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Toxoplasmosis

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Umar Amber
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12 views30 pages

Toxoplasmosis

Uploaded by

Umar Amber
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Course: Parasitology

Course code:MIC313
Credit hours: 3
INTRODUCTION
• Toxoplasma gondii is a protozoan parasite
responsible for toxoplasmosis.
• It affects a wide range of warm-blooded animals,
including humans.
• Emphasize its global impact: infecting an estimated
one-third of the world’s population.
• it can cause serious health problems in pregnant
women and people with weakened immune systems.
Morphology
Three key forms of the parasite:

1.Tachyzoites: Active, crescent-shaped,


rapidly dividing stage.

2.Bradyzoites: Dormant stage within tissue


cysts, responsible for chronic infections.

3.Oocysts: Environmentally resistant stage,


produced in the intestines of cats.
Morphological forms of toxoplasma
Transmission
1. Eating undercooked, contaminated meat
containing tissue cysts.

2. Ingestion of water or food contaminated with


oocysts from cat feces.

3. Vertical transmission (mother to fetus during


pregnancy).

4. Rare cases: Organ transplantation or blood


transfusion.
Transmission
Life Cycle Overview
The life cycle of Toxoplasma gondii is intricate
and involves two main hosts:
Definitive Host (Cats): Sexual reproduction
occurs exclusively in the intestines of cats,
leading to the production of oocysts.
Oocysts are excreted in cat feces, contaminating
the environment.
Intermediate Hosts (Humans and Other
Mammals/Birds): In these hosts, T. gondii
reproduces asexually, forming tachyzoites
(active stage) and bradyzoites (cysts).
Oocysts shed by cats are resistant and survive
in soil, water, or food for extended periods,
enabling transmission.
Humans and animals acquire the infection by
ingesting oocysts (from contaminated soil, water,
or vegetables) or tissue cysts (from
undercooked infected meat).
Vertical transmission (from mother to fetus) and
other rare routes, such as organ transplantation,
are also significant.
Toxoplasma gondii,Life-cycle
Pathogenesis
1. Host Cell Invasion:
Toxoplasma gondii uses specialized structures
called apical organelles (micronemes, rhoptries) to
invade host cells. Once inside, it creates a
protective compartment called the parasitophorous
vacuole, shielding it from the host's immune
system. This allows the parasite to multiply without
being detected or destroyed.
Pathogenesis
2.Tissue Damage:
The parasite spreads systemically, reaching
tissues such as the brain, muscles, and retina.
Inside these tissues, T. gondii forms cysts, which
may remain dormant for the host's lifetime. The
cysts' presence can cause inflammation and
disrupt normal tissue function, especially in
immunocompromised individuals.
Clinical Manifestations
Categorize symptoms based on infection type:

•Acute Toxoplasmosis: Flu-like symptoms (fever,


swollen lymph nodes).
•Chronic Infection: Often asymptomatic but may
reactivate in immunocompromised individuals.
•Congenital Toxoplasmosis: Severe effects on
the fetus, including neurological and ocular
damage.
•Severe Cases: Encephalitis, myocarditis, and
vision loss.
Toxoplasmosis
Clinical features
Toxoplasmosis in Pregnancy
In general :
The earlier in pregnancy the mother is
infected, the lower is the risk of an
infection of the fetus, but the severer is the
disease.
The later in pregnancy the mother is
infected, the higher is the possibility of
fetal infection, and the disease is less
severe (often subclinical infection)
Congenital Toxoplasmosis

When a pregnant woman is infected,


Toxoplasma gondii can cross the placental
barrier, leading to congenital toxoplasmosis in
the fetus.
First Trimester: The risk of transmission is
lower, but the consequences are more severe,
including miscarriage or major fetal anomalies.
Later Trimesters: The risk of transmission
increases, but symptoms may include
neurological damage, hydrocephalus, or ocular
issues.
Long-Term Effects on the Fetus:

• Children born with congenital toxoplasmosis


may face developmental delays, epilepsy,
hearing loss, or retinochoroiditis, even if
asymptomatic at birth.
• Vision problems and cognitive impairments can
emerge later in life.
Congenital Toxoplasmosis
Diagnosis
1. Serological Tests:
These are the most commonly used diagnostic
tools for Toxoplasma gondii.
IgM Detection: Indicates a recent or acute
infection. High levels of IgM are present during the
early stages of infection.
IgG Detection: Indicates past exposure. Rising
levels over time can confirm an active or recent
infection.
2. Molecular Methods:
Polymerase Chain Reaction (PCR) is a sensitive
and specific method to detect T. gondii DNA in
blood, cerebrospinal fluid (CSF), or amniotic fluid.
This is especially valuable for diagnosing
congenital toxoplasmosis or cases with central
nervous system involvement.
3. Prenatal Diagnosis
Amniocentesis allows for the detection of T.
gondii DNA in amniotic fluid, helping diagnose
congenital toxoplasmosis.
4. Histopathology: Tissue biopsies can reveal T.
gondii cysts or tachyzoites under the microscope.
This is typically used when other methods fail or
in cases requiring tissue-specific diagnosis.

5. Imaging Studies:
MRI or CT scans are essential for detecting
brain lesions in cases of toxoplasmic encephalitis,
particularly in immunocompromised individuals like
HIV/AIDS patients.
Treatment
Acute Infection:

The standard treatment includes a combination


of Pyrimethamine and Sulfadiazine, which
work together to inhibit folic acid synthesis in the
parasite.
Folinic Acid (Leucovorin) is added to
counteract the effects of folate depletion caused
by the treatment.
Congenital Cases:

For infections diagnosed during early


pregnancy, Spiramycin is the drug of choice, as
it reduces the risk of transmission to the fetus.
If fetal infection is confirmed later in pregnancy,
Pyrimethamine and Sulfadiazine are used, as
they are more effective in treating the infection
directly in the fetus.
Chronic Infection:
In immunocompromised patients, therapy aims
to prevent or manage reactivation of the
infection.
Special Cases:

For patients with toxoplasmic encephalitis


(commonly seen in AIDS patients), intensive
therapy with Pyrimethamine, Sulfadiazine, and
Folinic Acid is required for an extended
duration.
Prevention & Control
Provide actionable steps to prevent infection:

1. Properly cook meat to kill tissue cysts.

2. Wash fruits and vegetables thoroughly.

3. Practice hygiene when handling cats or


gardening.

4. Pregnant women should avoid cleaning litter


boxes.

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