Malaria 1

Malaria
Malaria
Classification and external resources

Ring-forms and gametocytes of Plasmodium falciparum in human blood.

ICD-10 [1]
B50.

ICD-9 [2]
084

OMIM [3]
248310

DiseasesDB [4]
7728

MedlinePlus [5]
000621

eMedicine [6] [7] [8]

med/1385 emerg/305 ped/1357

MeSH [9]
C03.752.250.552

Malaria is a mosquito-borne infectious disease of humans caused by eukaryotic protists of the genus Plasmodium. It
is widespread in tropical and subtropical regions, including much of Subsaharan Africa, Asia and the Americas. The
disease results from the multiplication of malaria parasites within red blood cells, causing symptoms that typically
include fever and headache, in severe cases progressing to coma, and death.
Four species of Plasmodium can infect and be transmitted by humans. Severe disease is largely caused by
Plasmodium falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae is
generally a milder disease that is rarely fatal. A fifth species, Plasmodium knowlesi, is a zoonosis that causes malaria
in macaques but can also infect humans[10] [11] .
Malaria transmission can be reduced by preventing mosquito bites by distribution of inexpensive mosquito nets and
insect repellents, or by mosquito-control measures such as spraying insecticides inside houses and draining standing
water where mosquitoes lay their eggs. Although many are under development, the challenge of producing a widely
available vaccine that provides a high level of protection for a sustained period is still to be met.[12] Two drugs are
also available to prevent malaria in travellers to malaria-endemic countries (prophylaxis).
A variety of antimalarial medications are available. In the last 5 years, treatment of P. falciparum infections in
endemic countries has been transformed by the use of combinations of drugs containing an artemisinin derivative.
Severe malaria is treated with intravenous or intramuscular quinine or, increasingly, the artemisinin derivative
Malaria 2

artesunate [13] which is superior to quinine in both children and adults.[14] Resistance has developed to several
antimalarial drugs, most notably chloroquine.[15]
Each year, there are more than 225 million cases of malaria,[16] killing around 781,000 people each year according to
the latest WHO Report [17]. The majority of deaths are of young children in sub-Saharan Africa.[18] Ninety percent
of malaria-related deaths occur in sub-Saharan Africa. Malaria is commonly associated with poverty, and can indeed
be a cause of poverty[19] and a major hindrance to economic development.

Signs and symptoms

Symptoms of malaria include fever, shivering, arthralgia (joint pain),
vomiting, anemia (caused by hemolysis), hemoglobinuria, retinal
damage,[21] and convulsions. The classic symptom of malaria is
cyclical occurrence of sudden coldness followed by rigor and then
fever and sweating lasting four to six hours, occurring every two days
in P. vivax and P. ovale infections, while every three days for P.
malariae.[22] P. falciparum can have recurrent fever every 36–48 hours
or a less pronounced and almost continuous fever. For reasons that are
poorly understood, but that may be related to high intracranial
pressure, children with malaria frequently exhibit abnormal posturing,
a sign indicating severe brain damage.[23] Malaria has been found to
cause cognitive impairments, especially in children. It causes
[20]
widespread anemia during a period of rapid brain development and Main symptoms of malaria.
also direct brain damage. This neurologic damage results from cerebral
malaria to which children are more vulnerable.[24] [25] Cerebral malaria
is associated with retinal whitening,[26] which may be a useful clinical
sign in distinguishing malaria from other causes of fever.[27]

Severe malaria is almost exclusively caused by P. falciparum infection,

and usually arises 6–14 days after infection.[28] Consequences of
severe malaria include coma and death if untreated—young children Typical fever patterns of malaria

and pregnant women are especially vulnerable. Splenomegaly

(enlarged spleen), severe headache, cerebral ischemia, hepatomegaly (enlarged liver), hypoglycemia, and
hemoglobinuria with renal failure may occur. Renal failure is a feature of blackwater fever, where hemoglobin from
lysed red blood cells leaks into the urine. Severe malaria can progress extremely rapidly and cause death within
hours or days.[28] In the most severe cases of the disease, fatality rates can exceed 20%, even with intensive care and
treatment.[29] In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria
can be as high as one in ten.[30] Over the longer term, developmental impairments have been documented in children
who have suffered episodes of severe malaria.[31]
Malaria 3

Cause
Malaria parasites are members of the genus Plasmodium (phylum
Apicomplexa). In humans malaria is caused by P. falciparum, P.
malariae, P. ovale, P. vivax and P. knowlesi.[32] [33] P. falciparum is
the most common cause of infection and is responsible for about 80%
of all malaria cases, and is also responsible for about 90% of the deaths
from malaria.[34] Parasitic Plasmodium species also infect birds,
reptiles, monkeys, chimpanzees and rodents.[35] There have been
documented human infections with several simian species of malaria,
namely P. knowlesi, P. inui, P. cynomolgi,[36] P. simiovale, P.
brazilianum, P. schwetzi and P. simium; however, with the exception
of P. knowlesi, these are mostly of limited public health importance.[37]

Malaria parasites contain apicoplasts, an organelle usually found in

plants, complete with their own functioning genomes. These apicoplast A Plasmodium sporozoite traverses the cytoplasm
[38] of a mosquito midgut epithelial cell in this
are thought to have originated through the endosymbiosis of algae
false-color electron micrograph.
and play a crucial role in various aspects of parasite metabolism e.g.
fatty acid bio-synthesis.[39] To date, 466 proteins have been found to be
produced by apicoplasts[40] and these are now being looked at as possible targets for novel anti-malarial drugs.

Life cycle
The parasite's secondary (intermediate) hosts are humans and other vertebrates. Female mosquitoes of the Anopheles
genus are primary hosts and transmission vectors. Young mosquitoes first ingest the malaria parasite by feeding on
an infected human carrier and the infected Anopheles mosquitoes carry Plasmodium sporozoites in their salivary
glands. A mosquito becomes infected when it takes a blood meal from an infected human. Once ingested, the
parasite gametocytes taken up in the blood will further differentiate into male or female gametes and then fuse in the
mosquito's gut. This produces an ookinete that penetrates the gut lining and produces an oocyst in the gut wall. When
the oocyst ruptures, it releases sporozoites that migrate through the mosquito's body to the salivary glands, where
they are then ready to infect a new human host. This type of transmission is occasionally referred to as anterior
station transfer.[41] The sporozoites are injected into the skin, alongside saliva, when the mosquito takes a subsequent
blood meal.
Only female mosquitoes feed on blood while male mosquitoes feed on plant nectar,[42] thus males 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.[43]

Recurrent malaria
Malaria recurs after treatment for three reasons. Recrudescence occurs when parasites are not cleared by treatment,
whereas reinfection indicates complete clearance with new infection established from a separate infective mosquito
bite; both can occur with any malaria parasite species. Relapse is specific to P. vivax and P. ovale and involves
re-emergence of blood-stage parasites from latent parasites (hypnozoites) in the liver. Describing a case of malaria as
cured by observing the disappearance of parasites from the bloodstream can, therefore, be deceptive. The longest
incubation period reported for a P. vivax infection is 30 years.[28] Approximately one in five of P. vivax malaria
cases in temperate areas involve overwintering by hypnozoites (i.e., relapses begin the year after the mosquito
bite).[44]
Malaria 4

Pathogenesis
Malaria develops via two phases: an exoerythrocytic and an
erythrocytic phase. The exoerythrocytic phase involves infection of the
hepatic system, or liver, whereas the erythrocytic phase involves
infection of the erythrocytes, or red blood cells. 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.
Within minutes of being introduced into the human host, the
sporozoites infect hepatocytes, multiplying asexually and
asymptomatically for a period of 8–30 days.[45] Once in the liver, these The life cycle of malaria parasites in the human
body. A mosquito infects a person by taking a
organisms differentiate to yield thousands of merozoites, which,
blood meal. First, sporozoites enter the
following rupture of their host cells, escape into the blood and infect bloodstream, and migrate to the liver. They infect
red blood cells, thus beginning the erythrocytic stage of the life liver cells (hepatocytes), where they multiply into
cycle.[45] The parasite escapes from the liver undetected by wrapping merozoites, rupture the liver cells, and escape
back into the bloodstream. Then, the merozoites
itself in the cell membrane of the infected host liver cell.[46]
infect red blood cells, where they develop into
ring forms, trophozoites and schizonts which in
Within the red blood cells, the parasites multiply further, again
turn produce further merozoites. Sexual forms
asexually, periodically breaking out of their hosts to invade fresh red (gametocytes) are also produced, which, if taken
blood cells. Several such amplification cycles occur. Thus, classical up by a mosquito, will infect the insect and
descriptions of waves of fever arise from simultaneous waves of continue the life cycle.

merozoites escaping and infecting red blood cells.

Some P. vivax and P. ovale sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but
instead produce hypnozoites that remain dormant for periods ranging from several months (6–12 months is typical)
to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are
responsible for long incubation and late relapses in these two species of malaria.[47]
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.[48] This "stickiness" is
the main factor giving rise to hemorrhagic complications of malaria. High endothelial venules (the smallest branches
of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage
of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red
blood cells can breach the blood brain barrier possibly leading to coma.[49]
Although the white blood cell surface adhesive proteins (called PfEMP1, for Plasmodium falciparum erythrocyte
membrane protein 1) are exposed to the immune system, they do not serve as good immune targets, because of their
extreme diversity; there are at least 60 variations of the protein within a single parasite and effectively limitless
versions within parasite populations.[48] The parasite switches between a broad repertoire of PfEMP17 surface
proteins, thus staying one step ahead of the pursuing immune system.
Some merozoites turn into male and female gametocytes. Since the gametocytes are formed in the blood of the
vertebrate host, the vertebrate host is the definitive host of the disease. If a mosquito pierces the skin of an infected
person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite
occurs in the mosquito's gut. New sporozoites develop and travel to the mosquito's salivary gland, completing the
cycle. Pregnant women are especially attractive to the mosquitoes,[50] and malaria in pregnant women is an
important cause of stillbirths, infant mortality and low birth weight,[51] particularly in P. falciparum infection, but
also in other species infection, such as P. vivax.[52]
Malaria 5

Genetic resistance
Malaria is thought to have been the greatest selective pressure on the human genome in recent history.[53] This is due
to the high levels of mortality and morbidity caused by malaria, especially the P. falciparum species. A number of
diseases may provide some resistance to it including sickle cell disease, thalassaemias, glucose-6-phosphate
dehydrogenase, Duffy antigens, and possibly others.

Diagnosis
The mainstay of malaria diagnosis has been the microscopic examination of blood.[54] Although blood is the sample
most frequently used to make a diagnosis, both saliva and urine have been investigated as alternative, less invasive
specimens.[55]
Areas that cannot afford laboratory diagnostic tests often use only a history of subjective fever as the indication to
treat for malaria. Using Giemsa-stained blood smears from children in Malawi, one study showed that when clinical
predictors (rectal temperature, nailbed pallor, and splenomegaly) were used as treatment indications, rather than
using only a history of subjective fevers, a correct diagnosis increased from 2% to 41% of cases, and unnecessary
treatment for malaria was significantly decreased.[56]

Blood films

Species Appearance Periodicity Liver persistent

Plasmodium vivax tertian yes

Plasmodium ovale tertian yes

Plasmodium falciparum tertian no

Plasmodium malariae quartan no

The most economic, preferred, and reliable diagnosis of malaria is microscopic examination of blood films because
each of the four major parasite species has distinguishing characteristics. Two sorts of blood film are traditionally
Malaria 6

used. Thin films are similar to usual blood films and allow species identification because the parasite's appearance is
best preserved in this preparation. Thick films allow the microscopist to screen a larger volume of blood and are
about eleven times more sensitive than the thin film, so picking up low levels of infection is easier on the thick film,
but the appearance of the parasite is much more distorted and therefore distinguishing between the different species
can be much more difficult. With the pros and cons of both thick and thin smears taken into consideration, it is
imperative to utilize both smears while attempting to make a definitive diagnosis.[57]
From the thick film, an experienced microscopist can detect parasite levels (or parasitemia) down to as low as
0.0000001% of red blood cells. Diagnosis of species can be difficult because the early trophozoites ("ring form") of
all four species look identical and it is never possible to diagnose species on the basis of a single ring form; species
identification is always based on several trophozoites.
One important thing to note is that P. malariae and P. knowlesi (which is the most common cause of malaria in
South-east Asia) look very similar under the microscope. However, P. knowlesi parasitemia increases very fast and
causes more severe disease than P. malariae, so it is important to identify and treat infections quickly. Therefore
modern methods such as PCR (see "Molecular methods" below) or monoclonal antibody panels that can distinguish
between the two should be used in this part of the world.[58]

Antigen tests
For areas where microscopy is not available, or where laboratory staff are not experienced at malaria diagnosis, there
are commercial antigen detection tests that require only a drop of blood.[59] Immunochromatographic tests (also
called: Malaria Rapid Diagnostic Tests, Antigen-Capture Assay or "Dipsticks") have been developed, distributed and
fieldtested. These tests use finger-stick or venous blood, the completed test takes a total of 15–20 minutes, and the
results are read visually as the presence or absence of colored stripes on the dipstick, so they are suitable for use in
the field. The threshold of detection by these rapid diagnostic tests is in the range of 100 parasites/µl of blood
(commercial kits can range from about 0.002% to 0.1% parasitemia) compared to 5 by thick film microscopy. One
disadvantage is that dipstick tests are qualitative but not quantitative – they can determine if parasites are present in
the blood, but not how many.
The first rapid diagnostic tests were using P. falciparum glutamate dehydrogenase as antigen.[60] PGluDH was soon
replaced by P.falciparum lactate dehydrogenase, a 33 kDa oxidoreductase [EC 1.1.1.27]. It is the last enzyme of the
glycolytic pathway, essential for ATP generation and one of the most abundant enzymes expressed by P.falciparum.
PLDH does not persist in the blood but clears about the same time as the parasites following successful treatment.
The lack of antigen persistence after treatment makes the pLDH test useful in predicting treatment failure. In this
respect, pLDH is similar to pGluDH. Depending on which monoclonal antibodies are used, this type of assay can
distinguish between all five different species of human malaria parasites, because of antigenic differences between
their pLDH isoenzymes.

Molecular methods
Molecular methods are available in some clinical laboratories and rapid real-time assays (for example, QT-NASBA
based on the polymerase chain reaction)[61] are being developed with the hope of being able to deploy them in
endemic areas.
PCR (and other molecular methods) is more accurate than microscopy. However, it is expensive, and requires a
specialized laboratory. Moreover, levels of parasitemia are not necessarily correlative with the progression of
disease, particularly when the parasite is able to adhere to blood vessel walls. Therefore more sensitive, low-tech
diagnosis tools need to be developed in order to detect low levels of parasitemia in the field.[62]
Malaria 7

Differential
Fever and septic shock are commonly misdiagnosed as severe malaria in Africa, leading to a failure to treat other
life-threatening illnesses. In malaria-endemic areas, parasitemia does not ensure a diagnosis of severe malaria,
because parasitemia can be incidental to other concurrent disease. Recent investigations suggest that malarial
retinopathy is better (collective sensitivity of 95% and specificity of 90%) than any other clinical or laboratory
feature in distinguishing malarial from non-malarial coma.[63]

Prevention
Methods used in order to prevent the spread of disease, or to protect
individuals in areas where malaria is endemic, include prophylactic
drugs, mosquito eradication and the prevention of mosquito bites.
The continued existence of malaria in an area requires a combination
of high human population density, high 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 sooner or later disappear from that area, as happened in
Anopheles albimanus mosquito feeding on a
North America, Europe and much of Middle East. However, unless the human arm. This mosquito is a vector of malaria
parasite is eliminated from the whole world, it could become and mosquito control is a very effective way of
re-established if conditions revert to a combination that favours the reducing the incidence of malaria.

parasite's reproduction. Many countries are seeing an increasing

number of imported malaria cases owing to extensive travel and migration.

Many researchers argue that prevention of malaria may be more cost-effective than treatment of the disease in the
long run, but the capital costs required are out of reach of many of the world's poorest people. Economic adviser
Jeffrey Sachs estimates that malaria can be controlled for US$3 billion in aid per year.[64]
A 2008 study that examined international financing of malaria control found large regional variations in the levels of
average annual per capita funding ranging from US$0.01 in Myanmar to US$147 in Suriname. The study found 34
countries where the funding was less than US$1 per capita, including 16 countries where annual malaria support was
less than US$0.5. The 16 countries included 710 million people or 50% of the global population exposed to the risks
of malaria transmission, including seven of the poorest countries in Africa (Côte d'Ivoire, Republic of the Congo,
Chad, Mali, Democratic Republic of the Congo, Somalia, and Guinea) and two of the most densely populated stable
endemic countries in the world (Indonesia and India).[65]
Brazil, Eritrea, India, and Vietnam, unlike many other developing nations, have successfully reduced the malaria
burden. Common success factors have included conducive country conditions, a targeted technical approach using a
package of effective tools, data-driven decision-making, active leadership at all levels of government, involvement
of communities, decentralized implementation and control of finances, skilled technical and managerial capacity at
national and sub-national levels, hands-on technical and programmatic support from partner agencies, and sufficient
and flexible financing.[66]

Medications
Several drugs, most of which are also used for treatment of malaria, can be taken preventively. Modern drugs used
include mefloquine (Lariam), doxycycline (available generically), and the combination of atovaquone and proguanil
hydrochloride (Malarone). Doxycycline and the atovaquone and proguanil combination are the best tolerated with
mefloquine associated with higher rates of neurological and psychiatric symptoms.[67] The choice of which drug to
use depends on which drugs the parasites in the area are resistant to, as well as side-effects and other considerations.
The prophylactic effect does not begin immediately upon starting taking the drugs, so people temporarily visiting
Malaria 8

malaria-endemic areas usually begin taking the drugs one to two weeks before arriving and must continue taking
them for 4 weeks after leaving (with the exception of atovaquone proguanil that only needs be started 2 days prior
and continued for 7 days afterwards). Generally, these drugs are taken daily or weekly, at a lower dose than would be
used for treatment of a person who had actually contracted the disease. Use of prophylactic drugs is seldom practical
for full-time residents of malaria-endemic areas, and their use is usually restricted to short-term visitors and travelers
to malarial regions. This is due to the cost of purchasing the drugs, negative side effects from long-term use, and
because some effective anti-malarial drugs are difficult to obtain outside of wealthy nations.
Quinine was used historically, however the development of more effective alternatives such as quinacrine,
chloroquine, and primaquine in the 20th century reduced its use. Today, quinine is not generally used for
prophylaxis. The use of prophylactic drugs where malaria-bearing mosquitoes are present may encourage the
development of partial immunity.[68]

Vector control
Efforts to eradicate malaria by eliminating mosquitoes have been successful in some areas. 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. In some areas, the draining of wetland breeding
grounds and better sanitation were adequate. 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 by 1951[69] (see National Malaria Eradication Program). In 2002, there were 1,059 cases of
malaria reported in the US, including eight deaths, but in only five of those cases was the disease contracted in the
United States.
Before DDT, malaria was successfully eradicated or controlled also in several tropical areas by removing or
poisoning the breeding grounds of the mosquitoes or the aquatic habitats of the larva stages, for example by filling or
applying oil to places with standing water. These methods have seen little application in Africa for more than half a
century.[70]
Sterile insect technique is emerging as a potential mosquito control method. Progress towards transgenic, or
genetically modified, insects suggest that wild mosquito populations could be made malaria-resistant. Researchers at
Imperial College London created the world's first transgenic malaria mosquito,[71] with the first
plasmodium-resistant species announced by a team at Case Western Reserve University in Ohio in 2002.[72]
Successful replacement of current populations with a new genetically modified population, relies upon a drive
mechanism, such as transposable elements to allow for non-Mendelian inheritance of the gene of interest. However,
this approach contains many difficulties and success is a distant prospect.[73] An even more futuristic method of
vector control is the idea that lasers could be used to kill flying mosquitoes.[74]

Indoor residual spraying

Indoor residual spraying (IRS) is the practice of spraying insecticides on the interior walls of homes in malaria
affected areas. After feeding, many mosquito species rest on a nearby surface while digesting the bloodmeal, so if
the walls of dwellings have been coated with insecticides, the resting mosquitos will be killed before they can bite
another victim, transferring the malaria parasite.
The first pesticide used for IRS was DDT.[69] 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 regions. The DDT resistance shown
by Anopheles mosquitoes can be compared to antibiotic resistance shown by bacteria. The overuse of anti-bacterial
soaps and antibiotics led to antibiotic resistance in bacteria, similar to how overspraying of DDT on crops led to
DDT resistance in Anopheles mosquitoes. 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
Malaria 9

1970s. Since the use of DDT has been limited or banned for agricultural use for some time, DDT may now be more
effective as a method of disease-control.
Although DDT has never been banned for use in malaria control and there are several other insecticides suitable for
IRS, some advocates have claimed that bans are responsible for tens of millions of deaths in tropical countries where
DDT had once been effective in controlling malaria. Furthermore, most of the problems associated with DDT use
stem specifically from its industrial-scale application in agriculture, rather than its use in public health.[75]
The World Health Organization (WHO) currently advises the use of 12 different insecticides in IRS operations,
including DDT as well as alternative insecticides (such as the pyrethroids permethrin and deltamethrin).[76] This
public health use of small amounts of DDT is permitted under the Stockholm Convention on Persistent Organic
Pollutants (POPs), which prohibits the agricultural use of DDT.[77] However, because of its legacy, many developed
countries previously discouraged DDT use even in small quantities.[78]
One problem with all forms of Indoor Residual Spraying is insecticide resistance via evolution of mosquitos.
According to a study published on Mosquito Behavior and Vector Control, mosquito species that are affected by IRS
are endophilic species (species that tend to rest and live indoors), and due to the irritation caused by spraying, their
evolutionary descendants are trending towards becoming exophilic (species that tend to rest and live out of doors),
meaning that they are not as affected—if affected at all—by the IRS, rendering it somewhat useless as a defense
mechanism.[79]

Mosquito nets and bedclothes

Mosquito nets help keep mosquitoes away from people and greatly reduce the infection and transmission of malaria.
The nets are not a perfect barrier and they are often treated with an insecticide designed to kill the mosquito before it
has time to search for 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.[80] Although ITNs are proven to be very
effective against malaria, less than 2% of children in urban areas in Sub-Saharan Africa are protected by ITNs. Since
the Anopheles mosquitoes feed at night, the preferred method is to hang a large "bed net" above the center of a bed
such that it drapes down and covers the bed completely.

Vaccination
Immunity (or, more accurately, tolerance) does occur naturally, but only in response to repeated infection with
multiple strains of malaria.[81] Vaccines for malaria are under development, with no completely effective vaccine yet
available. The first promising studies demonstrating the potential for a malaria vaccine were performed in 1967 by
immunizing mice with live, radiation-attenuated sporozoites, providing protection to about 60% of the mice upon
subsequent injection with normal, viable sporozoites.[82] Since the 1970s, there has been a considerable effort to
develop similar vaccination strategies within humans. It was determined that an individual can be protected from a P.
falciparum infection if they receive over 1,000 bites from infected yet irradiated mosquitoes.[83]

Other methods
Education in recognizing the symptoms of malaria has reduced the number of cases in some areas of the developing
world by as much as 20%. Recognizing the disease in the early stages can also stop the disease from becoming a
killer. Education can also inform people to cover over areas of stagnant, still water e.g. Water Tanks which are ideal
breeding grounds for the parasite and mosquito, thus cutting down the risk of the transmission between people. This
is most put in practice in urban areas where there are large centers of population in a confined space and
transmission would be most likely in these areas.
The Malaria Control Project is currently using downtime computing power donated by individual volunteers around
the world (see Volunteer computing and BOINC) to simulate models of the health effects and transmission dynamics
in order to find the best method or combination of methods for malaria control. This modeling is extremely computer
Malaria 10

intensive due to the simulations of large human populations with a vast range of parameters related to biological and
social factors that influence the spread of the disease. It is expected to take a few months using volunteered
computing power compared to the 40 years it would have taken with the current resources available to the scientists
who developed the program.[84]
An example of the importance of computer modeling in planning malaria eradication programs is shown in the paper
by Águas and others. They showed that eradication of malaria is crucially dependent on finding and treating the large
number of people in endemic areas with asymptomatic malaria, who act as a reservoir for infection.[85] The malaria
parasites do not affect animal species and therefore eradication of the disease from the human population would be
expected to be effective.
Other interventions for the control of malaria include mass drug administrations and intermittent preventive therapy.
Furthering attempts to reduce transmission rates, a proposed alternative to mosquito nets is the mosquito laser, or
photonic fence, which identifies female mosquitoes and shoots them using a medium-powered laser.[86] The device
is currently undergoing commercial development, although instructions for a DIY version of the photonic fence have
also been published.[87]
Another way of reducing the malaria transmitted to humans from mosquitoes has been developed by the University
of Arizona. They have engineered a mosquito to become resistant to malaria. This was reported on the 16 July 2010
in the journal PLoS Pathogens.[88] With the ultimate end being that the release of this GM mosquito into the
environment, Gareth Lycett, a malaria researcher from Liverpool School of Tropical Medicine told the BBC that "It
is another step on the journey towards potentially assisting malaria control through GM mosquito release."[89]

Treatment
When properly treated, a patient with malaria can expect a complete recovery.[90] The treatment of malaria depends
on the severity of the disease; whether patients who can take oral drugs have to be admitted depends on the
assessment and the experience of the clinician. Uncomplicated malaria is treated with oral drugs. The most effective
strategy for P. falciparum infection recommended by WHO is the use of artemisinins in combination with other
antimalarials artemisinin-combination therapy, ACT, in order to avoid the development of drug resistance against
artemisinin-based therapies.
Severe malaria requires the parenteral administration of antimalarial drugs. Until recently the most used treatment
for severe malaria was quinine but artesunate has been shown to be superior to quinine in both children [91] and
adults [92] . Treatment of severe malaria also involves supportive measures.
Infection with P. vivax, P. ovale or P. malariae is usually treated on an outpatient basis. Treatment of P. vivax
requires both treatment of blood stages (with chloroquine or ACT) as well as clearance of liver forms with
primaquine.

Epidemiology
It is estimated that malaria causes 250 million cases of

Countries which have regions where malaria is

[93]
endemic as of 2003 (coloured yellow).
Countries in green are free of indigenous cases of
malaria in all areas.
Malaria 11

fever
and
approximately
one
million
deaths Disability-adjusted life year for malaria per 100,000 inhabitants in 2002.  no
annually.[94] data  ≤10  10–50  50–100  100–250  250–500  500–1000  1000–1500  1500–2000  2000–2500  2500–3000  3000–3500  ≥3500
The vast
majority of cases occur in children under 5 years old;[95] pregnant women are also especially vulnerable. Despite
efforts to reduce transmission and increase treatment, there has been little change in which areas are at risk of this
disease since 1992.[96] Indeed, if the prevalence of malaria stays on its present upwards course, the death rate could
double in the next twenty years.[97] Precise statistics are unknown because many cases occur in rural areas where
people do not have access to hospitals or the means to afford health care. As a consequence, the majority of cases are
undocumented.[97]

Although co-infection with HIV and malaria does cause increased mortality, this is less of a problem than with
HIV/tuberculosis co-infection, due to the two diseases usually attacking different age-ranges, with malaria being
most common in the young and active tuberculosis most common in the old.[98] Although HIV/malaria co-infection
produces less severe symptoms than the interaction between HIV and TB, HIV and malaria do contribute to each
other's spread. This effect comes from malaria increasing viral load and HIV infection increasing a person's
susceptibility to malaria infection.[99]

Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and
much of Africa; however, it is in sub-Saharan Africa where 85– 90% of malaria fatalities occur.[100] The geographic
distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found
close to each other.[101] In drier areas, outbreaks of malaria can be predicted with reasonable accuracy by mapping
rainfall.[102] Malaria is more common in rural areas than in cities; this is in contrast to dengue fever where urban
areas present the greater risk.[103] For example, several cities in Vietnam, Laos and Cambodia are essentially
malaria-free, but the disease is present in many rural regions.[104] By contrast, in Africa malaria is present in both
rural and urban areas, though the risk is lower in the larger cities.[105] The global endemic levels of malaria have not
been mapped since the 1960s. However, the Wellcome Trust, UK, has funded the Malaria Atlas Project[106] to rectify
this, providing a more contemporary and robust means with which to assess current and future malaria disease
burden.

History
Malaria has infected humans for over 50,000 years, and Plasmodium may have been a human pathogen for the entire
history of the species.[107] Close relatives of the human malaria parasites remain common in chimpanzees.[108] Some
new evidence suggests that the most virulent strain of human malaria may have originated in gorillas.[109]
References to the unique periodic fevers of malaria are found throughout recorded history, beginning in 2700 BC in
China.[110] Malaria may have contributed to the decline of the Roman Empire,[111] and was so pervasive in Rome
that it was known as the "Roman fever".[112] 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.[113]
Malaria was once common in most of Europe and North America,[114] where it is no longer endemic,[115] though
imported cases do occur.[116]
Malaria was the most important health hazard encountered by U.S. troops in the South Pacific during World War II,
where about 500,000 men were infected.[117] According to Joseph Patrick Byrne, "Sixty thousand American soldiers
died of malaria during the African and South Pacific campaigns."[118]
Malaria 12

Prevention
An early effort at malaria prevention occurred in 1896, just before the mosquito malaria link was confirmed in India
by a British physician, Ronald Ross. An 1896 Uxbridge malaria outbreak prompted health officer, Dr. Leonard
White, to write a report to the Massachusetts State Board of Health, which led to study of mosquito-malaria links,
and the first efforts for malaria prevention.[119] Massachusetts State pathologist Theobald Smith, asked that White's
son collect mosquito specimens for further analysis, and that citizens 1) add screens to windows, and 2) drain
collections of water.[119] Carlos Finlay was also engaged in mosquito related research, and mosquito borne disease
theory, in the 1880s in Cuba, basing his work on the study of Yellow Fever.

Discovery of the malaria parasite

Scientific studies on malaria made their first significant advance in
1880, when a French army doctor working in the military hospital of
Constantine in Algeria named Charles Louis Alphonse Laveran
observed parasites for the first time, inside the red blood cells of people
suffering from malaria. He, therefore, proposed that malaria is caused
by this organism, the first time a protist was identified as causing
disease.[120] For this and later discoveries, he was awarded the 1907
Nobel Prize for Physiology or Medicine. The malarial parasite was
called Plasmodium by the Italian scientists Ettore Marchiafava and
Angelo Celli.[121]

Discovery of mosquito transmission Dr. Probert's Malarial Remedy,

"Will cure chills and fever, dyspepsia & c. Will
A year later, Carlos Finlay, a Cuban doctor treating patients with cure bilious fever, liver complaint & c.", c.1881,
yellow fever in Havana, provided strong evidence that mosquitoes New York

were transmitting disease to and from humans.[122] This work followed

earlier suggestions by Josiah C. Nott,[123] and work by Patrick Manson
on the transmission of filariasis.[124]
It was Britain's Sir Ronald Ross, working in the Presidency General
Hospital in Calcutta, who finally proved in 1898 that malaria is
transmitted by mosquitoes. He did this 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.[125] For this work, Ross received the 1902 Nobel Prize
in Medicine. After resigning from the Indian Medical Service, Ross
A continuous P. falciparum culture was
worked at the newly established Liverpool School of Tropical
established in 1976
Medicine and directed malaria-control efforts in Egypt, Panama,
Greece and Mauritius.[126] 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.
Malaria 13

Discovery of the liver stage

Shortt and Garnham discovered the pre-erythrocytic liver stage, first in the primate parasite P. cynomolgi and
subsequently the human malarias P. vivax [127] and P. falciparum [128] . Further work confirmed the transformation
of sporozoites from mosquitoes into liver forms, essentially completing documentation of the lifecycle [129] .

In vitro culture
The first successful continuous in vitro malaria culture was established in 1976 by William Trager and James B.
Jensen, which facilitated research into the molecular biology of the parasite and the development of new drugs.[130]
[131]

History of treatment
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 malaria. The Jesuits noted the efficacy of the practice and introduced the treatment to Europe during the
1640s, where it was rapidly accepted.[132] 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 and Joseph Bienaimé
Caventou.[133] . In the 20th century, chloroquine replaced quinine as treatment of both uncomplicated and severe
falciparum malaria until resistance supervened. Artemisinins, discovered by Chinese scientists in the 1970s, are now
recommended treatment for falciparum malaria, administered in combination with other antimalarials as well as in
severe disease.

Society and culture

Malaria is not just a disease commonly associated with poverty but also a cause of poverty and a major hindrance to
economic development. Tropical regions are affected most, however malaria’s furthest extent reaches into some
temperate zones with 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.[134] 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 countries where malaria is common, average per capita
GDP has risen (between 1965 and 1990) only 0.4% per year, compared to 2.4% per year in other countries.[135]
Poverty is both cause and effect, however, since the poor do not have the financial capacities to prevent or treat the
disease. The lowest income group in Malawi carries (1994) the burden of having 32% of their annual income used
on this disease compared with the 4% of household incomes from low-to-high groups.[136] In its entirety, the
economic impact of malaria has been estimated to cost Africa $12 billion USD 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.[95] In some countries with a heavy malaria
burden, the disease may account for as much as 40% of public health expenditure, 30–50% of inpatient admissions,
and up to 50% of outpatient visits.[137]
A study on the effect of malaria on IQ in a sample of Mexicans found that exposure during the birth year to malaria
eradication was associated with increases in IQ. It also increased the probability of employment in a skilled
occupation. The author suggests that this may be one explanation for the Flynn effect and that this may be an
important explanation for the link between national malaria burden and economic development.[138] A literature
review of 44 papers states that cognitive abilities and school performance were shown to be impaired in sub-groups
of patients (with either cerebral malaria or uncomplicated malaria) when compared with healthy controls. Studies
comparing cognitive functions before and after treatment for acute malarial illness continued to show significantly
Malaria 14

impaired school performance and cognitive abilities even after recovery. Malaria prophylaxis was shown to improve
cognitive function and school performance in clinical trials when compared to placebo groups.[139]

Counterfeit drugs
Sophisticated counterfeits have been found in several Asian countries such as Cambodia,[140] China,[141] Indonesia,
Laos, Thailand, Vietnam and are an important cause of avoidable death in those countries.[142] WHO have said that
studies indicate that up to 40% of artesunate based malaria medications are counterfeit, especially in the Greater
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.[143] 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.

War
Throughout history, the contraction of malaria (via natural outbreaks as well as via infliction of the disease as a
biological warfare agent) has played a prominent role in the fortunes of government rulers, nation-states, military
personnel, and military actions. "Malaria Site: History of Malaria During Wars" addresses the devastating impact of
malaria in numerous well-known conflicts, beginning in June 323 B.C. That site's authors note: "Many great warriors
succumbed to malaria after returning from the warfront and advance of armies into continents was prevented by
malaria. In many conflicts, more troops were killed by malaria than in combat."[144] The Centers for Disease Control
("CDC") traces the history of malaria and its impacts farther back, to 2700 BCE.[145]
In 1910, Nobel Prize in Medicine-winner Ronald Ross (himself a malaria survivor), published a book titled The
Prevention of Malaria that included the chapter: "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 and advised: "A specially selected medical officer should be placed in
charge of these operations with executive and disciplinary powers [...]."
Significant financial investments have been made to fund procure existing and create new anti-malarial agents.
During World War I and World War II, the supplies of the natural anti-malaria drugs, cinchona bark and quinine,
proved to be inadequate to supply military personnel and substantial funding was funnelled 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 the U.S. Army Medical
Research Institute of Infectious Diseases of the US Armed Forces.[144]
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) 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" and, during these activities, to "train
state and local health department officials in malaria control techniques and strategies." The CDC's Malaria Division
continued that mission, successfully reducing malaria in the United States, after which the organization expanded its
focus to include "prevention, surveillance, and technical support both domestically and internationally."[145]
Malaria 15

Popular culture
• Joseph Conrad, author of the novella Heart of Darkness (published in serial form in 1899 and as a novella in
1902), contracted malaria while on a four-month steamboat voyage along the Congo River.[146] One character in
the book, an ivory trader named Kurtz, dies from the disease[146] and the novella's narrator, Charles Marlow, is
weakened by it.
• In making the movie The African Queen (1951), most of the crew and the leading lady, Katharine Hepburn,
endured malaria.[147] [148] [149]
• In the movie Apocalypse Now (1979), Captain Benjamin L. Willard is a special operations veteran stationed in
Southeast Asia during the Vietnam war. Willard is assigned a classified mission to assassinate rogue soldier,
Colonel Walter E. Kurtz, who has gone insane and is commanding a legion of his own Montagnard troops in
neutral Cambodia. Upon finding Kurtz's location, Willard narrates: "It smelled like slow death in there, malaria,
and nightmares. This was the end of the river, all right."[150]
• In Barbara Kingsolver's novel, The Poisonwood Bible (1998), Ruth May – the youngest daughter of an American
Christian missionary who brings his family to live in the Belgian Congo of the late 1950s – stops taking her
quinine tablets and contracts malaria.[151]

Research
With the onset of drug resistant Plasmodium parasites, new strategies are required to combat the widespread disease.
One such approach lies in the introduction of synthetic pyridoxal-amino acid adducts, which are channelled into the
parasite. Thus, trapped upon phosphorylation by plasmodial PdxK (pyridoxine/pyridoxal kinase), the proliferation of
Plasmodium parasites is effectively hindered by a novel compound, PT3, a cyclic pyridoxyl-tryptophan methyl ester,
without harming human cells.[152]

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Malaria 21

External links
• WHO site on malaria (http://www.who.int/malaria/)
• Global Malaria action Plan (http://www.rollbackmalaria.org/gmap/)
• Malaria Atlas Project (http://www.map.ox.ac.uk/)
• Medicines for Malaria Venture (MMV) (http://www.mmv.org)
• World Malaria Report 2005 (http://www.rollbackmalaria.org/wmr2005/)
• Doctors Without Borders/Médecins Sans Frontières – Malaria (http://doctorswithoutborders.org/news/issue.
cfm?id=2395) information pages
• Medline Plus – Malaria (http://www.nlm.nih.gov/medlineplus/malaria.html)
• Who/TDR Malaria Database (http://www.wehi.edu.au/other_domains/MalDB/who.html)
• Anti malaria and sustainable development (http://www.antimalariaomd.org/en/index.php)
• Worldwide Antimalarial Resistance Network (WWARN) (http://www.wwarn.org)
• Malaria (http://www.dmoz.org/Health/Conditions_and_Diseases/Infectious_Diseases/Parasitic/Malaria/) at
the Open Directory Project
Article Sources and Contributors 22

Article Sources and Contributors

Malaria  Source: http://en.wikipedia.org/w/index.php?oldid=417462218  Contributors: .V., 100110100, 141.236.82.xxx, 62.253.64.xxx, A4, Abanima, Abendroth85, Acalamari, AccursedOne,
Adacus12, Adhib, Ahoerstemeier, Ajrodriguezm, Akamad, Alan.ca, Alex.tan, Alexius08, AlexiusHoratius, Alexsautographs, Alfie66, Algebraist, Allmightyduck, Alphax, AlwaysOnion,
Amaraiel, Amit0108, Ancient Apparition, Anclation, AndTheCrowdGoesWild, Andrew Benton, Andrew Hartford, Andrew Levine, AndrewDressel, AndrewLeeson, Andries, Andy tatem, Angus
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File:Plasmodium.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Plasmodium.jpg  License: Public Domain  Contributors: Original uploader was TimVickers at en.wikipedia
File:Symptoms of Malaria.png  Source: http://en.wikipedia.org/w/index.php?title=File:Symptoms_of_Malaria.png  License: Public Domain  Contributors: Mikael Häggström
File:Malaria fever.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Malaria_fever.svg  License: Creative Commons Attribution-Sharealike 3.0  Contributors: User:Brady8
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Wlodzimierz, Überraschungsbilder, 3 anonymous edits
Image:MalariacycleBig.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:MalariacycleBig.jpg  License: Public Domain  Contributors: Original uploader was TimVickers at
en.wikipedia
Image:Plasmodium vivax 01.png  Source: http://en.wikipedia.org/w/index.php?title=File:Plasmodium_vivax_01.png  License: Public Domain  Contributors: Photo Credit: Content Providers(s):
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Image:Plasmodium falciparum 01.png  Source: http://en.wikipedia.org/w/index.php?title=File:Plasmodium_falciparum_01.png  License: Public Domain  Contributors: Photo Credit: Content
Providers(s): CDC/Dr. Mae Melvin Transwiki approved by: w:en:User:Dmcdevit
Image:Mature Plasmodium malariae schizont PHIL 2715 lores.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Mature_Plasmodium_malariae_schizont_PHIL_2715_lores.jpg
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DO11.10, Mysid, Optigan13, 1 anonymous edits
Image:Malaria world map - DALY - WHO2002.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Malaria_world_map_-_DALY_-_WHO2002.svg  License: Creative Commons
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Robert's Malarial Remedy
File:P.falciparum Gelatine enrichment.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:P.falciparum_Gelatine_enrichment.jpg  License: Creative Commons Zero  Contributors:
Ernst Hempelmann
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