Malaria is a mosquito-borne infectious disease affecting humans and
other animals caused by parasitic protozoans (a group of single-celled
microorganisms) belonging to the
symptoms that typically include fever, tiredness, vomiting, and
headaches. In severe cases it can cause yellow skin, seizures,
coma, or death.
Symptoms usually begin ten to fifteen days after
being bitten. If not properly treated, people may have recurrences
of the disease months later. In those who have recently survived an
infection, reinfection usually causes milder symptoms. This partial
resistance disappears over months to years if the person has no
continuing exposure to malaria.
The disease is most commonly transmitted by an infected female
Anopheles mosquito. The mosquito bite introduces the parasites from
the mosquito's saliva into a person's blood. The parasites travel
to the liver where they mature and reproduce. Five species of
Plasmodium can infect and be spread by humans. Most deaths are
caused by P. falciparum because P. vivax, P. ovale, and
P. malariae generally cause a milder form of malaria. The
species P. knowlesi rarely causes disease in humans. Malaria
is typically diagnosed by the microscopic examination of blood using
blood films, or with antigen-based rapid diagnostic tests. Methods
that use the polymerase chain reaction to detect the parasite's DNA
have been developed, but are not widely used in areas where malaria is
common due to their cost and complexity.
The risk of disease can be reduced by preventing mosquito bites
through the use of mosquito nets and insect repellents, or with
mosquito control measures such as spraying insecticides and draining
standing water. Several medications are available to prevent
malaria in travellers to areas where the disease is common.
Occasional doses of the combination medication
sulfadoxine/pyrimethamine are recommended in infants and after the
first trimester of pregnancy in areas with high rates of malaria.
Despite a need, no effective vaccine exists, although efforts to
develop one are ongoing. The recommended treatment for malaria is a
combination of antimalarial medications that includes an
artemisinin. The second medication may be either mefloquine,
lumefantrine, or sulfadoxine/pyrimethamine.
Quinine along with
doxycycline may be used if an artemisinin is not available. It is
recommended that in areas where the disease is common, malaria is
confirmed if possible before treatment is started due to concerns of
increasing drug resistance. Resistance among the parasites has
developed to several antimalarial medications; for example,
chloroquine-resistant P. falciparum has spread to most malarial
areas, and resistance to artemisinin has become a problem in some
parts of Southeast Asia.
The disease is widespread in the tropical and subtropical regions that
exist in a broad band around the equator. This includes much of
Sub-Saharan Africa, Asia, and Latin America. In 2016, there were
216 million cases of malaria worldwide resulting in an estimated
731,000 deaths. Approximately 90% of both cases and deaths
occurred in Africa. Rates of disease have decreased from 2000 to
2015 by 37%, but increased from 2014 during which there were 198
Malaria is commonly associated with poverty and has
a major 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 negative effects
1 Signs and symptoms
2.1 Life cycle
2.2 Recurrent malaria
3.1 Genetic resistance
5.1 Mosquito control
5.2 Other methods
10 Society and culture
10.1 Economic impact
10.2 Counterfeit and substandard drugs
10.4 Eradication efforts
12 Other animals
14 Further reading
15 External links
Signs and symptoms
Main symptoms of malaria
The signs and symptoms of malaria typically begin 8–25 days
following infection; however, symptoms 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, gastroenteritis, and viral diseases. The
presentation may include headache, fever, shivering, joint pain,
vomiting, hemolytic anemia, jaundice, 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
Severe malaria is usually caused by P. falciparum (often referred
to as falciparum malaria).
Symptoms of falciparum malaria arise 9–30
days after infection. Individuals with cerebral malaria frequently
exhibit neurological symptoms, including abnormal posturing,
nystagmus, conjugate gaze palsy (failure of the eyes to turn together
in the same direction), opisthotonus, seizures, or coma.
Malaria has several serious complications. Among these is the
development of respiratory distress, which occurs in up to 25% of
adults and 40% of children with severe P. falciparum malaria.
Possible causes include respiratory compensation of metabolic
acidosis, noncardiogenic pulmonary oedema, concomitant pneumonia, and
severe anaemia. Although rare in young children with severe malaria,
acute respiratory distress syndrome occurs in 5–25% of adults and up
to 29% of pregnant women.
HIV with malaria
Renal failure is a feature of blackwater
fever, where hemoglobin from lysed red blood cells leaks into the
Infection with P. falciparum may result in cerebral malaria, a
form of severe malaria that involves encephalopathy. It is associated
with retinal whitening, which may be a useful clinical sign in
distinguishing malaria from other causes of fever. Enlarged
spleen, enlarged liver or both of these, severe headache, low blood
sugar, and hemoglobin in the urine with renal failure may occur.
Complications may include spontaneous bleeding, coagulopathy, and
Malaria in pregnant women is an important cause of stillbirths, infant
mortality, abortion and low birth weight, particularly in
P. falciparum infection, but also with P. vivax.
Main article: Plasmodium
Malaria parasites belong to the genus
Plasmodium (phylum Apicomplexa).
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 (~20%). 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
higher apes; however, except for P. knowlesi—a zoonotic species
that causes malaria in macaques—these are mostly of limited
public health importance.
Global warming is likely to affect malaria transmission, but the
severity and geographic distribution of such effects is
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, will
infect the insect and continue the life cycle.
In the life cycle of Plasmodium, 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 (tissue schizogony), 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 fertilized 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 fertilized, 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
Only female mosquitoes feed on blood; male mosquitoes feed on plant
nectar and do not transmit the disease. The females of the Anopheles
genus of mosquito prefer to feed at night. They usually start
searching for a meal at dusk and will continue throughout the night
until taking a meal.
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, relapse, 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
Relapse is when symptoms reappear after the parasites
have been eliminated from blood but persist as dormant hypnozoites in
Relapse commonly occurs between 8–24 weeks and is
commonly seen with P. vivax and P. ovale infections.
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.
Plasmodium falciparum biology
Micrograph 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
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 infections,
although their existence in P. ovale is uncertain.
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 in placental malaria. Sequestered red
blood cells can breach the blood–brain barrier and cause cerebral
Main article: Human genetic resistance to malaria
According to a 2005 review, due to the high levels of mortality and
morbidity caused by malaria—especially the P. falciparum
species—it has placed the greatest selective pressure on the human
genome in recent history. Several genetic factors provide some
resistance to it including sickle cell trait, thalassaemia traits,
glucose-6-phosphate dehydrogenase deficiency, and the absence of Duffy
antigens on red blood cells.
The impact of sickle cell trait on malaria immunity illustrates some
evolutionary trade-offs that have occurred because of endemic malaria.
Sickle cell trait
Sickle cell trait causes a change in the hemoglobin 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 hemoglobin 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 sickle or distort into a curved
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 hemoglobin 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 anemia. Although the shorter life expectancy
for those with the homozygous condition would tend to disfavor 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.
Main article: Diagnosis of malaria
The blood film is the gold standard for malaria diagnosis.
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 were malaria is common suggest high levels of
over diagnosis due to insufficient or inaccurate laboratory
Malaria is usually confirmed by the microscopic examination of blood
films or by antigen-based rapid diagnostic tests (RDT). In
some areas, RDTs need to 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 infections. 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 75–90% 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.
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
World Health Organization (WHO). It is deemed severe when any of
the following criteria are present, otherwise it is considered
Significant weakness such that the person is unable to walk
Inability to feed
Two or more convulsions
Low blood pressure (less than 70 mmHg in adults and 50 mmHg
Kidney failure or hemoglobin in the urine
Bleeding problems, or hemoglobin less than 50 g/L (5 g/dL)
Blood glucose less than 2.2 mmol/L (40 mg/dL)
Acidosis or lactate levels of greater than 5 mmol/L
A parasite level in the blood of greater than 100,000 per microlitre
(µL) in low-intensity transmission areas, or 250,000 per µL in
high-intensity transmission areas
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 greater 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:
severe malaria affecting the cardiovascular system and causing chills
and circulatory shock
severe malaria affecting the liver and causing vomiting and jaundice
severe malaria affecting the cerebrum
plasmodium introduced from the mother via the fetal circulation
Plasmodium falciparum malaria, pernicious malaria
Plasmodium ovale malaria
quartan malaria, malariae malaria,
Plasmodium malariae malaria
paroxysms every fourth day (quartan), counting the day of occurrence
as the first day
paroxysms daily (quotidian)
paroxysms every third day (tertian), counting the day of occurrence as
plasmodium introduced by blood transfusion, needle sharing, or
Plasmodium vivax malaria
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. There is no vaccine for
malaria. 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 will eventually disappear 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 become
re-established 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 program 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 anemia which is sometimes due to malaria. Giving children with
anemia in these areas preventive antimalarial medication improves red
blood cell levels slightly but did not affect the risk of death or
need for hospitalization.
Further information: Mosquito control
Man spraying kerosene oil in standing water,
Panama Canal Zone
Panama Canal Zone 1912
Vector control 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
picaridin. Insecticide-treated mosquito nets (ITNs) and indoor
residual spraying (IRS) have been shown to be highly effective in
preventing malaria among children in areas where malaria is
common. Prompt treatment of confirmed cases with
artemisinin-based combination therapies (ACTs) may also reduce
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 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.
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
World Health Organization recommends 12 insecticides in
IRS operations, including
DDT and the pyrethroids cyfluthrin and
deltamethrin. This public health use of small amounts of
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
There are a number of other methods to reduce mosquito bites and slow
the spread of malaria. Efforts to decrease mosquito larva by
decreasing the availability of open water in which they develop or by
adding substances to decrease their development is effective in some
locations. Electronic mosquito repellent devices which make very
high-frequency sounds that are supposed to keep female mosquitoes
away, do not have supporting evidence.
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. Recognizing the disease in the early stages
can prevent the disease 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.
There are a number of medications that can help prevent or interrupt
malaria in travelers 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, doxycycline , or the combination of
atovaquone/proguanil (Malarone)—are frequently used for
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.
The protective effect does not begin immediately, and people visiting
areas where malaria exists usually start taking the drugs one to two
weeks before arriving 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 preventative drugs is often not practical for those who
live in areas where malaria exists, and their use is usually only in
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 anti-malarial 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 anemia in the
mother. The use of preventative drugs where malaria-bearing
mosquitoes are present may encourage the development of partial
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
Simple or uncomplicated malaria may be treated with oral medications.
The most effective treatment for P. falciparum infection is the
use of artemisinins in combination with other antimalarials (known as
artemisinin-combination therapy, or ACT), which decreases resistance
to any single drug component. These additional antimalarials
include: amodiaquine, lumefantrine, mefloquine or
sulfadoxine/pyrimethamine. Another recommended combination is
dihydroartemisinin and piperaquine. ACT is about 90% effective
when used to treat uncomplicated malaria. 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). In the 2000s (decade), malaria with partial
resistance to artemisins emerged in Southeast Asia. Infection
with P. vivax, P. ovale or P. malariae usually do not
require hospitalization. Treatment of P. vivax requires both
treatment of blood stages (with chloroquine or ACT) and clearance of
liver forms with primaquine. Treatment with tafenoquine prevents
relapses after confirmed P. vivax malaria.
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 are medical emergencies
since mortality rates are high (10% to 50%).
Cerebral malaria is
the form of severe and complicated malaria with the worst neurological
symptoms. 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.
Drug resistance poses a growing problem in 21st-century malaria
treatment. 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.
Disability-adjusted life year
Disability-adjusted life year for malaria per 100,000 inhabitants in
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
During childhood, malaria causes anemia 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,
Malaria prophylaxis was shown to improve cognitive
function and school performance in clinical trials when compared to
Distribution of malaria in the world: ♦ Elevated
occurrence of chloroquine- or multi-resistant malaria
♦ Occurrence of chloroquine-resistant malaria
Plasmodium falciparum or chloroquine-resistance
♦ No malaria
Deaths due to malaria per million persons in 2012
The WHO estimates that in 2015 there were 214 million new cases of
malaria resulting in 438,000 deaths. Others have estimated the
number of cases at between 350 and 550 million for falciparum
malaria The majority of cases (65%) occur in children under 15
years old. 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. 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 the
turn of millennium 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 (86.15),
Angola (56.93) and
Burkina Faso (50.66). A 2010 estimate indicated the deadliest
countries per population were Burkina Faso,
Mozambique and Mali.
Malaria Atlas Project
Malaria Atlas Project aims to map global endemic levels of
malaria, providing a means with which 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. 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 in which 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
Greater Mekong Subregion of Southeast
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.
History of malaria
History of malaria and Mosquito-malaria theory
Ancient malaria oocysts preserved in Dominican amber
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 recorded 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
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 River.
The presence of stagnant water in these places was preferred by
mosquitoes for breeding grounds. Irrigated gardens, swamp-like
grounds, runoff from agriculture, and drainage problems from road
construction led to the increase of standing water.
Ronald Ross received the Nobel Prize for Physiology or
Medicine in 1902 for his work on malaria.
The term malaria originates from Medieval Italian: mala aria—"bad
air"; 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 in Algeria—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 in Havana, 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.
Chinese traditional Chinese medicine researcher
Tu Youyou received the
Nobel Prize for Physiology or Medicine
Nobel Prize for Physiology or Medicine in 2015 for her work on
antimalarial drug artemisin.
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 in Calcutta, 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
Liverpool School of Tropical Medicine
Liverpool School of Tropical Medicine and directed
malaria-control efforts in Egypt, Panama,
Greece and Mauritius.
The findings of Finlay and Ross were later confirmed by a medical
board headed by
Walter Reed in 1900. Its recommendations were
William C. Gorgas
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.
Artemisia annua, source of the antimalarial drug artemisin
The first effective treatment for malaria came from the bark of
cinchona tree, which contains quinine. This tree grows on the slopes
of the Andes, mainly in Peru. The indigenous peoples of
Peru made a
tincture of cinchona to control fever. Its effectiveness against
malaria was found and the Jesuits introduced the treatment to Europe
around 1640; by 1677, it was included in the
London Pharmacopoeia as
an antimalarial treatment. It was not until 1820 that the active
ingredient, quinine, was extracted from the bark, isolated and named
by the French chemists
Pierre Joseph Pelletier
Pierre Joseph Pelletier and Joseph Bienaimé
Quinine became the predominant malarial medication until the 1920s
when other medications began to be developed. 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
The medicinal value of
Artemisia annua has been used by Chinese
herbalists in traditional Chinese medicines for 2,000 years. In 1596,
Li Shizhen recommended tea made from qinghao specifically to treat
malaria symptoms in his "Compendium of Materia Medica". Artemisinins,
discovered by Chinese scientist
Tu Youyou and colleagues in the 1970s
from the plant Artemisia annua, became the recommended treatment for
P. falciparum malaria, administered in severe cases in
combination with other antimalarials. Tu says she was influenced
by a traditional Chinese herbal medicine source, The Handbook of
Prescriptions for Emergency Treatments, written in 340 by Ge
Hong. For her work on malaria,
Tu Youyou received the 2015 Nobel
Prize in Physiology or Medicine.
Plasmodium vivax 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
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 rough field hospital on Guadalcanal,
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 resistant mosquitoes in many
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
Egypt by removing or poisoning the breeding grounds of the
mosquitoes or the aquatic habitats of the larva stages, for example by
applying the highly toxic arsenic compound
Paris Green to places with
Malaria vaccines have been an elusive goal of research. The first
promising studies demonstrating the potential for a malaria vaccine
were performed in 1967 by immunizing 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
Society and culture
See also: World
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
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 ($1,526 USD versus $8,268 USD). 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.
Child with malaria in Ethiopia
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
Sophisticated counterfeits have been found in several Asian countries
such as Cambodia, China, Indonesia, Laos, Thailand, and
Vietnam, and are an important 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
Mekong region and have established a rapid alert system to
enable information about counterfeit drugs to be rapidly reported to
the 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
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
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
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."
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."
Significant financial investments have been made to procure existing
and create new anti-malarial agents. During
World War I
World War I and World War
II, inconsistent supplies of the natural anti-malaria drugs cinchona
bark and quinine prompted substantial funding into research and
development of other drugs and vaccines. American military
organizations conducting such research initiatives include the Navy
Medical Research Center,
Walter Reed Army Institute of Research, and
U.S. Army Medical Research Institute of Infectious Diseases
U.S. Army Medical Research Institute of Infectious Diseases of the
US Armed Forces.
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".
Members of the
Malaria Commission of the
League of Nations
League of Nations collecting
larvae on the Danube delta, 1929
Several notable attempts are being made to eliminate the parasite from
sections of the world, or to eradicate it worldwide. In 2006, the
Malaria No More
Malaria No More set a public goal of eliminating malaria
from Africa by 2015, and the organization plans to dissolve if that
goal is accomplished. Several malaria vaccines 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[update], The Global Fund to Fight AIDS,
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
Project, focus on analysing climate and weather information required
to accurately predict the spread of malaria based on the availability
of habitat of malaria-carrying parasites. The
Advisory Committee (MPAC) of the
World Health Organization
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 the
long-term goal of malaria eradication.
Malaria has been successfully eliminated or greatly reduced in certain
Malaria was once common in the United States and southern
Europe, but vector control programs, in conjunction 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 USA in the early 20th century by such methods, and
the use of the pesticide
DDT and other means eliminated it from the
remaining pockets in the South in the 1950s as part of the National
Malaria Eradication Program. Bill Gates has said that he thinks
global eradication is possible by 2040.
Malaria Eradication Research Agenda (malERA) initiative was a
consultative process to identify which areas of research and
development (R&D) needed to be addressed for the worldwide
eradication of malaria.
A vaccine against malaria called RTS,S, was approved by European
regulators in 2015. It is undergoing pilot trials in select
countries in 2016.
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 is
common in the 1990s, but trials showed it to be insufficiently
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 anti-malarial 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.
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
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.
Genomics 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
lifecycle 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.
Gene drive is a technique for changing wild populations, for instance
to combat insects so they cannot transmit diseases (in particular
mosquitoes in the cases of malaria and zika).
Nearly 200 parasitic
Plasmodium species have been identified that
infect birds, reptiles, and other mammals, and about 30 species
naturally infect non-human primates. Some malaria parasites that
affect non-human primates (NHP) serve as model organisms for human
malarial parasites, such as P. coatneyi (a model for
P. falciparum) and P. cynomolgi (P. vivax). Diagnostic
techniques used to detect parasites in NHP are similar to those
employed for humans.
Malaria parasites that infect rodents are
widely used as models in research, such as P. berghei. Avian
malaria primarily affects species of the order Passeriformes, and
poses a substantial threat to birds of Hawaii, the Galapagos, and
other archipelagoes. The parasite P. relictum is known to play a
role in limiting the distribution and abundance of endemic Hawaiian
Global warming is expected to increase the prevalence and
global distribution of avian malaria, as elevated temperatures provide
optimal conditions for parasite reproduction.
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