Advanced Medical Parasitology

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Advanced medical parasitology

‫املرحلة الرابعة‬

‫طفيليات نظري‬

Sporozoa

Phylum Apicomplexa

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Toxoplasma gondii

The cause of toxoplasmosis: Obligate intracellular parasite.

Distribution: worldwide-distributed para. 20% - 75% of the population are


seropositive without any symptomatic episode.

Final hosts (definitive host): is the house or domestic cat and other cats and other
felidae.

Intermediate hosts: human being (considered as a dead end host) and wide range
of mammals (cattle, sheep, mouse and pig), birds and Hippopotamus amphibious.

Mode of transmission: (In human and other mammals (intermediate hosts))

1- Congenital via placenta, that is from mother or pregnant woman to the fetus.
2- Acquired by contaminated food and drinks especially infected meat (Ingestion
of undercooked infected meat).
3- Ingestion of the oocyst from fecally contaminated hands (oocyst during the
cleaning of cat litter box) or food, milk and water.
4- Organ transplantation or blood transfusion

Morphology : Trachyzoites are 3x6 um , pear – shaped organisms .

Toxoplasma gondii

Life cycle: Cats get infected by ingestion of cysts and the organisms penetrate the
submucosal epithelial cells where they undergo several generations of mitosis,
finally resulting in development of microgametocytes and macrogametocytes.
Fertilized macrogametes develops into oocysts that are discharged into the gut
lumen and excreted. Oocyst sporulate in the worm environment and are infectious
to a variety of animals including rodents and man. Sporozoites released from the
oocyst in the small intestine penetrate the intestinal mucosa and find their way into
macrophages where they divide very rapidly (trachyzoites) and form a cyst- like
which may occupy the whole cell.

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Infected cell bursts and release the trachyzoites to inter other cells including
muscles and nerve cell. (bradyzoites), these cysts are infectious to carnivores
(including humans).

Reproduction: 1. By binary fission

2. endodyogony.

Toxoplasmosis

Pathogenicity: the host’s ingestion of either tissue cysts containing bradyzoites or


oocysts containing sporozoites, the parasites are released from the cysts by a
digestive process. invasion of the viscera leads to enlargement of these viscera, such
as cardiomegaly. In pregnant women and immunodeficient hosts the parasite
causes serious consequences. Congenital infections occur in about 1_5 per 1000
pregnancies of which 5_ 10 % result in miscarriage (abortion) and 8_10 % result in
serious brain and eye damage to the fetus. 10_13 % of babies will have visual
handicaps. Although some of infected women will give birth to a normal offspring,
a small proportion of babies will develop active retino_ chorditis or mental
retardation in childhood or young adulthood.

In immunocompetent adults, toxoplasmosis may produce flu_ like symptoms:


associated with lymphadenopathy. The parasite may invade brain, liver, lungs and
other organs, and often death.

Post_ natal infection may lead to lymphadenitis, myalgia, headache, splenomegaly,


myocarditis, meningoencephalitis and pneumonia. Acute toxoplasmosis is
characterized by lesion in the heart, liver, lungs and brain.

Laboratory diagnosis
A. Pathogenic
1) Smears from Lymph node, bone marrow, spleen. For organism detection.
2) Body fluids (in acute infection) or from tissue (chronic infection) inoculated
intraperitonealy into young laboratory mice for demonstrations of the organisms.
B. Serological
Serology remains the primary approach for the diagnosis of toxoplasmosis.

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1) Indirect fluorescent antibody (IFA) test and ELISA test including IgM and IgG
kits.

Toxoplasmosis is normally diagnosed serologically by detection of parasite-specific


IgG and IgM antibodies.
IgM antibodies can be detected as early as one week after the primary infection, peak
within two to four weeks, then drop to below the detection limit within a few weeks; in
some cases persistence at low titers lasts longer. IgG antibodies appear somewhat later,
peak after two to four months and persist for many years. A high or rising IgG titer with
contemporal detection of IgM indicates an acute primary infection.
nnot be diagnosed by serological methods.

2) sabin-feldman dye test


depends upon the appearance in 2-3 weeks of antibody that will render the membrane
of laboratory cultured living Toxoplasma gondii impermeable to alkaline methylene
blue , so that the organism are unstained in presence of positive specimen.

C. Molecular diagnosis by PCR


Treatment: pyrimethamine, sulfadiazine or spiramycin.

In pregnant women: IgG titers show past infection whereas IgM titers

means recent acute infection.

Definitions

Endodyogeny:

Trophozoite (tachyzoite): It is oval to crescent-shaped with a pointed anterior end


and a rounded posterior end. An ovoid nucleus is present in the posterior end of the
parasite. Tachyzoite is the multiplying form seen during the acute stage of the infection.
It can invade any type of cell in a host and once inside a cell, it multiplies within a
vacuole by a process known as endodyogeny, or by binary fission or schizogony.
Tachyzoites divide until they fill the host cell, which then liberates them, and they
reinvade (or ingested by) other macrophages, repeating the process. The cell which
contains them, when becomes merely a bag full of tachyzoites, called(Pseudocyst).

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Tissue cyst:
It is spherical. This is the chronic stage of the infection. The tissue cysts can be found
in any organ of the body but are commonly found in the brain ,skeletal and heart
muscles. The cyst contain hundreds of bradyzoite ( cystozoites). Bradyziotes multiply
slowly.
Oocyst: This stage is only present in cats and other felines but not in humans. It is
oval. Each cyst is surrounded by a thick resistant wall. The oocyst librated from the
intestinal epithelial cell while still immature; it completes its development while
passing down the gut and after expulsion in the feces. Its contents are divided first into
two cells; these then secrete cyst walls to form 2 sporocyst. The content of each
sporocyst then divide once more to produce infective sporozoites.

In cat (definitive host):


Ingestion of the organism ( bradyzoite from tissue cyst) invades the mucosal cells of
the cat’s small intestine, and then they form schizont (asexual) and gametocytes
(sexual). After sexual fusion of gametes, zygotes are formed and a thin wall protect the
zygote and an oocyst develops, then exit into the gut lumen, then passes out via feces
as an oocyst with single sporoblast. Within each oocyst, 2 sporocysts form (zygote
divide into 2 sporoblast) in about 3-4 days, four sporozoite forms within each sporocyst
(i.e. 8 sporozoite) (infective oocyst).
In human and other mammals (intermediate hosts)
Swallowing the oocyst or tissue cyst initiate the development of ASEXUAL CYCLE.
This process occurs mainly in macrophages.
The sporozoites from the ingested oocyst and bradyzoites from the tissue cyst invade
the mucosal epithelial cell of the small intestine in which they multiply as tachyzoites
by endodyogeny. The tachyzoites divide until they fill the host cell which then liberates
them, and the tachyzoite reinvade (or ingested by) other macrophages, repeating the
process and form pseudocyst.
The multiplying tachyzoites also spread to distant extra - intestinal organ (e.g. brain,
eye, liver, spleen, heart, skeletal muscle and placenta of pregnant mother) by invading
lymphatics and blood.
The multiplication of tachyzoites constitutes the acute phase of infection.
If the host lives, and the infection is untreated, the host’s immune system becomes
effective and tachyzoites are destroyed, but the the parasite usually responds to this

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by entering other cells (muscle cells, neurons, and perhaps others) and secreting a
thin but tough cyst wall around itself form a tissue cyst and initiate the chronic
phase of the disease. A tissue cyst contains hundreds of bradyzoites.
If another intermediate host eats uncooked meat containing this tissue cyst ,
bradyzoites emerge in the duodenum and repeat the cycle.

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