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6 Plasmodium

Malaria is caused by four species of Plasmodium, with P. vivax and P. falciparum being the most common. The disease is transmitted by female Anopheles mosquitoes and has a complex life cycle involving both sexual and asexual phases, leading to symptoms such as fever, chills, and anemia. Diagnosis is typically made through microscopic examination of blood smears, and treatment varies depending on the Plasmodium species identified.

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0% found this document useful (0 votes)
27 views38 pages

6 Plasmodium

Malaria is caused by four species of Plasmodium, with P. vivax and P. falciparum being the most common. The disease is transmitted by female Anopheles mosquitoes and has a complex life cycle involving both sexual and asexual phases, leading to symptoms such as fever, chills, and anemia. Diagnosis is typically made through microscopic examination of blood smears, and treatment varies depending on the Plasmodium species identified.

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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

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