Oscillaria malariae Laveran, 1881
Plasmodium malariae Marchiafava and Celli, 1885
Laverania malariae Feletti and Grassi, 1890
Ematozoo falciforme Antolisei and Angelini, 1890
Haemamoeba immaculata Grassi, 1891
Haemamoeba laverani Labbe, 1894
Haematozoon falciforme Thayer and Hewetson, 1895
Haematozoon falciparum Welch, 1897
Haemosporidium sedecimanae Lewkowicz, 1897
Haemosporidium undecimanae Lewkowicz, 1897
Haemosporidium vigesimotertianae Lewkowicz, 1897
Plasmodium falciparum is a unicellular protozoan parasite of humans,
and the deadliest species of
Plasmodium that cause malaria in
humans. It is transmitted through the bite of a female Anopheles
mosquito. It is responsible for roughly 50% of all malaria cases.
It causes the disease's most dangerous form called falciparum
malaria. It is therefore regarded as the deadliest parasite in
humans, causing a conservative estimate of one million deaths every
year. It is also associated with the development of blood cancer
(Burkitt's lymphoma) and is clasiified as Group 2A carcinogen.
The species originated from the malarial parasite
Laverania found in
gorillas, around 10,000 years ago.
Alphonse Laveran was the first to
identify the parasite in 1880, and named it Oscillaria malariae.
Ronald Ross discovered its transmission by mosquito in 1897. Giovanni
Battista Grassi elucidated the complete transmission from a female
anopheline mosquito to humans in 1898. In 1897, William H. Welch
created the name
Plasmodium falciparum, which ICZN formally adopted in
1954. P. falciparum assumes several different forms during its life
cycle. The human-infective stage are sporozoites from the salivary
gland of a mosquito. The sporozoites grow and multiply in the liver to
become merozoites. These merozoites invade the erythrocytes (RBCs) to
form trophozoites, schizonts and gametocytes, during which the
symptoms of malaria are produced. In the mosquito, the gametocytes
undergo sexual reproduction to a zygote, which turns into ookinete.
Ookinete forms oocyts from which sporozoites are formed.
As of the latest World
Malaria Report of the World Health
Organization, there were 216 million cases of malaria worldwide in
2016, up from 211 million cases in 2015. This resulted in an estimated
445,000 deaths. The rate of infection decreased from 2000 to 2015
by 37%, but there is a steady increase from 2014's 198 million
cases. Almost every malarial death is caused by P. falciparum, and
91% of death occurs in Africa. Children under five years of age are
most affected, accounting for two-third of the total deaths. In
Sub-Saharan Africa, over 75% of cases were due to P. falciparum,
whereas in most other malarial countries, other, less virulent
plasmodial species predominate.
1.2 Origin and evolution
3 Life cycle
3.1 In humans
3.1.1 Liver stage or exo-erythrocytic schizogony
3.1.2 Blood stage or erythrocytic schizogony
3.2 Incubation period
3.3 In mosquitoes
4 Interaction with human immune system
4.1 Immune response
4.2 Immune system evasion
6 Distribution and epidemiology
7.2 Uncomplicated malaria
7.3 Severe malaria
9 Influence on the human genome
10 See also
12 Further reading
13 External links
Laveran's drawing of various stages of P. falciparum as seen on fresh
Falciparum malaria was familiar to Ancient Greeks, who gave the
general name pyretos (meaning fever).
Hippocrates (c. 460-370 BCE)
gave several descriptions on tertian fever and quartan fever. It
was prevalent throughout the Ancient Egypt and Roman civilisation.
It the Romans who gave the name of the disease "malaria"—mala for
air, and aria for air, as they believed that the disease was spread by
contaminated air, or miasma. It is hypothesised that the fall of the
Roman Empire was in part due to malaria epidemic.
A German physician Johann Heinrich Meckel must have been the first to
see P. falciparum but not knowing what it was. In 1847 he reported the
presence of black pigment granules from the blood and spleen of a
patient who died of malaria. The French Army physician Charles Louis
Alphonse Laveran, while working at the Bône Hospital in Algeria,
correctly identified the parasite as a causative pathogen of malaria
in 1880. He presented his discovery before the French Academy of
Medicine in Paris, and published it in The Lancet, in 1881. He gave
the scientific name Oscillaria malariae. But his discovery was
received with skepticism mainly because by that time leading
physicians such as Theodor Albrecht
Edwin Klebs and Corrado
Tommasi-Crudeli claimed that they had discovered a bacterium (which
they called Bacillus malariae) as the pathogen of malaria. Laveran's
discovery was widely accepted only after five years when Camillo Golgi
confirmed the parasite using better microscope and staining technique.
Laveran was awarded the Nobel Prize in Physiology or Medicine in 1907
for his work. In 1900, the Italian zoologist Giovanni Battista Grassi
Plasmodium species based on the timing of fever in the
patient; malignant tertian malaria was caused by
(now P. falciparum), benign tertian malaria by Haemamoeba vivax (now
P. vivax), and quartan malaria by Haemamoeba malariae (now P.
malariae). The British physician
Patrick Manson formulated the
mosquito-malaria theory in 1894; until that time, malarial parasites
were believed to be spread in air as miasma (a Greek word for
pollution). His colleague Ronald Ross, a British Army surgeon,
traveled to India to prove the theory. Ross discovered in 1897 that
malarial parasite lived in certain mosquitoes. The next year, he
demonstrated that a malarial parasite of birds could be transmitted by
mosquitoes from one bird to another. Around the same time, Grassi
demonstrated that P. falciparum was transmitted in humans only by
female anopheline mosquito (in his case
Anopheles claviger). Ross,
Manson and Grassi were nominated for the Nobel Prize in Physiology or
Medicine in 1902. Under controversial circumstances, only Ronald Ross
was selected for the award.
There was a long debate on the taxonomy. It was only in 1954 the
International Commission on Zoological Nomenclature officially
approved the binominal
Plasmodium falciparum. The valid genus
Plasmodium was created by two Italian physicians Ettore Marchiafava
Angelo Celli in 1885. The species name was introduced by an
William Henry Welch
William Henry Welch in 1897. It is derived from
the Latin falx, meaning "sickle" and parum meaning "like or equal to
Origin and evolution
P. falciparum is now generally accepted to have evolved from Laverania
(a subgenus of
Plasmodium found in apes) species present in gorilla in
Western Africa. Genetic diversity indicates that the human
protozoan emerged around 10,000 years ago. The closest relative of
P. falciparum is P. praefalciparum, a parasite of gorillas, as
supported by mitochondrial, apicoplastic and nuclear DNA
sequences. These two species are closely related to the
chimpanzee parasite P. reichenowi, which was previously thought to be
the closest relative of P. falciparum. P. falciparum was also once
thought to originate from a parasite of birds.
Levels of genetic polymorphism are extremely low within the P.
falciparum genome compared to that of closely related, ape infecting
Plasmodium (including P. praefalciparum). This
suggests that the origin of P. falciparum in humans is recent, as a
single P. praefalciparum strain became capable of infecting
humans. The genetic information of
Plasmodium falciparum has
signaled a recent expansion that coincides with the agricultural
revolution. It is likely that the development of extensive agriculture
increased mosquito population densities by giving rise to more
breeding sites, which may have triggered the evolution and expansion
Blood smear from a P. falciparum culture (K1 strain - asexual forms) -
several red blood cells have ring stages inside them. Close to the
center is a schizont and on the left a trophozoite.
P. falciparum does not have a fixed structure but undergoes continuous
change during the course of its life cycle. A sporozoite is
spindle-shaped and 10-15 μm long. In the liver it grows into an ovoid
schizont of 30-70 μm in diameter. Each schizont produces merozoites,
each of which is roughly 1.5 μm in length and 1 μm in diameter. In
the erythrocyte the merozoite form a ring-like structure, becoming a
trophozoite. A trophozoites feed on the haemoglobin and forms a
granular pigment called haemozoin. Unlike those of other Plasmodium
species, the gametocytes of P. falciparum are elongated and
crescent-shaped, by which they are sometimes identified. A mature
gametocyte is 8-12 μm long and 3-6 μm wide. The ookinete is also
elongated measuring about 18-24 μm. An oocyst is rounded and can grow
up to 80 μm in diameter. Microscopic examination of a blood film
reveals only early (ring-form) trophozoites and gametocytes that are
in the peripheral blood. Mature trophozoites or schizonts in
peripheral blood smears, as these are usually sequestered in the
tissues. On occasion, faint, comma-shaped, red dots are seen on the
erythrocyte surface. These dots are Maurer's cleft and are secretory
organelles that produce proteins and enzymes essential for nutrient
uptake and immune evasion processes.
The apical complex, which is actually a combination of organelles, is
an important structure. It contains secretory organelles called
rhoptries and micronemes, which are vital for mobility, adhesion, host
cell invasion, and parasitophorous vacuole formation. As an
apicomplexan, it harbours a plastid, an apicoplast, similar to plant
chloroplasts, which they probably acquired by engulfing (or being
invaded by) a eukaryotic alga and retaining the algal plastid as a
distinctive organelle encased within four membranes. The apicoplast is
involved in the synthesis of lipids and several other compounds and
provides an attractive drug target. During the asexual blood stage of
infection, an essential function of the apicoplast is to produce the
isoprenoid precursors isopentenyl pyrophosphate (IPP) and
dimethylallyl pyrophosphate (DMAPP) via the MEP (non-mevalonate)
In 1995 the
Genome Project was set up to sequence the genome
of P. falciparum. The genome of its mitochondrion was reported in
1995, that of the nonphotosynthetic plastid known as the apicoplast in
1996, and the sequence of the first nuclear chromosome (chromosome
2) in 1998. The sequence of chromosome 3 was reported in 1999 and the
entire genome was reported on 3 October 2002. The roughly
24-megabase genome is extremely AT-rich (about 80%) and is organised
into 14 chromosomes. Just over 5,300 genes were described. Many genes
involved in antigenic variation are located in the subtelomeric
regions of the chromosomes. These are divided into the var, rif, and
stevor families. Within the genome, there exist 59 var, 149 rif, and
28 stevor genes, along with multiple pseudogenes and truncations. It
is estimated that 551, or roughly 10%, of the predicted
nuclear-encoded proteins are targeted to the apicoplast, while 4.7% of
the proteome is targeted to the mitochondria.
Humans are the intermediate hosts in which asexual reproduction
occurs, and female anopheline mosquitos are the definitive hosts
harbouring the sexual reproduction stage.
Life cycle of Plasmodium
Infection in humans begins with the bite of an infected female
Anopheles mosquito. Out of about 460 species of
more than 70 species transmit falciparum malaria. Anopheles
gambiae is one of the best known and most prevalent vectors,
particularly in Africa.
The infective stage called sporozoites released from the salivary
glands through the proboscis of the mosquito enter the bloodstream
during feeding. The mosquito saliva contains antihemostatic and
anti-inflammatory enzymes that disrupt blood clotting and inhibit the
pain reaction. Typically, each infected bite contains 20-200
sporozoites. The immune system clears the sporozoites from the
circulation within 30 minutes. But a few escape and quickly invade
liver cells (hepatocytes). The sporozoits move in the blood stream
by gliding, which is driven by motor made up of proteins actin and
myosin beneath their plasma membrane.
Liver stage or exo-erythrocytic schizogony
Entering the hepatocytes, the parasite loses its apical complex and
surface coat, and transforms into a trophozoite. Within the
parasitophorous vacuole of the hepatocyte, it undergoes 13-14 rounds
of mitosis and meiosis which produce a syncytial cell (coenocyte)
called a schizont. This process is called schizogony. A schizont
contains tens of thousands of nuclei. From the surface of the
schizont, tens of thousands of haploid (1n) daughter cells called
merozoites emerge. The liver stage can produce up to 90,000
merozoites, which are eventually released into the bloodstream in
parasite-filled vesicles called merosomes.
Blood stage or erythrocytic schizogony
Merozoites use the apicomplexan invasion organelles (apical complex,
pellicle and surface coat) to recognize and enter the host erythrocyte
(red blood cell). The parasite first binds to the erythrocyte in a
random orientation. It then reorients such that the apical complex is
in proximity to the erythrocyte membrane. The parasite forms a
parasitophorous vacuole, to allow for its development inside the
erythrocyte. This infection cycle occurs in a highly synchronous
fashion, with roughly all of the parasites throughout the blood in the
same stage of development. This precise clocking mechanism has been
shown to be dependent on the human host's own circadian rhythm.
Within the erythrocyte, the parasite metabolism depends on the
digestion of hemoglobin. The clinical symptoms of malaria such as
fever, anemia, and neurological disorder are produced during the blood
The parasite can also alter the morphology of the erythrocyte, causing
knobs on the erythrocyte membrane. Infected erythrocytes are often
sequestered in various human tissues or organs, such as the heart,
liver and brain. This is caused by parasite-derived cell surface
proteins being present on the erythrocyte membrane, and it is these
proteins that bind to receptors on human cells. Sequestration in the
brain causes cerebral malaria, a very severe form of the disease,
which increases the victim's likelihood of death.
After invading the erythrocyte, the parasite loses its specific
invasion organelles (apical complex and surface coat) and
de-differentiates into a round trophozoite located within a
parasitophorous vacuole. The young trophozoite (or "ring" stage,
because of its morphology on stained blood films) grows substantially
before undergoing schizogony.
At the schizont stage, the parasite replicates its DNA multiple times
and multiple mitotic divisions occur asynchronously. Each
schizont forms 16-18 merozoites. The red blood cells are ruptured
by the merozoites. The liberated merozoites invade fresh erythrocytes.
A free merozoite is in the bloodstream for roughly 60 seconds before
it enters another erythrocyte.
The duration of each blood stage is approximately 48 hours. This gives
rise to the characteristic clinical manifestations of falciparum
malaria, such as fever and chills, corresponding to the synchronous
rupture of the infected erythrocytes.
Not all of the merozoites divide into schizonts; some get
differentiated into sexual forms, male and female gametocytes. These
gametocytes take roughly 7–15 days to reach full maturity, through
the process called gametocytogenesis. These gametocytes are taken up
by a female
Anopheles mosquito during a blood meal.
The time of appearance of the symptoms from infection (called
incubation period) in P. falciparum infection is 11 days, but may
range from 11 to 14 days. Parasites can be detected from blood samples
by the 10th day after infection (pre-patent period).
Within the mosquito midgut, the female gamete maturation process
entails slight morphological changes, becoming more enlarged and
spherical. The male gametocyte undergoes a rapid nuclear division
within 15 minutes, producing eight flagellated microgametes by a
process called exflagellation. The flagellated microgamete
fertilizes the female macrogamete to produce a diploid cell called a
zygote. The zygote then develops into an ookinete. The ookinete is a
motile cell, capable of invading other organs of the mosquito. It
traverses the peritrophic membrane of the mosquito midgut and crosses
the midgut epithelium. Once through the epithelium, the ookinete
enters the basal lamina, and settles to an immotile oocyst. For
several days, the oocyst undergoes 10 to 11 rounds of cell division to
create a syncytial cell (sporoblast) containing thousands of nuclei.
Meiosis takes place inside the sporoblast to produce over 3,000
haploid daughter cells called sporozoites on the surface of the mother
cell. Immature sporozoites break through the oocyst wall into the
haemolymph. They migrate to the mosquito salivary glands where they
undergo further development and become infective to humans.
Interaction with human immune system
A single anopheline mosquito can transmit hundreds of P. falciparum
sporozoites in a single bite under experimental conditions. But in
nature the number is generally less than 80. The sporozoites do
not enter the blood stream directly and remain in the skin tissue for
2 to 3 hours. About 15–20% sporozoites enter the lymphatic system
where they actiavate dendritic cells, which send them for destruction
by T lymphocytes (CD8+ T cells). At 48 hours after infection,
Plasmodium-specific CD8+ T cells can be detected in the lymph nodes
connected to the skin cells. Most of the sporozites remaining in
the skin tissue are subsequently killed by the innate immune system.
The sporozoite glycoprotein specifically activates mast cells. The
mast cells then produce signalling molecules such as
TNFα and MIP-2,
which activate cell eaters (professional phagocytes) such as
neutrophils and macrophages.
Only small number (0.5-5%) of sporozoites enter the blood stream into
the liver. In the liver, the activated CD8+ T cells from the lymph
bind the sporozoites through the circumsporozoite protein (CSP).
Antigen presentation by dendritic cells in the skin tissue to T cells
is also a crucial process. From this stage onward the parasites
produce different proteins that help in suppressing communication of
the immune cells. Even at the height of the infection when RBCs
are ruptured, the immune signals are not strong enough to activate
macropages or natural killer cells.
Immune system evasion
Although P. falciparum is easily recognized by human immune system
while in the bloodstream, it evades immunity by producing over 2,000
cell membrane antigens The initial infective stage sporozoites
produce circumsporozoite protein (CSP), which binds to
hepatocytes. Binding to and entry into the hepatocytes is aided by
another protein, thrombospondin-related anonymous protein (TRAP).
TRAP and other secretory proteins (including sporozoite microneme
protein essential for cell traversal 1, SPECT1 and SPECT2) from
microneme allow the sporozoite to move through the blood, avoiding
immune cells and penetrating hepatocytes.
During erythrocyte invasion, merozoites release merozoite cap
protein-1 (MCP1), apical membrane antigen 1 (AMA1),
erythrocyte-binding antigens (EBA), myosin A tail domain interacting
protein (MTIP), and merozoite surface proteins (MSPs). Of these
MSPs, MSP1 and MSP2 are primarily responsible for avoiding immune
cells. The virulence of P. falciparum is mediated by erythrocyte
membrane proteins, which are produced by the schizonts and
trophozoites inside the erythrocytes and are displayed on the
PfEMP1 is the most important, capable of acting
as both an antigen and an adhesion molecule.
Main article: Malaria
The clinical symptoms of falciparum malaria are produced by the
rupture of schizont and destruction of erythrocytes. Most of the
patients experience fever (>92% of cases), chills (79%), headaches
(70%), and sweating (64%). Dizziness, malaise, muscle pain, abdominal
pain, nausea, vomiting, mild diarrhea, and dry cough are also
generally associated. High heartrate, jaundice, pallor, orthostatic
hypotension, enlarged liver, and enlarged spleen are also
P. falciparum works via sequestration, a distinctive property not
shared by any other Plasmodium. The mature schizonts change the
surface properties of infected erythrocytes, causing them to stick to
blood vessel walls (cytoadherence). This leads to obstruction of the
microcirculation and results in dysfunction of multiple organs, such
as the brain in cerebral malaria.
P. falciparum is responsible for (almost) all severe human illnesses
and deaths due to malaria, in a condition called complicated or severe
malaria. Complicated malaria occurs more commonly in children under
age 5, and sometimes in pregnant women (a condition specifically
called pregnancy-associated malaria). Women become susceptible to
severe malaria during their first pregnancy. Susceptibility to severe
malaria is reduced in subsequent pregnancies due to increased antibody
levels against variant surface antigens that appear on infected
erythrocytes. But increased immunity in mother increases
susceptibility to malaria in newborn babies.
Distribution and epidemiology
The Z(T) normalized index of temperature suitability for P. falciparum
displayed by week across an average year.
P. falciparum is found in all continents except Europe. According to
the WHO World
Malaria Report 2017, 216 million people suffered from
malaria in 2016, which was an increase from 211 million in 2015.
445,000 people died from it. The infection is most prevalent in
Africa, and accounts for about 90% of the total death. Children under
five years of age are most affected and 70% of deaths occurred in this
age group. 80% of the infection is found in Sub-Saharan Africa, 7% in
the South-East Asia, and 2% in the Eastern Mediterranean. Nigeria has
the highest incidence with 27% of the total global cases. Outside
Africa, India has the highest incidence with 4.5% of the global
burden. Europe is regarded as a malaria-free region. Historically,
the parasite and its disease had been most well known in Europe. But
medical programmes, such as insecticide spraying, drug therapy and
environmental engineering since the early 20th century resulted in
complete eradication in the 1970s. It is estimated that
approximately 2.4 billion people are at constant risk of
See also: History of malaria
In 1640, Huan del Vego first employed the tincture of the cinchona
bark for treating malaria; the native Indians of
Peru and Ecuador had
been using it even earlier for treating fevers. Thompson (1650)
introduced this "Jesuits' bark" to England. Its first recorded use
there was by John Metford of
Northampton in 1656. Morton (1696)
presented the first detailed description of the clinical picture of
malaria and of its treatment with cinchona.
Gize (1816) studied the
extraction of crystalline quinine from the cinchona bark and Pelletier
and Caventou (1820) in
France extracted pure quinine alkaloids, which
they named quinine and cinchonine. The total synthesis of
quinine was achieved by American chemists R.B. Woodward and W.E.
Doering in 1944. Woodward received the Nobel Prize in Chemistry in
Attempts to make synthetic antimalarials began in 1891. Atabrine,
developed in 1933, was used widely throughout the Pacific in World War
II, but was unpopular because of its adeverse effects. In the late
1930s, the Germans developed chloroquine, which went into use in the
North African campaigns. Creating a secret military project called
Mao Zedong encouraged Chinese scientists to find new
antimalarials after seeing the casualties in the Vietnam War. Tu
Youyou discovered artemisinin in the 1970s from sweet wormwood
(Artemisia annua). This drug became known to Western scientists in the
late 1980s and early 1990s and is now a standard treatment. Tu won the
Nobel Prize in Physiology or Medicine in 2015.
According to WHO guidelines 2010, artemisinin-based combination
therapies (ACTs) are the recommended first-line antimalarial
treatments for uncomplicated malaria caused by P. falciparum. WHO
recommends combinations such as artemether/lumefantrine,
The choice of ACT is based on the level of resistance to the
constituents in the combination.
Artemisinin and its derivatives are
not appropriate for monotherapy. As second-line antimalarial
treatment, when initial treatment does not work, an alternative ACT
known to be effective in the region is recommended, such as artesunate
plus tetracycline or doxycycline or clindamycin, and quinine plus
tetracycline or doxycycline or clindamycin. Any of these combinations
is to be given for 7 days. For pregnant women, the recommended
first-line treatment during the first trimester is quinine plus
clindamycin for 7 days. Artesunate plus clindamycin for 7 days is
indicated if this treatment fails. For travellers returning to
nonendemic countries, atovaquone/proguanil, artemether/lumefantrineany
and quinine plus doxycycline or clindamycin are recommended.
For adults, intravenous (IV) or intramuscular (IM) artesunate is
Quinine is an acceptable alternative if parenteral
artesunate is not available.
For children, especially in the malaria-endemic areas of Africa,
artesunate IV or IM, quinine (IV infusion or divided IM injection),
and artemether IM are recommended.
Parenteral antimalarials should be administered for a minimum of 24
hours, irrespective of the patient's ability to tolerate oral
medication earlier. Thereafter, complete treatment is recommended
including complete course of ACT or quinine plus clindamycin or
RTS,S is the only candidate as malaria vaccine to have gone through
clinical trials. Analysis of the results of the phase III trial
(conducted between 2011 and 2016) revealed a rather low efficacy
(20-39% depending on age, with up to 50% in 5–17-month aged babies),
indicating that the vaccine will not lead to full protection and
International Agency for Research on Cancer
International Agency for Research on Cancer (IARC) has classified
malaria due to P. falciparum as Group 2A carcinogen, meaning that the
parasite is probably a cancer-causing agent in humans. Its
association with a blood cell (lymphocyte) cancer called Burkitt's
lymphoma is established. Burkit's lymphoma was discovered by Denis
Burkitt in 1958 from African children, and he later speculated that
the cancer was likely due to certain infectious diseases. In 1964, a
virus, later called Eppstein-Barr virus (EBV) after the discoverers,
was identified from the cancer cells. The virus was subsequently
proved to be the direct cancer agent, and is now classified as Group 1
carcinogen. In 1989, it was realised that EBV requires other
infections such as with malaria to cause lymphocyte transformation. It
was reported that the incidence of
Burkitt's lymphoma decreased with
effective treatment of malaria over several years. The actual role
played by P. falciparum remained unclear for the next two-and-half
decades. EBV had been known to induce lymphocytes to become cancerous
using its viral proteins (antigens such as EBNA-1, EBNA-2, LMP-1, and
LMP2A). From 2014, it became clear that P. falciparum
contributes to the development of the lymphoma. P. falciparum-infected
erythrocytes directly bind to
B lymphocytes through the CIDR1α domain
of PfEMP1. This binding activates toll-like receptors (
TLR7 and TLR10)
causing continuous activation of lymphocytes to undergo proliferation
and differentiation into plasma cells, thereby increasing the
IgM and cytokines. This in turn activates an enzyme
called activation-induced cytidine deaminase (AID), which tends to
cause mutation in the DNA (by double-strand break) of an EBV-infected
lymphocytes. The damaged DNA undergoes uncontrolled replication, thus
making the cell cancerous.
Influence on the human genome
Further information: Genetic resistance to malaria
The high mortality and morbidity caused by P. falciparum has
placed great selective pressure on the human genome. Several genetic
factors provide some resistance to
Plasmodium infection, including
sickle cell trait, thalassaemia traits, glucose-6-phosphate
dehydrogenase deficiency, and the absence of Duffy antigens on red
blood cells. The presence of P. falciparum in human
populations has exerted selective pressure on the human genome. E. A.
Beet, a doctor working in
Southern Rhodesia (now Zimbabwe) had
observed in 1948 that sickle-cell disease was related to lower rate of
malaria infection. This suggestion was reiterated by J. B. S.
Haldane in 1948, who suggested that thalassaemia could provide similar
protection. This hypothesis has since been confirmed and extended
to hemoglobin E, hemoglobin C and
Malaria Atlas Project
List of parasites (human)
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Profile at Scientists Against Malaria
Clinical Identification Case 1
Clinical Identification Case 2
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Control and prevention
Sterile insect technique
Sickle cell anaemia
Diagnosis and treatment
Diagnosis of malaria
Malaria antigen detection tests
Society and malaria
Diseases of poverty
Millennium Development Goals
History of malaria
Malaria Eradication Program
Malaria and the Caribbean
Malaria Atlas Project
Bill and Melinda Gates Foundation
Imagine No Malaria
Malaria No More
Africa Fighting Malaria
Malaria Network Trust
The Global Fund to Fight AIDS, Tuberculosis and Malaria
Protozoan infection: SAR and
Archaeplastida (A07, B50–B54,B58, 007,
Coccidia: Cryptosporidium hominis/Cryptosporidium parvum
Algaemia: Prototheca wickerhamii