Plasmodium vivax
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Mature P. vivax trophozoite
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P.
vivax
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Plasmodium
vivax is a protozoal parasite and a human pathogen. The most frequent and
widely distributed cause of recurring (Benign tertian) malaria, P. vivax is one of the four
species of malarial parasite that commonly infect humans. It is less virulent
than Plasmodium
falciparum, which is the deadliest of the four, and is seldom
fatal. P. vivax is carried by the female Anopheles mosquito, since it is the
only female of the species that bites.
Health
Epidemiology
P. vivax is found
mainly in the United States, Latin America, and in some parts of Africa. P.
vivax can cause death due to splenomegaly (a pathologically enlarged
spleen), but more often it causes debilitating – but non-fatal – symptoms.[1][2] Overall it accounts for 65% of
malaria cases in Asia and South America.
Treatment
Chloroquine remains the treatment of choice
for vivax malaria,[3] 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). Chloroquine resistance is an increasing problem in other parts of
the world, such as Korea,India.[4]
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.[5] Where an artemisinin-based
combination therapy has been adopted as the first-line treatment for
P. falciparum malaria, it may also be
used for P. vivax malaria in combination with primaquine for radical cure.[3] An exception is artesunate plus sulfadoxine-pyrimethamine (AS+SP), which is not
effective against P. vivax in many places.[3] Mefloquine is a good alternative and in
some countries is more readily available.[6] Atovaquone-proguanil is an effective
alternative in patients unable to tolerate chloroquine.[7] Quinine may be used to treat vivax
malaria but is associated with inferior outcomes.
Thirty-two to
100% of patients will relapse following successful treatment of P. vivax
infection if a radical cure (eradication of liver stages) is not given.[8][9][10] Eradication of the liver stages
is achieved by giving primaquine, after
checking the patients G6PD status to reduce the risk of haemolysis.[11] However, in severe G6PD
deficiency, primaquine is contraindicated and should not be used.[3] Recently, this point has taken
particular importance for the increased incidence of vivax malaria among
travelers.[12] At least a 14-day course of
primaquine is required for the radical treatment of P. vivax.[3]
Eradication
efforts in Korea
P. vivax is the only
indigenous 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 peninsula 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.[13][14]
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 corpuscle 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.
It has been
suggested that P. vivax has horizontally
acquired genetic material from humans. [15]
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
The infection
of Plasmodium vivax takes place in human when an infected female
anopheles mosquito sucks blood from a healthy person. During feeding, the
mosquito injects saliva to prevent blood clotting (along with sporozoites),
thousands of sporozoites are inoculated into human blood; within a half-hour
the sporozoites reach the liver. There they enter hepatic cells, transform into
the tropozoite form and feed on hepatic cells, and reproduce asexually. This
process gives rise to thousands of merozoites (plasmodium daughter cells) in
the circulatory system and the liver.
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".[16] Different strains of P. vivax
have their own characteristic relapse pattern and timing.[17] The earlier stage is
exo-erythrocytic generation.
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
(Fy6) to penetrate red blood cells. This antigen does not occur in the majority
of humans in West Africa [phenotype Fy (a-b-)]. As a result P. vivax
occurs less frequently in West Africa.[19]
The parasitised
red blood cell is up to twice as large as a
normal red cell and Schüffner's dots
(also known as Schüffner's stippling 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.
Sexual stage
The sexual
stage includes following processes by which P. vivax reproduces
sexually:
- Transfer to mosquito
- Gametogenesis
- Microgametes
- Macrogametes
- Fertilization
- Ookinite
- Oocyst
- Sporogony
Mosquito stage
the life cycle
in mosquitoes include:
Formation of
gametes
Development of
gametes from gametocytes is known as gametogony. When a female Anopheles
mosquito bites an infected person, gametocytes and other stages of the parasite
are transferred to the stomach where further development occur.
The
microgametocytes becomes very active and its nucleus undergoes fission to give
6-8 daughter nuclei which becomes arranged at the periphery. The cytoplasm
develops long thin flagella like projections, then a nucleus enter into each
one of these extensions. These cytoplasmic extensions later break off as mature
male gametes (microgametes). This process of formation of flagella like
microgametes or male gametes is known as exflagellation. Macrogametocytes show
very little change. It develops a cone of reception at one side and becomes
mature as female gamete / macrogameto cytes.
Fertilization
Male gametes
move actively in the stomach of mosquito in search of female gamete. Male
gamete then enters into female gamete through the cone of reception and the
complete fusion of 2 gametes result in the formation of zygote. (synkaryon).
Process of fusion of male and female gamete is called as syngamy. Fusion of 2
dissimilar gametes is known as anisogamy. The zygote remains inactive for
sometime but it soon elongates, becomes vermiform (worm-like) and motile. It is
now known as ookinete. The pointed ends of ookinete penetrate the wall of
stomach and comes to lie below its outer epithelial layer. Here it becomes
spherical and develops a cyst wall around itself. The cyst wall is derived
partly from the stomach tissues and partly produced by the zygote itself. At
this stage, it is known as the oocyst. The oocyst absorbs nourishment and grow
in size. These oocyst protrude (bulge) from the surface of stomach giving it a
kind of blistered appearance. In a highly infected mosquito, as many as 1000
oocyst may be seen.
Sporogony
The nucleus of
oocyst divides repeatedly to form large number of daughter nuclei. At the same
time, the cytoplasm develops large vacuoles and forms numerous cytoplasmic
masses. These cytoplasmic masses then elongate and a daughter nuclei migrates
into each one of them. The resulting sickle-shaped bodies is known as
sporozoites. This phase of asexual multiplication is known as sporogony and is
completed in about 10–21 days. The oocyst then burst and sporozoites are
released into the body cavity of mosquito from where they eventually reach the
salivary glands of mosquito through blood. The mosquito now becomes infectiv .
Salivary glands of a single infected mosquito may contain as many as 200,000
sporozoites. When the mosquito bites a healthy person, thousands of sporozoites
are infected into the blood along with the saliva and the cycle starts again.
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. Diagnosis can be
done with the strip fast test of antibodies,
Taxonomy
P. vivax can be divided
into two clades one that appears to have origins in the Old World and a second
that originated in the New World.[20] The distinction can be made on
the basis of the structure of the A and S forms of the rRNA.
A rearrangement of these genes appears to have occurred in the New World
strains. It appears that a gene conversion occurred in an Old World strain and
this strain gave rise to the New World strains. The timing of this event has
yet to be established.
At present both
types of P. vivax circulate in the Americas. The monkey parasite - Plasmodium
simium - is related to the Old World strains rather than to the
New World strains.
A specific name
- Plasmodium collinsi - has been proposed for the New World strains but
this suggestion has not been accepted to date.
Sumber : http://en.wikipedia.org/wiki/Plasmodium_vivax
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