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PROTOZOA

Sitti Wahyuni, MD, PhD


Department of Parasitology
Medical Faculty, Hasanuddin University

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Introduction
• a single cell-like microorganisms
• Able to performs all of the functions of life (metabolism and
reproduction)
• some are free-living and some need dependent on other
organism
• > 50,000 species have been described
• Anton van Leeuwenhoek: the first person saw protozoa
using simple lenses microscopes
• has genetic material encased in a nuclear membrane
(unlike bacteria and viruses)
• many infections are inapparent or mild in normal individual
• can be life-threatening in immunosuppressed patients
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Morphology

• Unicellular eukaryotes
• Size < 50 μm in size
• Form:
– nearly spherical/ovoidal,
– bizarre contours.
– radial symmetry, some bilateral symmetry
– possess a longitudinal torsion to their body

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Fundamental structures
• Nucleus: reproduction
• Cell-wall: protection
• Cytoplasm
– Endoplasm : consist of foreign bodies, contractile
vacuole, chromatoid bodies, food vacuoles,
chromotoidal bodies, mitochondria
– Ectoplasm : functions as the locomotor apparatus for
the procurement and ingestion ofood, respiration,
discharge of metabolic wastes and protection
Ectoplasm might be: Cilium, Pseudopodia, Flagella,
Undulating membrane
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Nucleus :

Nucleus consist of:


-nucleolus
-nucleus membare
-achromatic reticulum
-nucleoplasm
-karyosom
-chromatin

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Nutrition

• All protozoa is holozoic; require organic


materials, which may be particulate or in
solution.
• Food that are obtain from host may
– predigested substances present in the host's
digestive tract, in the blood stream or lymphatic
vessels
– Host tissue cell

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• Engulf food by:
– temporary mouth, perform digestion and absorption in
a food vacuole, and eject the waste substances.
– permanent mouth (cytosome or micropore), through
which ingested food passes to become enclosed in food
vacuoles.
• Undigest or waste food is exreted via
– Cytopig
– osmosis pressure
– contractile vacuole

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Life Cycle
• Have certain of optimal condition for their development
• Able to adjust to wide ranges of temperature, of pH,
salinity, light, and nutriment
• Life cycle stages
– Trophozoite: any stage in a protozoan’s life refers to
the motile form, feeding, multiplying stage
– Cyst: the non motile form which is protected by a
distinct membrane or cyst well. This is an infective
stage of the parasite.
– Trophozoite-cyst
• Excystation:
• Endcystation

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Other protozoa live stages:
• Hemoflagellates: amastigote, promastigote,
epimastigote, and trypomastigote designate
trophozoite stages that differ in the absence or
presence of a flagellum and in the position of the
kinetoplast associated with the flagellum.
• Toxoplasma gondii: tachyzoite and bradyzoite
• Plasmodium: merozoite (the form resulting from
fission of a multinucleate schizont) and sexual
stages such as gametocytes and gametes.

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Reproduction
• Asexual:
– Binary fission: the organelles are duplicated and the
protozoan then divides into two complete organisms
• longitudinal division in the flagellates
• transverse division in the ciliates
• No no apparent anterior-posterior axis in amebas
– Sporogony: Reproduction by division of a spore
• Sexual
– Syngamy: The fusion of two gametes in fertilization.
– Conjugation: two similar organisms come together on
their oral surfaces and reciprocally exchange a mature
microgamete (division product of the micronucleus), so
that a micronucleus with diploid number of
chromosomes (zygote) is produced in each of the pairing
individuals
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• Both asexual and sexual: Apicomplexa
• Endodyogeny (Toxoplasma): Two daughter cells form
within the parent cell, which then ruptures, releasing
the smaller progeny which grow to full size before
repeating the process
• Schizogony in Apicomplexa: the nucleus divides a
number of times, and then the cytoplasm divides into
smaller uninucleate merozoites.
• Production of gametes (gamogony) fertilization
(zygote) encystation of the zygote to form an oocyst
 formation of infective sporozoites (sporogony)
within the oocyst

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Classification
• Based on organelle locomotion
– Mastigophora: movement with flagella:
Trichomonas, Giardia
– Sarcodina: pseudopodia, e.g. Entamoeba
histolytica
– Apicomplexa (apical complex) no locomotor
apparatus; cryptosporidium, malaria, toxoplasma
– Ciliophora: movement with cilia: Balantidium coli

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Protozoa classification
Rhizopod Ciliata Flagellata Sporozoa
(Amoeboid) (Cilia +) (Flagel +) (Gamet +)
Intestine E. coli B. coli G. lamblia Isospora spp.
E. Histollitica T. hominis Eimeria spp.
I. butchii
D. fragilis
Mouth E. ginggivalis T. tenax
T. vaginalis
Blood Leishmania Plasmodium
spp. spp.
Trypanosoma
spp.
Tissue Naegleria fowleri Tx. gondii
Achantamoeba Sc. lindemanii
spp. Pn. carini

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Host resistant to protozoa

• Resistance: ability of a host to defend itself


against a pathogen.
• Mechanisms are not yet well understood.
• Two main groups of mechanisms:
1. nonspecific mechanism: host, age, sex, genetic,
soluble host that is lethal to parasite, phagocytic
cells
2. specific mechanism(s) involving the immune
system: T cells, B cells

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Nonspecific mechanisms
• Genetic factors control the susceptibility of red blood cells to invasion or
growth of plasmodia, the agents of malaria
– Heterozygous/homozygous individuals for the sickle cell hemoglobin
trait are more resistant to Plasmodium falciparum
– Individuals lack the Duffy factor on their red blood cells are not
susceptible to P vivax.
– Thalassaemia and glucose-6-phosphate dehydrogenase deficiency,
may contribute to survival of individuals in various malaria-endemic
regions.
• Trypanolytic factor presence in human serum confers resistance against
Trypanosoma brucei brucei (agent of sleeping sickness) in animals)
• Fever and the sex of the host, may also contribute to the host's resistance
to various protozoan parasites.

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Specific mechanism (Immunity)

• Humoral immunity
– Malaria and trypanosome infections: antibody
– T cruzi and T brucei gambiense infections:
antibody-dependent cytotoxic
• Cellular immunity
– Leishmaniasis and toxoplasmosis.

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Disease pathogenesis
Mechanism Example
Toxic parasite products:
High molecular weight (e.g. Presumably all parasitic protozoal infections
hydrolytic enzimes)

Low molecular weight African trypanosomiasis


Immediate type hypersensitivity Malaria, African trypanosomiasis
Delayed type hypersensitivity Leishmaniasis, Amebiasis, Toxoplasmosis

Autoimmunity American trypanosomiasis


Immunosupression Malaria, African trypanosomiasis, possibly
many protozoal infection

Mechanical tissue damage Malaria

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Protozoa immunoescape
• Antigenic masking: covering itself with host antigens.
• Blocking of serum factors: blocks the binding of specific antibody or
lymphocytes to the parasite surface antigens.
• Intracellular location: Protects from the direct effects of the host's
immune response. By concealing the parasite antigens, this strategy
also delays detection by the immune system.
• Antigenic Variation: Change their surface antigens during the
course of an infection. Parasites carrying the new antigens escape
the immune response to the original antigens.
• Immunosuppression:
– delay detection of antigenic variants
– reduce the ability of the immune system to inhibit the growth of
and/or to kill the parasites.

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Protozoa immunoescape

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