PLASMODIUM
DISEASE
Malaria is caused by four plasmodia:
• Plasmodium vivax
• Plasmodium ovale
• Plasmodium malariae
• Plasmodium falciparum.
P. vivax and P. falciparum are more common
causes of malaria than are P. ovale and P.
malariae.
PROPERTIES
The vector and definitive host for plasmodia
is the female Anopheles mosquito.
There are two phases in the life cycle:
sexual cycle,
It occurs primarily in mosquitoes,
asexual cycle
occurs in humans, the intermediate hosts.
Sexual cycle is called sporogony because
sporozoites are produced
Asexual cycle is called schizogony because
schizonts are made.
The life cycle in humans begins with the
introduction of sporozoites into the blood from
the saliva of the biting mosquito.
The sporozoites are taken up by hepatocytes
within 30 minutes.
This "exoerythrocytic" phase consists of cell
multiplication and differentiation into
merozoites.
P. vivax and P. ovale produce a latent form
(hypnozoite) in the liver; this form is the cause
of relapses seen with vivax and ovale malaria.
Merozoites are released from the liver cells and
infect red blood cells.
During the erythrocytic phase, the organism
differentiates into a ring-shaped trophozoite .
The ring form grows into an ameboid form and
then differentiates into a schizont filled with
merozoites.
After release, the merozoites infect other
erythrocytes.
This cycle in the red blood cell repeats at regular
intervals typical for each species.
The periodic release of merozoites causes
the typical recurrent symptoms of chills,
fever, and sweats seen in malaria patients.
The sexual cycle begins in the human red
blood cells when some merozoites develop
into male and others into female
gametocytes.
The gametocyte-containing red blood cells
are ingested by the female Anopheles
mosquito and, within her gut, produce a
female macrogamete and eight sperm
like male microgametes.
After fertilization, the diploid zygote
differentiates into a motile ookinete that
burrows into the gut wall, where it grows into
an oocyst within which many haploid
sporozoites are produced.
The sporozoites are released and migrate to
the salivary glands, ready to complete the
cycle when the mosquito takes her next
blood meal.
PATHOGENESIS & EPIDEMIOLOGY
Most of the pathologic findings of malaria
result from the destruction of red blood
cells.
Red cells are destroyed both by the release
of the merozoites and by the action of the
spleen to first sequester the infected red
cells and then to lyse them.
The enlarged spleen characteristic of
malaria.
Malaria caused by P. falciparum is more
severe than that caused by other plasmodia.
It is characterized by infection of far more
red cells than the other malarial species and
by occlusion of the capillaries with
aggregates of parasitized red cells.
This leads to life-threatening hemorrhage
and necrosis, particularly in the brain
(cerebral malaria).
Furthermore, extensive hemolysis and kidney
damage occur, with resulting
hemoglobinuria.
The dark color of the patient's urine has
given rise to the term "blackwater fever."
The hemoglobinuria can lead to acute renal
failure.
The timing of the fever cycle is 72 hours for
P. malariae and 48 hours for the other
plasmodia
Disease caused by P. malariae is called
quartan malaria because it recurs every
fourth day, whereas malaria caused by the
others is called tertian malaria because it
recurs every third day.
Tertian malaria is subdivided into
malignant malaria, caused by P. falciparum,
and benign malaria, caused by P. vivax and P.
ovale.
P. falciparum causes a high level of
parasitemia, because it can infect red cells of
all ages. In contrast, P. vivax infects only
reticulocytes and P. malariae infects only
mature red cells; therefore, they produce
much lower levels of parasites in the blood.
CLINICAL FINDINGS
Malaria presents with abrupt onset of fever
and chills, accompanied by headache,
muscle and joint pain about 2 weeks after
the mosquito bite.
The fever spike, which can reach 41°C, is
frequently accompanied by shaking chills,
nausea, vomiting, and abdominal pain.
Patients usually feel well between the febrile
episodes.
Splenomegaly is seen in most patients, and
hepatomegaly occurs in roughly one-third.
Anemia is prominent.
Untreated malaria caused by P. falciparum is
potentially life-threatening as a result of
extensive brain (cerebral malaria) and kidney
(blackwater fever) damage.
Cerebral malaria
Many parasitized cells can be found in the
capillaries of the brain in the late stages,
haemorrhaging from small blood vessels can
occur.
LAB DIAGNOSIS
Diagnosis rests on microscopic examination
of blood, using both thick and thin Giemsa-
stained smears.
The thick smear is used to screen for the
presence of organisms, and the thin smear is
used for species identification.
It is important to identify the species,
because the treatment of different species
can differ.
Using a malaria rapid diagnostic test (RDT) to
detect malaria antigen.
MAKING THICK AND THIN BLOOD
FILMS
STAINING MALARIA PARASITES
Fix the slide
Stains
Field’s
stain
Giemsa stain
PLASMODIUM FALCIPARUM
Trophozoites
Small rings, occasionally larger rings in
heavy infections.
Often with double chromatin dot.
PLASMODIUM FALCIPARUM
Schizonts
Only seen occasionally in severe infections.
Usually with 2 or 4 merozoites and pigment.
PLASMODIUM FALCIPARUM
Gametocytes
Banana shaped.
Rounded forms may be seen if film dries
slowly.
PLASMODIUM VIVAX
Trophozoites
Large and amoeboid. Cytoplasm fragmented
in thick films.
Fine pigment.
PLASMODIUM VIVAX
Schizonts
Large, round or irregular in form. Contain up
to 24 or more merozoites and fine pigment
PLASMODIUM VIVAX
Gametocytes
Large, round or irregular in form (small forms
also).
Scattered pigment.
PLASMODIUM VIVAX
host cell will be enlarged, irregular in shape,
pale
Staining and Schuffner’s dots present.
PLASMODIUM OVALE
Low prevalence, mainly in West Africa.
Trophozoites
Small and compact
Small amount of pigment.
PLASMODIUM OVALE
Schizonts
Small and compact.
Contain up to 12 merozoites.
PLASMODIUM OVALE
Gametocytes
Small and round.
Host cell
About 20–30% of cells may become oval with
fimbriated ends.
Schuffner’s dots are prominent
PLASMODIUM MALARIAE
Low prevalence
Trophozoites
Thick, neat, densely stained.
Yellow-brown pigment in late trophozoites.
Schizonts
Small with neatly arranged (up to 12)
merozoites.
ANY QUESTIONS