Medical Parasitology

Lectures 46-47-48
Introduction to Protozoa 1
Introduction to Intestinal Protozoa
Introduction to Blood Protozoa

Subkingdom Protozoa

ILOs:

 Identify medically important protozoa.

 Understand life cycle’s needs for common protozoa.
 Recall and differentiate the infective and diagnostic stages of common protozoa
 Demonstrate different types of protozoal infections.
 Explain host-parasite relationships in protozoa.

Medical Protozoology: It is the study of protozoa of medical importance.

Protozoa are unicellular organisms which are capable of performing all the physiologic functions of life
(locomotion, nutrition, reproduction, excretion, respiration etc.…).
Structure:
 Protozoa are the smallest, simplest and most primitive of all parasitic organisms.
 The body is composed of cytoplasm and nucleus together with other organelles as mitochondria,
endoplasmic reticulum and Golgi apparatus.
1- Cytoplasm: consists of an outer thin hyaline ectoplasm and inner voluminous granular endoplasm.
The ectoplasm functions including: ingestion of food, excretion of waste products, respiration, protection and
locomotion
The endoplasm is concerned with metabolism and reproduction. It contains:
a. Food vacuoles containing food during digestion.
b. Volutin granules for storing food such as glycogen vacuoles (carbohydrates) and chromatoid bodies(protein).
c. Excretory vacuoles for collecting waste products and discharging them to outside the ectoplasm by

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bursting or by anal opening (cytopyge).

Nucleus is concerned with reproduction. It consists of nuclear membrane, nucleoplasm (nuclear sap) and
chromatin. It may be one or more, vesicular or compact.

1. Vesicular nucleus: The chromatin is concentrated in a mass (karyosome) or distributed between the
karyosome and the inner surface of nuclear membrane (peripheral chromatin) eg. Entamoeba sp.

2. Compact nucleus: The chromatin is distributed diffusely and filling the nucleus eg. Balantidium sp.

Nucleus also may be one or more,

 single (Trichomonas sp.), doubled (Giardia sp., Balantidium sp.) or several (cyst stages of
Entamoeba sp.).
Locomotion: Protozoa move by one of the following organs of locomotion:

o Pseudopodia: It is a protrusion of ectoplasm followed by endoplasm leading to amoeboid movement

(Entamoeba trophozoite).

o Flagella: It is a thread-like organelle arising from a basal granule in the cytoplasm (kinetoplast).

It may be single (Trypanosoma), 3-5 (Trichomonas) or 8 (Giardia).

o Cilia:
Numerous short
hair- like threads
covering the whole
organism
(Balantidium).

o Gliding and twisting: in which the movement is propagated through myonemes (Toxoplasma,
Sarcocystis).

o Some protozoa are lacking organs of locomotion as the erythrocytic stages of Plasmodium.

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Nutrition: Protozoa feed by one of the following methods:

1. Pseudopodia: as Entamoeba trophozoites, the ingested food is surrounded by a vacuole.
2. Diffusion: by absorption of fluids through the surface as in malarial parasites.
3. Permanent mouth: by a cytostome as in Trichomonas and Balantidium coli.

Reproduction: Protozoa reproduce by one of the following:

1. Asexual reproduction:
a. Simple binary division: There is division of the nucleus into two segments followed by division of the
cytoplasm. The plane of division is either longitudinal as in flagellates, transverse as in ciliates or in any
direction as in Entamoeba.
b. Schizogony: The nucleus divides into several fragments followed by division of the cytoplasm forming
new individuals as in Plasmodium.
c. Endodyogeny or internal budding: Two buds (or more) appear from the mother nucleus forming two
daughter cells within the mother cell, which later is consumed, as in Toxoplasma gondii.
d. Cyst formation: Under unfavorable conditions, the organism forms thick wall, then the nucleus divides
into several divisions as in Entamoeba.
2. Sexual reproduction:
a. Gametogony: Two sex cells meet each other, one is the male “microgametocyte”, and the other is the
female “macrogametocyte”. The resultant stage is termed „zygote‟ which may be motile “ookinete” or
non-motile as in sporozoa.
b. Conjugation: It is a temporary union of two organisms for exchange of nuclear material, as in
Balantidium coli.

Simple and multiple binary divisions

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Schizogony

Conjugation

Classification of Phylum Protozoa:

According to the organ of locomotion According to the habitat

1- Class Rhizopoda (Amoebae) → move by 1- Intestinal protozoa: Amoebae, flagellates,

pseudopodia. ciliates and intestinal coccidian
2- Class Ciliata (Ciliates) → move by cilia. 2- Blood protozoa: Blood flagellates,
3- Class Zoomastigophora (Flagellates) → moveby Plasmodium species and Babesia
flagella. 3- Tissue protozoa: Toxolasma, Sarcocystis and
4- Class Sporozoa (& Coccidia) → move by tissue flagellates
gliding. 4- Buccal protozoa: Entamoeba gingivaiis &
5- No organ for locomotion: As Plasmodia Trichomonas tenax
5- Urogenital protozoa: Trichomonas vaginalis

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Introduction to Intestinal Protozoa

Subphylum: Sarcodina
Class: Rhizopoda
Family Endamoebidae
Genus Entamoeba
1- Pathogenic Amoebae: Entamoeba histolytica
Host: It is mainly a parasite of human beings. No reservoir hosts.
Habitat: in the large intestine (intestinal amoebiasis or dysentery). It may reach the liver, lung and brain
causing amoebicabscesses (extra intestinal amoebiasis).
Diagnostic stage: Quadrinucleated cyst or trophozoite.
Infective stage: Quadrinucleated cyst.
Mode of infection: Faecal-oral transmission which means: eating raw vegetables (salad), fruits or drinking
water contaminated with quadrinucleated cysts. Flies and food handlers (cyst passer) are a source of
infection.
Life cycle:
• After the quadrinucleated cysts (infective stage) are swallowed with contaminated food or water, no
changes occur in an acidic environment (stomach), once the PH becomes neutral or slightly alkaline a
single trophozoite with 4 nuclei is liberated. The trophozoite divides by binary fission giving rise to
multiple daughter trophozoites.
• They may invade the mucosa of the caecum and
flexures. The ulcers may reach up to the
rectum; it is inverted flask shaped lesion
with extension to the peritoneum.
• After repeated multiplication, encystation takes
place.
• Entamoeba histolytica causes intestinal
amoebiasis and extra-intestinal amoebiasis
like liver, lung, heart, brain abscesses and
skin lesions.

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2- Potentially pathogenic free-living amoebae

Naegleria sp & Acanthamoeba sp.
• They are normal inhabitants of soil and water where they feed on bacteria.
• A few members have the ability to become parasites when an opportunity to enter a vertebrate exists.
• Two of them are able to infect humans and they belong to two genera:
1- Naegleria causes Primary amoebic meningoencephalitis (PAM)
2-Acanthamoeba: causes
• Granulomatous amebic encephalitis (GAE)
• Granulomatous skin lesion (primarily immunocompromised)
• Amoebic keratitis
1-Naegleria fowleri
N. fowleri is found in fresh water, soil, heated swimming pools and sewage.
Morphology: it exists in 3 forms:
1) Trophozoite (amoeboid):
• It is an invasive, reproductive form
• Pear shaped with broad anterior and tapered posterior ends with blunt single pseudopodia.
• The nucleus is vesicular with large central karyosome with no peripheral chromatin.
• Has a sucker like structure called "Amoebastome".
2) Flagellate form:
• Transient, non-dividing, non-feeding form.
• Similar shape as the trophozoite form, except it has two flagella at the anterior broad end.
• N. fowleri amoeboid forms are found in cerebrospinal fluid (CSF) and tissue. Amoeboid form can
turn into temporary flagellated form which usually reverts back to the amoeboid stage.
3) Resistant cyst form:
• Under unfavorable condition amoeboid stage transform to flagellated form then cyst stage.
• Cyst found in nature and culture (never in host tissue).
Portal of entry: Trophozoites infect humans or animals by inhalation or aspiration of water or dust containing
the organism. The organisms then penetrate the olfactory neuro-epithelium and reach upto the brain.

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Forms of Naegleria fowleri

2- Acanthamoeba spp.
At least 5 species of Acanthamoeba have been identified in human tissues. Free-living trophozoites and
cysts occur in soil, fresh and sea water; sewage, contact lens equipment; ventilating, and air conditioning
systems.
Morphology:
Acanthamoeba spp. has two forms; cysts and trophozoites, both are found in host tissues.

1) Trophozoites:
• Occur only as amoeboid form.
• Larger in size than Naegleria.
• Have multiple spines like pseudopodia "Acanthopodia".
2) Cyst:
• Rounded with double cyst wall (outer wrinkled wall) and single nucleus with similar criteria of the
trophozoite.
• It has characteristic opercula for exacystation.
Portal of entry:
The trophozoites are the infective forms and gain entry into the body through the respiratory tract
(airborne cyst changes to trophozoite), ulcerated or broken skin and invade the central nervous system by
hematogenous dissemination.
Acanthamoeba spp. cysts and trophozoites are found in tissue.

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Intestinal flagellates
Giardia lamblia (Giardia intestinalis)
Giardiasis
Habitat: Upper part of small intestine (duodenum) and gall bladder.
Host: human (more common in children than adult), beaver, muskrat etc.
Diagnostic stage: cyst or trophozoite
Infective stage: cyst.
Mode of infection: Faeco-oral rout. Infection occurs by ingestion of the cyst stage (infective stage) with food
or water, day care, oral-anal sex. In the duodenum the cyst wall dissolves releasing the trophozoites,
which attach to the mucosal membrane by the ventral sucking disc.

Life cycle of Giardia lamblia

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PHYLUM: APICOMPLEXA
 The phylum Apicomplexa contains organisms that possess a certain combination of structures "the apical
complex" structures; that aid in penetrating the host cell.

 The apical complex structures are seen only with the electron microscope.

 These protozoan parasites are characterized by being intracellular parasites.

 Reproduction involves both asexual (schizogony) and sexual (gametogony). Following gametogony, a zygote is
formed which divides to produce spores (sporogony) hens the name sporozoa was given to them.

 The most important classes of medical significance are the Coccidia or alimentary sporozoa (Cystoisospora and
Cryptosporidium) and blood sporozoa (Toxoplasma, Plasmodium and Babesia).

1. Genus: Isospora (Cystoisospora)

This genus infects man and a wide range of animal hosts. The only species in man is Isospora hominis
(Cystoisospora belli). It is most commonly observed in immunocompromised individuals.
Habitat: Inside the Epithelial lining of the small intestine (duodenum and jejunum).
Geographical distribution: World-wide
Definitive Host: Man.
Mode of infection: Ingestion of food and water contaminated with sporulated oocyst (infective stage).
Oocysts:
The oocysts are elliptical (elongated) in shape. The size ranges from 25 – 30 µm. The wall issmooth and thin.
The oocyst contains two sporocysts, each with four curved, sausage-shaped nucleated sporozoites
(Disporocystic tetrazoic).
 Diagnostic stage: Unsporulated oocyst.
 Infective stage: Sporulated oocyst.
 Life cycle: It is divided into three phases, schizogony, gametogony and
sporulation.

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2- Genus Cyclospora
Cyclospora cayetanensis: causes an intestinal infection called cyclosporiasis.
Geographical distribution: More common in tropical and sub-tropical regions.
Forms of oocyst: acid-fast-stained and Oocysts exhibit blue auto fluorescence by UV fluorescence microscope.

 Unsporulated oocyst: It is spherical, 8-10μ, with central morula, containing 6-9 retractile granules. Since
sporulation requires 5-10 days, unsporulated oocyst is the form usually seen in Faeces.

 Mature sporulated oocyst: It contains 2 sporocysts; each contains 2 crescent

shaped sporozoites (disporocystic dizoic).
Habitat: Jujenal enterocytes.
Definitive host: Man (C. cayetanensis is a host-specific parasite, completing its life cycle
phases in man).
Infective stage: Mature sporulated oocysts.
Mode of infection: By ingestion of food or drink contaminated with sporulated oocysts.

3- Genus Cryptosporidium
Important species: C. parvum and C. hominis
 These are parasites of the brush border of the epithelial cells of intestine, gall bladder and respiratory
tract.
Habitat: This genus is remarkable in that, unlike other members of the Eimeriidae, it does not enter the cells
of the host and lacks host specificity so that cross infection occurs between domestic and laboratory animals
and man.
Definitive Host: Wide range of vertebrate hosts, including Man.
Geographical distribution: World-wide Zoonotic disease.
Oocysts: acid-fast-stained
The minute oocysts (cysts) (4- 4.5 µm), each with four sporozoites. Two types of oocysts are produced:
the first, the majority, are thick-walled and are passed in faeces. The second are thin walled which
mostly rupture within the host intestine and causes autoinfection. Oocysts not killed by chlorination.
Diagnostic stage: Sporulated oocyst containing 4 sporozoites.
Infective stage: Sporulated oocyst containing 4 sporozoites.

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Mode of infection:

 Faecal-oral route by ingestion of thick-walled oocysts in contaminated food or water (not killed by
chlorination).

 Internal autoinfection by thin walled oocysts, which release sporozoites in situ.

 Zoonotic transmission from the reservoir animals.

Life cycle: It is divided into three phases, schizogony, gametogony and sporulation. Sporulation takes place
within the host.

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4- Microsporidia
 They cause an intestinal infection called microsporidiosis (microsporidiasis), predominantly associated with
immune suppression causing diarrhea, and also cause hepatitis, neurologic, disseminated infection.
 They are obligate intracellular spore-forming parasites.
 It includes 6 genera of medical importance e.g.: Enterocytozoon, Encephalitozoon, and Microsporidium.
Habitate: They infect a variety of cell types in
Hosts: many different species of animals.
 Microsporidia spores are all round and oblong, about 1 -4 µm in size, Gram-
stained, acid-fast-stained, with a characteristic feature of microsporidia is the
polar tube or polar filament found in the spore used to infiltrate host cells.
Mode of transmission: of microsporidia is by

 Inhaling, ingesting or otherwise contracting spores (for example ocular or

sexually transmitted).

 Contact with infected animals may also transmit the disease (zoonoic infection) but cases are rare.

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Balantidium coli (Ciliates)

Host: It is a parasite of pigs in which it lives as a commensal. Rodents, occasionally horses, cattle andman can
be also infected. Balantidium coli is a zoonotic parasite causing balantidiasis.
Habitat: Large intestine of multiple hosts.
Morphology:
The parasite has trophozoite and cyst stages; they are the largest protozoa infecting man.
Diagnostic stage: cyst and trophozoite.
Infective stage: cyst
Mode of infection:
Faeco-oral rout, Infection of a new host is by ingestion of the cysts contaminatingfood or hands. Most of the
human cases are due to close association to pigs.

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Urogenital flagellates
Trichomonas vaginalis
It is a pathogenic flagellate. The parasite is only present in the trophozoite stage, which is the most resistant
of the parasitic protozoa. Reproduction takes place by longitudinal binary fission.
Habitat:
T. vaginalis restricted to the genitourinary tract of both sexes; in the vagina and urethra of female and in
the prostate, seminal vesicles and urethra of male (Sexually Transmitted Infection STI) (Trichomoniasis).
Diagnostic stage: Trophozoite.
Infective stage: Trophozoite.
Transmission:
• Sexual intercourse is the main route.
• Contaminated toilet articles and toilet seats.
• Newborn infants may attract infection through the birth canal.

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Introduction to Blood Protozooa

Haemoflagellates
This family includes two important genera:
1. Genus Leishmania.
2. Genus Trypansoma.
Some common features of these parasites are:
1. All members of the family have similar life cycle. They require insect vector as intermediatehost.
2. They live in blood and tissues of their vertebrate host (man) and in the gut of their vector.
3. No sexual cycle is known, multiplication is by binary fission.
4. Haemoflagellates exist in two or more of morphological stages.
Parasite Amastigote Promastigote Epimastigote Trypomastigote
T. gambiense Vector
Vector and
& -------------- ------------------ ,blood,CSF.lymph
culture
rhodesiense node
Vector and
T. cruzi Tissue ------------------ Vector and blood
culture
Vector and
Leishmania sp Tissue ------------------ ---------------------------
culture

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1. Genus Leishmania
Members of this genus are parasites of man, dogs and rodents. They are obligate intracellular parasites.They
have heteroxenous life cycle. They occur in two forms:
• Leishmania (amastigote) form: It occurs in the definitive host as intracellular parasites and
multiplies as Leishmania bodies in macrophages and other phagocytic cells of the reticuloendothelial
system (e.g. spleen).
• Leptomonad (promastigote) form: It occurs in the culture or in the gut of the vector.
Diagnostic stage: amastigote in host tissue scrapping and biopsies while leptomonad form in culture
Vectors: members of family Psycodidae Phlebotomus sp (Old World)
Lutzomyia sp (New World)
Infective stage: leptomonad form (promastigotes).

• Life cycle:
• When the female sand fly bites an infected person with Leishmania sp it takes the organisms (Leishmania
bodies) with the blood meal.
• Leishmania bodies (amastigote) change to leptomonad (promastigote) form.
• The promastigotes multiply (binary division) while attaching to the gut epithelium (Salivary glands are
not infected).
• When the sand fly bites a healthy person, it regurgitates the infective stage (leptomonad form) in the
biting site where inoculation of the infective stage takes place.
• In the vertebrate host (man), leptomonad (promastigotes) forms are phagocytozed by host macrophages
and transform into amastigotes, and multiply by binary fission.
• The amastigotes form breaks the infected cells and re-infect other cells (reticulo-endothelial cells) and
ready to repeat its life cycle.
• In case of the old world “L. tropica “, the parasites produce dermal leishmaniasis, usually a self-healing
lesion called "oriental sore". The reaction is confined to the skin; thus, the parasites do not circulate in
the blood to the internal organs.
• Whereas in L. donovani, the parasites migrate to endothelial cells of the reticuloendothelial system and
polymorphonuclear leukocytes of the blood, spleen, lymph and bone marrow, and produce visceral
leishmaniasis, which can be fatal if untreated.

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• In the new world, mucocutaneous leishmaniasis initiates with a lesion at the biting site but the parasites
can undergo metastasis to the nose and mouth and cause a disfiguring and untreatable disease.
1- Cutaneous leishmaniasis
Host: Man, (dogs and rodents are reservoir hosts).
Vector: Phlebotomus papatasii and Lutzomyia sp (sand fly)
Disease: Cutaneous leishmaniasis
Geographical distribution:
It is present where the vector (sand fly) is present, more than 90% of the world's cases of cutaneous
leishmaniasis occur in Afghanistan, Algeria, Egypt, Iran, Iraq, Saudi Arabia, Syria, and in new world
in Brazil and Peru.
2- Visceral leishmaniasis

"Kala-azar fever, Dumdum fever, black fever"

Host: Dogs and rodents are reservoir hosts, except in India man is the only reservoir.
Vector: Phlebotomus papatasii and Lutzomyia sp (sand fly)
Disease: visceral leishmaniasis disease.
Geographical distribution:
Middle East, Mediterranean region, part of Africa; India, Africa and China, as well as new world
visceral leismaniasis.
Transmission:
The organisms can be transmitted not only by sandflies but also congenitally and parenterally (e.g.,
through blood transfusions or sharing of needles).

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2. Genus Trypanosoma
They are elongated leaf-like organisms.
Classification of Trypanosomes according to their methods of transmission.
I. Section Salivaria (Anterior station):
Transmission is by injection of the infective stage (metacyclic trypansome) which is present in saliva
of insect. T. gambiense and T. rhodesiense.
II. Section Stercoraria (Posterior station): T. cruzi.
I. Section Salivaria (Anterior station)
African trypanosomes
T. gambiense and T. rhodesiense
• T. gambiense causes “West African, Gambian African trypanosomiasis or chronic sleeping sickness.
• T. rhodesiense causes east African or Rhodesian African trypanosomiasis or acute sleepingsickness.

Vector: Glossina palpalis (Tsetse fly) in T. gambiense, Glossina moristans in T. rhodesiense

(Biological transmission).

Habitat: Blood, lymph channel throughout the body, CSF, connective tissue, intracellular space, brain
Infective stage: Metacylic trypanosomes; which is a short stumpy form.
Transmission:
• The disease is mostly transmitted through the bite of an infected tsetse fly but there are other ways in
which people are infected with sleeping sickness.
• Mother-to-child infection: the trypanosome can cross the placenta.
• Accidental infections have occurred in laboratories due to pricks from contaminated needle or via
blood transfusion.

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Life cycle of Trypanosoma gambiense & rhodesiense

*************
2- Section Stercoraria (posterior station)
Trypanosoma cruzi
American trypanosomiasis “Chaga‟s disease”
Host: Man, specially infants and young children.
Habitat: Tissues of mesenchymal origin as heart muscle, smooth muscles, thyroid gland, bonemarrow, lung,
brain and macrophage-phagocyte (reticuloendothelial system.)
Geographical distribution: Central and South America.
Vector: Triatoma megista (Kissing bugs or cone-nose, winged-bugs).
Infective stage: Metacylic trypanosomes Transmission:
1- Bite of reduviid bug which defecate during the process of feeding. Insect deposits infective faeces near
or at the bite site
2- Accidental ingestion of bug.
3- Transmission by blood transfusion or via the placenta from mother to child may occur (congenital
transmission).
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4- Organ transplants using organs from infected donors.

Morphology:
1- Trypomastigote form:

• Size: 20 micr.
• Shape: C-shaped, monomorphic posterior end is pointed.
• Undulating membrane: Narrow and is not much folded.
• Nucleus: Central
• Kinetoplast: Oval and situated near the posterior end.
2- Amastigote form:

• On the entry to the host cells trypomastigote form changes to amastigote when they enter
blood, they change to trypomastigote form.
Life cycle:
In the vector:
1- When the winged bug bites an infected patient it takes the trypanosomes (trypomastigoteform), which
pass to the gut. They turn into leishmanoid (amastigote) forms, which multiply by binary fission and
turn into crithidial (epimastigote) forms pass to the rectum. In the rectum it turns into metacyclic
trypanosome, which is the infective stage.
2- The metacyclic trypanosomes pass out in the faeces. They can penetrate the mucous membranes or skin
actively. Triatomids commonly defecate after feeding and most human infections occur when faeces
are rubbed into the eyes or mucous membranes following a bite (posterior station).
In man:
1. The metacyclic trypanosomes enter the cells of the reticuloendothelial system and striatedmuscles
especially of the heart where they transform into leishmanoid form.
2. They multiply by binary fission, destroying the host cells and forming cyst-like nests of parasites
(pseudocyst).
3. The leishmanoid form turns into trypanosome form, which re-enter the blood to be picked upby the
winged bugs and repeat its life cycle.

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Life cycle of Trypansoma cruzi

**********
Family: Sarcocystidae
1. Genus: Toxoplasma
Toxoplasma gondii is an obligate intracellular parasite. The predator host is mainly the domestic cat,while
man, animals (cattle, sheep, goat, pig) and birds (chicken, pigeon) serve as prey hosts.
Morphology:
Trophzoite: Banana-shaped or crescentic with one end rounded and broad while the other end is pointed.
Nucleus: vesicular, lying central or towards the broad end.
Developmental stages:
1. Oocysts:
These are found in the faeces of cats, unsporulated Sporulation occurs in the soil within 1-3 days. The
sporulated oocyst contains 2 sporocysts each with 4 sporozoites (Disporocystic tetrazoic oocyst).
2. Schizonts:
Occur mainly in the intestine of cats. The trophozoite nucleus divides, followed by cytoplasmic

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divisions leading to formation of 32 merozoites.

3. Gamonts:
Occur most commonly in the intestine of cats. The macrogamete and microgamete unite to
form the zygote within the oocyst, which passes to the lumen of the intestine unsporulated.
4. Tachyzoites:
Occur in many cell types of the prey host as neurons, endothelium, liver, lung, glandular or epithelial
cells, muscle cells, foetal membrane and leucocytes. In acute infection they may be found free in blood
and peritoneal exudate.
5. Bradyzoites:
These are contained in cysts and occur mainly in the muscle, liver, lung and brain. There may be
several thousands of the organisms in one cyst.
Life cycle:
1. In the predator host:
• Most cats become infected by ingestion of Toxoplasma infected animals, usually rodents, whose
tissues contain tachyzoite or bradyzoite cysts.
• The cyst wall is digested in the cat’s stomach.
• The released zoites penetrate the intestinal epithelium to start a cycle of schizogony with
repeated generation followed by gametogony with formation of oocysts that release to the lumen
of intestine and pass with cats’ stool within 3-10 days.
• Sporulation of oocysts occurs in soil; it takes 1-3 day at temperature 24oC. The oocyst forms 2
sporocysts each have 4 sporozoites (Disporocystic tetrazoic).
2. In the prey host:
• When the sporulated oocyst is ingested by the prey host the sporozoites are liberated and penetrate
the intestinal wall, circulate with blood and are called tachyzoites.
• When a tachyzoite enters a cell, it multiplies by endodyogeny within a vacuole formed by the host
cell.
• When 8-16 tachyzoites have accumulated the cell ruptures and new host cells are infected. This
process forms the acute phase of toxoplasmosis.
• The parasitaemia continues for sometimes until the antibodies appear in the plasma. These
antibodies limit the invasiveness of the tachyzoites and result in the formation of cysts

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containing thousands of organisms, which are termed bradyzoites. This process forms the
chronic or latent form of toxoplasmosis. If the host immunity wanes, the cyst may rupture,
releasing the bradyzoites, which become active and acquires the invasive character of
tachyzoites.
Mode of Infection of Toxoplasmosis:
1. Ingestion of sporulated oocysts in contaminated vegetables or water or during handling of littertrays.
2. Further spread of oocysts may occur by flies, which can contaminate vegetables, meat and animal fodder.
3. Ingestion of tachyzoites or bradyzoites in cysts in undercooked meat or during handling infected raw
meat.
4. Transplacental, occurs in pregnant animals or humans when exposed for the first time to T.gondii
infection.

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2-Genus: Sarcocystis
It is an obligatory heteroxenous parasite that has a carnivorous predator host (dogs, cats and man) and a
wide variety of prey hosts (sheep, cattle, buffalo, pig, camels, birds, fish and man).
Morphology:
• Cysts are microscopic, appear as bluish cytoplasmic inclusions.
• Cyst wall is very thin, but sometimes acquires fine processes projecting outwards called
cytophaneres.
• From its inner most layer, internal septa divide the cyst into compartments.
• The spores are banana-like with one end broad and rounded, while the other end is tapering. The
nucleus lies at the broad end.
Developmental stages:
1. Oocysts:
These are developed in the small intestine of the predator host, where sporulation takes place. The
sporulated oocyst has a smooth wall and contains two sporocysts each has four sporozoites
(disporocystic tetrazoic). The oocyst wall is fragile, so the sporocysts are usually released in the
lumen and passed with faeces of the predator host. The sporocysts have often been mistaken for
oocysts of Cryptosporidium.
2. Gamonts:
These are developed directly from the released sporozoites and differentiate into macro and
microgamet that unite to form the oocyst.
3. Schizonts:
These are found in the endothelial cells of blood vessels in the prey hosts.
4. Bradyzoite cysts: (Sarcocyst or Miescher’s tubules).
These are present in the muscles of the prey hosts. It may be micro or macroscopic cysts appear as
whitish streaks with spindle or fusiform-shape, running in the direction of the muscle fibers.
Transmission:
1. Ingestion of sporocysts (contain four sporozoites) in contaminated food or water by dog or cat faeces.
2. Flies may mechanically contaminate food or drink with the sporocysts. 3-Infection to the final host,
including man, occurs by ingestion of bradyzoite cysts in the muscles through eating raw or
undercooked meat.
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Life cycle of Sarcocystis spp.

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Genus: Plasmodium
Members of this genus are the cause of malaria. Four species of plasmodia may give rise to malaria in man:
1. Plasmodium vivax producing benign tertian malaria. It is widely spread in tropics and some
temperate zones. It is found in Egypt (in the Delta).
2. P. malariae producing quartan malaria. It is present in the tropics and subtropics.
3. P. falciparum causing malignant subtertian malaria. It is distributed in the tropics and
subtropics. It is called malignant because it is misleading in diagnosis.
4. P. ovale causing ovale tertian malaria. It is confined mainly to the tropics.
Vector: female Anopheles mosquito.
Transmission and Infective stages:
1. Biological: through the bite of female Anopheles mosquito. Infective stage is the sporozoite.

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2. Mechanical: through blood transfusion of an infected donor or among drug addicts. Infectivestage is
the schizont or merozoite.
3. Congenital: this occurs through placental defects or during labour (connatal). Infective stage isthe merozoite.
Life cycle of Plasmodium:
The life cycle of the parasite is completed in two different hosts.
1. Asexual cycle “Schizogony” occurs in man.
a) Liver cycle take place within the hepatic cells and is called “Pre-erythrocytic and exo- Erythrocytic
cycle.
Pre-erythrocytic and exo-erythrocytic cycles:
When the female Anopheles bites a man, it injects the sporozoites into his blood. then reach the liver
cells to start a pre-erythrocytic cycle where they multiply producing schizonts. Rupture of these
schizonts release merozoites most of them invade quickly the red blood cells to begin the erythrocytic
cycle.
In P. vivax and P. ovale some merozoites re-invade liver cells and differentiate into nonsexual
hypnozoites that remain dormant for weeks, or even years.
The activated hypnozoites undergo exoerythrocytic schizogony, forming a wave of merozoites that
cause a relapse.

b) Blood cycle or Erythrocytic cycle which take place inside the RBCs
This cycle begins with the entrance of the zoites inside the red blood cell, where it grows and
reproduces on the expense of the haemoglobin of the infected red blood cell.
The developmental stages inside the R.B.Cs. are:
- Ring stage. - Trophozoite.
- Schizont. - Gametocyte.
The entire cycle of shcizogony occupies a period of 48 h in P. vivax, P. ovale, 36-48 h in P.falciparum,
and 72 h in P. malariae. Then the red blood cell ruptures releasing merozoites and haemozoin pigment,
which is the cause of the malarial paroxysm. The free merozoites while circulating in the blood stream
attack new red blood cells and the cycle is repeated several times.
2. Sexual cycle, “Gametogony” and “Sporogony” occur in the female Anopheles mosquito (arthropod
host)
• When the female Anopheles mosquito sucks up blood from a malarial patient, it takes up both the

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sexual and asexual forms. In the stomach of mosquito, all forms die except the gametocytes, which are
transformed within few minutes into gametes (Gametogony).
• Fertilization takes place between the male (microgametocyte) and female gametes (macrogametocyte)
resulting in “zygote”.
• The zygote elongates and becomes motile and is called “ookinete”.
• It takes a spherical shape and becomes surrounded by a cyst wall and is called “oocyst”.
• The oocyst increases in size, the nucleus divides into a large number of nuclei each becomes surrounded
by the cytoplasm, giving rise to slender bodies with pointed ends termed “sporozoites”. The occyst
(now known as sporocyst) ruptures and the sporozoites reach the salivary glands. Infection to man is
by the saliva injected by the mosquito during biting to prevent blood coagulation.

Life cycle of Plasmodium

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Genus: Babesia
Babesia microti
Human babesiosis is a zoonosis, acquired by tick bite when individuals accidentally interact with the natural life
cycle of the parasite; causing haemolytic malaria like disease.
Host: All domestic animals and accidentally man.
Vector: Hard ticks (Ixodes) are the vector inside which the transovarian infection occurs via the egg from one
tick generation to the next hens coinfection with Borrelia occurs.
Infective stage: sporozoites.
Transmission: hard tick bite.

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