TOXOPLASMOSIS

Toxoplasma gondii

Dr. Shatarupa Chakraborty

 INTRODUCTION
Toxoplasma gondii is a
protozoan, obligate
intracellular parasite
Cause Toxoplasmosis
Infects most species of warm-
blooded animals, including
humans.
Members of the cat family
Felidae- the only known
definitive host for the sexual
stages - the main reservoirs of
infection.
Alter the behavior in Rodents-
Manipulation hypothesis (
Decrease the aversion of
rodents towards cats urine)
Toxoplasma oocyst fecal floatation.
 TAXONOMY

Phylum Apicomplexa
Class Conoidasida
Subclass Coccidiasina
Order Eucoccidiorida
Suborder Eimeriorina
Family Sarcocystidae
Subfamily Toxoplasmatinae
Genus Toxoplasma
Geographical distribution:
Worldwide, one of the most common human infections
More common in warm climates
In France and C. America
Infection is more common in warm climates and lower
altitudes than cold climates and mountainous regions.
 STRUCTURE/MORPHOLOGY

Crescent shaped, pointed anterior, round posterior, 2 by 6

Micrometer
Conoid: Rotate, tilt, extent
Rhoptries: Secretory function associated with host cell
penetration
A Pellicle, apical rings, microneme, micropore, microtubules,
ER, apicoplast( multi-membrane plastid like organelle)
Site of infection:
Small intestine
Brain
Eye
Fetal stage
Skeleton muscles
Signs & symptoms:
Body aches
Swollen lymph nodes
Headache
Fever
Fatigue
Occasionally, a sore throat
People with weakened immune system
Headache
Confusion
Poor coordination
Blurred vision caused by severe inflammation of your retina (ocular
toxoplasmosis).
Host :
Intermediate host:
Human, cattle, birds, rodents, pigs, and sheep.
Humans get the disease through ingestion of a
cyst, infected raw meat, trans placental, organ
transplantation or blood transfusion.
Definitive host:
Mainly domestic and wild cats.
Cats can become infected by ingesting
sporulated oocyst or infected rodent or a bird.
 LIFE CYCLE
The three stages of T. gondii
(i) Tachyzoites (trophozoites): rapidly proliferate and
destroy infected cells during acute infection.
(ii) Bradyzoites: slowly multiply in tissue cysts.
(iii) Sporozoites in oocysts.
Cats become infected with T. gondii by carnivorism or by
ingestion of oocysts
 LIFE CYCLE
(i) Tachyzoites (trophozoites): rapidly proliferate and destroy infected cells during
acute infection.
(ii) Bradyzoites: slowly multiply in tissue cysts.
(iii) Sporozoites in oocysts.
LIFE CYCLE
Tachyzoites:
Motile & Quickly Multiplying
Sporozoites Stage-convert Into Tachyzoites.
Tachyzoites Spread Throughout The Body
Via The Blood Stream.
Tachyzoites Stage-convert To Bradyzoites To Form Tissue
Cysts.
Merozoites:
Divide Quickly.
Bradyzoites Convert Into Merozoites
Inside Intestinal .
Bradyzoites:
Dividing Stage Of The Parasite.
Bradyzoites Released From The Cyst Before Converting
To The Proliferative Tachyzoite Stage.
Tachyzoites Then Convert Back To Bradyzoites.
Reproduce Inside Host Cells To Form Tissue Cysts In
The New Host.
Sporozoites:
Sporozoites are the stage of the
parasite residing within oocytes.
warm-blooded host consumes an
oocyst, sporozoites are released from it.
 EPIDEMIOLOGY / TRANSMISSION
Toxoplasmosis is one of the most common infections
of humans throughout the world(30 50% of global
population exposed or chronically infected)
Infection is more common in warm climates and at
lower altitudes.
Distribution is probably related to conditions favoring
the sporulation and survival of oocysts.
Variations in the prevalence of infection between
geographic areas and between population groups
within the same locale are probably due to
differences in exposure.
Eg 1: A high prevalence of infection in France (65 to 85%) has been related
to a preference for eating raw or undercooked meat.
Eg 2: A high prevalence in Central America has been related to the
frequency of stray cats in a climate favoring the survival of oocysts.
 EPIDEMIOLOGY / TRANSMISSION

Human infection may be acquired in several ways:

Ingestion of undercooked infected meat containing T. gondii
cysts
Ingestion of the oocyst from fecally contaminated hands, food,
or water.
Organ transplantation or blood transfusion
Transplacental transmission
Accidental inoculation of tachyzoites
The two major routes of transmission to humans are
oral and congenital.
In human, The tachyzoites are pressured by the hosts
immune response to transform into bradyzoites and
form tissue cysts; these cysts may remain throughout
the life of the host
Clinical disease may appear if the host becomes
immuno suppressed and the cysts rupture, releasing the
parasites.
 EPIDEMIOLOGY / TRANSMISSION

The transmission rate from mother to

fetus ranges from 11% in the first
trimester to 90% in the late third
trimester, with an overall transmission
rate is 40 to 50%.
CLINICAL SIGNIFICANCE/ PATHOGENECITY

Toxoplasmosis can be categorized into

four groups:
1- Acquired in the immunocompetent patient
2 - Acquired or reactivated in the
immunodeficient patient
3 - Congenital
4 Ocular
Methods of diagnosis and their
interpretations may differ for each clinical
category.
Acquired in the immunocompetent patient

Generally an asymptomatic infection.

10 to 20% of patients with acute infection
may develop cervical Lymphadenopathy
and/or a flu-like illness.
The clinical course is benign and self-
limited
Symptoms usually resolve within weeks to
months.
Acquired or reactivated in the immunodeficient patient

Immunodeficient patients often have

central nervous system(CNS) disease but
may have myocarditis or pneumonitis.
In patients with AIDS, Toxoplasmic
encephalitis is the most common cause of
intracerebral mass lesions
Toxoplasmosis in immunosuppressive
drugs using patients due to either newly
acquired or reactivated latent infection.
 Congenital Infection
Congenital toxoplasmosis results from an acute
primary infection acquired by the mother during
pregnancy.
The incidence and severity vary with the
trimester during which infection was acquired.
Treatment of the mother may reduce the severity
of symptoms in the infant, So an accurate
diagnosis is extremely important
Many infants with subclinical infection at birth will
subsequently develop signs or symptoms of
congenital toxoplasmosis
Treatment may help prevent subsequent
symptoms.
 Ocular Infection
Ocular toxoplasmosis, an important cause of
Chorioretinitis in the United States, may be the
result of congenital or acquired infection
Congenitally infected patients are often
asymptomatic until the second or third decade of
life
Lesions develop in the eye presumably due to
cyst rupture and subsequent release of
tachyzoites and bradyzoites.
Chorioretinitis is characteristically bilateral in
congenital infection but is often unilateral in
individuals with acute acquired T. gondii infection.
 DIAGNOSIS
DIRECT EXAMINATION :
Microscopy
Antigen Detection
Nucleic Acid Detection Techniques
SEROLOGIC TESTS :
Determination of Immune Status
Diagnosis of Acute Acquired Infections
Diagnosis of Congenital Infection
Diagnosis of Infection in the Newborn
 DIRECT EXAMINATION

MICROSCOPY:
The slides should be air dried,
fixed in methanol, and stained
with Giemsa for microscopic
examination.
Tachyzoites may be observed as
free organisms or within host
cells such as leukocytes.
Well preserved tachyzoites are
crescent shaped and stain well
Degenerating organisms may be
oval and stain poorly.
Tissue imprints stained with
Giemsa may reveal T. gondii cysts.
 DIRECT EXAMINATION
ANTIGEN DETECTION:
Immunologic methods are used to identify
parasites in tissue sections or tissue cultures
For detecting tachyzoites in tissue sections
Fluorescein isothiocyanate-labeled antisera
Peroxidase-labeled antisera
Enzyme immunoassay(EIA) antigen detection
Due to lack sensitivity for human samples it is not
recommended.
NUCLEIC ACID DETECTION:
Important use of PCR appears to be in the prenatal
diagnosis of congenital toxoplasmosis
PCR of amniotic fluid has been shown to be more
sensitive for the confirmation of fetal infection
 SEROLOGIC TESTS
Many tests are there for the detection of
antibodies to Toxoplasma:
Methylene blue dye test (DT)
Commercial kits for agglutination tests
Indirect fluorescent antibody (IFA) tests
Enzyme immunoassay(EIA)
The serologic tests, however does not give a
clear idea about the surety of infection.
The specificity and sensitivity rates from
time to time, is used to select a Toxoplasma-
specific antibody accordingly
Diagnosis of Acute Acquired Infections
If an acute acquired infection is suspected,
the serum is tested for the presence of
Toxoplasma-specific antibodies
A negative result in DT, IgG IFA or EIA
excludes the diagnosis of acute Toxoplasma
infection in an immunocompetent person.
The presence of typical Lymphadenopathy,
a high DT or IgG IFA titer (300 IU/ml or
1:1,000), and the presence of specific IgM
are indicative of acute infection
 Diagnosis of Congenital Infection

Diagnosis of congenital toxoplasmosis involves:

Diagnosing acute infection in a pregnant woman
Demonstrating infection in the fetus
Documenting infection in the newborn infant
Amniotic fluid PCR is the recommended test of
choice to establish the intrauterine diagnosis of
congenital toxoplasmosis
If collected, fetal blood should be tested for
Toxoplasma specific IgG, IgM, and IgA antibodies
Demonstrating Toxoplasma-specific IgM or IgA
antibodies in fetal serum or isolating the parasite
from fetal leukocytes is a definitive diagnosis of
fetal infection.
 Diagnosis of Infection in the Newborn

Diagnosis is made through a combination of

serologic testing, parasite isolation, and
nonspecific findings
An attempt should be made to isolate T. gondii
from the placenta, amniotic fluid, and cord blood
The childs serum should be tested for total IgG
and IgM antibody levels and Toxoplasma-specific
IgG, IgM, and IgA antibodies.
A child with suspected congenital toxoplasmosis
should have a thorough general, neurologic, and
ophthalmologic examination and a computed
tomographic scan of the head
 Diagnosis of Ocular Infection
Toxoplasma Chorioretinitis results from
both acute infection and congenital
infection
In addition to demonstrating IgG antibody
to Toxoplasma in the serum of a person
with compatible eye lesions,
demonstration of the local production of
antibody and detection of parasite DNA
in aqueous humor have been used to
document active ocular toxoplasmosis
Treatment:
Sulphonamides
Pyrimethamine
Spiramycine
Atovaquone
Clindamycin
Spiramycin during pregnancy
Antibiotics and steroid tablets
during an infection
Pathogenesis:
Infection with Toxoplasma in immunocompetent
persons is generally an asymptomatic infection.
The clinical course is benign and self-limited;
symptoms usually resolve within a few months to a year.
Immunodeficient patients often have central nervous
system (CNS) disease but may have retinochoroiditis,
or pneumonitis. In patients with AIDS, toxoplasma
encephalitis is the most common cause of
intracerebral mass lesions and is thought to be
caused by reactivation of chronic infection.
Lymphadenitis is the most common in humans.
Children exhibit Hydrocephalous, retinochoroiditis, convulsion
and intracerebral calsifications.
Congenital neurological defects in infants.
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