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Table 7.3 Post-diagnosis evaluation, monitoring during treatment, and follow-up of infants with
congenital cytomegalovirus infection
Post-diagnosis evaluation: Asymptomatic or symptomatic cCMVI at birth
Physical, neurologic, and neurodevelopmental examination
Laboratory tests: complete blood count, kidney and liver function tests, coagulation studies (in
patients with liver disease), and quantitative CMV PCR in whole blood or plasma (used for
monitoring of infant receiving antiviral therapy)
Hearing assessment: auditory brainstem response
Ophthalmic assessment
Cranial imaging with ultrasound, computed tomography, or magnetic resonance imaging
(depending on clinical presentation)
Monitoring during antiviral treatment
Absolute neutrophil counts should be monitored weekly for 6weeks, then at week 8, and then
monthly for the duration of antiviral treatment
Liver function tests should be monitored monthly during treatment
Long-term follow-up
Audiological testing (all children with cCMVI)
Neurologic consultation and developmental assessments (on a case-by-case basis)
Ophthalmologic evaluations (in cases with clinically detectable disease)
Dental visits
CMV cytomegalovirus, cCMVI congenital cytomegalovirus infection, PCR polymerase chain
reaction
M. Polat et al.
testing method’s low and highly variable sensitivity [21, 35]. Serologic methods are
not recommended for routine diagnosis of cCMVI. A positive serologic test for
CMV immunoglobulin (Ig) G antibody may indicate the passive transfer from the
mother; however, a negative test makes cCMVI unlikely. The CMV IgM antibody is
insensitive and may be falsely negative in more than 50% of infected newborns [1, 2].
Once the diagnosis of cCMVI is conrmed virologically, a multidisciplinary and
comprehensive evaluation should be performed to detect the presence of end-organ
involvement, even in asymptomatic newborns, to determine subclinical or subtle
symptoms (Table7.3). Findings might also help determine potential candidates for
antiviral treatment and counseling about prognosis and long-term outcomes [21, 35].
7.10 Newborn Screening forCongenital
Cytomegalovirus Infection
As the most common congenital infection and a signicant public health problem
worldwide, cCMVI meets many criteria for screening. Cytomegalovirus is more
common and causes more cases of congenital disabilities than the several metabolic
or endocrine disorders included in newborn screening panels. Unlike other causes
of SNHL in children, cCMVI-related SNHL is potentially treatable, making screening and early diagnosis highly important. Early diagnosis improves patient outcomes and may provide opportunities for timely antiviral treatment and earlier
interventions. On the other side, delay in diagnosis and initiating interventions lead
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to poor patient outcomes, such as speech and language delays and cognitive and
hearing impairments.
Most infants born with cCMVI are asymptomatic or have nonspecic clinical
presentations that do not prompt the physician to order a CMV test that must be
performed within the rst 3weeks of life. Detection of CMV after this period cannot distinguish congenital from postnatal infection, which is not associated with
SNHL and developmental disabilities. All of these, coupled with the substantial
health and economic burden of the disease that mainly stems from long-term cognitive and hearing impairments, many CMV experts advocate the implementation of
targeted and/or universal newborn screening for cCMVI.Despite the potential benets mentioned above, it is possible that a false- or true positive screening result,
since most infants with cCMVI never develop SNHL or other sequelae, may lead to
increased parental stress and inappropriate antiviral treatment, or unnecessary medical visits and tests [21, 36, 37].
Although cCMVI is the leading nonhereditary cause of SNHL in children and is
more common than any other screened newborn disorders, there is no universal
neonatal screening program to identify infected infants. The main goals of newborn
screening for cCMVI include identifying asymptomatic infants at risk for delayed
HL, requiring more frequent audiologic assessment, and early identifying infected
infants with subtle, nonspecic, or atypical symptoms that might benet from antiviral treatment [36, 37].
The two types of proposed newborn screening for cCMVI are the universal
(screening of all newborns) and targeted (testing of newborns who fail newborn
hearing screening) programs [1, 37]. The hearing-targeted CMV screening approach
has been implemented in many hospitals. In the USA, Utah became the rst state to
mandate CMV screening in 2013, and a 2015 cost-benet analysis found targeted
newborn screening to be cost-effective [38]. However, this screening approach is
insufcient to detect all CMV-infected infants since most infants with cCMVI have
normal hearing at birth. A recent study from seven medical centers in the USA demonstrated that the targeted screening approach failed to detect 43% of infants with
CMV-related SNHL in the newborn period and identify infants with cCMVI at risk
of late-onset SNHL [39].
Without universal screening, asymptomatic and many symptomatic cCMVIs
presenting with milder or nonspecic symptoms will go undiagnosed [24]. For
these reasons, many experts advocate for universal newborn screening, which
appears to be cost-effective. However, the most reliable and cost-effective method
for universal newborn screening for cCMVI has yet to be determined. It may
include the detection of CMV DNA by PCR in saliva (both liquid and dried) and
urine samples collected at birth or DBS samples from newborn screening Guthrie
cards [1]. It has been demonstrated that saliva and urine are reliable samples for
neonatal cCMVI screening [40]. Previous reports revealed that DBS PCR has
lower sensitivity than traditional methods, possibly because not all infected infants
are viremic at birth or the methods used [41]. However, recent studies demonstrated improved sensitivity for DBS, possibly because of improved PCR testing
methodologies [42].
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7.11 Treatment
Treatment of cCMVI includes supportive treatment, antiviral treatment, hearing
amplication and/or cochlear implantation, speech-language therapy, physical therapy, and special education [1].
Antiviral treatment (intravenous ganciclovir or oral valganciclovir) is recommended only for newborns with moderate to severe symptomatic cCMV disease to
improve hearing and neurodevelopmental outcomes [21, 35]. Antiviral treatment
should be initiated within the rst 30days of life, and the standard duration of treatment is 6months. There is no denitive clinical evidence or benet in starting antiviral therapy beyond the rst 30days of life, and this issue is an area of active study.
The clinical benet and safety of antiviral treatment in infants with asymptomatic
cCMVI, including those with isolated SNHL, are unknown. Two international consensus groups recommend that asymptomatic infants with or without isolated SNHL
should not receive antiviral treatment [21, 35]. Several clinical trials are underway
to determine whether valganciclovir treatment is benecial in asymptomatic infants
with and without SNHL.
In infants with severe, life-threatening diseases or gastrointestinal disorders
affecting drug absorption, intravenous ganciclovir is preferred initially. Antiviral
treatment’s commonly reported side effects are neutropenia, thrombocytopenia,
hepatotoxicity, and catheter-related events during ganciclovir treatment, such as
infection or extravasation [1, 21, 35]. Therefore, blood tests should be monitored
regularly during antiviral treatment. In animal models, ganciclovir is gonadal toxic
and carcinogenic, but these long-term adverse effects have not been reported in
humans [43].
In addition to antiviral treatment, managing symptomatic infants with severe disease includes supportive measures, such as control of seizures, nutritional support,
and platelet transfusion [1].
If undetected or untreated, HL can lead to speech and language delays and cognitive impairments in children. Therefore, a multidisciplinary team should manage
children with cCMVI-associated SNHL, including otolaryngologists, speechlanguage pathologists, and HL educators. The treatment of children with cCMVIrelated SNHL is not different from any child with SNHL.The rst stage of treatment
is early amplication. Cochlear implantation can be considered for children with
severe to profound HL who do not receive adequate hearing amplication benets [33].
7.12 Long-term Follow-Up
To detect late complications and sequelae, long-term follow-up is necessary for all
children, asymptomatic and symptomatic, with cCMVI (Table7.3).
Due to the absence of well-dened predictors of SNHL, monitoring all infants
with asymptomatic or symptomatic cCMVI is essential. Additionally, the
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late-onset and progressive nature of SNHL in children with cCMVI necessitates
long-term audiologic follow-up for early detection and intervention of HL.Most
changes seem to occur within the rst few years of life, and most children with
cCMVI will develop progressive HL into adolescence. Considering these ndings, hearing evaluations are recommended every 3–6months for the rst 3years
of life and annually through adolescence. If HL is determined, audiological
assessments should be carried out into adulthood to monitor the progression of
HL [1, 21, 35].
Neurodevelopmental assessments should be performed regularly to determine
cognitive and motor disabilities. Neurology consultation may be required in children with cerebral palsy or seizure management. Repeat ophthalmologic evaluations should be performed to follow up on symptomatic infants with chorioretinitis
or other abnormalities present at birth and to monitor for the development of late
sequelae, such as later-onset retinitis, strabismus, and vision impairment. Congenital
CMVI is also associated with hypoplasia and hypocalcication of tooth enamel.
Therefore, regular dental visits are also required for the long-term care of these
children [1, 44].
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7.13 Prevention
Currently, no effective and safe therapies are available to treat maternal and fetal
CMVI.Therefore, prevention rather than treatment is a promising option for reducing the risk of cCMVI.Until today, several promising interventions have been proposed to prevent cCMVI [45].
At present, no licensed vaccine is available to prevent CMVI.Randomized trials
of CMV hyperimmune globulin use to prevent cCMVI have not shown a benet
[46]. A recent randomized study by Shahar-Nissan etal. [47] reported a 70% reduction in vertical transmission of CMV with the oral valaciclovir treatment after primary maternal infection acquired early in pregnancy. However, the routine use of
antiviral therapy to prevent cCMVI during pregnancy is not recommended due to
insufcient clinical evidence [21].
A signicant risk factor for maternal CMVI is close contact with young children
who excrete the virus in saliva and urine for months or years. Several studies have
shown that most pregnant women are unaware and uninformed about cCMVI and
its consequences in infants. Similarly, low awareness rates have also been reported
among healthcare providers [1, 21]. This lack of awareness is a critical problem,
given that the only way to prevent maternal CMVI is through hygiene precautions
and behavioral interventions. Therefore, all pregnant women, seropositive and seronegative, should be educated about cCMVI and preventive measures, such as careful hand-washing after exposure to young children’s body uids, avoiding kissing
children on the mouth, and not sharing food, drink, or oral utensils with young
children [21, 45]. The www.nationalcmv.org website may be advised as a good
resource for families and professionals.
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7.14 Conclusion
Congenital CMVI is the leading cause of nongenetic SNHL in children worldwide.
The recognition of cCMVI as a cause of SNHL is underestimated for the following
reasons. First, there is a lack of awareness about cCMVI among healthcare workers
and the general population. Second, there is no universal systematic newborn
screening for cCMVI.Third, most maternal and newborn infections are asymptomatic and, therefore, not tested and diagnosed with cCMVI at birth. Also, most children with cCMVI have normal hearing at birth and develop subsequent late-onset
HL, at which point a retrospective diagnosis is challenging. Consequently, universal
neonatal hearing screening programs will miss many of these children even if combined with targeted testing for cCMVI.
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40. Yamamoto AY, Mussi-Pinhata MM, Marin LJ, etal. Is saliva as reliable as urine for detection
of cytomegalovirus DNA for neonatal screening of congenital CMV infection? J Clin Virol.
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41. Lazzarotto T, Blázquez-Gamero D, Delforge ML, et al. Congenital cytomegalovirus infection: a narrative review of the issues in screening and management from a panel of European
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42. Dollard SC, Dreon M, Hernandez-Alvarado N, etal. Sensitivity of dried blood spot testing for
detection of congenital cytomegalovirus infection. JAMA Pediatr. 2021;175:e205441.
43. Gwee A, Curtis N, Connell TG, Garland S, Daley AJ.Ganciclovir for the treatment of congenital cytomegalovirus: what are the side effects? Pediatr Infect Dis J. 2014;33:115.
44. Swanson EC, Schleiss MR.Congenital cytomegalovirus infection: new prospects for prevention and therapy. Pediatr Clin North Am. 2013;60:335–49.
45. Tol I, Heath PT, Khalil A.Prevention strategies for congenital cytomegalovirus infection. Curr
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M. Polat et al.
Congenital Toxoplasmosis andHearing
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Loss
EdaKepenekli, AyşeEnginArısoy, EminSamiArısoy,
andArmandoG.Correa
8.1 Introduction
Normal hearing is one of the most critical factors affecting the neurocognitive
development of humans. While the peripheral part of structures related to hearing is
fully formed until birth, the central part takes up to 2years after delivery to mature.
In this maturation period, the quantity and quality of external stimuli reaching the
infant are critical. Therefore, early diagnosis and treatment of hearing loss (HL) are
vital to neuromotor development, speech development, and socialization [1].
E. Kepenekli (*)
Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine,
Marmara University, İstanbul, Türkiye
e-mail: ekepenekli@yahoo.com
A. E. Arısoy
Division of Neonatology, Department of Pediatrics, Faculty of Medicine, Kocaeli University,
Kocaeli, Türkiye
e-mail: arisoyengin@yahoo.com
E. S. Arısoy
Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine,
Kocaeli University, Kocaeli, Türkiye
e-mail: emin.sami.arisoy@gmail.com
A. G. Correa
Division of Academic General Pediatrics, Department of Pediatrics, Baylor College of
Medicine, Houston, TX, USA
Section of International and Destination Medicine, Texas Children’s Hospital,
Houston, TX, USA
e-mail: acorrea@bcm.edu
8
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_8
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Permanent congenital HL occurs in 2–4 of every 1000 live births [2, 3]; inherited
disorders cause more than half, and acquired causes, including congenital infections, about a quarter [2]. Almost all congenital infections can adversely affect fetal
hearing function development. Because congenital toxoplasmosis may also result in
hearing impairment, it should be considered among the preventable causes of hearing loss. Current guidelines on early hearing detection and intervention recommend
that infants with congenital infections be monitored to detect late-onset hearing
loss, even if the initial audiological evaluation was normal [4].
E. Kepenekli et al.
8.2 Etiology andEpidemiology
Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii, an obligate
intracellular protozoan that infects almost all warm-blooded animals. It is estimated
that about one-third of the world’s human population is infected with T. gondii.
Infection rates vary extensively from 10 to 80% between geographical regions.
Socioeconomic status and hygiene behaviors are important factors determining the
prevalence of infection [5].
The prevalence of T. gondii infection was reported at quite different rates in epi-
demiological studies conducted in different geographical areas or populations. The
incidence and prevalence data may also differ over the years. Europe, Central
America, Brazil, and Central Africa have the highest rates of T. gondii infections
[6]. Among European countries, seroprevalence rates vary widely between regions.
For example, while the overall seroprevalence was reported as 10.7% in pregnant
women in Norway [7], it was 37–42% in France [8]. The seroprevalence and incidence rates, reported to be higher in the past years, have been decreasing in recent
years. In France, seropositivity for toxoplasmosis was decreased in pregnant women,
from 83% in 1965 to 37% in 2010 [8].
The differences in the seroprevalence for toxoplasmosis are also observed for
congenital toxoplasmosis as 18–34, 20–24, and 6–8 per 10,000 live births in South
America, Africa, Europe, and North America, respectively [9]. The global congenital toxoplasmosis burden is estimated to be 190,000 cases annually [9].
In the last 20years, a dramatic decrease occurred in the incidence and prevalence
of toxoplasmosis, even in countries with a high prevalence of T. gondii infections [8,
10]. It is thought that this is related to raising awareness in the population, especially
about food preparation hygiene, educating pregnant women, and prenatal screening
[6, 10, 11]. In some countries, prenatal screening for toxoplasmosis is strongly recommended [6, 11]. A signicant decrease in congenital toxoplasmosis incidence
after prenatal screening programs was reported [6, 11].
8.3 Life Cycle ofToxoplasma gondii andTransmission
Toxoplasma gondii can live in animals in three forms; tachyzoite, bradyzoite, and
oocyst [5]. Tachyzoite is the rapid-proliferating form, and bradyzoite is the slowproliferating form in animals and humans [6]. Oocysts are found in cat feces. The
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sexual life cycle of T. gondii occurs mainly in felines, and the asexual cycle occurs
in humans and animals [6].
Cats become infected directly by ingesting oocysts or ingesting intermediate
hosts’ tissue or organs harboring bradyzoite-containing tissue cysts [12]. Then, the
sexual life cycle begins in the cat’s intestine, and macrogametocytes and microgametocytes develop from ingested bradyzoites and/or oocysts and fuse to form
zygotes [13, 14]. The zygotes become encapsulated within a thick wall and are
dispersed as oocysts. Oocysts are resistant to ultraviolet light, chlorinated water, and
ozone. Thus, oocysts can survive and contaminate water sources, soil, and the environment through cat feces. Oocysts are responsible for the spread of infection from
cats to humans or animals [5, 15].
Humans and animals may acquire toxoplasmosis from oocyst-contaminated soil
and vegetables. When orally ingested, oocysts reach the intestines and rupture to
release sporozoites. Then, sporozoites transform into tachyzoites. Tachyzoites can
spread throughout the body via the bloodstream and lymphatics. If the host’s
immune response is adequate, tachyzoites reaching the end organs are conned to
tissue cysts and transform into bradyzoites. Bradizoites are responsible for the
chronic stage of infection and can persist throughout the host’s life. A cyst may
contain several or hundreds of bradyzoites responsible for latent infection [15].
Tissue cysts can be found in the eye, brain, heart, and skeletal muscles [5, 15]. The
shape of the cysts may differ according to the involved organ; a spherical shape in
the brain parenchyma and a more elongated shape in the muscle are seen [5].
Transmission of T. gondii to humans also occurs by eating undercooked meat
containing tissue cysts. Cysts are found in the muscles of pigs and cattle, and their
ingestion by humans is critical for transmitting toxoplasmosis to humans.
Bradyzoites, more resistant to temperature changes than tachyzoites, should be
stayed for 3days at minus (−) 12°C or be exposed to a temperature above 67°C to
lose the infectivity potential [15]. Therefore, it is essential to cook the meat at the
appropriate temperatures for bradyzoites’ inactivation [5, 6, 15].
Congenital toxoplasmosis happens due to transplacental transmission of the
tachyzoites to the fetus [5]. Rarely, the infection can be transmitted to humans by
transplantation of an infected organ or transfusion of blood products containing
tachyzoites [5, 6].
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8.4 Clinical Features
The incubation period is around 1 week for acquired toxoplasma infection.
Parasitemia occurs through the spread of tachyzoites and is responsible for acute
symptoms, generally lasting 2weeks after infection. Following the acute phase, the
latent phase begins with transforming the tachyzoites into bradyzoites [15].
Toxoplasmosis is usually asymptomatic, benign, and self-limited in immunocompetent individuals [6]. Severe end-organ damage may occur in immunocompromised patients and congenitally infected infants. Patients with congenital infections
are at high risk for retinal disease throughout their lives, even if they are asymptomatic in early life [6].
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