TOXOPLASMOSIS: Diagnosis, Treatment and Prevention in Congenitally Exposed Infants

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TOXOPLASMOSIS: Diagnosis,

Treatment and Prevention in


Congenitally Exposed Infants
Astra Parahita
INTRODUCTION
Coccidian protozoan
Multiplies only in living cells
Sexual reproduction
Definitive host: cat
Asexual reproduction
Intermediate host: man, bird,
rodent
Toxoplasma
gondii
Toxoplasmosis is an important zoonotic parasitic disease worldwide
Congenital Toxoplasmosis
Pregnant woman is infected
Parasites cross the placenta
Fetus is Infected
Damaging effect
EPIDEMIOLOGY
Prevalence: varies greatly around the world
Prevalence depend on food production and
harvesting practices, water treatment,
environment, climate, and exposure to soil or
sand
Prevalence rates of IgG antibodies to T. gondii
in women of childbearing age provide insight
into the prevalence of congenital
toxoplasmosis
PATHOPHYSIOLOGY
Toxoplasma gondii:
Obligate intra-cellular protozoan parasite
Primary host: cats (humans intermediate
host)

The Cycle of Exposure
VERTICAL TRANSMISSION
Transplacental transmission occurs in 40% of
pregnancies in which the mother is exposed
for the first time during the course of the
pregnancy
90% mother will be asymptomatic
50% expectant mothers who give birth to
infants congenitally infected with T. gondii
have no recollection of symptoms or any
obvious exposure to the parasite
VERTICAL TRANSMISSION
(2)

Symptomatic mother: flu-like symptoms (fever, malaise,
cervical lymphadenopathy)
Mothers infected prior to conception rarely transmit the
parasite to the fetus except parasite becomes reactivated
because of the immune suppression of the mother
Majority of the fetus is exposed during the last trimester
Symptoms in the infant: mild asymptomatic
Infection during the first trimester clinical manifestations
more severe, spontaneous abortion
Infection during the second trimester clinical
manifestations mild severe, depend on individual factors
RISK FACTORS
CLINICAL PRESENTATION
Majority: asymptomatic/ subclinical symptoms difficult to
diagnose
Minority: present with symptoms within the first few weeks to
months of life
Redflags in the history that would allude to the possibility of
congenital toxoplasmosis: hydrocephalus, retinochoroiditis,
calcifications in the central nervous system in the newborn
The signs and symptoms may be less specific and may not be
present until late in infancy and childhood
Symptoms: convulsions, palsies, growth or mental retardation,
visual or hearing impairment, learning disabilities, organomegaly,
lymphadenopathy, fever, rash
Differential diagnoses: other congenital infections such as CMV,
rubella, herpes viral infections

Ocular Toxoplasmosis
Symptoms: vary depending on the age of the patient
(reduced visual acuity, strabismus, leukocoria,
photophobia, pain, nystagmus)
Most common manifestation: retinochoroiditis
(Toxoplasmosis affects the retina and the underlying
choroid)
Retinochoroiditis: macular-pigmented lesions with a
central necrotic area primarily found on the retina and
can be observed by funduscopic examination
In more than 50%, the lesions are found on the
posterior pole of the retina and are unilateral
Ocular Toxoplasmosis
(2)

A gray-white area of retinal necrosis with or without exudates with
adjacent swelling of the optic disc, vitreitis, vasculitis, andhemorrhage
A headlight in the fog refers to the retinal inflammation seen through
an infected and opaque vitreous
Active inflammation and infection in the eye typically lasts about 6 weeks,
at which time the lesion will begin to regress, leaving behind a
characteristic pigmented scar on the retina
Ocular toxoplasmosis can lead to long-term effects
It has been associated with glaucoma, cataracts, vitreous opacification,
retinal hemorrhage or detachment, and optic atrophy
All of these conditions can lead to permanent blindness
Ocular lesions can recur in adolescence and adulthood, even after
treatment in infancy.
Follow-up of these patients is extremely important to prevent further
damage to the eyes
CNS Toxoplasmosis
May or may not have overt neurologic symptoms
Symptoms: convulsions, abnormal tearing of the
eye, nystagmus, strabismus, hearing and visual
impairments, and growth and developmental
delays
Many of these symptoms overlap with symptoms
of ocular toxoplasmosis
Toxoplasmosis can also cause hydrocephalus and
microcephaly
SNHL and Toxoplasmosis
Toxoplasmosis also has been associated with
sensorineural hearing loss
Child with a history of toxoplasmosis should
be evaluated on a regular basis and referred
to an audiologist and ear, nose and throat
specialist for follow-up
DIAGNOSTIC TEST
The prevention and treatment of congenital toxoplasmosis begins with identifying
infection in pregnant women
Antibody testing that measures the amount of IgG and IgM is used to confirm
exposure to T. gondii
IgG and IgM levels rise within 2 weeks of being exposed to the parasite
Elevated IgG levels confirm a patient has been exposed to the parasite but do not
differentiate between a recent exposure and an exposure that occurred in the past
because IgG will persist at a low level throughout the life
of the patient
IgM antibody levels can be used to confirm an acute exposure, and the degree of
elevation can be used to discern when the exposure occurred
IgM antibodies are almost always present following an acute exposure, they can
persist in some patients at high levels for up to 18 months, leading to an
inaccurate assessment of when the exposure occurred
A significant increase in specific antibody titers or seroconversion during
pregnancy is usually considered diagnostic of a recent exposure
DIAGNOSTIC TEST
(2)

DIAGNOSTIC TEST
(3)

The Sabin FeldmanDye test is performed by a reference laboratory and is
considered the gold-standard diagnostic
test for toxoplasmosis
This test detects a change in T. gondiispecific antibody titers (IgG) over a
3-week period or detects a single elevated (IgG) antibody titer
A four-fold increase in titer levels over a three-week period or a single titer
above 250 IU/ml is considered highly suggestive of infection
Polymerase chain reaction testing of amniotic fluid is the preferred
method for providing confirmation of fetal exposure
This test should be performed at or after 18 weeks gestation and only in
women with preliminary positive serologic results indicative of acute
exposure
Polymerase chain reaction testing of cerebrospinal fluid also can be used
to confirm the presence of infection in the central nervous system after
birth
TREATMENT
Goal: to arrest the replication of the parasite and prevent further
damage to the organs involved
It is especially important to stop replication in the eye to prevent
irreversible damage to the retina and optic nerve that can lead to
permanent blindness
Debate exists about the appropriate length of therapy
3 months of therapy may be sufficient to eradicate the parasite and
prevent long-termeffects aswell as decrease the burden of long-
term medication usage on the affected infant and family
Decisions concerning whether therapy should be continued or
discontinued be based on patient response to therapy, severity of
symptoms, the age of the patient at the time of diagnosis
Treatment for Infant
Medication Mechanism of
Action
Dose Length of Therapy Advese Effect
Sulfadiazine Inhibits folic
acid synthesis
100 mg/kg/day every 12 1 year Bone marrow
suppression, fever,
vasculitis, rash, nausea,
vomiting, neprhopathy

Pyrimethamine Inhibits
tetrahydrofolic
acid synthase
1 mg/kg/day
1 mg/kg/day three times per week
First 6 months
Second 6 months
Bone marrow
suppression, rash,
seizures, fever,
vomiting, diarrhea,
hematuria
Leucovorin A reduced
form folic acid
5-10 mg every 3 days
10 mg three times per week
First 6 months
Second 6 months
Rash, erythema,
urticaria, wheezing,
thrombocytosis,
hypersensitivity
Treatment for Expectant Mother
Treatment for Expectant Mother
(2)
Pyrimethamine is contraindicated during the first
trimester of pregnancy because of the
teratogenic effects
Sulfadiazine may be used alone during the first
trimester and pyrimethamine may be added after
this crucial period of fetal development
Although not yet approved by the FDA,
Spiramycin is used to prevent transplacental
infection in many other countries
NEONATAL SCREENING
Controversial topic in populations with a low prevalence
Not believed to be cost-effective, nor is treatment during
pregnancy guaranteed to prevent congenital toxoplasmosis
Screening in the neonatal period may be a more feasible
IgM and IgG antibody testing is used
Positive serologic results demonstrate that the mother has
been exposed and do not definitively indicate congenital
toxoplasmosis in the infant
The results simply allow the primary care provider to be
aware of the possibility and provide further follow-up as
indicated.
NEONATAL SCREENING
(2)

Prevalence of congenital toxoplasmosis is 1 in
12,000 live births
Early treatment significantly decreases the
neurologic and ophthalmologic effects
Early screening and treatment can significantly
decrease the long-term sequelae
Screening Question
PATIENT EDUCATION
Prevention of congenital toxoplasmosis begins
with preventing primary infection
T. gondii can be avoided by implementing
relatively simple strategies in daily life
Most pregnant women in the US knew
toxoplasmosis was associated with cat litter
but did not know about exposure in the
environment through food, water, dirt, sand,
or soil
PATIENT EDUCATION
(2)

Limiting contact with dirt, sand, or soil
Hand washing
Wearing gloves while gardening
The skins of all raw fruit and vegetables
should be washed and then peeled away
Never ingest raw meat
Cook all meat to an internal temperature of at
least 152F
PATIENT EDUCATION
(3)

Contact with cat litter should be avoided or
gloves should be worn while changing the litter
box and hands should be washed thoroughly
afterward
Frequent litter changes should be done
Box should be thoroughly cleaned with
disinfecting agents
Preventing a cat from hunting outdoors or eating
raw
Keep indoor-only cats and feed them only canned
or dry food
CONCLUSION
Many questions are still to be solved
Management (both for mother and child)
Choice of a specific therapy
The research pertaining to anti-toxoplasmic
treatment is lacking. The majority of studies
are retrospective, and few randomized control
trials exist that look at medication efficacy
THANK YOU

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