Parasite Disease (Malaria)

MALARIA
Disease Name: Malaria

Other name: "Paludism" or Paludeen fever"
Disease Category: Parasite Disease
Disease description: Malaria is a worldwide problem with two-thirds of the world's
population living in malarious areas and if global warming eventuates, this proportion
could increase to three-quarters by 2010. At a conservative estimate there are 250 million
new infections per year. The problem is getting worse because of increasing anti-malaria
drug resistance by parasites, as well as increasing resistance to insecticides by
mosquitoes. It is a vector-borne infectious disease caused by protozoan parasites and
widespread in tropical and subtropical regions, including parts of the Americas, Asia,
and Africa. Each year, there are approximately 515 million cases of malaria, killing
between one and three million people, the majority of whom are young children in Sub-
Saharan Africa.Malaria is commonly associated with poverty, but is also a cause of
poverty and a major hindrance to economic development. The disease is caused by
protozoan parasites
of the genus Plasmodium. This group of human-pathogenic Plasmodium species is
usually referred to as malaria parasites.
Patient with Malaria in Tanzanian malaria Deadly Reign

Malaria parasites are transmitted by female Anopheles mosquitoes.
The parasites multiply within red blood cells, causing symptoms that
include symptoms of anemia , as well as other general symptoms such
as fever, chills, nausea, flu-like illness, and in severe cases, coma and
death. Malaria transmission can be reduced by preventing mosquito
bites with 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. Malaria infections are
treated through the use of antimalarial drugs, such
as quinine orartemisinin derivatives, although drug resistance is
increasingly common.
Types of malaria:
There are 4 types of malaria that infect humans:
• Plasmodium vivax, abbreviated as P.v.
• Plasmodium malariae, abbreviated as P.m.
• Plasmodium ovale, abbreviated as P.o. and
• Plasmodium falciparum, abbreviated as P.f.
Malaria and HIV/AIDS (WHO):

Malaria and HIV are two of the most devastating global health problems of our time.
Together they cause more than 4 million deaths a year. Both are diseases of poverty, and
both are causes of poverty. To a considerable extend, both are concentrated in the same
geographical regions. The resulting co-infection and interaction between the two diseases
have major public health implications.
 HIV-infected people must be considered particularly vulnerable to malaria;
 Antenatal care needs to address both diseases and their interactions;
 Where both diseases occur, more attention must be given to specific diagnosis for
febrile patients.
Source:http://www.who.int/malaria/malariandhivaids.html
Socio-economic effects:
Malaria is not just a disease commonly associated with poverty, but is also a cause of
poverty and a major hindrance to economic development. The disease has been
associated with major negative economic effects on regions where it is widespread. A
comparison of average per capita GDP in 1995, adjusted to give parity of purchasing
power, between malarious and non-malarious countries demonstrates a fivefold
difference ($1,526 USD versus $8,268 USD). Moreover, 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. However, correlation does not demonstrate
causation, and the prevalence is at least partly because these regions do not have the
financial capacities to prevent malaria. 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. 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.
History of Malaria:
Charles Louis Alphonse Laveran Sir Ronald Ross

Malaria has infected humans for over 50,000 years, and may have been a
human pathogen for the entire history of our species. Indeed, close relatives of the human
malaria parasites remain common in chimpanzees, our closest relatives. References to the
unique periodic fevers of malaria are found throughout recorded history, beginning in
2700 BC in China. The term malaria originates from Medieval Italian: mala aria — "bad
air"; and the disease was formerly called ague or marsh fever due to its association with
swamps.
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 this protozoan caused malaria;
the first time protozoa were identified as causing disease. For this and later discoveries,
he was awarded the 1907 Nobel Prize for Physiology or Medicine. The protozoan was
called Plasmodium by the Italian scientists Ettore Marchiafava and Angelo Celli. A year
later, Carlos Finlay, a Cuban doctor treating patients 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 Patrick
Manson on the transmission of filariasis.
However, 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 and isolating malaria parasites from the salivary glands of mosquitoes that had fed
on infected birds. For this work Ross received the 1902 Nobel Prize in Medicine. After
resigning from the Indian Medical Service, Ross worked at the newly
established Liverpool School of Tropical Medicine and directed malaria-control efforts
in Egypt, Panama, Greece and Mauritius. The findings of Finlay and Ross were later
confirmed by a medical board headed by Walter Reed in 1900, and its recommendations
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 this disease.
The first effective treatment for malaria was the bark of cinchona tree, which
contains quinine. This tree grows on the slopes of the Andes, mainly in Peru. This natural
product was used by the inhabitants of Peru to control malaria, and the Jesuits introduced
this practice to Europe during the 1640s where it was rapidly accepted. However, 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.
In the early twentieth century, before antibiotics, patients with syphilis were
intentionally infected with malaria to create a fever, following the work of Julius
Wagner-Jauregg. By accurately controlling the fever with quinine, the effects of both
syphilis and malaria could be minimized. Although some patients died from malaria, this
was preferable to the almost-certain death from syphilis.
Although the blood stage and mosquito stages of the malaria life cycle were identified in
the 19th and early 20th centuries, it was not until the 1980s that the latent liver form of
the parasite was observed. The discovery of this latent form of the parasite finally
explained why people could appear to be cured of malaria but still relapse years after the
parasite had disappeared from their bloodstreams.
Geographical Distribution and impact:
Malaria causes about 400–900 million cases of fever and approximately one to three
million deaths annually this represents at least one death every 30 seconds. The vast
majority of cases occur in children under the age of 5 years; 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. Indeed, if the
prevalence of malaria stays on its present upwards course, the death rate could double in
the next twenty years. 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.
Consequently, the majority of cases are undocumented.
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. 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.
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. The geographic distribution of malaria
within large regions is complex, and malaria-afflicted and malaria-free areas are often
found close to each other. In drier areas, outbreaks of malaria can be predicted with
reasonable accuracy by mapping rainfall. Malaria is more common in rural areas than in
cities; this is in contrast to dengue fever where urban areas present the greater risk. For
example, the cities of Vietnam, Laos and Cambodia are essentially malaria-free, but the
disease is present in many rural regions. By contrast, in Africa malaria is present in both
rural and urban areas, though the risk is lower in the larger cities. The
global endemic levels of malaria have not been mapped since the 1960s. However,
the Wellcome Trust, UK, has funded the Malaria Atlas Project to rectify this, providing a
more contemporary and robust means with which to assess current and future
malaria disease burden.
Symptoms of malaria:
Include fever, shivering, arthralgia (joint pain), vomiting, anemia (caused
by hemolysis), hemoglobinuria, and convulsions. There may be a feeling of tingling in
the skin, particularly with malaria caused by P. falciparum. The classical 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 for P. malariae. 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 which may be related to high intracranial pressure,
children with malaria frequently exhibit abnormal posturing, a sign indicating severe
brain damage. Malaria has been found to cause cognitive impairments, especially in
children. It causes widespread anemia during a period of rapid brain development and
also direct brain damage. This neurologic damage results from cerebral malaria to which
children are more vulnerable.
Severe malaria is almost exclusively caused by P. falciparum infection and usually arises
6-14 days after infection. Consequences of severe malaria includecoma and death if
untreated—young children 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 may cause 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. In the most severe cases of the disease fatality rates can exceed
20%, even with intensive care and treatment. 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. Over the longer term, developmental impairments have been documented in children
who have suffered episodes of severe malaria.
Chronic malaria is seen in both P. vivax and P. ovale, but not in P. falciparum. Here, the
disease can relapse months or years after exposure, due to the presence of latent parasites
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. 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
Pathogen Description:
A plasmodium is also the macroscopic form of the protist known as a slime mould.
Plasmodium is a genus of parasitic protozoa. Infection with this genus is known as
malaria. The parasite always has two hosts in its life cycle: a mosquito vector and a
vertebrate host. Of the 200 known species of Plasmodium, at least 10 species infect
humans. Other species infect other animals, including birds, reptiles and rodents.
The genus Plasmodium was created in 1885 by Marchiafava and Celli. Currently over
200 species are recognized. New species continue to be described.
The genus is currently (2006) in need of reorganization as it has been shown that
parasites belonging to the genera Haemocystis and Hepatocystis appear to be closely
related to Plasmodium. It is likely that other species such as Haemoproteus meleagridis
will be included in this genus once it is revised.
Domain: Eukaryota
Superphylum:Alveolata
Phylum:Apicomplexa
Class:Aconoidasida
Order:Haemosporida
Family:Plasmodiidae
Genus: Plasmodium
Evolution:
The life cycle is probably best understood in terms of its evolution. At the present time
(2007) DNA sequences are available from fewer than sixty species of Plasmodium and
most of these are from species infecting either rodent or primate hosts. The evolutionary
outline given here should be regarded as speculative and subject to revision as data
becomes available.
The Apicomplexa — the phylum to which Plasmodium belongs - are thought to have
originated within the Dinoflagellates — a large group of photosynthetic protozoa. It is
thought that the ancestors of the Apicomplexa were originally prey organisms that
evolved the ability to invade the intestinal cells and subsequently lost their photosynthetic
ability. Many of the species within the Apicomplexia still possess a plastid (the organelle
in which photosynthesis occurs in eukaryotes): some that do not have evidence of plastid
genes within their genome. These plastids - unlike those found in algae - are not
photosynthetic. Its function is not known but there is some suggestive evidence that it
may be involved in reproduction.
Some extant dinoflagelates, however, can invade the bodies of jellyfish and continue to
photosynthesize, which is possible because jellyfish bodies are almost transparent. In
other organisms with opaque bodies this ability would most likely rapidly be lost. The
recent (2008) description of a photosynthetic protist related to the Apicomplexia with a
functional plastid supports this hypothesis.
Current (2007) theory suggests that the genera Plasmodium, Hepatocystis and
Haemoproteus evolved from one or more Leukocytozoon species. Parasites of the genus
Leukocytozoan infect white blood cells (leukocytes), liver and spleen cells and are
transmitted by 'black flies' (Simulium species) — a large genus of flies related to the
mosquitoes.
It is thought that Leukocytozoon evolved from a parasite that spread by the orofaecal
route and which infected the intestinal wall. At some point this parasite evolved the
ability to infect the liver. This pattern is seen in the genus Cryptosporidium to which
Plasmodium is distantly related. At some later point this ancestor developed the ability to
infect blood cells and to survive and infect mosquitoes. Once vector transmission was
firmly established the previous orofecal route of transmission was lost.
Leukocytes, hepatocytes and most spleen cells actively phagocytose particulate matter
making entry into the cell easier for the parasite. The mechanism of entry of Plasmodium
species into erythrocytes is still very unclear taking as it does less than 30 seconds. It is
not yet known if this mechanism evolved before mosquitoes became the main vectors for
transmission of Plasmodium.
The genus Plasmodium evolved (presumably from its Leukocytozoon ancestor) about 130
million years ago, a period that is coincidental with the rapid spread of the angiosperms
(flowering plants). This expansion in the angiosperms is thought to be due to at least one
genomic duplication event. It seems probable that the increase in the number of flowers
led to an increase in the number of mosquitoes and their contact with vertebrates.
Mosquitoes evolved in what is now South America about 230 million years ago. There
are over 3500 species recognised but to date their evolution has not been well worked out
so a number of gaps in our knowledge of the evolution of Plasmodium remain. There is
evidence of a recent expansion of Anopheles gambiae and Anopheles arabiensis
populations in the late Pleistocene in Nigeria.
Presently it seems probable that birds were the first group infected by Plasmodium
followed by the reptiles—probably the lizards. At some point primates and rodents
became infected. The remaining species infected outside these groups seem likely to be
due to relatively recent events.
All Plasmodium species examined to date have 14 chromosomes, one mitochondrion and
one plastid. The chromosomes whose length is known vary from 500 kilobases to 3.5
megabases in length. It is presumed that this is the pattern throughout the genus. The
typical chormosome number of Leukcytozoon has not yet been established.
Mosquito vectors and the Plasmodium life cycle:

The parasite's primary (definitive) hosts and transmission vectors are female mosquitoes
of the Anopheles genus. 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 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. The sporozoites are injected into
the skin, alongside saliva, when the mosquito takes a subsequent blood meal. Only
female mosquitoes feed on blood, 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.
Malaria in humans develops via two phases: an exoerythrocytic (exo=outside;
erythrocutic=red blood cell), i.e., mainly in the liver (hepatic), and an erythrocyte 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. Within 30 minutes of
being introduced into the human host, they infect hepatocytes, multiplying asexually and
asymptomatically for a period of 6–15 days. Once 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, thus beginning 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 hosts 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 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 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. 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.[Although the red 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 perhaps limitless versions within parasite populations.
Like a thief changing disguises or a spy with multiple passports, the parasite switches
between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of
the pursuing immune system.
Some merozoites turn into male and female gametocytes. 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, thereby defining
the mosquito as the definitive host of the disease. New sporozoites develop and travel to
the mosquito's salivary gland, completing the cycle. Pregnant women are especially
attractive to the mosquitoes, and malaria in pregnant women is an important cause
of stillbirths, infant mortality and low birth weight, particularly
in P.falciparum infection, but also in other species infection, such as P. vivax.
The life cycle of malaria parasites in the human body. A mosquito infects a pregnant
woman, first in the liver and then in the bloodstream. First, sporozoites enter the
bloodstream, and migrate to the liver. They infect liver cells (hepatocytes), where they
multiply into merozoites, rupture the liver cells, and escape back into the bloodstream.
Then, the merozoites infect red blood cells (erythrocytes), where they develop into ring
forms, then trophozoites (a feeding stage), then multinucleated schizonts (a reproduction
stage), then merozoites again. The merozoites rupture the blood cells and return to the
bloodstream to infect more blood cells. Only the ring forms circulate in the bloodstream;
the other red blood cells stick (adhere) to the walls (endothelium) of small blood vessels
(venules), preventing the infected red blood cells from traveling to the spleen and being
destroyed.
Malaria Risk: The level of malaria risk may differ according to altitude, population size,
seasons, etc., so be sure to read all of the information for each location. Malaria risk also
changes with time. While updates are being made constantly, this map does not guarantee
lack of malaria risk.
Diagnosis: Malaria must be recognized promptly in order to treat the patient in time and
to prevent further spread of infection in the community.
Malaria should be considered a
potential medical emergency
and should be treated
accordingly. Delay in
diagnosis and treatment is a
leading cause of death in
malaria patients in the United
States.
Fig.: Little girl with suspected malaria seen at the Moronacocha Health Center, in the
outskirts of Iquitos, on the Peruvian Amazon. The clinical suspicion was confirmed when
the blood smear (being taken here by a health worker) confirmed the presence of malaria
parasites.
Malaria can be suspected based on the patient's symptoms and the physical findings at
examination. However, for a definitive diagnosis to be made, laboratory tests must
demonstrate the malaria parasites or their components.
Diagnosis of malaria can be difficult:
Where malaria is not endemic any more (such as the United States), health care providers
are not familiar with the disease. Clinicians seeing a malaria patient may forget to
consider malaria among the potential diagnoses and not order the needed diagnostic tests.
Laboratorians may lack experience with malaria and fail to detect parasites when
examining blood smears under the microscope.
In some areas, malaria transmission is so intense that a large proportion of the population
is infected but not made ill by the parasites. Such carriers have developed just enough
immunity to protect them from malarial illness but not from malarial infection. In that
situation, finding malaria parasites in an ill person does not necessarily mean that the
illness is caused by the parasites.
In many malaria-endemic countries, lack of resources is a major barrier to reliable and
timely diagnosis. Health personnel are undertrained, underequipped and underpaid. They
often face excessive patient loads, and must divide their attention between malaria and
other equally severe infectious diseases such as pneumonia, diarrhea, tuberculosis and
HIV/AIDS.
Clinical Diagnosis:
Clinical diagnosis is based on the patient's symptoms and on physical findings at
examination.
The first symptoms of malaria (most often fever, chills, sweats, headaches, muscle pains,
nausea and vomiting) are often not specific and are also found in other diseases (such as
the "flu" and common viral infections). Likewise, the physical findings are often not
specific (elevated temperature, perspiration, tiredness).
In severe malaria (caused by Plasmodium falciparum), clinical findings (confusion,
coma, neurologic focal signs, severe anemia, respiratory difficulties) are more striking
and may increase the suspicion index for malaria.
Thus, in most cases the early clinical findings in malaria are not typical and need to be
confirmed by a laboratory test.
"Presumptive Treatment":
In highly endemic areas (particularly in Africa), the great prevalence of asymptomatic
infections and lack of resources (such as microscopes and trained microscopists) have led
peripheral health facilities to use "presumptive treatment". Patients who suffer from a
fever that does not have any obvious cause are presumed to have malaria and are treated
for that disease, based only on clinical suspicion, and without the benefit of laboratory
confirmation.
This practice is dictated by practical considerations and allows the treatment of a
potentially fatal disease.
But it also leads frequently to incorrect diagnoses and unnecessary use of antimalarial
drugs. This results in additional expenses and increases the risk of selecting for drug-
resistant parasites.
Microscopic Diagnosis:
Malaria parasites can be identified by examining under the microscope a drop of the
patient's blood, spread out as a "blood smear" on a microscope slide. Prior to
examination, the specimen is stained (most often with the Giemsa stain) to give to the
parasites a distinctive appearance. This technique remains the gold standard for
laboratory confirmation of malaria. However, it depends on the quality of the reagents, of
the microscope, and on the experience of the laboratorian.
Fig.Blood smear stained with Giemsa, showing a white blood cell (on left side) and
several red blood cells, two of which are infected with Plasmodium falciparum (on right
side).
Alter
nate methods for laboratory diagnosis include:
Antigen Detection:
Various test kits are available to detect antigens derived from malaria parasites. Such
immunologic ("immunochromatographic") tests most often use a dipstick or cassette
format, and provide results in 2-15 minutes. These "Rapid Diagnostic Tests" (RDTs)
offer a useful alternative to microscopy in situations where reliable microscopic diagnosis
is not available. Malaria RDTs are currently used in some clinical settings and programs.
However, before malaria RDTs can be widely adopted, several issues remain to be
addressed, including improving their accuracy; lowering their cost; and ensuring their
adequate performance under adverse field conditions. The World Health Organization's
Regional Office for the Western Pacific (WHO/WPRO) provides technical information,
including a list of commercially available malaria RDTs,
at http://www.wpro.who.int/rdt/.
On June 13, 2007, the U.S. Food and Drug Administration (FDA) approved the first RDT
for use in the United States. This RDT is approved for use by hospital and commercial
laboratories, not by individual clinicians or by patients themselves. It is recommended
that all RDTs are followed-up with microscopy to confirm the results and if positive, to
quantify the proportion of red blood cells that are infected. The use of this RDT may
decrease the amount of time that it takes to determine that a patient is infected with
malaria.
Rapid Diagnostic Test:

A Rapid Diagnostic Test (RDT) is an alternate way of quickly establishing the diagnosis
of malaria infection by detecting specific malaria antigens in a person's blood. RDTs have
recently become available in the United States.
Binax NOW is the only brand of malaria RDT approved for use in the United States. The
picture above demonstrates a positive test for Plasmodium falciparum. (Howden BP et
al.)Chronic falciparum malaria causing massive splenomegaly 9 years after leaving an
endemic area.
A blood specimen collected from the patient is applied to the sample pad on the test card
along with certain reagents. After 15 minutes, the presence of specific bands in the test
card window indicate whether the patient is infected with Plasmodium falciparum or one
of the other 3 species of human malaria. It is recommended that the laboratory maintain a
supply of blood containing P. falciparum for use as a positive control.
Advantages:
High quality malaria microscopy is not always immediately available in every clinical
setting where patients might seek medical attention. Although this practice is
discouraged, many healthcare settings either save blood samples for malaria microscopy
until a qualified person is available to perform the test, or send the blood samples to
commercial or reference laboratories. These practices have resulted in long delays in
diagnosis. The laboratories associated with these healthcare settings may now use an
RDT to more rapidly determine if their patients are infected with malaria.
Disadvantages:
The use of the RDT does not eliminate the need for malaria microscopy. The RDT may
not be able to detect some infections with lower numbers of malaria parasites circulating
in the patient’s bloodstream. Also, there is insufficient data available to determine the
ability of this test to detect the 2 less common species of malaria, P. ovale and P.
malariae. Therefore all negative RDT’s must be followed by microscopy to confirm the
result.
In addition, all positive RDTs should also followed by microscopy. The currently
approved RDT detects 2 different malaria antigens; one is specific for P. falciparum and
the other is found in all 4 human species of malaria. Thus, microscopy is needed to
determine the species of malaria that was detected by the RDT. In addition, microscopy is
needed to quantify the proportion of red blood cells that are infected, which is an
important prognostic indicator.
Molecular Diagnosis:
Parasite nucleic acids are detected using polymerase chain reaction (PCR). This
technique is more accurate than microscopy. However, it is expensive, and requires a
specialized laboratory (even though technical advances will likely result in field-operated
PCR machines).
Other techniques related to malaria diagnosis are:
Serology:
Serology detects antibodies against malaria parasites, using either indirect
immunofluorescence (IFA) or enzyme-linked immunosorbent assay (ELISA). Serology
does not detect current infection but rather measures past experience.
Drug Resistance Tests:

Drug resistance tests are performed in specialized laboratories to assess the susceptibility
to antimalarial compounds of parasites collected from a specific patient. Two main
laboratory methods are available:
In vitro tests: The parasites are grown in culture in the presence of increasing
concentrations of drugs; the drug concentration that inhibits parasite growth is used as
endpoint;
Molecular characterization: molecular markers assessed by PCR or gene sequencing
allow also the prediction, to some degree, of resistance to some drugs; however, the
predictive values of these molecular tests are still being evaluated.
Drug-resistant:
The development of resistance to drugs poses one of the greatest threats to malaria
control and has been linked to recent increases in malaria morbidity and mortality. Drug
resistance has been confirmed in only 2 of the 4 human malaria parasite species,
Plasmodium falciparum and P. vivax.
Drug-resistant P. falciparum:
Chloroquine resistant P. falciparum (CRPF) first developed independently in 3 to 4 foci
in Southeast Asia, Oceania , and South America in the late 1950's and early 1960's. Since
then, Chloroquine resistance has spread to nearly all areas of the world where falciparum
malaria is transmitted.
P. falciparum has also developed resistance to nearly all of the other currently available
antimalarial drugs, such as sulfadoxine/ pyrimethamine, mefloquine, halofantrine, and
quinine. Although resistance to these drugs tends to be much less widespread
geographically, in some areas of the world, the impact of multi-drug resistant malaria can
be extensive.
Drug-resistant P. vivax:
Chloroquine resistant P. vivax (CRPV) malaria was first identified in 1989 among
Australians living in or traveling to Papua New Guinea. CRPV has also now been
identified in Southeast Asia, on the Indian subcontinent, and in South America. Vivax
malaria, particularly from Oceania, also exhibits decreased susceptibility to primaquine.
Tests for Drug Resistance:
There are 4 basic methods for testing malaria for drug resistance: in vivo tests, in vitro
tests, molecular characterization, and animal models. Of these, only the first 3 are
routinely done.
In vivo tests: In these tests, patients with clinical malaria are given a treatment dose of an
antimalarial drug under observation and are monitored over time for either failure to clear
parasites or for reappearance of parasites.
In vitro tests: In these tests, blood samples from malaria patients are obtained and the
malaria parasites are exposed to different concentrations of antimalarial drugs in the
laboratory. Some methods call for adaptation of parasites to culture first, while others put
blood directly from patients into the test system.
Molecular characterization: For some drugs (chloroquine, SP and similar drugs,
atovaquone), molecular markers have been identified that confer resistance. Molecular
techniques, such as polymerase chain reaction (PCR) or gene sequencing can identify
these markers in blood taken from malaria-infected pat.
Prevalence and incidence statistics for Malaria:

 Incidence (annual) of Malaria: 1,800 cases annually (1997); 1,666 annual cases
notified in USA 1999 (MMWR 1999)
 Incidence Rate: approx 1 in 151,111 or 0.00% or 1,800 people in USA
Incidence extrapolations for USA for Malaria: 1,799 per year, 149 per month,
34 per week, 4 per day, 0 per hour, 0 per minute, 0 per second.
 Worldwide incidence of Malaria: 300 to 500 million people develop malaria
 Prevalance of Malaria: In the United States, approximately 1,000 cases are
reported annually, which researchers estimate represent only 25 to 50 percent of
actual cases. (Source: excerpt from Microbes in Sickness and in Health -
Publications, National Institute of Allergy and Infectious Diseases: NIAID)
 Worldwide prevalence of Malaria: Each year, 300 to 500 million people
develop malaria and 1.5 to 3 million–mostly children–die, according to the World
Health Organization (WHO). (Source: excerpt from Malaria, NIAID Fact Sheet:
NIAID)
 Incidence statistics about Malaria:
 The following statistics relate to the incidence of Malaria:
 1.39 per 100,000 in Canada 2000
 2.4 new cases per 100,000 population for malaria notified in Australia 2002
(Yohannes K, Roche P, Blumer C et al. 2004, Australia’s Health 2004, AIHW)
 466 new cases of malaria was notified in Australia 2002 (Yohannes K, Roche P,
Blumer C et al. 2004, Australia’s Health 2004, AIHW)
 Malaria incidence statistics for various countries:
 125 registered cases in Argentina 2002 (Regional Core Health Data Initiative, Pan
American Health Organization, 2003)
 928 registered cases in Belize 2002 (Regional Core Health Data Initiative, Pan
 14,276 registered cases in Bolivia 2002 (Regional Core Health Data Initiative,
Pan American Health Organization, 2003)
 349,873 registered cases in Brazil 2002 (Regional Core Health Data Initiative,
 740 registered cases in Canada 2002 (Regional Core Health Data Initiative, Pan
 5 registered cases in Chile 2002 (Regional Core Health Data Initiative, Pan
 195,719 registered cases in Colombia 2002 (Regional Core Health Data Initiative,
 1,021 registered cases in Costa Rica 2002 (Regional Core Health Data Initiative,
 29 registered cases in Cuba 2002 (Regional Core Health Data Initiative, Pan
 1,296 registered cases in the Dominican Republic 2002 (Regional Core Health
Data Initiative, Pan American Health Organization, 2003)
 86,757 registered cases in Ecuador 2002 (Regional Core Health Data Initiative,
 117 registered cases in El Salvador 2002 (Regional Core Health Data Initiative,
 12 registered cases in Guadeloupe 2002 (Regional Core Health Data Initiative,
 35,540 registered cases in Guatemala 2002 (Regional Core Health Data Initiative,
 21,895 registered cases in Guyana 2002 (Regional Core Health Data Initiative,
 17,223 registered cases in Honduras 2002 (Regional Core Health Data Initiative,
 7 registered cases in Jamaica 2002 (Regional Core Health Data Initiative, Pan
 11 registered cases in Martinique 2002 (Regional Core Health Data Initiative, Pan
 4,289 registered cases in Mexico 2002 (Regional Core Health Data Initiative, Pan
 7,466 registered cases in Nicaragua 2002 (Regional Core Health Data Initiative,
 2,244 registered cases in Panama 2002 (Regional Core Health Data Initiative, Pan
 2,778 registered cases in Paraguay 2002 (Regional Core Health Data Initiative,
 1 registered case in Puerto Rico 2002 (Regional Core Health Data Initiative, Pan
 2 registered cases in Saint Lucia 2002 (Regional Core Health Data Initiative, Pan
 13,091 registered cases in Suriname 2002 (Regional Core Health Data Initiative,
 8 registered cases in Trinidad and Tobago (Regional Core Health Data Initiative,
 446 registered cases in the US 2002 (Regional Core Health Data Initiative, Pan
 24 registered cases in Uruguay 2002 (Regional Core Health Data Initiative, Pan
 29,491 registered cases in Venezuela 2002 (Regional Core Health Data Initiative,
Death statistics for Malaria:

 The following are statistics from various sources about deaths and Malaria:
 Malaria death statistics by worldwide region:
 About 1,136,000 deaths from malaria in Africa 2002 (The World Health Report,
WHO, 2004)
 About 1,000 deaths from malaria in The Americas 2002 (The World Health
Report, WHO, 2004)
 About 65,000 deaths from malaria in South East Asia 2002 (The World Health
Report, WHO, 2004)
 About 2,000 deaths from malaria in Europe 2002 (The World Health Report,
WHO, 2004)
 About 57,000 deaths from malaria in Eastern Mediterranean 2002 (The World
Health Report, WHO, 2004)
 About 11,000 deaths from malaria in Western Pacific 2002 (The World Health
Report, WHO, 2004)
Society statistics for Malaria

Hospitalization statistics for Malaria:
 The following are statistics from various sources about hospitalizations and
Malaria:
 0.011% (1,432) of hospital consultant episodes were for plasmodium falciparum
malaria in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 86% of hospital consultant episodes for plasmodium falciparum malaria required
hospital admission in England 2002-03 (Hospital Episode Statistics, Department
of Health, England, 2002-03)
 61% of hospital consultant episodes for plasmodium falciparum malaria were for
men in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 39% of hospital consultant episodes for plasmodium Falciparum malaria were for
women in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 94% of hospital consultant episodes for plasmodium falciparum malaria required
emergency hospital admission in England 2002-03 (Hospital Episode Statistics,
Department of Health, England, 2002-03)
 3.9 days was the mean length of stay in hospitals for plasmodium falciparum
England, 2002-03)
 3 days was the median length of stay in hospitals for plasmodium falciparum
England, 2002-03)
 33 was the mean age of patients hospitalized for plasmodium falciparum malaria
in England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
 81% of hospital consultant episodes for plasmodium falciparum malaria occurred
in 15-59 year olds in England 2002-03 (Hospital Episode Statistics, Department
 0% of hospital consultant episodes for plasmodium falciparum malaria occurred
in people over 75 in England 2002-03 (Hospital Episode Statistics, Department of
Health, England, 2002-03)
 1% of hospital consultant episodes for plasmodium falciparum malaria were
single day episodes in England 2002-03 (Hospital Episode Statistics, Department
 0.009% (4,475) of hospital bed days were for plasmodium falciparum malaria in
England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
 0.002% (275) of hospital consultant episodes were for plasmodium vivax malaria
2002-03)
 79% of hospital consultant episodes for plasmodium vivax malaria required
hospital admission in England 2002-03 (Hospital Episode Statistics, Department
 61% of hospital consultant episodes for plasmodium vivax malaria were for men
2002-03)
 39% of hospital consultant episodes for plasmodium vivax malaria were for
women in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 97% of hospital consultant episodes for plasmodium vivax malaria required
emergency hospital admission in England 2002-03 (Hospital Episode Statistics,
Department of Health, England, 2002-03)
 2.7 days was the mean length of stay in hospitals for plasmodium vivax malaria in
2002-03)
 2 days was the median length of stay in hospitals for plasmodium vivax malaria in
2002-03)
 29 was the mean age of patients hospitalised for plasmodium vivax malaria in
2002-03)
 75% of hospital consultant episodes for plasmodium vivax malaria occurred in
15-59 year olds in England 2002-03 (Hospital Episode Statistics, Department of
 1% of hospital consultant episodes for plasmodium vivax malaria occurred in
people over 75 in England 2002-03 (Hospital Episode Statistics, Department of
 0% of hospital consultant episodes for plasmodium vivax malaria were single day
episodes in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 0.001% (617) of hospital bed days were for plasmodium vivax malaria in England
2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03)
 0.004% (441) of hospital consultant episodes were for unspecified malaria in
2002-03)
 81% of hospital consultant episodes for required hospital admission in England
 61% of hospital consultant episodes for unspecified malaria were for men in
2002-03)
 39% of hospital consultant episodes for unspecified malaria were for women in
2002-03)
 96% of hospital consultant episodes for required emergency hospital admission in
2002-03)
 3 days was the mean length of stay in hospitals for unspecified malaria in England
 2 days was the median length of stay in hospitals for unspecified malaria in
2002-03)
 30 was the mean age of patients hospitalized for unspecified malaria in England
 77% of hospital consultant episodes for unspecified malaria occurred in 15-59
year olds in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 0% of hospital consultant episodes for unspecified malaria occurred in people
over 75 in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 1% of hospital consultant episodes for unspecified malaria were single day
episodes in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
 0.002% (1,082) of hospital bed days were for unspecified malaria in England
The following table attempts to extrapolate the above incidence rate for Malaria to the
populations of various countries and regions.
Country/Region Extrapolated Incidence Population Estimated Used
Malaria in North America (Extrapolated Statistics)
USA 1,943 293,655,4051
Canada 215 32,507,8742
Mexico 694 104,959,5942
Malaria in Central America (Extrapolated Statistics)
Belize 1 272,9452
Guatemala 94 14,280,5962
Nicaragua 35 5,359,7592
Malaria in Caribbean (Extrapolated Statistics)
Puerto Rico 25 3,897,9602
Malaria in South America (Extrapolated Statistics)
Brazil 1,218 184,101,1092
Chile 104 15,823,9572
Colombia 279 42,310,7752
Paraguay 40 6,191,3682
Peru 182 27,544,3052
Venezuela 165 25,017,3872
Malaria in Northern Europe (Extrapolated Statistics)
Denmark 35 5,413,3922
Finland 34 5,214,5122
Iceland 1 293,9662
Sweden 59 8,986,4002
Malaria in Western Europe (Extrapolated Statistics)
Britain (United Kingdom) 398 60,270,708 for UK2
Belgium 68 10,348,2762
France 399 60,424,2132
Ireland 26 3,969,5582
Luxembourg 3 462,6902
Monaco 0 32,2702
Netherlands (Holland) 107 16,318,1992
United Kingdom 398 60,270,7082
Wales 19 2,918,0002
Malaria in Central Europe (Extrapolated Statistics)
Austria 54 8,174,7622
Czech Republic 8 1,0246,1782
Germany 545 82,424,6092
Hungary 66 10,032,3752
Liechtenstein 0 33,4362
Poland 255 38,626,3492
Slovakia 35 5,423,5672
Slovenia 13 2,011,473 2
Switzerland 49 7,450,8672
Malaria in Eastern Europe (Extrapolated Statistics)
Belarus 68 10,310,5202
Estonia 8 1,341,6642
Latvia 15 2,306,3062
Lithuania 23 3,607,8992
Russia 952 143,974,0592
Ukraine 315 47,732,0792
Malaria in the Southwestern Europe (Extrapolated Statistics)
Azerbaijan 52 7,868,3852
Portugal 69 10,524,1452
Spain 266 40,280,7802
Georgia 31 4,693,8922
Malaria in the Southern Europe (Extrapolated Statistics)
Italy 384 58,057,4772
Greece 70 10,647,5292
Malaria in the Southeastern Europe (Extrapolated Statistics)
Albania 23 3,544,8082
Bosnia and Herzegovina 2 407,6082
Bulgaria 49 7,517,9732
Croatia 29 4,496,8692
Macedonia 13 2,040,0852
Romania 147 22,355,5512
Serbia and Montenegro 71 10,825,9002
Malaria in Northern Asia (Extrapolated Statistics)
Mongolia 18 2,751,3142
Malaria in Central Asia (Extrapolated Statistics)
Kazakhstan 100 15,143,7042
Tajikistan 46 7,011,556 2
Uzbekistan 174 26,410,4162
Malaria in Eastern Asia (Extrapolated Statistics)
China 8,595 1,298,847,6242
Hong Kong s.a.r. 45 6,855,1252
Japan 842 127,333,0022
Macau s.a.r. 2 445,2862
North Korea 150 22,697,5532
South Korea 319 48,233,7602
Taiwan 150 22,749,8382
Malaria in Southwestern Asia (Extrapolated Statistics)
Turkey 455 68,893,9182
Malaria in Southern Asia (Extrapolated Statistics)
Afghanistan 188 28,513,6772
Bangladesh 935 141,340,4762
Bhutan 14 2,185,5692
India 7,048 1,065,070,6072
Pakistan 1,053 159,196,3362
Sri Lanka 131 19,905,1652
Malaria in Southeastern Asia (Extrapolated Statistics)
East Timor 6 1,019,2522
Indonesia 1,577 238,452,9522
Laos 40 6,068,1172
Malaysia 155 23,522,4822
Philippines 570 86,241,6972
Singapore 28 4,353,8932
Thailand 429 64,865,5232
Vietnam 547 82,662,8002
Malaria in the Middle East (Extrapolated Statistics)
Gaza strip 8 1,324,9912
Iran 446 67,503,2052
Iraq 167 25,374,6912
Israel 41 6,199,0082
Jordan 37 5,611,2022
Kuwait 14 2,257,5492
Lebanon 24 3,777,2182
Saudi Arabia 170 25,795,9382
Syria 119 18,016,8742
United Arab Emirates 16 2,523,9152
West Bank 15 2,311,2042
Yemen 132 20,024,8672
Malaria in Northern Africa (Extrapolated Statistics)
Egypt 503 76,117,4212
Libya 37 5,631,5852
Sudan 259 39,148,1622
Malaria in Western Africa (Extrapolated Statistics)
Congo Brazzaville 19 2,998,0402
Ghana 137 20,757,0322
Liberia 22 3,390,6352
Niger 75 11,360,5382
Nigeria 117 12,5750,3562
Senegal 71 10,852,1472
Sierra leone 38 5,883,8892
Malaria in Central Africa (Extrapolated Statistics)
Central African Republic 24 3,742,4822
Chad 63 9,538,5442
Congo Kinshasa 385 58,317,0302
Rwanda 54 8,238,6732
Malaria in Eastern Africa (Extrapolated Statistics)
Ethiopia 472 71,336,5712
Kenya 218 32,982,1092
Somalia 54 8,304,6012
Tanzania 238 36,070,7992
Uganda 174 26,390,2582
Malaria in Southern Africa (Extrapolated Statistics)
Angola 72 10,978,5522
Botswana 10 1,639,2312
South Africa 294 44,448,4702
Swaziland 7 1,169,2412
Zambia 72 11,025,6902
Zimbabwe 24 1,2671,8602
Malaria in Oceania (Extrapolated Statistics)
Australia 131 19,913,1442
New Zealand 26 3,993,8172
Papua New Guinea 35 5,420,2802
Source: http://www.wrongdiagnosis.com/m/malaria/stats-country.htm
Plasmodium Falciparum
Plasmodium falciparum is a protozoan parasite, one of the species of Plasmodium that

cause malaria in humans. It is transmitted by Anopheles mosquitoes. P. falciparum is the
most dangerous of these infections as P. falciparum malaria has the highest rates of
complications and mortality. In addition it accounts for 80% of all human malarial
infections and 90% of the deaths. It is more prevalent in sub-Saharan Africa than in other.
Taxonomic Classification:
regions of the world.

Kingdom:Protista
Phylum:Apicomplexa
Class:Aconoidasida
Order:Haemosporida
Family:Plasmodiidae
Genus:Plasmodium
Species: P. falciparum
Blood smear of Plasmodium falciparum
Life Cycle:
Plasmodium falciparum has a complicated life-cycle, requiring both a human and a

mosquito host, and differentiating multiple times during its transmission/infection
process.
Human Infection:
P. falciparum is transmitted to humans by the females of the Anopheles species of
mosquito. There are about 460 species of Anopheles mosquito, but only 68 transmit
malaria. Anopheles gambiae is one of the best malaria vectors since it is long-lived,
prefers feeding on humans, and lives in areas near human habitation. A. gambiae is found
in Africa.
Prior to transmission, Plasmodium falciparum resides within the salivary glad of the
mosquito. The parasite is in its sporozoite stage at this point. As the mosquito takes its
blood meal, it injects a small amount of saliva into the skin wound. The saliva contains
antihemostatic and anti-inflammatory enzymes that disrupt the clotting process and
inhibit the pain reaction.Typically, each infected bite contains 5-200 sporozoites which
proceed to infect the human vector.Once in the human bloodstream, the sporozoites only
circulate for a matter of minutes before infecting liver cells.
Liver Stage:
After circulating in the bloodstream, the P. falciparum sporozoites enter hepatocytes. At
this point, the parasite loses its apical complex and surface coat, and transforms into a
trophozoite. Within the parasitophorous vacuole of the hepatocyte, P. falciparum
undergoes schizogonic development. In this stage, nucleus divides multiple times with a
concomitant increase in cell size, but without cell segmentation. This exoerythrocytic
schizogony stage of P. falciparum has a minimum duration of roughly 5.5 days. After
segmentation, the parasite cells are differentiated into merozoites.
After maturation, the merozoites are released from the hepatocytes and enter the
erythrocytic portion of their life-cycle. Note that these cells do not reinfect hepatocytes.
Merozoite:
After release from the hepatocytes, the merozoites enter the bloodstream prior to
infecting red blood cells. At this point, the merozoites are roughly 1.5 μm in length and 1
μm in diameter, and use the apicomplexan invasion organelles (apical complex, pellicle
and surface coat) to recognize and enter the host erythrocyte.
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. A tight junction is
formed between the parasite and erythrocyte. As it enters the red blood cell, the parasite
forms a parasitophorous vesicle, to allow for its development inside the erythrocyte.
Trophozoite:
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 in the red blood cell cytoplasm. The young trophozoite (or
"ring" stage, because of its morphology on stained blood films) grows substantially
before undergoing schizogonic division.
Schizont:
At the schizont stage, the parasite replicates its DNA multiple times without cellular
segmentation. These schizonts then undergo cellular segmentation and differentiation to
form roughly 16-18 merozoite cells in the erythrocyte.The merozoites burst from the red
blood cell, and proceed to infect other erythrocytes. The parasite is in the bloodstream for
roughly 60 seconds before it has entered another 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.Specifically, human body temperature changes, as a result of the circadian
rhythm, seem to play a role in the development of P. falciparum within the erythrocytic
stage.
Within the red blood cell, the parasite metabolism depends greatly on the digestion of
hemoglobin.
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 red blood cell 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.The parasite can also alter the
morphology of the red blood cell, causing knobs on the erythrocyte membrane.
Plasmodium erythrocytic cycle
Gametocyte Differentiation:
During the erythrocytic stage, some merozoites develop into male and female
gametocytes. This process is called gametocytogenesis.The specific factors and causes
underlying this sexual differentiation are largely unknown. These gametocytes take
roughly 8-10 days to reach full maturity. Note that the gametocytes remain within the
erythrocytes until taken up by the mosquito host.
Mosquito Stage:
P. falciparum is taken up by the female Anopheles mosquito as it takes its bloodmeal

from an infected human.
Gametogenesis:
Upon being taken up by the mosquito, the gametocytes leave the erythrocyte shell and
differentiate into gametes. The female gamete maturation process entails slight
morphological changes, as it becomes enlarged and spherical. On the other hand, the
male gamete maturation involves significant morphological development. The male
gamete's DNA divides three times to form eight nuclei. Concurrently, eight flagella are
formed. Each flagella pairs with a nucleus to form a microgamete, which separates from
the parasite cell. This process is referred to as exflagellation.
Gametogenesis has been shown to be caused by: 1) a sudden drop in temperature upon
leaving the human host, 2) a rise in pH within the mosquito, and 3) xanthurenic acid
within the mosquito.
Fertilization:
Fertilization of the female gamete by the male gamete occurs rapidly after
gametogenesis. The fertilization event produces a zygote. The zygote then develops into
an ookinete. The zygote and ookinete are the only diploid stages of P. falciparum.
Ookinete:
The diploid ookinete is an invasive form of P. falciparum within the mosquito. It

traverses the peritrophic membrane of the mosquito midgut and cross the midgut
epithelium. Once through the epithelium, the ookinete enters the basil lamina, and forms
an oocyst.
During the ookinete stage, genetic recombination can occur. This takes place if the
ookinete was formed from male and female gametes derived from different populations.
This can occur if the human host contained multiple populations of the parasite, or if the
mosquito fed of multiple infected individuals within a short time-frame.
Sporogony:
Over the period of a 1-3 weeks, the oocyst grows to a size of tens to hundreds of microns.
During this time, multiple nuclear divisions occur. After oocyst maturation is complete,
the oocyst divides to form multiple haploid sporozoites. Immature sporozoites break
through the oocyst wall into the haemolymph. The sporozoites then migrate to the
salivary glands an complete their differentiation. Once mature, the sporozoites can
proceed to infect a human host during a subsequent mosquito bite.
Genome:
The genome of Plasmodium falciparum (clone 3D7) was fully sequenced in 2002. The
parasite has a 23 megabase genome, divided into 14 chromosomes.The genome codes for
approximately 5,300 genes. About 60% of the putative proteins have little or no
similarity to proteins in other organisms, and thus currently have no functional
assignment. It is estimated 52.6% of the genome is a coding region, with 53.9% of the
putative genes containing at least one intron.
Haploid/Diploid:
It is haploid during nearly all stages of its life-cycle, except for a brief period after
fertilization when it is diploid from the ookinete to sporogenic stages within the mosquito
gut.
AT Richness:
The P. falciparum genome has an AT content of roughly 80.6%.Within the intron and
intergenic regions, this AT composition rises to roughly 90%. The putative exons contain
an AT content of 76.3%. The parasite's AT content is very high in comparison to other
organisms. For example, the entire genomes of Saccharomyces cerevisiae and
Arabidopsis thaliana have AT contents of 62% and 65%, respectively.
Promoters:
Subtelomeric regions:
The subtelomeric regions of P. falciparum chromosomes show a high degree of

conservation within the genome, and contain significant amounts of repeated structure.
These conserved regions can be divided into five subtelomeric blocks. The blocks contain
tandem repeats in addition to non-repetitive regions.
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.
Transcriptome:
A transcriptome analysis has been conducted on the intraerythrocytic development cycle

of P. falciparum.Roughly 60% of the genome is transcriptionally active during this
portion of the parasite's life cycle. Whereas many genes appear to have stable mRNA
levels throughout the cycle, many of the genes are transcriptionally regulated in a
continuous cascade.
The transition from early trophozoite to trophozoite to schizont correlates with the
ordered induction of genes related to transcription/translation machinery, metabolic
synthesis, energy metabolism, DNA replication, protein degradation, plastid functions,
merozoite invasion, and motility.
Closely adjacent genes along the chromosome do not exhibit common transcription
characteristics. Thus, genes are likely individually regulated along the parasite
chromosome.
Conversely, the apicoplast genome is polycistronic and most of its genes are coexpressed
during the intraerythrocytic development cycle.
Proteome:
There are 5,268 predicted proteins in Plasmodium falciparum, and roughly 60% share
little or no similarity to proteins in other organisms and thus are without functional
assignment. Of the predicted proteins, 31% contain at least one transmembrane domain,
and 17.3% have a signal peptide or signal anchor.
It is estimated that 10.4% of the proteome is targeted to the apicoplast.
It is estimated that 4.7% of the proteome is targeted to the mictochondria.
The parasite has different subsets of its proteome expressed during various stages of its
developmental cycle.In one study, of the 2,415 proteins were identified in four
stages(sporozoite, merozoite, trophozoite, gametocyte), representing 46% of the
theoretical number of proteins.Only 6% of the proteins were found in all of the four
stages. Of the proteins found, 51% were annotated as hypothetical proteins.
Merozoites contained high levels of cell recognition and invasion proteins. Trophozoites
contained proteins implicated in erythrocyte remodeling and hemoglobin digestion.
Gametocytes contained high amounts of gametocyte-specific transcription factors and
cell cycle/DNA processing proteins. The gametocytes had low levels of polymorphic
surface antigens. Sporozoites contained large amounts of proteins related to invasion, as
well as members of the var and rif families.
Metabolism:
While all of the metabolic pathways of Plasmodium falciparum have yet to be fully
elucidated, the presence and components of many can be predicted through genomic
analysis.
Hemoglobin metabolism:
During the erythrocytic stage of the parasite's life cycle, it uses intracellular hemoglobin
as a food source. The protein is broken down into peptides, and the heme group is
released and detoxified by biocrystallization in the form of hemozoin.
Heme biosynthesis by the parasite has been reported.

Carbohydrate metabolism:
During erythrocytic stages, the parasite produces its energy mainly through anaerobic
glycolysis, with pyruvate being converted into lactate.
Genes encoding for the TCA cycle enzymes are present in the genome, but it is unclear
whether the TCA cycle is used for oxidation of glycolytic products to be used for energy
production, or for metabolite intermediate biosynthesis.It has been hypothesized that the
main function of the TCA cycle in P. falciparum is for production of succinyl-CoA, to be
used in heme biosynthesis.
Genes for nearly all of the pentose phosphate pathway enzymes have been identified
from the genome sequence.
Protein metabolism:
It has been hypothesized that the parasite obtains all, or nearly all, of its amino acids by
salvaging from the host or through the degradation of hemoglobin. This is supported by
the fact that genomic analysis has found no enzymes necessary for amino acid
biosynthesis, except for glycine-serine, cysteine-alanine, aspartate-asparagine, proline-
ornithine, and glutamine-glutamate interconversions.
Lipid metabolism:
Nucleotide metabolism
P. falciparum is unable to biosynthesize purines.Instead, the parasite is able to transport

and interconvert host purines.
Conversely, the parasite can produce pyrimidines de novo using glutamine, bicarbonate,
and aspartate.
Human Immune System Evasion
Variable Genes
var family:
The var genes encode for the P. falciparum erythrocyte membrane protein 1 (PfEMP1)
proteins. The genes are found in the subtelomeric regions of the chromosomes. There
exist an estimated 59 var genes within the genome.
The proteins encoded by the var genes are ultimately transported to the erythrocyte
membrane and cause the infected erythrocytes to adhere to host endothelial receptors.
Due to transcriptional switching between var genes, antigenic variation occurs which
enables immune evasion by the parasite.
rif family:
The rif genes encode for repetitive interspersed family (rifin) proteins. The genes are
found in the subtelomeric regions of the chromosomes. There exist an estimated 149 rif
genes within the genome.
Rifin protein are ultimately transported to the erythrocyte membrane. The function of
these proteins is currently unknown.
stevor family:
The stevor genes encode for the sub-telomeric variable open reading frame (stevor)
proteins. The genes are found in the subtelomeric regions of the chromosomes. There
exist an estimated 28 stevor genes within the genome.
The function of the stevor proteins is currently unknown.
Microscopic appearance:
Among medical professionals, the preferred method to diagnose malaria and determine
which species of Plasmodium is causing the infection is by examination of a blood film
microscopically in a laboratory. Each species has distinctive physical characteristics that
are apparent under a microscope. In P. falciparum, only early trophozoites and
gametocytes are seen in the peripheral blood. It is unusual to see mature trophozoites or
schizonts in peripheral blood smears as these are usually sequestered in the tissues. The
parasitised erythrocytes are not enlarged and it is common to see cells with more than one
parasite within them (multiply parasitised erythrocytes). Occasionally, faint comma-
shaped red dots are seen on the red cell surface called "Maurer's dots". The comma
shaped dots can also appear as pear shaped blotches.
Treatment and drug resistance:
Attempts to make synthetic antimalarials began in 1891. Atabrine was developed in 1928,
was used widely throughout the Pacific in World War II but was deeply unpopular
because of the yellowing of the skin it caused. In the late 1930s, the Germans developed
chloroquine, which went into use in the North African campaigns. Mao Zedong
encouraged Chinese scientists to find new antimalarials after seeing the casualties in the
Vietnam War. Artemisinin was discovered in the 1970s based on a medicine described in
China in the year 340. This new drug became known to Western scientists in the late
1980s and early 1990s and is now a standard treatment. In 1976 P. falciparum was
successfully cultured in vitro for the first time which facilitated the development of new
drugs substantially.
Vaccination:
Although an antimalarial vaccine is urgently needed, infected individuals never develop a
sterilizing (complete) immunity, making the prospects for such a vaccine dim. The
parasites live inside cells, where they are largely hidden from the immune response.
Infection has a profound effect on the immune system including immune suppression.
Dendritic cells suffer a maturation defect following interaction with infected erythrocytes
and become unable to induce protective liver-stage immunity. Infected erythrocytes
directly adhere to and activate peripheral blood B cells from nonimmune donors. The var
gene products, a group of highly expressed surface antigens, bind the Fab and Fc
fragments of human immunoglobulins in a fashion similar to protein A to Staphylococcus
aureus and this may offer some protection to the parasite from the human immune
system. Despite the poor prospects for a fully protective vaccine, it may be possible to
develop a vaccine that would reduce the severity of malaria for children living in endemic
areas.
Plasmodium vivax:
The parasite Plasmodium vivax is the most frequent and widely distributed cause of
benign, but recurring (tertian), malaria. It is one of four species of parasite that commonly
cause malaria infection in humans. It is less virulent than Plasmodium falciparum, the
deadliest of the four, and seldom fatal. P. vivax is passed on by the female Anopheles
mosquito, since it is the only sex of the species that bites.
Kingdom:Protista
Phylum:Apicomplexa
Class:Aconoidasida
Order:Haemosporida
Family:Plasmodiidae
Genus:Plasmodium
Species:P. vivax
Mature P. vivax trophozoite

Epidemiology :
Plasmodium vivax is found mainly in Asia, Latin America, and in some parts of Africa.
P. vivax can cause death due to enlarged spleen, but more often it causes debilitating, but
not deadly, symptoms.
Treatment:
Chloroquine remains the treatment of choice for vivax malaria, except in Indonesia's Irian
Jaya (Western New Guinea) region and the geographically contiguous Papua New
Guinea, where chloroquine resistance is common (up to 20% resistance). When
chloroquine resistance is common or when chloroquine is contraindicated, then
artesunate is the drug of choice, except in the U.S. where it is not approved for
use;mefloquine is a good alternative and in some countries is more readily
available.Atovaquone-proguanil is an effective alternative in patients unable to tolerate
chloroquine.Quinine may be used to treat vivax malaria but is associated with inferior
outcomes.
32 to 100% of patients will relapse following successful treatment of P. vivax infection if

a radical cure (eradication of liver stages) is not given. Eradication of the liver stages is
achieved by giving primaquine, after checking the patients G6PD status to reduce the risk
of haemolysis. Recently, this point has taken particular importance for the increased
incidence of vivax malaria among travelers.
Eradication Efforts in Korea:
P. vivax is the only indiginous malaria parasite on the Korean peninsula. In the years
following the Korean War (1950-53), malaria-eradication campaigns successfully
reduced the number of new cases of the disease in North Korea and South Korea. In
1979, World Health Organization declared the Korean vivax malaria-free but the disease
unexpectedly re-emerged in the late 1990s and still persists today. Several factors
contributed to the re-emergence of the disease, including reduced emphasis on malaria
control after 1979, floods and famine in North Korea, emergence of drug resistance and
possibly global warming. Most cases are identified along the Korean Demilitarized Zone.
As such, vivax malaria offers the two Koreas a unique opportunity to work together on an
important health problem that affects both countries.
Biology:
P. vivax can reproduce both asexually and sexually, depending on its life cycle stage.
Asexual forms:
• Immature trophozoites (Ring or signet-ring shaped), about 1/3 of the diameter of a
RBC.
• Mature trophozoites: Very irregular and delicate (described as amoeboid); many
pseudopodial processes seen. Presence of fine grains of brown pigment (malarial
pigment) or hematin probably derived from the haemoglobin of the infected red
blood cell.
• Schizonts (also called meronts): As large as a normal red cell; thus the parasitized
corpuslce becomes distended and larger than normal. there are about sixteen
merozoites.
Sexual forms: Gametocytes: Round. The gametocytes of P. vivax are commonly found in
the peripheral blood at about the end of the first week of parasitemia.
Life Cycle
The incubation period for the infection usually ranges from ten to seventeen days and
sometimes up to a year. Persistent liver stages allow relapse up to five years after
elimination of red blood cell stages and clinical cure.
Human Infection:
Liver Stage
The P. vivax sporozoite enters a hepatocyte and begins its exoerythrocytic schizogony
stage. This is characterized by multiple rounds of nuclear division without cellular
segmentation. After a certain number of nuclear divisions, the parasite cell will segment
and merozoites are formed.
There are situations where some of the sporozoites do not immediately start to grow and
divide after entering the hepatocyte, but remain in a dormant, hypnozoite stage for weeks
or months. The duration of latency is variable from one hypnozoite to another and the
factors that will eventually trigger growth are not known; this explains how a single
infection can be responsible for a series of waves of parasitaemia or "relapses".Different
strains of P. vivax have their own characteristic relapse pattern and timing.
Erythrocytic Cycle:
P. vivax preferentially penetrates young red blood cells (reticulocytes). In order to

achieve this, merozoites have two proteins at their apical pole (PvRBP-1 and PvRBP-2).
The parasite uses the Duffy blood group antigens (Fya and Fyb) as receptors to penetrate
red blood cells. These antigens do not occur in the majority of humans in West Africa
[phenotype Fy (a-b-)]. As a result P. vivax does not occur in West Africa.[15]
Microscopically, the parasitised red blood cell is up to twice as large as a normal red cell
and Schüffner's stippling (also known as Schüffner's dots or Schüffner's granules) is seen
on the infected cell's surface, the spotted appearance of which varies in color from light
pink, to red, to red-yellow, as coloured with Romanovsky stains. The parasite within it is
often wildly irregular in shape (described as "amoeboid"). Schizonts of P. vivax have up
to twenty merozoites within them. It is rare to see cells with more than one parasite
within them. Merozoites will only attach to immature blood cell (reticulocytes) and
therefore it is unusual to see more than 3% of all circulating erythrocytes parasitised.
Laboratory Considerations:
P. vivax and P. ovale that has been sitting in EDTA for more than half-an-hour before the
blood film is made will look very similar in appearance to P. malariae, which is an
important reason to warn the laboratory immediately when the blood sample is drawn so
they can process the sample as soon as it arrives. Blood films are preferably made within
half-an-hour of the blood being drawn and must certainly be made within an hour of the
blood being drawn.
Plasmodium ovale:
Plasmodium ovale is a species of parasitic protozoa that causes tertian malaria in

humans. It is closely related to Plasmodium falciparum and Plasmodium vivax, which are
responsible for most malaria. It is rare compared to these two parasites, and substantially
less dangerous than P. falciparum.
Kingdom: Protista
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemosporida
Family: Plasmodiidae
Genus: Plasmodium
Species: P. ovale
Plasmodium ovale trophozoite, Giemsa stain.
Epidemiology:
P. ovale is very limited in its range. It is endemic mainly to West Africa, the Philippines,
eastern Indonesia, and Papua New Guinea.
Diagnosis:
The microscopic appearance of P. ovale is very similar to that of P. vivax and if there are
only a small number of parasites seen, it may be impossible to distinguish the two species
on morphological grounds alone. There is no difference between the medical treatment of
P. ovale and P. vivax, and therefore some laboratory diagnoses report "P. vivax/ovale",
which is perfectly acceptable as treatment for the two are very similar. Schüffner's dots
are seen on the surface of the parasitised red blood cell, but these are larger and darker
than in P. vivax and are sometimes called "James's dots". About twenty percent of the
parasitized cells are oval in shape (hence the species name) and some of the oval cells
also have fimbriated edges (the so-called "comet cell"). The mature schizonts of P. ovale
never have more than twelve nuclei within them and this is the only reliable way of
distinguishing between the two species.
they can process the sample as soon as it arrives.
Treatment:
Standard treatment is concurrent treatment with chloroquine and primaquine. The

combination atovaquone-proguanil may be used in those patients who are unable to take
chloroquine for whatever reason.
Biology:
Life Cycle:
Human Infection:
Liver Stage
The P. ovale sporozoite enters a hepatocyte and begins its exoerythrocytic schizogony
stage. This is characterized by multiple rounds of nuclear division without cellular
segmentation. After a certain number of nuclear divisions, the parasite cell will segment
and merozoites are formed.
There are situations where some of the sporozoites do not immediately start to grow and
divide after entering the hepatocyte, but remain in a dormant, hypnozoite stage for weeks
or months. The duration of latency is variable from one hypnozoite to another and the
factors that will eventually trigger growth are not known; this explains how a single
infection can be responsible for a series of waves of parasitaemia or "relapses".
Erythrocytic Cycle:
While similar to P. vivax, P. ovale is able to infect individuals who are negative for the
Duffy blood group, which is the case for many residents of sub Saharan Africa. This
explains the greater prevalence of P. ovale (rather than P. vivax) in most of Africa.
Plasmodium malariae
Plasmodium malariae is a parasitic protozoa that causes malaria in humans and animals.
It is closely related to Plasmodium falciparum and Plasmodium vivax which are
responsible for most malarial infection. While found worldwide, it is a so-called "benign
malaria" and is not nearly as dangerous as that produced by P. falciparum or P. vivax. P.
malariae causes fevers that recur at approximately three-day intervals (a quartan fever),
longer than the two-day (tertian) intervals of the other malarial parasites.\
Kingdom: Protista
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemosporida
Family: Plasmodiidae
Genus: Plasmodium
Species: P. malariae
Giemsa-stained micrograph of a mature Plasmodium malariae schizont
Signs and symptoms:
Plasmodium malariae causes a long-lasting, chronic infection that in some cases can last
a lifetime. In some patients P. malariae can cause serious complications such as the
nephrotic syndrome.
Biology
Life cycle:
P. malariae is the only human malaria parasite that causes fevers that recur at
approximately three-day intervals (therefore occurring evey fourth day, a quartan fever),
longer than the two-day (tertian) intervals of the other malarial parasites.
Human Infection:
Liver Stage:
Within the hepatocytes, the exoerythrocytic schizogony stage of P. malariae has a
minimum duration of roughly 15 days.
Erythrocytic Cycle:
The total length of the intraerythrocytic development is roughly 72 hours for P. malariae.
At the schizont stage, after schizogonic division, there are roughly 6-8 parasite cells in
the erythrocyte.
Sexual Stage
Mosquito Stage
Laboratory considerations:
they can process the sample as soon as it arrives.
Microscopically, the parasitised red blood cell (erythrocyte) is never enlarged and may
even appear smaller than that of normal red blood cells. The cytoplasm is not decolorized
and no dots are visible on the cell surface. The food vacuole is small and the parasite is
compact. Cells seldom host more than one parasite. Band forms, where the parasite forms
a thick band across the width of the infected cell, are characteristic of this species (and
some would say is diagnostic). Large grains of malarial pigment are often seen in these
parasites: more so than any other Plasmodium species. 8 merozoites
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Parasite Disease (Malaria)

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Parasite Disease (Malaria)

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MALARIA

Disease Name: Malaria

Patient with Malaria in Tanzanian malaria Deadly Reign

Malaria and HIV/AIDS (WHO):

Charles Louis Alphonse Laveran Sir Ronald Ross

Geographical Distribution and impact:

Mosquito vectors and the Plasmodium life cycle:

Rapid Diagnostic Test:

Drug Resistance Tests:

Prevalence and incidence statistics for Malaria:

Death statistics for Malaria:

Society statistics for Malaria

Plasmodium falciparum is a protozoan parasite, one of the species of Plasmodium that

regions of the world.

Blood smear of Plasmodium falciparum

Plasmodium falciparum has a complicated life-cycle, requiring both a human and a

Plasmodium erythrocytic cycle

P. falciparum is taken up by the female Anopheles mosquito as it takes its bloodmeal

The diploid ookinete is an invasive form of P. falciparum within the mosquito. It

The subtelomeric regions of P. falciparum chromosomes show a high degree of

A transcriptome analysis has been conducted on the intraerythrocytic development cycle

It is estimated that 10.4% of the proteome is targeted to the apicoplast.

It is estimated that 4.7% of the proteome is targeted to the mictochondria.

Heme biosynthesis by the parasite has been reported.

P. falciparum is unable to biosynthesize purines.Instead, the parasite is able to transport

Human Immune System Evasion

The function of the stevor proteins is currently unknown.

Treatment and drug resistance:

Mature P. vivax trophozoite

32 to 100% of patients will relapse following successful treatment of P. vivax infection if

Eradication Efforts in Korea:

P. vivax preferentially penetrates young red blood cells (reticulocytes). In order to

Plasmodium ovale is a species of parasitic protozoa that causes tertian malaria in

Plasmodium ovale trophozoite, Giemsa stain.

Standard treatment is concurrent treatment with chloroquine and primaquine. The

Giemsa-stained micrograph of a mature Plasmodium malariae schizont

Signs and symptoms:

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