infection by a bite. First, sporozoites enter the bloodstream, and migrate to the liver. They infect liver cells
, where they multiply into merozoites, rupture the liver cells, and return to the bloodstream. The merozoites infect red blood cells, where they develop into ring forms, trophozoites and schizonts that in turn produce further merozoites. Sexual forms
are also produced, which, if taken up by a mosquito, infect the insect and continue the life cycle.
In the life cycle
, a female Anopheles
mosquito (the definitive host
) transmits a motile infective form (called the sporozoite
) to a vertebrate host such as a human (the secondary host), thus acting as a transmission vector
. A sporozoite travels through the blood vessels to liver cells (hepatocytes
), where it reproduces asexually
), producing thousands of merozoites
. These infect new red blood cells and initiate a series of asexual multiplication cycles (blood schizogony) that produce 8 to 24 new infective merozoites, at which point the cells burst and the infective cycle begins anew.
Other merozoites develop into immature gametocytes
, which are the precursors of male and female gametes
. When a fertilised mosquito bites an infected person, gametocytes are taken up with the blood and mature in the mosquito gut. The male and female gametocytes fuse and form an ookinete
—a fertilised, motile zygote
. Ookinetes develop into new sporozoites that migrate to the insect's salivary glands
, ready to infect a new vertebrate host. The sporozoites are injected into the skin, in the saliva, when the mosquito takes a subsequent blood meal.
Only female mosquitoes feed on blood; male mosquitoes feed on plant nectar and do not transmit the disease. Females of the mosquito genus Anopheles
prefer to feed at night. They usually start searching for a meal at dusk, and continue through the night until they succeed.
Malaria parasites can also be transmitted by blood transfusions
, although this is rare.
Symptoms of malaria can recur after varying symptom-free periods. Depending upon the cause, recurrence can be classified as either recrudescence
, or reinfection. Recrudescence is when symptoms return after a symptom-free period. It is caused by parasites surviving in the blood as a result of inadequate or ineffective treatment.
Relapse is when symptoms reappear after the parasites have been eliminated from the blood but persist as dormant hypnozoites
in liver cells.
Relapse commonly occurs between 8–24 weeks and is often seen in P. vivax
and P. ovale
However, relapse-like P. vivax
recurrences are probably being over-attributed to hypnozoite activation. Some of them might have an extra-vascular merozoite origin, making these recurrences recrudescences, not relapses.
One newly recognised, non-hypnozoite, possible contributing source to recurrent peripheral P. vivax
parasitemia is erythrocytic forms in bone marrow. P. vivax
malaria cases in temperate
areas often involve overwintering
by hypnozoites, with relapses beginning the year after the mosquito bite.
Reinfection means the parasite that caused the past infection was eliminated from the body but a new parasite was introduced. Reinfection cannot readily be distinguished from recrudescence, although recurrence of infection within two weeks of treatment for the initial infection is typically attributed to treatment failure.
People may develop some immunity
when exposed to frequent infections.
of a placenta
from a stillbirth
due to maternal malaria. H&E stain
. Red blood cells are anuclear; blue/black staining in bright red structures (red blood cells) indicate foreign nuclei from the parasites.
Electron micrograph of a Plasmodium falciparum-infected red blood cell (center), illustrating adhesion protein "knobs"
Malaria infection develops via two phases: one that involves the liver
(exoerythrocytic phase), and one that involves red blood cells, or erythrocytes
(erythrocytic phase). When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver where they infect hepatocytes, multiplying asexually and asymptomatically for a period of 8–30 days.
After a potential dormant period in the liver, these organisms differentiate
to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells to begin the erythrocytic stage of the life cycle.
The parasite escapes from the liver undetected by wrapping itself in the cell membrane
of the infected host liver cell.
Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their host cells to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.
Some P. vivax
sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead, produce hypnozoites that remain dormant for periods ranging from several months (7–10 months is typical) to several years.
After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in P. vivax
although their existence in P. ovale
The parasite is relatively protected from attack by the body's immune system
because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen
. To avoid this fate, the P. falciparum
parasite displays adhesive proteins
on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen.
The blockage of the microvasculature causes symptoms such as those in placental malaria.
Sequestered red blood cells can breach the blood–brain barrier
and cause cerebral malaria.
The impact of sickle cell trait on malaria immunity illustrates some evolutionary trade-offs that have occurred because of endemic malaria. Sickle cell trait causes a change in the haemoglobin molecule in the blood. Normally, red blood cells have a very flexible, biconcave shape that allows them to move through narrow capillaries
; however, when the modified haemoglobin S
molecules are exposed to low amounts of oxygen, or crowd together due to dehydration, they can stick together forming strands that cause the cell to distort into a curved sickle shape. In these strands, the molecule is not as effective in taking or releasing oxygen, and the cell is not flexible enough to circulate freely. In the early stages of malaria, the parasite can cause infected red cells to sickle, and so they are removed from circulation sooner. This reduces the frequency with which malaria parasites complete their life cycle in the cell. Individuals who are homozygous
(with two copies of the abnormal haemoglobin beta allele
) have sickle-cell anaemia
, while those who are heterozygous (with one abnormal allele and one normal allele) experience resistance to malaria without severe anaemia. Although the shorter life expectancy for those with the homozygous condition would tend to disfavour the trait's survival, the trait is preserved in malaria-prone regions because of the benefits
provided by the heterozygous form.
Liver dysfunction as a result of malaria is uncommon and usually only occurs in those with another liver condition such as viral hepatitis
or chronic liver disease
. The syndrome is sometimes called malarial hepatitis
While it has been considered a rare occurrence, malarial hepatopathy has seen an increase, particularly in Southeast Asia and India. Liver compromise in people with malaria correlates with a greater likelihood of complications and death.
Ring-forms and gametocytes
of Plasmodium falciparum
in human blood
Owing to the non-specific nature of the presentation of symptoms, diagnosis of malaria in non-endemic areas requires a high degree of suspicion, which might be elicited by any of the following: recent travel history, enlarged spleen
, fever, low number of platelets
in the blood, and higher-than-normal levels of bilirubin
in the blood combined with a normal level of white blood cells
Reports in 2016 and 2017 from countries where malaria is common suggest high levels of over diagnosis due to insufficient or inaccurate laboratory testing.
Malaria is usually confirmed by the microscopic examination of blood films
or by antigen
-based rapid diagnostic tests
In some areas, RDTs must be able to distinguish whether the malaria symptoms are caused by Plasmodium falciparum
or by other species of parasites since treatment strategies could differ for non-P. falciparum
Microscopy is the most commonly used method to detect the malarial parasite—about 165 million blood films were examined for malaria in 2010.
Despite its widespread usage, diagnosis by microscopy suffers from two main drawbacks: many settings (especially rural) are not equipped to perform the test, and the accuracy of the results depends on both the skill of the person examining the blood film and the levels of the parasite in the blood. The sensitivity
of blood films ranges from 75 to 90% in optimum conditions, to as low as 50%. Commercially available RDTs are often more accurate than blood films at predicting the presence of malaria parasites, but they are widely variable in diagnostic sensitivity and specificity depending on manufacturer, and are unable to tell how many parasites are present.
However, incorporating RDTs into the diagnosis of malaria can reduce antimalarial prescription. Although RDT does not improve the health outcomes of those infected with malaria, it also does not lead to worse outcomes when compared to presumptive antimalarial treatment.
In regions where laboratory tests are readily available, malaria should be suspected, and tested for, in any unwell person who has been in an area where malaria is endemic. In areas that cannot afford laboratory diagnostic tests, it has become common to use only a history of fever as the indication to treat for malaria—thus the common teaching "fever equals malaria unless proven otherwise". A drawback of this practice is overdiagnosis
of malaria and mismanagement of non-malarial fever, which wastes limited resources, erodes confidence in the health care system, and contributes to drug resistance.
Although polymerase chain reaction
-based tests have been developed, they are not widely used in areas where malaria is common as of 2012, due to their complexity.
Malaria is classified into either "severe" or "uncomplicated" by the World Health Organization
It is deemed severe when any
of the following criteria are present, otherwise it is considered uncomplicated.
Cerebral malaria is defined as a severe P. falciparum
-malaria presenting with neurological symptoms, including coma (with a Glasgow coma scale
less than 11, or a Blantyre coma scale
less than 3), or with a coma that lasts longer than 30 minutes after a seizure.
Various types of malaria have been called by the names below:
An Anopheles stephensi
mosquito shortly after obtaining blood from a human (the droplet of blood is expelled as a surplus). This mosquito is a vector of malaria, and mosquito control is an effective way of reducing its incidence.
Methods used to prevent malaria include medications, mosquito elimination and the prevention of bites. As of 2020, there is one vaccine for malaria
(known as RTS,S
) which is licensed for use.
The presence of malaria in an area requires a combination of high human population density, high anopheles mosquito population density and high rates of transmission from humans to mosquitoes and from mosquitoes to humans. If any of these is lowered sufficiently, the parasite eventually disappears from that area, as happened in North America, Europe, and parts of the Middle East. However, unless the parasite is eliminated from the whole world, it could re-establish if conditions revert to a combination that favors the parasite's reproduction. Furthermore, the cost per person of eliminating anopheles mosquitoes rises with decreasing population density, making it economically unfeasible in some areas.
Prevention of malaria may be more cost-effective than treatment of the disease in the long run, but the initial costs
required are out of reach of many of the world's poorest people. There is a wide difference in the costs of control (i.e. maintenance of low endemicity) and elimination programs between countries. For example, in China—whose government in 2010 announced a strategy to pursue malaria elimination in the Chinese provinces
—the required investment is a small proportion of public expenditure on health. In contrast, a similar programme in Tanzania would cost an estimated one-fifth of the public health budget.
In areas where malaria is common, children under five years old often have anaemia
, which is sometimes due to malaria. Giving children with anaemia in these areas preventive antimalarial medication improves red blood cell levels slightly but does not affect the risk of death or need for hospitalisation.
refers to methods used to decrease malaria by reducing the levels of transmission by mosquitoes. For individual protection, the most effective insect repellents
are based on DEET
However, there is insufficient evidence that mosquito repellents can prevent malaria infection.
Insecticide-treated mosquito nets
(ITNs) and indoor residual spraying
(IRS) are effective, have been commonly used to prevent malaria, and their use has contributed significantly to the decrease in malaria in the 21st century.
ITNs and IRS may not be sufficient to completely eliminate the disease as these interventions depend on how many people use nets, how many gaps in insecticide there are (low coverage areas), if people are not protected when outside of the home, and an increase in mosquitoes that are resistant to insecticides.
Modifications to people's houses to prevent mosquito exposure may be an important long term prevention measure.
Walls where indoor residual spraying of DDT has been applied. The mosquitoes remain on the wall until they fall down dead on the floor.
A mosquito net in use.
Mosquito nets help keep mosquitoes away from people and reduce infection rates and transmission of malaria. Nets are not a perfect barrier and are often treated with an insecticide designed to kill the mosquito before it has time to find a way past the net. Insecticide-treated nets (ITNs) are estimated to be twice as effective as untreated nets and offer greater than 70% protection compared with no net.
Between 2000 and 2008, the use of ITNs saved the lives of an estimated 250,000 infants in Sub-Saharan Africa.
About 13% of households in Sub-Saharan countries owned ITNs in 2007
and 31% of African households were estimated to own at least one ITN in 2008. In 2000, 1.7 million (1.8%) African children living in areas of the world where malaria is common were protected by an ITN. That number increased to 20.3 million (18.5%) African children using ITNs in 2007, leaving 89.6 million children unprotected
and to 68% African children using mosquito nets in 2015.
Most nets are impregnated with pyrethroids
, a class of insecticides with low toxicity
. They are most effective when used from dusk to dawn.
It is recommended to hang a large "bed net" above the center of a bed and either tuck the edges under the mattress or make sure it is large enough such that it touches the ground.
ITN is beneficial towards pregnancy outcomes in malaria-endemic regions in Africa but more data is needed in Asia and Latin America.
In areas of high malaria resistance, piperonyl butoxide combined with pyrethroids in ITN is effective in reducing malaria infection rates.
Indoor residual spraying
Indoor residual spraying is the spraying of insecticides on the walls inside a home. After feeding, many mosquitoes rest on a nearby surface while digesting the bloodmeal, so if the walls of houses have been coated with insecticides, the resting mosquitoes can be killed before they can bite another person and transfer the malaria parasite.
As of 2006, the World Health Organization
recommends 12 insecticides in IRS operations, including DDT
and the pyrethroids cyfluthrin
This public health use of small amounts of DDT is permitted under the Stockholm Convention
, which prohibits its agricultural use.
One problem with all forms of IRS is insecticide resistance
. Mosquitoes affected by IRS tend to rest and live indoors, and due to the irritation caused by spraying, their descendants tend to rest and live outdoors, meaning that they are less affected by the IRS.
It is uncertain whether the use of IRS together with ITN is effective in reducing malaria cases due to wide geographical variety of malaria distribution, malaria transmission, and insecticide resistance.
Housing is a risk factor for malaria and modifying the house as a prevention measure may be a sustainable strategy that does not rely on the effectiveness of insecticides such as pyrethroids
The physical environment inside and outside the home that may improve the density of mosquitoes are considerations. Examples of potential modifications include how close the home is to mosquito breeding sites, drainage and water supply near the home, availability of mosquito resting sites (vegetation around the home), the proximity to live stock and domestic animals, and physical improvements or modifications to the design of the home to prevent mosquitoes from entering.
Other mosquito control methods
People have tried a number of other methods to reduce mosquito bites and slow the spread of malaria. Efforts to decrease mosquito larvae by decreasing the availability of open water where they develop, or by adding substances to decrease their development, are effective in some locations.
Electronic mosquito repellent devices, which make very high-frequency sounds that are supposed to keep female mosquitoes away, have no supporting evidence of effectiveness.
There is a low certainty evidence that fogging
may have an effect on malaria transmission.
Larviciding by hand delivery of chemical or microbial insecticides into water bodies containing low larval distribution may reduce malarial transmission.
There is insufficient evidence to determine whether larvivorous fish can decrease mosquito density and transmission in the area.
There are a number of medications that can help prevent or interrupt malaria in travellers to places where infection is common. Many of these medications are also used in treatment. In places where Plasmodium
is resistant to one or more medications, three medications—mefloquine
, or the combination of atovaquone/proguanil
)—are frequently used for prevention.
Doxycycline and the atovaquone/proguanil are better tolerated while mefloquine is taken once a week.
Areas of the world with chloroquine
-sensitive malaria are uncommon.
Antimalarial mass drug administration to an entire population at the same time may reduce the risk of contracting malaria in the population.
The protective effect does not begin immediately, and people visiting areas where malaria exists usually start taking the drugs one to two weeks before they arrive, and continue taking them for four weeks after leaving (except for atovaquone/proguanil, which only needs to be started two days before and continued for seven days afterward).
The use of preventive drugs is often not practical for those who live in areas where malaria exists, and their use is usually given only to pregnant women and short-term visitors. This is due to the cost of the drugs, side effects
from long-term use, and the difficulty in obtaining antimalarial drugs outside of wealthy nations.
During pregnancy, medication to prevent malaria has been found to improve the weight of the baby at birth and decrease the risk of anaemia
in the mother.
The use of preventive drugs where malaria-bearing mosquitoes are present may encourage the development of partial resistance.
Giving antimalarial drugs to infants through intermittent preventive therapy can reduce the risk of having malaria infection, hospital admission, and anaemia.
Mefloquine is more effective than sulfadoxine-pyrimethamine in preventing malaria for HIV-negative pregnant women. Cotrimoxazole is effective in preventing malaria infection and reduce the risk of getting anaemia in HIV-positive women. Giving sulfadoxine-pyrimethamine for three or more doses as intermittent preventive therapy is superior than two doses for HIV-positive women living in malaria-endemic areas.
Prompt treatment of confirmed cases with artemisinin-based combination therapies (ACTs) may also reduce transmission.
Community participation and health education
strategies promoting awareness of malaria and the importance of control measures have been successfully used to reduce the incidence of malaria in some areas of the developing world.
Recognising the disease in the early stages can prevent it from becoming fatal. Education can also inform people to cover over areas of stagnant, still water, such as water tanks that are ideal breeding grounds for the parasite and mosquito, thus cutting down the risk of the transmission between people. This is generally used in urban areas where there are large centers of population in a confined space and transmission would be most likely in these areas. Intermittent preventive therapy
is another intervention that has been used successfully to control malaria in pregnant women and infants,
and in preschool children where transmission is seasonal.
An advertisement for quinine
as a malaria treatment from 1927.
Malaria is treated with antimalarial medications
; the ones used depends on the type and severity of the disease. While medications against fever
are commonly used, their effects on outcomes are not clear.
Providing free antimalarial drugs to households may reduce childhood deaths when used appropriately. Programmes which presumptively treat all causes of fever with antimalarial drugs may lead to overuse of antimalarials and undertreat other causes of fever. Nevertheless, the use of malaria rapid-diagnostic kits can help to reduce over-usage of antimalarials.
Simple or uncomplicated malaria may be treated with oral medications. Artemisinin drugs are effective and safe in treating uncomplicated malaria.
Artemisinin in combination with other antimalarials (known as artemisinin-combination therapy
, or ACT) is about 90% effective when used to treat uncomplicated malaria.
The most effective treatment for P. falciparum
infection is the use of ACT, which decreases resistance to any single drug component. Artemether-lumefantrine (six-dose regimen) is more effective than the artemether-lumefantrine (four-dose regimen) or other regimens not containing artemisinin derivatives in treating falciparum malaria.
Another recommended combination is dihydroartemisinin
. Artemisinin-naphthoquine combination therapy showed promising results in treating falciparum malaria. However, more research need to establish its efficacy as a reliable treatment.
Artesunate plus mefloquine performs better than mefloquine alone in treating uncomplicated falciparum malaria in low transmission settings. Atovaquone-proguanil is effective against uncomplicated falciparum with a possible failure rate of 5% to 10%; the addition of artesunate may reduce failure rate.
Azithromycin monotherapy or combination therapy has not shown effectiveness in treating plasmodium or vivax malaria. Amodiaquine plus sulfadoxine-pyrimethamine may achieve less treatment failures when compared to sulfadoxine-pyrimethamine alone in uncomplicated falciparum malaria. There is insufficient data on chlorproguanil-dapsone in treating uncomplicated falciparum malaria.
The addition of primaquine with artemisinin-based combination therapy for falciparum malaria reduces its transmission at day 3-4 and day 8 of infection. Sulfadoxine-pyrimethamine plus artesunate is better than sulfadoxine-pyrimethamine plus amodiaquine in controlling treatment failure at day 28. However, the latter is better than the former in reducing gametocytes in blood at day 7.
Infection with P. vivax
, P. ovale
or P. malariae
usually does not require hospitalisation. Treatment of P. vivax
requires both treatment of blood stages (with chloroquine or ACT) and clearance of liver forms with primaquine
Artemisinin-based combination therapy is as effective as chloroquine in treating uncomplicated P. vivax
Treatment with tafenoquine
prevents relapses after confirmed P. vivax
However, for those treated with chloroquine for blood stage infection, 14 days of primaquine treatment is required to prevent relapse. Shorter primaquine regimens may lead to higher relapse rates.
There is no difference in effectiveness between primaquine given for seven or 14 days for prevention of relapse in vivax malaria. The shorter regimen may be useful for those with treatment compliance problems.
To treat malaria during pregnancy, the WHO
recommends the use of quinine plus clindamycin
early in the pregnancy (1st trimester), and ACT in later stages (2nd and 3rd trimesters).
There is limited safety data on the antimalarial drugs in pregnancy.
Severe and complicated malaria
Cases of severe and complicated malaria are almost always caused by infection with P. falciparum
. The other species usually cause only febrile disease.
Severe and complicated malaria cases are medical emergencies since mortality rates are high (10% to 50%).
Recommended treatment for severe malaria is the intravenous
use of antimalarial drugs. For severe malaria, parenteral
artesunate was superior to quinine in both children and adults.
In another systematic review, artemisinin derivatives (artemether and arteether) were as efficacious as quinine in the treatment of cerebral malaria in children.
Treatment of severe malaria involves supportive measures that are best done in a critical care unit
. This includes the management of high fevers
and the seizures that may result from it. It also includes monitoring for poor breathing effort
, low blood sugar, and low blood potassium
Artemisinin derivatives have the same or better efficacy than quinolones in preventing deaths in severe or complicated malaria.
Quinine loading dose
helps to shorten the duration of fever and increases parasite clearance from the body. There is no difference in effectiveness when using intrarectal quinine compared to intravenous or intramuscular quinine in treating uncomplicated/complicated falciparum malaria.
There is insufficient evidence for intramuscular arteether to treat severe malaria.
The provision of rectal artesunate before transfer to hospital may reduce the rate of death for children with severe malaria.
Cerebral malaria is the form of severe and complicated malaria with the worst neurological symptoms.
There is insufficient data on whether osmotic agents such as mannitol or urea are effective in treating cerebral malaria.
Routine phenobarbitone in cerebral malaria is associated with fewer convulsions
but possibly more deaths.
There is no evidence that steroids would bring treatment benefits for cerebral malaria.
There is insufficient evidence to show that blood transfusion is useful in either reducing deaths for children with severe anaemia or in improving their haematocrit
in one month.
There is insufficient evidence that iron chelating agents such as deferoxamine and deferiprone improve outcomes of those with malaria falciparum infection.
poses a growing problem in 21st-century malaria treatment.
In the 2000s (decade), malaria with partial resistance to artemisins emerged in Southeast Asia.
Resistance is now common against all classes of antimalarial drugs apart from artemisinins
. Treatment of resistant strains became increasingly dependent on this class of drugs. The cost of artemisinins limits their use in the developing world.
Malaria strains found on the Cambodia–Thailand border are resistant to combination therapies that include artemisinins, and may, therefore, be untreatable.
Exposure of the parasite population to artemisinin monotherapies in subtherapeutic doses for over 30 years and the availability of substandard artemisinins likely drove the selection of the resistant phenotype.
Resistance to artemisinin has been detected in Cambodia, Myanmar, Thailand, and Vietnam,
and there has been emerging resistance in Laos.
Resistance to the combination of artemisinin and piperaquine was first detected in 2013 in Cambodia, and by 2019 had spread across Cambodia and into Laos
(with up to 80 percent of malaria parasites resistant in some regions).
There is insufficient evidence in unit packaged antimalarial drugs in preventing treatment failures of malaria infection. However, if supported by training of healthcare providers and patient information, there is improvement in compliance of those receiving treatment.
When properly treated, people with malaria can usually expect a complete recovery.
However, severe malaria can progress extremely rapidly and cause death within hours or days.
In the most severe cases of the disease, fatality rates
can reach 20%, even with intensive care and treatment.
Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. Chronic
infection without severe disease can occur in an immune-deficiency syndrome associated with a decreased responsiveness to Salmonella
bacteria and the Epstein–Barr virus
During childhood, malaria causes anaemia during a period of rapid brain development, and also direct brain damage resulting from cerebral malaria.
Some survivors of cerebral malaria have an increased risk of neurological and cognitive deficits, behavioural disorders
, and epilepsy
Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials
when compared to placebo
Deaths due to malaria per million persons in 2012
Past and current malaria prevalence in 2009
The WHO estimates that in 2018 there were 228 million new cases of malaria resulting in 405,000 deaths.
Children under 5 years old are the most affected, accounting for 67% (272,000) of malaria deaths worldwide in 2018.
About 125 million pregnant women are at risk of infection each year; in Sub-Saharan Africa
, maternal malaria is associated with up to 200,000 estimated infant deaths yearly.
There are about 10,000 malaria cases per year in Western Europe, and 1300–1500 in the United States.
The United States eradicated malaria in 1951.
About 900 people died from the disease in Europe between 1993 and 2003.
Both the global incidence of disease and resulting mortality have declined in recent years. According to the WHO and UNICEF, deaths attributable to malaria in 2015 were reduced by 60%
from a 2000 estimate of 985,000, largely due to the widespread use of insecticide-treated nets and artemisinin-based combination therapies.
In 2012, there were 207 million cases of malaria. That year, the disease is estimated to have killed between 473,000 and 789,000 people, many of whom were children in Africa.
Efforts at decreasing the disease in Africa since 2000 have been partially effective, with rates of the disease dropping by an estimated forty percent on the continent.
Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; in Sub-Saharan Africa, 85–90% of malaria fatalities occur.
An estimate for 2009 reported that countries with the highest death rate per 100,000 of population were Ivory Coast
(56.93) and Burkina Faso
A 2010 estimate indicated the deadliest countries per population were Burkina Faso, Mozambique
The Malaria Atlas Project
aims to map global levels of malaria
, providing a way to determine the global spatial limits of the disease and to assess disease burden
This effort led to the publication of a map of P. falciparum
endemicity in 2010 and an update in 2019.
As of 2010, about 100 countries have endemic malaria.
Every year, 125 million international travellers visit these countries, and more than 30,000 contract the disease.
The geographic distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found close to each other.
Malaria is prevalent in tropical and subtropical regions because of rainfall, consistent high temperatures and high humidity, along with stagnant waters where mosquito larvae readily mature, providing them with the environment they need for continuous breeding.
In drier areas, outbreaks of malaria have been predicted with reasonable accuracy by mapping rainfall.
Malaria is more common in rural areas than in cities. For example, several cities in the Greater Mekong Subregion
of Southeast Asia are essentially malaria-free, but the disease is prevalent in many rural regions, including along international borders and forest fringes.
In contrast, malaria in Africa is present in both rural and urban areas, though the risk is lower in the larger cities.
is likely to affect malaria transmission, but the degree of effect and the areas affected is uncertain.
Greater rainfall in certain areas of India, and following an El Niño
event is associated with increased mosquito numbers.
Since 1900 there has been substantial change in temperature and rainfall over Africa.
However, factors that contribute to how rainfall results in water for mosquito breeding are complex, incorporating the extent to which it is absorbed into soil and vegetation for example, or rates of runoff and evaporation.
Recent research has provided a more in-depth picture of conditions across Africa, combining a malaria climatic suitability model with a continental-scale model representing real-world hydrological processes.
Although the parasite responsible for P. falciparum
malaria has been in existence for 50,000–100,000 years, the population size of the parasite did not increase until about 10,000 years ago, concurrently with advances in agriculture
and the development of human settlements. Close relatives of the human malaria parasites remain common in chimpanzees. Some evidence suggests that the P. falciparum
malaria may have originated in gorillas.
References to the unique periodic fevers of malaria are found throughout history.
Hippocrates described periodic fevers, labelling them tertian, quartan, subtertian and quotidian.
The Roman Columella
associated the disease with insects from swamps.
Malaria may have contributed to the decline of the Roman Empire
and was so pervasive in Rome that it was known as the "Roman fever
Several regions in ancient Rome were considered at-risk for the disease because of the favourable conditions present for malaria vectors. This included areas such as southern Italy, the island of Sardinia
, the Pontine Marshes
, the lower regions of coastal Etruria
and the city of Rome
along the Tiber
. The presence of stagnant water in these places was preferred by mosquitoes for breeding grounds. Irrigated gardens, swamp-like grounds, run-off from agriculture, and drainage problems from road construction led to the increase of standing water.
The term malaria originates from MediaevalItalian
: mala aria
"; the disease was formerly called ague
or marsh fever
due to its association with swamps and marshland.
The term first appeared in the English literature about 1829.
Malaria was once common in most of Europe and North America,
where it is no longer endemic,
though imported cases do occur.
Scientific studies on malaria made their first significant advance in 1880, when Charles Louis Alphonse Laveran
—a French army doctor working in the military hospital of Constantine
—observed parasites inside the red blood cells of infected people for the first time. He, therefore, proposed that malaria is caused by this organism, the first time a protist
was identified as causing disease.
For this and later discoveries, he was awarded the 1907 Nobel Prize for Physiology or Medicine
. A year later, Carlos Finlay
, a Cuban doctor treating people with yellow fever
, provided strong evidence that mosquitoes were transmitting disease to and from humans.
This work followed earlier suggestions by Josiah C. Nott
and work by Sir Patrick Manson
, the "father of tropical medicine", on the transmission of filariasis
In April 1894, a Scottish physician, Sir Ronald Ross
, visited Sir Patrick Manson at his house on Queen Anne Street, London. This visit was the start of four years of collaboration and fervent research that culminated in 1897 when Ross, who was working in the Presidency General Hospital
, proved the complete life-cycle of the malaria parasite in mosquitoes.
He thus proved that the mosquito was the vector for malaria in humans by showing that certain mosquito species transmit malaria to birds. He isolated malaria parasites from the salivary glands of mosquitoes that had fed on infected birds.
For this work, Ross received the 1902 Nobel Prize in Medicine. After resigning from the Indian Medical Service
, Ross worked at the newly established Liverpool School of Tropical Medicine
and directed malaria-control efforts in Egypt
The findings of Finlay and Ross were later confirmed by a medical board headed by Walter Reed
in 1900. Its recommendations were implemented by William C. Gorgas
in the health measures undertaken
during construction of the Panama Canal
. This public-health work saved the lives of thousands of workers and helped develop the methods used in future public-health campaigns against the disease.
, source of the antimalarial drug artemisinin
Quinine was the predominant malarial medication until the 1920s when other medications began to appear. In the 1940s, chloroquine replaced quinine as the treatment of both uncomplicated and severe malaria until resistance supervened, first in Southeast Asia and South America in the 1950s and then globally in the 1980s.
was used between 1917 and the 1940s for malariotherapy
—deliberate injection of malaria parasites to induce a fever to combat certain diseases such as tertiary syphilis
. In 1927, the inventor of this technique, Julius Wagner-Jauregg
, received the Nobel Prize in Physiology or Medicine for his discoveries. The technique was dangerous, killing about 15% of patients, so it is no longer in use.
U.S. Marines with malaria in a field hospital on Guadalcanal
, October 1942
The first pesticide used for indoor residual spraying was DDT
Although it was initially used exclusively to combat malaria, its use quickly spread to agriculture
. In time, pest control, rather than disease control, came to dominate DDT use, and this large-scale agricultural use led to the evolution of pesticide-resistant
mosquitoes in many regions. The DDT resistance shown by Anopheles
mosquitoes can be compared to antibiotic resistance
shown by bacteria. During the 1960s, awareness of the negative consequences of its indiscriminate use increased, ultimately leading to bans on agricultural applications of DDT in many countries in the 1970s.
Before DDT, malaria was successfully eliminated or controlled in tropical areas like Brazil and Egypt by removing or poisoning the breeding grounds of the mosquitoes or the aquatic habitats of the larval stages, for example by applying the highly toxic arsenic compound Paris Green
to places with standing water.
have been an elusive goal of research. The first promising studies demonstrating the potential for a malaria vaccine were performed in 1967 by immunising mice with live, radiation-attenuated
sporozoites, which provided significant protection to the mice upon subsequent injection with normal, viable sporozoites. Since the 1970s, there has been a considerable effort to develop similar vaccination strategies for humans.
The first vaccine, called RTS,S
, was approved by European regulators in 2015.
Society and culture
Malaria clinic in Tanzania
Malaria is not just a disease commonly associated with poverty
: some evidence suggests that it is also a cause of poverty and a major hindrance to economic development
Although tropical regions
are most affected, malaria's furthest influence reaches into some temperate zones that have extreme seasonal changes. The disease has been associated with major negative economic effects on regions where it is widespread. During the late 19th and early 20th centuries, it was a major factor in the slow economic development of the American southern states.
A comparison of average per capita GDP
in 1995, adjusted for parity of purchasing power
, between countries with malaria and countries without malaria gives a fivefold difference (US$1,526 versus US$8,268). In the period 1965 to 1990, countries where malaria was common had an average per capita GDP that increased only 0.4% per year, compared to 2.4% per year in other countries.
Poverty can increase the risk of malaria since those in poverty do not have the financial capacities to prevent or treat the disease. In its entirety, the economic impact of malaria has been estimated to cost Africa US$12 billion every year. The economic impact includes costs of health care, working days lost due to sickness, days lost in education, decreased productivity due to brain damage from cerebral malaria, and loss of investment and tourism.
The disease has a heavy burden in some countries, where it may be responsible for 30–50% of hospital admissions, up to 50% of outpatient
visits, and up to 40% of public health spending.
Cerebral malaria is one of the leading causes of neurological disabilities in African children.
Studies comparing cognitive functions before and after treatment for severe malarial illness continued to show significantly impaired school performance and cognitive abilities even after recovery.
Consequently, severe and cerebral malaria have far-reaching socioeconomic
consequences that extend beyond the immediate effects of the disease.
Counterfeit and substandard drugs
have been found in several Asian countries such as Cambodia
, and Vietnam
, and are a major cause of avoidable death in those countries.
The WHO said that studies indicate that up to 40% of artesunate-based malaria medications are counterfeit, especially in the Greater Mekong
region. They have established a rapid alert system to rapidly report information about counterfeit drugs to relevant authorities in participating countries.
There is no reliable way for doctors or lay people to detect counterfeit drugs without help from a laboratory. Companies are attempting to combat the persistence of counterfeit drugs by using new technology to provide security from source to distribution.
Another clinical and public health concern is the proliferation of substandard antimalarial medicines resulting from inappropriate concentration of ingredients, contamination with other drugs or toxic impurities, poor quality ingredients, poor stability and inadequate packaging.
A 2012 study demonstrated that roughly one-third of antimalarial medications in Southeast Asia and Sub-Saharan Africa failed chemical analysis, packaging analysis, or were falsified.
World War II poster
Throughout history, the contraction of malaria has played a prominent role in the fates of government rulers, nation-states, military personnel, and military actions.
In 1910, Nobel Prize in Medicine
-winner Ronald Ross (himself a malaria survivor), published a book titled The Prevention of Malaria
that included a chapter titled "The Prevention of Malaria in War." The chapter's author, Colonel C. H. Melville, Professor of Hygiene at Royal Army Medical College
in London, addressed the prominent role that malaria has historically played during wars: "The history of malaria in war might almost be taken to be the history of war itself, certainly the history of war in the Christian era. ... It is probably the case that many of the so-called camp fevers, and probably also a considerable proportion of the camp dysentery, of the wars of the sixteenth, seventeenth and eighteenth centuries were malarial in origin."
In British-occupied India the cocktail gin and tonic
may have come about as a way of taking quinine, known for its antimalarial properties.
Malaria was the most significant health hazard encountered by U.S. troops in the South Pacific during World War II
, where about 500,000 men were infected.
According to Joseph Patrick Byrne, "Sixty thousand American soldiers died of malaria during the African and South Pacific campaigns."
Additionally, initiatives have been founded such as Malaria Control in War Areas (MCWA), established in 1942, and its successor, the Communicable Disease Center (now known as the Centers for Disease Control and Prevention
, or CDC) established in 1946. According to the CDC, MCWA "was established to control malaria around military training bases in the southern United States and its territories, where malaria was still problematic".
Several notable attempts are being made to eliminate the parasite from sections of the world or eradicate it worldwide
. In 2006, the organization Malaria No More
set a public goal of eliminating malaria from Africa by 2015, and the organization claimed they planned to dissolve if that goal was accomplished. In 2007, World Malaria Day
was established by the 60th session of the World Health Assembly
. As of 2018, they are still functioning.
Only one malaria vaccine
is licensed for use, while several others are in clinical trials,
which are intended to provide protection for children in endemic areas and reduce the speed of transmission of the disease. As of 2012, The Global Fund to Fight AIDS, Tuberculosis, and Malaria
has distributed 230 million insecticide-treated nets intended to stop mosquito-borne transmission of malaria.
The U.S.-based Clinton Foundation
has worked to manage demand and stabilize prices in the artemisinin market.
Other efforts, such as the Malaria Atlas Project, focus on analysing climate and weather information required to accurately predict malaria spread based on the availability of habitat of malaria-carrying parasites.
The Malaria Policy Advisory Committee
(MPAC) of the World Health Organization
(WHO) was formed in 2012, "to provide strategic advice and technical input to WHO on all aspects of malaria control and elimination".
In November 2013, WHO and the malaria vaccine funders group set a goal to develop vaccines designed to interrupt malaria transmission with malaria eradication's long-term goal.
Malaria has been successfully eliminated or significantly reduced in certain areas. Malaria was once common in the United States and southern Europe, but vector control programs, combined with the monitoring and treatment of infected humans, eliminated it from those regions. Several factors contributed, such as the draining of wetland
breeding grounds for agriculture and other changes in water management
practices, and advances in sanitation, including greater use of glass windows and screens in dwellings.
Malaria was eliminated from most parts of the United States in the early 20th century by such methods. The use of the pesticide
DDT and other means eliminated it from the South's remaining pockets in the 1950s as part of the National Malaria Eradication Program
In 2015 the WHO targeted a 90% reduction in malaria deaths by 2030,
and Bill Gates
said in 2016 that he thought global eradication would be possible by 2040.
In 2018, WHO announced that Paraguay was free of malaria, after an eradication effort that began in 1950.
As of 2019, the eradication process is ongoing, but it will be difficult to achieve a world free of malaria with the current approaches and tools. Approaches may require investing more in research and greater universal health care.
Continuing surveillance will also be important to prevent the return of malaria in countries where the disease has been eliminated.
The Malaria Eradication Research Agenda (malERA) initiative was a consultative process to identify which areas of research and development (R&D) must be addressed for worldwide eradication of malaria.
A vaccine against malaria called RTS,S/AS01 (RTS,S)
was approved by European regulators in 2015.
As of 2019 it is undergoing pilot trials in 3 sub-Saharan African countries – Ghana, Kenya and Malawi – as part of the WHO's Malaria Vaccine Implementation Programme (MVIP).
Immunity (or, more accurately, tolerance
) to P. falciparum
malaria does occur naturally, but only in response to years of repeated infection.
An individual can be protected from a P. falciparum
infection if they receive about a thousand bites from mosquitoes that carry a version of the parasite rendered non-infective by a dose of X-ray irradiation
The highly polymorphic
nature of many P. falciparum
proteins results in significant challenges to vaccine design. Vaccine candidates that target antigens on gametes, zygotes, or ookinetes in the mosquito midgut aim to block the transmission of malaria. These transmission-blocking vaccines induce antibodies
in the human blood; when a mosquito takes a blood meal from a protected individual, these antibodies prevent the parasite from completing its development in the mosquito.
Other vaccine candidates, targeting the blood-stage of the parasite's life cycle, have been inadequate on their own.
For example, SPf66
was tested extensively in areas where the disease was common in the 1990s, but trials showed it to be insufficiently effective.
In 2021, researchers from the University of Oxford
reported findings from a Phase IIb trial
of a candidate malaria vaccine, R21/Matrix-M, which demonstrated efficacy of 77% over 12-months of follow-up. This vaccine is the first to meet the World Health Organization
's Malaria Vaccine Technology Roadmap goal of a vaccine with at least 75% efficacy.
Malaria parasites contain apicoplasts
, organelles usually found in plants, complete with their own genomes
. These apicoplasts are thought to have originated through the endosymbiosis
of algae and play a crucial role in various aspects of parasite metabolism
, such as fatty acid biosynthesis
. Over 400 proteins have been found to be produced by apicoplasts and these are now being investigated as possible targets for novel antimalarial drugs.
With the onset of drug-resistant Plasmodium
parasites, new strategies are being developed to combat the widespread disease. One such approach lies in the introduction of synthetic pyridoxal
-amino acid adducts
, which are taken up by the parasite and ultimately interfere with its ability to create several essential B vitamins
Antimalarial drugs using synthetic metal-based complexes
are attracting research interest.
- (+)-SJ733: Part of a wider class of experimental drugs called spiroindolone. It inhibits the ATP4 protein of infected red blood cells that cause the cells to shrink and become rigid like the aging cells. This triggers the immune system to eliminate the infected cells from the system as demonstrated in a mouse model. As of 2014, a Phase 1 clinical trial to assess the safety profile in human is planned by the Howard Hughes Medical Institute.
- NITD246 and NITD609: Also belonged to the class of spiroindolone and target the ATP4 protein.
liver-stage parasites selectively is emerging as an alternative strategy in the face of resistance to the latest frontline combination therapies against blood stages of the parasite.
In a research conducted in 2019, using experimental analysis with knockout (KO) mutants of Plasmodium berguei
the authors were able to identify genes that are potentially essential in the liver stage. Moreover, they generated a computational model to analyse pre–erytrocytic development and liver–stage metabolism. Combining both methods they identified seven metabolic subsystems that become essential compared to the blood stage. Some of these metabolic pathways are fatty acid synthesis and elongation, tricarboxylic acid, amino acid and heme metabolism among others.
Specifically, they studied 3 subsystems: fatty acid synthesis and elongation, and amino sugar biosynthesis. For the first two pathways they demonstrated a clear dependence of the liver stage on its own fatty acid metabolism.
They proved for the first time the critical role of amino sugar biosynthesis in the liver stage of P. berghei. The uptake of N–acetyl–glucosamine appears to be limited in the liver stage, being its synthesis needed for the parasite development.
These findings and the computational model provide a basis for the design of antimalarial therapies targeting metabolic proteins.
In silico study, identified molecule 3j as the potent and selective inhibitor of PfLDH out of 30 in-house synthesized Quinolines based molecules compared to Chloroquine (referenced inhibitor). Molecule 3j showed high selectivity and novel binding mechanism for PfLDH without having a profound effect on the activity of human LDH. 
A non-chemical vector control strategy involves genetic manipulation of malaria mosquitoes. Advances in genetic engineering
technologies make it possible to introduce foreign DNA into the mosquito genome and either decrease the lifespan of the mosquito, or make it more resistant to the malaria parasite. Sterile insect technique
is a genetic control method whereby large numbers of sterile male mosquitoes are reared and released. Mating with wild females reduces the wild population in the subsequent generation; repeated releases eventually eliminate the target population.
is central to malaria research. With the sequencing
of P. falciparum
, one of its vectors Anopheles gambiae
, and the human genome
, the genetics of all three organisms in the malaria life cycle can be studied.
Another new application of genetic technology is the ability to produce genetically modified
mosquitoes that do not transmit malaria, potentially allowing biological control
of malaria transmission.
In one study, a genetically-modified strain of Anopheles stephensi
was created that no longer supported malaria transmission, and this resistance was passed down to mosquito offspring.
is a technique for changing wild populations, for instance to combat or eliminate insects so they cannot transmit diseases (in particular mosquitoes in the cases of malaria, zika
dengue and yellow fever).
In December 2020, a review article found that malaria-endemic regions had lower reported COVID-19
case fatality rates on average than regions where malaria was not known to be endemic.
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