Blood and Tissue
Protozoa
Zainab Ali
zali77805@gmail.com
The medically important organisms in this category of
protozoa consist of
 the sporozoans Plasmodium and Toxoplasma
 the flagellates Trypanosoma and Leishmania
Plasmodium
 Disease Malaria
 Almost 300 million cases per year
 Almost 10% world population is affected
 There are approximately 156 named species
of Plasmodium which infect various species of
vertebrates.
 Four species are considered true parasites of humans, as
they utilize humans almost exclusively as a natural
intermediate host: P. falciparum, P. vivax, P. ovale and P.
malariae.
Vector Anopheles (female)
Definitive host Mosquito
Intermediate host Humans
Sexual Stage Sporogony
Asexual Stage Shizogony
Disease Ratio in Pakistan
 All areas (including all cities)
 P. vivax 70%,
 P. falciparum 30%
Life Cycle
 The malaria parasite life cycle involves two hosts.
 During a blood meal, a malaria-infected female Anopheles mosquito
inoculates sporozoites into the human host .
 Sporozoites infect liver cells and mature into schizonts , which rupture
and release merozoites . (Of note, in P. vivax and P. ovale a dormant stage
[hypnozoites] can persist in the liver and cause relapses by invading the
bloodstream weeks, or even years later.) After this initial replication in the
liver (exo-erythrocytic schizogony ), the parasites undergo asexual
multiplication in the erythrocytes (erythrocytic schizogony ).
 Merozoites infect red blood cells . The ring stage trophozoites mature into
schizonts, which rupture releasing merozoites . Some parasites
differentiate into sexual erythrocytic stages (gametocytes) . Blood stage
parasites are responsible for the clinical manifestations of the disease.
 The gametocytes, male (microgametocytes) and female
(macrogametocytes), are ingested by an Anopheles mosquito during a
blood meal .
 The parasites’ multiplication in the mosquito is known as the sporogonic
cycle .
 While in the mosquito’s stomach, the microgametes penetrate the
macrogametes generating zygotes .
 The zygotes in turn become motile and elongated (ookinetes) which
invade the midgut wall of the mosquito where they develop into oocysts .
 The oocysts grow, rupture, and release sporozoites , which make their
way to the mosquito’s salivary glands. Inoculation of the sporozoites into
a new human host perpetuates the malaria life cycle .
Pathogenesis
 Pathogenesis is concerned with destruction of RBCs
 RBCs Destruction
Merozoites
•Destruction
of RBCs
Spleen
• first sequester the
infected red cells and then
to lyse them.
•Spleenomegaly
•Hyperplasia of
lymphocytes and
macrophages.
Timing of Fever
 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.
 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.
Clinical Findings
 From Book
 Malaria caused by the other three plasmodia is usually
self-limited, with a low mortality rate.
 However, relapses of P. vivax and P. ovale malaria can
occur up to several years after the initial illness as a result
of hypnozoites latent in the liver.
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. Ring-shaped trophozoites can be seen within infected
red blood cells. The gametocytes of P. falciparum are crescent-shaped
("banana-shaped"), whereas those of the other plasmodia are spherical.
If more than 5% of red blood cells are parasitized, the diagnosis is
usually P. falciparum malaria.
 If blood smears do not reveal the diagnosis, then a PCR-based test for
Plasmodium nucleic acids or an ELISA test for a protein specific for P.
falciparum can be useful.
P. falciparum
 P. falciparum rings have delicate cytoplasm and one or two small
chromatin dots. Rbcs that are infected are not enlarged; multiple
infection of Rbcs is more common in P. falciparum than in other
species.
 P. falciparum gametocytes are crescent or sausage shaped. The
chromatin is in a single mass (macrogamete) or diffuse
(microgamete).
 As P. falciparum trophozoites grow and mature, they tend to retain
their ring-like shape and sometimes trace amounts of yellow
pigment can be seen within the cytoplasm. Growing trophozoites
in P. falciparum can appear slightly amoeboid in shape.
P. vivax
 P. vivax rings have large chromatin dots and cytoplasm
can become ameboid as they develop.
 P. vivax trophozoites show amoeboid cytoplasm, large
chromatin dots, and have fine, yellowish-brown pigment
Treatment
 Chloroquine is the drug of choice for acute malaria caused
by sensitive strains.
 Chloroquine kills the merozoites, thereby reducing the
parasitemia, but does not affect the hypnozoites of P. vivax
and P. ovale in the liver. These are killed by primaquine,
which must be used to prevent relapses.
 For chloroquine-resistant strains of P. falciparum, either
mefloquine or a combination of quinine and doxycycline is
used. A combination of atovaquone and proguanil
(Malarone), in a fixed dose, is available for the treatment of
malaria caused by chloroquine-resistant P. falciparum
Blood and Tissue Protozoa pptx (2)..pptx

Blood and Tissue Protozoa pptx (2)..pptx

  • 1.
    Blood and Tissue Protozoa ZainabAli zali77805@gmail.com
  • 2.
    The medically importantorganisms in this category of protozoa consist of  the sporozoans Plasmodium and Toxoplasma  the flagellates Trypanosoma and Leishmania
  • 3.
    Plasmodium  Disease Malaria Almost 300 million cases per year  Almost 10% world population is affected  There are approximately 156 named species of Plasmodium which infect various species of vertebrates.  Four species are considered true parasites of humans, as they utilize humans almost exclusively as a natural intermediate host: P. falciparum, P. vivax, P. ovale and P. malariae.
  • 4.
    Vector Anopheles (female) Definitivehost Mosquito Intermediate host Humans Sexual Stage Sporogony Asexual Stage Shizogony
  • 5.
    Disease Ratio inPakistan  All areas (including all cities)  P. vivax 70%,  P. falciparum 30%
  • 6.
  • 7.
     The malariaparasite life cycle involves two hosts.  During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host .  Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ).  Merozoites infect red blood cells . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease.
  • 8.
     The gametocytes,male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal .  The parasites’ multiplication in the mosquito is known as the sporogonic cycle .  While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes .  The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts .  The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle .
  • 9.
    Pathogenesis  Pathogenesis isconcerned with destruction of RBCs  RBCs Destruction Merozoites •Destruction of RBCs Spleen • first sequester the infected red cells and then to lyse them. •Spleenomegaly •Hyperplasia of lymphocytes and macrophages.
  • 10.
    Timing of Fever 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.
  • 11.
     Malaria causedby 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.
  • 12.
    Clinical Findings  FromBook  Malaria caused by the other three plasmodia is usually self-limited, with a low mortality rate.  However, relapses of P. vivax and P. ovale malaria can occur up to several years after the initial illness as a result of hypnozoites latent in the liver.
  • 13.
    Diagnosis  Diagnosis restson 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. Ring-shaped trophozoites can be seen within infected red blood cells. The gametocytes of P. falciparum are crescent-shaped ("banana-shaped"), whereas those of the other plasmodia are spherical. If more than 5% of red blood cells are parasitized, the diagnosis is usually P. falciparum malaria.  If blood smears do not reveal the diagnosis, then a PCR-based test for Plasmodium nucleic acids or an ELISA test for a protein specific for P. falciparum can be useful.
  • 14.
    P. falciparum  P.falciparum rings have delicate cytoplasm and one or two small chromatin dots. Rbcs that are infected are not enlarged; multiple infection of Rbcs is more common in P. falciparum than in other species.  P. falciparum gametocytes are crescent or sausage shaped. The chromatin is in a single mass (macrogamete) or diffuse (microgamete).  As P. falciparum trophozoites grow and mature, they tend to retain their ring-like shape and sometimes trace amounts of yellow pigment can be seen within the cytoplasm. Growing trophozoites in P. falciparum can appear slightly amoeboid in shape.
  • 16.
    P. vivax  P.vivax rings have large chromatin dots and cytoplasm can become ameboid as they develop.  P. vivax trophozoites show amoeboid cytoplasm, large chromatin dots, and have fine, yellowish-brown pigment
  • 18.
    Treatment  Chloroquine isthe drug of choice for acute malaria caused by sensitive strains.  Chloroquine kills the merozoites, thereby reducing the parasitemia, but does not affect the hypnozoites of P. vivax and P. ovale in the liver. These are killed by primaquine, which must be used to prevent relapses.  For chloroquine-resistant strains of P. falciparum, either mefloquine or a combination of quinine and doxycycline is used. A combination of atovaquone and proguanil (Malarone), in a fixed dose, is available for the treatment of malaria caused by chloroquine-resistant P. falciparum