MALARIA PARASITE - Plasmodium falciparum
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MALARIA
PARASITE
Plasmodium
falciparum
Malaria
is a
vector-borne
infectious
disease
caused
by
protozoan
parasites.
It is
widespread
in
tropical
and
subtropical
regions,
including
parts of
the
Americas,
Asia,
and
Africa.
Each
year, it
causes
disease
in
approximately
650
million
people
and
kills
between
one and
three
million,
most of
them
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.
Malaria
is one
of the
most
common
infectious
diseases
and an
enormous
public-health
problem.
The
disease
is
caused
by
protozoan
parasites
of the
genus
Plasmodium.
The most
serious
forms of
the
disease
are
caused
by
Plasmodium
falciparum
and
Plasmodium
vivax,
but
other
related
species
(Plasmodium
ovale,
Plasmodium
malariae,
and
sometimes
Plasmodium
knowlesi)
can also
infect
humans.
This
group of
human-pathogenic
Plasmodium
species
is
usually
referred
to as
malaria
parasites.
Malaria
parasites
are
transmitted
by
female
Anopheles
mosquitoes.
The
parasites
multiply
within
red
blood
cells,
causing
symptoms
that
include
symptoms
of
anemia
(light
headedness,
shortness
of
breath,
tachycardia
etc.),
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.
No
vaccine
is
currently
available
for
malaria;
preventative
drugs
must be
taken
continuously
to
reduce
the risk
of
infection.
These
prophylactic
drug
treatments
are
often
too
expensive
for most
people
living
in
endemic
areas.
Most
adults
from
endemic
areas
have a
degree
of
long-term
recurrent
infection
and also
of
partial
resistance;
the
resistance
reduces
with
time and
such
adults
may
become
susceptible
to
severe
malaria
if they
have
spent a
significant
amount
of time
in
non-endemic
areas.
They are
strongly
recommended
to take
full
precautions
if they
return
to an
endemic
area.
Malaria
infections
are
treated
through
the use
of
antimalarial
drugs,
such as
quinine
or
artemisinin
derivatives,
although
drug
resistance
is
increasingly
common.
Symptoms
Symptoms
of
malaria
include
fever,
shivering,
arthralgia
(joint
pain),
vomiting,
anemia
caused
by
hemolysis,
hemoglobinuria,
and
convulsions.
There
may be
the
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
include
coma 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).
Pathogenesis
The life
cycle of
malaria
parasites
in the
human
body.
The
various
stages
in this
process
are
discussed
in the
text.
Malaria
in
humans
develops
via two
phases:
an
exoerythrocytic
(hepatic)
and an
erythrocytic
phase.
When an
infected
mosquito
pierces
a
person's
skin to
take a
blood
meal,
sporozoites
in the
mosquito's
saliva
enter
the
bloodstream
and
migrate
to the
liver.
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.[46]
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.
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.
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