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When symptomatic, toxoplasmosis may present with mild symptoms, such as
fever, u-like syndrome, lymphadenopathy, hepatosplenomegaly, infectious mononucleosis, arthralgia, or rarely with severe end-organ involvement, such as chorioretinitis, pneumonia, central nervous system (CNS) infections, and myocarditis.
Severe toxoplasmosis is more common in patients with high parasite load and countries with more virulent and antigenic sub-types, such as Mexico, Colombia, French
Guiana, and Brazil [5, 6, 15, 16].
Chorioretinitis has particular importance for a person infected with T. gondii
because it is the most common late manifestation of infection. The patients usually
suffer from blurred vision. Rarely, chorioretinitis may also present with photophobia, epiphora, and scotoma. Fundoscopic examination shows focal necrotizing retinitis. Vision loss, retinal detachment, and neovascularization on the optic nerve and
retina may occur. Cataracts, microphthalmia, strabismus, and nystagmus are the
other ocular complications of Toxoplasma infections [6, 17]. Approximately 90% of
children who do not receive appropriate treatment may develop new retinal lesions
later in life. These lesions usually develop in late childhood or adolescence. In cases
that received proper treatment, chorioretinitis attacks may also be seen in the following years [6, 18].
Toxoplasma gondii is an important opportunistic pathogen in immunocompromised patients. Reactivation of bradyzoites in tissue cysts may occur in these
patients, resulting in prolonged fever, meningoencephalitis, brain abscess, lower
respiratory tract infection, myocarditis, hepatitis, skin rash, uveitis, chorioretinitis,
disseminated disease, multi-organ failure, and death [5, 6, 15]. Hematopoietic stem
cell and solid organ transplant recipients are at risk of severe toxoplasmosis without
antimicrobial prophylaxis. Toxoplasma infection has particular importance for
pregnant women. In pregnant women, the fetus may be infected transplacentally
when the primary infection develops or the reactivation of bradyzoites in tissue
cysts during latent infection [5, 6, 15, 16].
E. Kepenekli et al.
8.5 Congenital Toxoplasmosis
Primary T. gondii infection in pregnant women is usually asymptomatic. During
primary or reactivated toxoplasma infection in pregnant women, the probability of
transmission to the fetus is 50% [5]. The transmission rate varies according to the
stage of pregnancy, geographical region, and subtypes of the parasite [5].
The probability of maternofetal transmission is low in early pregnancy; this risk
becomes almost 100% in the last weeks. If the fetus is infected early in pregnancy,
the risk for severe congenital toxoplasmosis is high [6, 15, 16]. However, if the fetal
infection occurs in late pregnancy, neonates are usually born asymptomatic. The
treatment for toxoplasmosis during pregnancy reduces the risk of developing complications in the newborn but does not eliminate the risk [5, 6, 19]. The severity of
congenital toxoplasmosis mostly depends on the timing of fetal infection, genotypic
subtypes of T. gondii strains, parasite burden, and immune responses of infants and
pregnant women [6, 20].
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Congenital toxoplasmosis is 90% asymptomatic in the neonatal period. The
physical examination of a newborn with congenital toxoplasmosis is usually normal. If there is a high index of suspicion for intrauterine infection, additional tests,
including cerebrospinal uid (CSF) examination, neuroimaging, and ophthalmologic examination, should be performed [6, 15]. These tests are abnormal in half of
the asymptomatic infants with congenital toxoplasmosis [21].
In early infancy, clinical ndings may present in only 10–30% of infants with
congenital toxoplasmosis [6, 15]. In neonates with symptomatic congenital toxoplasmosis, microcephaly, microphthalmia, seizures, rash, jaundice, generalized
lymphadenopathy, hepatosplenomegaly, strabismus, meningoencephalitis, hepatitis, retinitis, choroiditis, HL, anemia, and thrombocytopenia may occur [5, 15].
Severe congenital toxoplasmosis manifestations usually result from the primary
infection of pregnant women in the rst trimester [6, 15].
The classic triad of congenital toxoplasmosis consists of chorioretinitis, cerebral
calcications, and hydrocephalus. Retinal involvement is usually characterized by
unilateral macular scars [6]. Cerebral calcications may be seen as small, focal, and
scattered lesions. Cerebrospinal uid shows mononuclear pleocytosis and increased
protein levels. However, these ndings occur in <10% of patients [6].
Even if congenital toxoplasmosis is asymptomatic in the perinatal period, it may
present with chorioretinitis, vision problems, HL, learning disabilities, endocrine
abnormalities including growth retardation, and precocious puberty, or severe
developmental delay later [5, 6, 15, 16].
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8.6 Diagnosis
The diagnosis of toxoplasmosis is often challenging due to the interpretation of
diagnostic tests. Many different techniques can be used for the diagnosis of
Toxoplasma infections. Test selection is made by considering the patient’s age, clinical status, and whether the tests are available. The most commonly used diagnostic
method is serological tests [5, 6, 15, 16].
Isolation of T. gondii from sterile body uids, or blood, inoculated into the mice
or cell cultures indicates acute infection [16]. Toxoplasma can also be isolated from
tissues in acute and chronic (latent) infections. If the placental infection exists, the
fetus is often infected with T. gondii. Tachyzoites may be demonstrated in histo-
pathological examination of tissues or cytologic preparations of body uids. Tissue
cysts can also be shown by specic immunoperoxidase staining in tissue specimens,
including the placenta and fetus [16].
Toxoplasma-specic immunoglobulin (Ig) M and IgG tests are widely available
in commercial laboratories. The results should be conrmed in reference laboratories when serological tests are positive in pregnant women and newborns.
Toxoplasma-specic IgM test results may be falsely positive. Conrmatory tests
may include IgM, IgA, IgE, IgG avidity, and differential agglutination [15].
Toxoplasma-specic IgM becomes positive 1–2weeks after infection, reaches
the peak level in 1month, and decreases to undetectable levels in 6–9 months.
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Rarely, it may remain positive for years. This prolonged Toxoplasma-specic IgM
positivity is the most common diagnostic error in pregnant women [16]. Toxoplasma-
specic IgM positivity may indicate a recent infection, latent infection, or a falsepositive result [15]. The acute infection is excluded if Toxoplasma-specic IgM by
enzyme-linked immunosorbent assay (ELISA) or immunosorbent agglutination
assay (ISAGA) methods is negative [16].
Toxoplasma-specic IgG antibodies reach the highest level 1month to 5months
after infection and usually remain positive lifelong [15, 16]. If Toxoplasma-specic
IgG is positive in low-titers and Toxoplasma-specic IgM is negative, it may indi-
cate the infection occurred at least 6months ago. Toxoplasma-specic IgG avidity
tests can help differentiate between recent and chronic infections. If the avidity of
the Toxoplasma-specic IgG test is high, it indicates that the infection was acquired
before, not within the last 3months. If the avidity of the Toxoplasma-specic IgG
test is low, it indicates that the infection may have been acquired within the previous
3months [16]. Avidity tests are helpful when Toxoplasma-specic IgG is positive in
the rst trimester of pregnancy [16].
An acute (recent) infection diagnosis can be made when an initially negative test
result turns positive or if the specic-antibody levels rise fourfold or more in serum
samples taken at least 3weeks apart [16].
Differential agglutination tests can help distinguish acute and chronic infections
[16]. High agglutination with acetone xation suggests acute infection; high agglutination with formalin xation indicates chronic infection. For the most accurate
evaluation of infection in pregnant women, differential agglutination tests should be
combined with the Sabin–Feldman dye test, IgM ELISA, IgA ELISA, IgE ELISA/
ISAGA, and avidity studies [16].
For the accurate diagnosis of congenital infection, it is essential to determine
when it is acquired or reactivated in pregnant women. A positive result of
Toxoplasma-IgM should be conrmed with additional tests (IgG avidity, IgA-, and
IgE-specic antibodies) [5, 6, 15, 16].
Polymerase chain reaction (PCR), an essential, widely used diagnostic test, can
detect the deoxyribonucleic acid (DNA) segments of T. gondii in both tissue sam-
ples, such as muscle, myocardium, placenta, and brain parenchyma, and sterile
body uids, including blood, CSF, vitreous uid, bronchoalveolar lavage uid, and
urine [6, 15]. When PCR positivity is detected in tissue samples, it primarily indicates that this may be due to bradyzoites responsible for latent infection or tachyzoites responsible for acute illness [15]. In a study conducted on 339 pregnant women
in France, PCR tests in amniotic uid and umbilical cord blood sampling were
entirely compatible with diagnosing congenital infection [16].
E. Kepenekli et al.
8.6.1 Diagnosis ofCongenital Toxoplasmosis
Early diagnosis of congenital toxoplasmosis and, thus, early initiation of antimicrobial therapy are crucial to reducing morbidity and mortality. Serological screening
during pregnancy, screening of newborns in the postnatal period, or diagnostic tests
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performed on amniotic uid or a neonate born with compatible clinical ndings
provide the congenital toxoplasmosis diagnosis [6, 15, 22].
The indications for the evaluation of a newborn for congenital toxoplasmosis are
listed below [6, 23];
1. Serologic evidence of primary T. gondii infection during pregnancy
2. Serologic evidence of past infection with T. gondii in a pregnant woman with
immunodeciency
3. Infants born with compatible clinical ndings
4. Infants with a positive result for Toxoplasma-specic IgM if newborn screening
is performed.
Given the potential difculty in interpreting serologic tests in newborns, all
infants with a presumed diagnosis of congenital toxoplasmosis should undergo
additional clinical, laboratory, and neuroimaging evaluations for evidence of
infection.
Tests that can be used to demonstrate fetal infection are as follows: (1)
Toxoplasma-PCR in amniotic uid, (2) Fetal ultrasonography, which can detect
anatomical abnormalities, (3) Histopathological examination of placental tissue,
fetus, or newborn, and (4) Toxoplasma-PCR in placental tissue [5, 16].
In neonates, serologic evaluation should be performed with Toxoplasma-specic
IgG, IgM, and IgA measurements and Toxoplasma-PCR test in blood or sterile body
uids, including urine and CSF. Toxoplasma-specic IgM and/or IgA and IgG positivity suggest the diagnosis of congenital toxoplasmosis. Transfusion of blood products may cause false-positive serological test results. If an infant is still positive for
Toxoplasma-specic IgG after 12months, this also supports the diagnosis of congenital toxoplasmosis [5, 15].
A newborn with positive Toxoplasma-specic IgG but negative IgM and IgA
tests and no supporting ndings for congenital toxoplasmosis should be monitored
with serological tests. Repeating the Toxoplasma-specic IgG test is recommended
every 4–6weeks. If initial Toxoplasma-specic IgG positivity is due to transplacen-
tally transmitted maternal antibodies, the IgG level is expected to decrease gradually and disappear before 1year of age [15]. If initial serological tests are performed
in the rst 10days of life, tests should be repeated later to exclude false positivities
[6]. The pyrimethamine and sulfadiazine treatments during pregnancy may affect
the infant’s serological test results for toxoplasmosis [6].
Complete blood count, liver function tests, serum total IgM, IgG, IgA, albumin,
CSF analysis including cell count, protein, and glucose levels, CSF IgG level, CSF
dye test, Toxoplasma-specic IgM, head and abdominal ultrasonography, and brain
magnetic resonance (MR) imaging should be performed in a newborn with suspected congenital infection [5, 6, 15, 16]. In a newborn with congenital toxoplasmo-
sis with CNS involvement, CSF protein level increases and glucose level decreases.
Maternal serologic tests, including the Sabin–Feldman dye test, Toxoplasma-
specic IgM, IgA, IgE, and differential agglutination, should also be performed
during newborns’ evaluation for congenital toxoplasmosis [16].
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E. Kepenekli et al.
Calcications localized to the brain parenchyma can be detected by ultrasonography, computed tomography (CT), or MR imaging. Among the imaging methods,
CT is recommended as it is more sensitive to calcications [5, 15]. Dilated eye
examination and audiological assessments should be performed on every neonate
evaluated for congenital infection.
If initial laboratory test results are within normal limits despite high clinical suspicion, serological evaluation should be repeated every 4weeks until 3months of
age [6].
8.7 Treatment
Acute-acquired toxoplasma infections usually do not require specic antimicrobial
therapy. However, Toxoplasma-specic treatment should be given in the following
indications: (1) Infection during pregnancy, (2) Ocular involvement, (3) Severe endorgan damage, (4) Infection in patients with immunodeciencies, and (5) Congenital
toxoplasmosis.
When congenital toxoplasmosis is strongly suspected or a denite diagnosis is
made, antimicrobial therapy should be started as soon as possible. The preferred
regimen is the combination of pyrimethamine, sulfadiazine, and folinic acid. The
treatment should be given for at least 12months. The treatment regimen and doses
are summarized in Table8.1 [15].
In children and adolescents with severe acute toxoplasmosis or severe reactivated toxoplasmosis, if the preferred drug regimen (pyrimethamine, sulfadiazine,
and folinic acid) is not available or drug-related adverse effects have developed, the
following antimicrobial therapy options can be given [15]:
1. Trimethoprim-sulfamethoxazole (TMP-SMX) monotherapy, intravenous or
peroral)
2. Pyrimethamine+folinic acid+clindamycin
3. Pyrimethamine+folinic acid+atovaquone
Table 8.1 Drugs and doses used in the treatment of toxoplasmosis
Drugs
Doses First 2days: 1mg/kg
a
Adapted and modied from Ref [15, 16]
b
Only given if the cerebrospinal uid protein is ≥1 g/dL or detection of vision treating
chorioretinitis
Pyrimethamine Sulfadiazine
every 12h orally
Then, 1mg/kg once daily
for at least 2–6months
Remaining months to
complete 12months:
1mg/kg once daily,
3days/a week
50mg/kg every
12h orally (for
12months)
a
Folinic acid
(leucovorin)
10mg/dose,
3days/a week
orally
Prednisone
0.5mg/kg every
12h (maximum
20mg/dose)
b
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4. Pyrimethamine+folinic acid+clarithromycin
5. Pyrimethamine+folinic acid+azithromycin
6. Atovaquone+sulfadiazine
Alternative therapies should be changed to the preferred drug regimen when
available.
Spiramycin treatment is recommended in pregnant women with Toxoplasma
infection [13]. However, if fetal infection occurs despite spiramycin treatment, a
combination of pyrimethamine, sulfadiazine, and folinic acid should be started [6,
16]. If antitoxoplasmal therapy during pregnancy is started within the rst 3weeks
after seroconversion, the probability of maternofetal transmission is reduced by
52% [24].
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8.8 Prophylaxis
Primary or secondary prophylaxis with TMP-SMX is indicated in patients with primary and secondary immunocompromising conditions, including hematopoietic
stem cell and solid organ transplantation and human immunodeciency virus (HIV)
infection.
In HIV-infected patients, if the absolute CD4(+) T-cell count is low and
Toxoplasma-specic IgG is positive, antimicrobial prophylaxis against toxoplasmosis should be given. Trimethoprim-SMX is the preferred agent for primary prophylaxis and can be given thrice per week [25]. Alternative regimens also can be given,
such as dapsone + pyrimethamine + leucovorin and atovaquone ± pyrimethamine±leucovorin [25].
Toxoplasmosis is a rare but fatal infection after solid organ transplantation. Since
T. gondii tends to settle in the muscles, the disease can be problematic, especially
after heart transplantation [26]. If the donor is seropositive and the recipient is seronegative, the risk of T. gondii infection in the posttransplant period is high. If appro-
priate antimicrobial prophylaxis is not given in this patient group, 50–70% of
patients may develop toxoplasmosis [26]. Although rare, toxoplasmosis was also
transmitted by liver, kidney, and lung transplantation. Although no standard recommendation for antimicrobial prophylaxis exists in these patient groups, primary prophylaxis is given with TMP-SMX or TMP-SMX +pyrimethamine for 6weeks to
6 months, especially after heart transplantation [26]. Sulfadiazine, dapsone,
clindamycin, and atovaquone are the other alternative agents for prophylaxis against
toxoplasmosis.
When acute Toxoplasma infection is detected during pregnancy, antimicrobial
therapy is given to prevent congenital T. gondii infection in the infant, regardless of
whether the mother has symptoms or not [27]. The parents should be informed that
this prophylaxis approach does not eliminate the infection risk in the fetus. When
acute infection is detected in the mother, treatment should be started as soon as possible, preferably before amniocentesis. Treatment should be initiated before
tachyzoites in the fetus transform into bradyzoites, known to be resistant to
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antimicrobial therapy, within the rst 3 weeks after seroconversion occurs.
Spiramycin or pyrimethamine-sulfadiazine treatment is given to pregnant women.
Studies report that pyrimethamine-sulfadiazine is more successful in prophylaxis [28].
E. Kepenekli et al.
8.9 Complications andPrognosis
A fetus with disseminated congenital toxoplasmosis may die in utero or within the
rst few days of life. In infants with severe congenital toxoplasmosis, although early
diagnosis and treatment have been applied in the neonatal period, neurocognitive
and visual functions may be affected later in life. However, symptomatic infants
without signs of severe disease or asymptomatic infants can recover completely
without sequelae with early diagnosis and treatment [15]. Asymptomatic and symptomatic newborns should be followed up regarding neurocognitive, ocular, and
hearing functions.
In long-term follow-up, motor and cerebellar dysfunctions, microcephaly, and
intellectual disabilities can be noticed [6]. An infant with congenital toxoplasmosis
may present with seizures later. A study conducted in the United States of America
(USA) in 2011 reported that when prenatal or postnatal treatment was not applied
for toxoplasmosis, more than 90% of infants had mental or visual impairment when
they reached the age of 12 [29]. Therefore, monitoring and supporting neurocognitive functions during or after treatment is vital in improving the patient’s quality
of life.
Infants diagnosed with congenital toxoplasmosis should be examined every
3months in the rst 2years of life, every 6months in the third year, and once a year
after that until they can report vision problems [6].
All infants with congenital toxoplasmosis should be evaluated for hearing function and kept on close follow-up. Hearing screening programs are routinely performed in many countries. However, hearing should be monitored with auditory
brainstem response (ABR) tests in infants with congenital toxoplasmosis. These
tests are more sensitive than automated tests used in routine screening to evaluate
hearing functions [6].
It is also reported that congenital toxoplasmosis may result in precocious puberty
and growth retardation by disrupting the hypothalamohypophyseal axis [6, 30].
8.10 Prevention
Another compelling feature of toxoplasmosis is that it is impossible to suggest a
single protection method because T. gondii can transmit to humans by different
mechanisms. Increasing knowledge and awareness about toxoplasmosis and its
transmission in society are essential. However, special consideration should be
given to pregnant women and those with primary or acquired immunodeciency at
high risk for severe complications of toxoplasmosis.
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To prevent the transmission of toxoplasmosis, the following precautions should
be recommended:
1. Contact with cat feces should be avoided. Cat litter should be changed daily, and
hands should be washed carefully after this process.
2. Domestic cats should be prevented from hunting birds or rodents infected with
T. gondii.
3. Gloves should be worn during contact with the soil, and hands should be washed
carefully after removing the gloves. Contamination of water with soil or waste
should be prevented.
4. Meat should be well cooked. Bradyzoite-containing tissue cysts will be inacti-
vated when their internal temperature rises above 65.5°C.Keeping the meat in
the freezer for at least 2days at minus (−) 20°C also inactivates the bradyzoites.
Foods should be prevented from being contaminated with raw meat. Shellsh
should not be consumed raw.
5. Vegetables and fruits should be washed carefully, and the materials and benches
used while preparing the food should be adequately cleaned [15].
The approaches to prevent congenital toxoplasmosis in infants can be summarized as follows; performing serological screening in pregnant women, treating the
acute maternal infection with spiramycin, and administering pyrimethamine, sulfadiazine, and folinic acid when a fetal infection is documented. Therapeutic abortion
should be discussed with parents when fetal abnormalities are detected by ultrasound or MR imaging to prevent the birth of a severely affected infant [16].
Standard isolation precautions are recommended when a patient with congenital
or acquired toxoplasmosis is hospitalized [15].
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8.11 Screening Programs
In some countries, including Austria, Denmark, France, Slovenia, and only a few
states in the USA, prenatal serological screening is mandatory to detect congenital
toxoplasmosis early [6, 11]. In the study of Prusa etal. [11], the cost of the screening
program implemented in Austria and the costs of diagnosing and treating infants with
congenital toxoplasmosis who would be born in the absence of screening were compared and was reported that prenatal serological screening is cost-saving. However,
pregnant women are not screened routinely for toxoplasmosis in many countries.
In newborn screening programs, blood samples taken for routine metabolic
screening are tested for Toxoplasma-specic IgM; if positive, detailed serological
testing is performed on the mother and the infant [6].
8.12 Congenital Toxoplasmosis andHearing Loss
Hearing loss is one of the most important but challenging to detect complications of
congenital toxoplasmosis. In cases with congenital toxoplasmosis, educationally
signicant HL was reported as 10–15% and all HLs up to 30% [31–33].
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E. Kepenekli et al.
In the ear involvement of congenital toxoplasmosis, severe inammation, necrosis, and calcium deposits are seen in histopathological examinations, similar to the
lesions seen in CNS involvement [34, 35]. The calcium deposits are primarily found
in the spiral ligament of the cochlea [35]. Another important mechanism in HL
caused by congenital toxoplasmosis is that the T. gondii tachyzoites can also dam-
age the auditory pathways during brain involvement [5, 32]. In these cases, tachyzoites were found in the middle ear uid, temporal bones, internal auditory canal,
spiral ligament, stria vascularis, and saccular macula [5, 34]. Antimicrobial therapy
suppresses the replication of T. gondii and reduces inammation, and cell destruc-
tion caused.
Inammatory changes caused by tachyzoites are not observed in the presence of
encysted organisms, bradyzoites [34]. The mechanism responsible for HL is thought
to be the host’s inammatory response to tachyzoites. It has also been reported that
vacuolization and nucleus–nucleolus distinction are lost in cochlear neurons.
Therefore, neuronal pathways of hearing are also affected. Thus, timely initiation of
antimicrobial therapy, suppressing the replication of tachyzoites, can decrease hearing damage [34].
In the 1940s, the relationship between toxoplasmosis and HL began to draw
attention, demonstrating parasites in the mastoid and temporal bones in autopsies of
cases with toxoplasmosis. A study by Kelemen [35] in 1958 emphasized the effect
of congenital toxoplasmosis on hearing; autopsy ndings of two infants showed the
CNS and hearing effects. In the following years, studies focused on the long-term
effects of congenital toxoplasmosis on hearing and treatment success in preventing
complications. In 1980, Wilson etal. [36] reported clinical outcomes of 24 cases
with asymptomatic congenital toxoplasmosis without treatment. They reported chorioretinitis in 19 patients and varying degrees of HL in ve cases (Tables 8.2
and 8.3).
Table 8.2 Summary of studies reporting hearing outcomes in infants with congenital
toxoplasmosis
Degree of hearing impairment Results
Normal
Mild >20–40 25–40 25–50dB 0 3 2
Moderate >40–60 >40 51–80dB 0 2 1
Severe >60 >70–90 0 0 1
Profound >90 0 0
Total number
of cases
Db indicates decibel, Db/HL decibel/hearing loss, N/A not applicable
a
Adapted from Ref. [32, 36, 37]
a
Auditory
brainstem
responses
(Db/HL)
≤20
McGee
Wilson
Audiogram
(Db/HL)
0–20 <25dB 30 14 15
etal. (1980)
[36]
etal.
(1992) [32]
n
30 19 19
Wilson
etal.
(1980) [36]
n
De Andrade
etal. (2008)
[37]
n
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Table 8.3
comes in infants with congenital toxoplasmosis
Study/
Reference
number
Stagno
etal.
(1977)
[38]
Wilson
etal.,
(1980)
[36]
McGee
etal.
(1992)
[32]
McAuley
etal.
(1994)
[22]
McLeod
etal.
(2006)
[39]
Andrade
etal.
(2008)
[37]
Summary of studies reporting diagnostic tools, treatment modalities, and hearing out-
Number
of cases
1
19 Toxoplasma-IgM
30 Toxoplasma-IgM
7 Serological test in
68 Serological test in
19 IgM/IgA
Diagnostic
criterion Treatment Audiometric test
Toxoplasmaspecic- IgG
antibody
persistence after
12months
testing in
neonatal/cord
blood and
Toxoplasmaspecic- IgG
persistence after
6months
testing in
neonates (17
infants) or in CSF
(two infants),
and/or
Toxoplasmaspecic IgM or
Sabin–Feldman
dye test in
maternal blood
plus clinical
ndings of
congenital
toxoplasmosis
the reference
laboratory
the reference
laboratory
<6months and
IgG persistence
after 12months
None Air-bone
None/
insufcient
>12months ABR 0% (0/30) (in
None ABR, soundeld,
>12months ABR, soundeld,
Partial
/12months
a
Prevalence of
hearing loss
0% (0/1)
conduction used to
exclude conductive
hearing loss
Pure-tone and
speech reception
threshold
audiometry
and behavioral
audiography
and behavioral
audiography
Interacoustics
pediatric
audiometer,
impedanciometer,
behavioral
audiometry,
otoacoustic
emissions, and
BAEP
26% (5/19)
six cases,
conductive
type hearing
loss was
detected due
to acute otitis
media)
14% (1/7)
0% (0/68)
21%, (4/19)
(continued)
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