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Toxoplasma gondii
and toxoplasmosis
Cheng Yanbin
April 2005
Toxoplasma gondii
Infects most species of warm blooded
animals,including humans.
Cause the disease toxoplasmosis.
Found in almost every country.
Estimated to infect 50% of the
population of some countries.
Most of infections are asymptomatic.
Morphology I
Trophozoite (tachyzoite & bradyzoite)
banana form or crescent-shape, 4~7
µm by 2~4 µm. (Pseuocyst)
Cyst: spherical, has a think wall
around the masses of bradyzoites.
Morphology II
Mature oocyst: contains two
sporocysts that contains 4
sporozoites.
Life cycle
Cats are the final host;
Mammals, birds and humans are the
intermediate host;
The common infectious stages:
A) The tachyzoites (in groups or
clones);
B) The bradyzoites (in tissue cysts);
C) The sporozoites (in oocysts) .
Life cycle
Human infection may be acquired in
several ways:
A) ingestion of undercooked infected meats
containing Toxoplasma cysts;
B) ingestion of the oocyst from fecally
contaminated hands or food;
C) organ transplantation or blood
transfusion;
D) transplacental transmission;
E) accidental inoculation of tachyzoites
Life cycle
In the human body, the actively
proliferating trophozoites or
tachyzoites are usually seen in the
early, more acute phages of the
infection. The cysts are formed in
chronic infections and are found
primarily in muscle, brain and other
organs. It is a result of the host
immune response.
Clinical diseases
The majority of infections are nosymptoms. The most severe symptoms
are seen with congenital, transpacental
infections or infections in the
compromised patients.
Mechanism: When the trophozoites are
actively proliferating, they invade adjacent
cells from the original infected cells as it
ruptures. This process create s focal
lesions. The organisms can be
disseminated via the lymphatic liquid and
the blood stream to other tissues.
Congenial infections
It may be particularly severe if the
mother acquires the infection during the
first or second trimester of pregnancy.
Symptoms in these infants may include
retinochoroiditis, cerebral calcification,
hydrocephalus or microcephaly.
Symptoms of CNS involvement may not
appear until several years later.
Asymptomatic congenital infections
were common in prospective studies.
Acquired infections
In 90% of cases, no clinical symptoms
are seen during the acute infection.
However, rare symptoms seen in
acquired acute infections would include
chorioretinitis, myositis, and
symptomatic heart, lung, liver, or CNS
involvement.
Infections acquired can be categorized
into four groups:
Lymphadenitis, fever, headache, and myalgia,
with a possibility of spenomegaly.
Typhus-like exanthemous form with
myocarditis, meningoencephalitis, atypical
pneumonia, and possibly death;
CNS involvement, which is usually fatal;
Retinochoroiditis, which may be severe,
requiring enucleation.
The most common manifestation in adults is
local or generalized lymphadenopathy, and
the nodes most commonly involved are those
of the neck.
Infections in the
immunocompromised
patients
Infections in the compromised patients can
lead to severe complications (Hodgkin’s
disease, non- Hodgkin’s lymphomas,
leukemias, solid tumors, AIDS and
transplant recipients).
The CNS is primarily involved, with diffuse
encephalopathy, meningoencephalitis or
cerebral mass lesions
Laboratory diagnosis
Observation of T.g in patient specimens,
such as bronchoalveolar lavage
material, or lymph node biopsy.
Isolation of T.g from blood or other body
fluids, by intraperitoneal into mice or
tissue culture.
Serological tests using killed antigens.
Detection of T.g DNA by PCR.
Treatment
Treatment is not needed for a healthy
person who is not pregnant.
Treatment may be recommended for
pregnant women or persons who have
weakened immune systems.
Oral administration of pyrimethamine,
usually accompanied by sulfadiazine, is
the treatment of choice at this time.