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10 Congenital Syphilis andHearing Loss
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amniotic uid analyzes of pregnant women with early syphilis [16]. This nding
indicates that spirochetes cross the fetal membranes, reach the amniotic uid, and
cause infection in the fetus. Findings consistent with CS are detected in utero, and
immunoglobulin (Ig) M antibodies specic for T. pallidum are detected in blood
samples taken from fetuses or newborns [16]. Moreover, the Langerhans cell layer
persists throughout pregnancy.
Mother-to-child transmission of syphilis varies with the stage of maternal syphilis. The highest transmission rates are detected in early syphilis, especially secondary syphilis [16]. Shefeld etal. [17] determined the vertical transmission rates as
29%, 59%, 50%, and 13% during primary, secondary, early latent, and late latent
infection, respectively. Transmission can also occur through contact with infected
maternal lesions during delivery. Breastfeeding is not considered a route for infection unless the mother has an infectious lesion on her breast [3, 12].
Syphilis is also associated with increased sexual transmission of HIV.However,
the contribution of syphilis and HIV coinfection to MTCT of either syphilis or HIV
has not been elucidated fully [3].
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10.4 Pathogenesis
Treponema pallidum spirochetemia leads to disseminated infection and widespread
inammation of the fetus’s almost all visceral organs [3, 12, 18]. Perivascular struc-
ture and interstitial stroma, rather than the parenchyma, are intensely affected. The
liver, gastrointestinal system, kidneys, spleen, and bone are frequently involved in
symptomatic CS. Skeletal changes are attributed to syphilitic granulation of the
periosteum and epiphyses that interfere with bone formation. Extramedullary hematopoiesis in the fetus is prominent [3, 12]. The placenta of the neonates with CS
presents enlarged villi, the proliferation of the vascular structures, and inammation
[3, 19]. The umbilical cord may also show signs of inammation, necrosis, and
abscess-like foci called necrotizing funisitis [19]. Histochemical staining may yield
spirochetes within both the umbilical cord and placenta.
10.5 Clinical Presentation
Transplacental transmission of syphilis can result in adverse fetal outcomes [2, 3,
12]. In a comprehensive meta-analysis, Gomez etal. [20] documented that 52% of
the pregnancies with untreated syphilis ended up with complications, including
fetal loss or stillbirth (21%), neonatal death (9%), prematurity or low birth weight
(LBW, <2500g; 6%), and symptomatic CS (15%).
Clinical ndings appear broadly from asymptomatic infection limited to only
laboratory or radiologic abnormalities to life-threatening involvement of multiple
organ systems. In a South African study of 50 newborns diagnosed with early symptomatic CS, 34 infants required intensive care and 38% died [21].
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E. M. Kara et al.
Table 10.1 Clinical, laboratory, and radiologic ndings of congenital syphilis
Early congenital syphilis (rst 2years of life)
Physical examination ndings:
Hepatomegaly with or without jaundice
Splenomegaly
Skin rash
Adenopathy (characteristically epitrochlear)
Rhinitis (snufes)
Condyloma lata
Mucus patch
Pseudo paralysis of parrot
Eye: chorioretinitis, cataract
Central nervous system: asymptomatic, cranial nerve palsies, seizures.
Laboratory ndings:
Blood analysis: anemia, thrombocytopenia, hypoglycemia, increased liver transaminases,
direct hyperbilirubinemia.
Cerebrospinal uid analysis: pleocytosis, elevated protein levels
Radiographic ndings:
Periostitis, osteochondritis, pneumonia alba
Other: Nephrotic syndrome, pancreatitis, myocarditis, fever, gastrointestinal malabsorption,
hypopituitarism (diabetes insipidus)
Late congenital syphilis (>2years)
Eye: interstitial keratitis, chorioretinitis
Eight nerve deafness
Hutchinson’s teeth, Mulberry molars
Rhagades
Central nervous system: mental retardation, hydrocephalus, seizures, optic nerve atrophy,
cranial nerve palsies
Bone and joint: frontal bossing, saddle nose deformity, protuberant mandible, short maxilla,
saber shin, high palatal arch, Higoumenakis sign (sternoclavicular joint thickening), Clutton
joints
a
Adapted and modied from Ref. [22, 23]
a
Congenital syphilis is divided into two clinical syndromes according to the presentation time as early or late CS [3]. Clinical, laboratory, and radiologic ndings of
CS are summarized in Table10.1.
10.5.1 Early Congenital Syphilis
Early CS is the disease in which clinical ndings are observed in the rst two years
of life [2, 3, 12, 22]. Most neonates born to untreated syphilitic mothers may appear
normal at birth and develop the symptoms of the disease months later. In untreated
cases, clinical ndings occur most frequently in the rst 3months.
Bone involvement, sometimes the only manifestation of CS, occurs in up to 80%
of infants born to mothers with untreated syphilis. Periostitis and osteochondritis
have diagnostic values, mainly in the femur and humerus [3]. Although skeletal
changes may heal spontaneously in the rst year of age, they may be very painful
initially, leading to disability in the child termed pseudoparalysis of Parrot. Long
bone involvement may also cause pathologic fractures.
ab
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135
Almost all symptomatic CS cases have hepatomegaly which may also be together
with splenomegaly. Jaundice may also be observed at physical examination.
Biochemical ndings of liver dysfunction, most commonly after the initiation of
therapy due to immune response, and elevated serum alkaline phosphatase levels
are expected [20, 24].
Neonates with CS may have white, translucent nasal discharge, usually appearing in the rst week of life. Snufes may be hemorrhagic or purulent in the case of
bacterial superinfection. It lasts longer than the common cold. The darkeld examination may yield spirochetes [2, 3].
Generalized non-tender-rm lymphadenopathy may be as large as 1 cm.
Lymphadenopathy in the epitrochlear region is highly suggestive of CS [2]. An
erythematous maculopapular rash may be observed during the rst weeks of life.
The rash then may desquamate and appear in a coppery color. Palm and soles are
usually affected, and peeling can occur (Fig.10.1a, b). If the infant has thrombocytopenia, petechial lesions may also be seen. Infectious vesiculobullous lesions
called “pemphigus syphiliticus” are characteristic of CS [2, 3, 12]. Less commonly,
easily bleeding ssures around the mucocutaneous junctions may be observed. Flat,
wart-like lesions called “condylomata lata” containing spirochetes can also be
encountered.
Central nervous system (CNS) invasion by T. pallidum occurs in approximately
50% of infants with clinical, laboratory, or radiographic signs of CS [2, 3, 12].
Involvement of CNS may be asymptomatic at birth. Cerebrospinal uid (CSF) analysis can yield pleocytosis, increased protein levels, and a reactive Venereal Disease
Fig. 10.1 (a, b) Peeling on hands and feet in an infant with congenital syphilis (Courtesy of Tuğçe
Tural Kara, MD)
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Research Laboratory (VDRL) test. Symptomatic infants generally present with two
clinical syndromes. The “acute syphilitic leptomeningitis” form usually occurs in the
rst year of life and is hardly indistinguishable from bacterial meningitis [2]. Yet, the
CSF ndings mostly mimic aseptic meningitis. In the other scenario, the infant may
come to clinical attention with signs of progressive hydrocephalus, neurodevelopmental regression, and seizures [2, 3, 12, 25]. The presentation, which typically
occurs at the end of the rst year, is called “chronic meningovascular syphilis.”
Early CS can rarely manifest itself with non-immune hydrops, hematologic
abnormalities, ocular ndings (loss of eyebrows, glaucoma, chorioretinitis, etc.),
myocarditis, pneumonia, gastrointestinal involvement (necrotizing enterocolitis),
nephrotic syndrome, failure to thrive, or prolonged fever. However, the latter is
prominent when the infant’s mother is affected late in the pregnancy [25].
E. M. Kara et al.
10.5.2 Late Congenital Syphilis
In late CS, the clinical ndings occur after 2years of age [3]. The disease results
from chronic inammation rather than active infection; therefore, patients are not
contagious [2, 16]. Although some clinical ndings can be preventable by treating
the expectant mother in the late pregnancy or the neonate after birth, particular
manifestations like keratitis and saber shins may occur even with treatment [2].
In the nineteenth century, British surgeon and pathologist Jonathan Hutchinson
dened the classical triad of “interstitial keratitis, 8th nerve deafness and the defects
in the incisor teeth” as characteristic of CS [26]. In addition to these, there are specic ndings related to various systems. For instance, infants with CS have characteristic facial features, including frontal bossing, saddle nose, protuberant mandible,
and short maxilla, resulting from osteochondritis [25]. An ophthalmologic examination may also reveal corneal scarring, glaucoma, and optic atrophy. Interstitial keratitis is quite specic for CS, is usually bilateral, and can occur at any time in the rst
three decades of life [25, 27, 28].
Dental developmental disorders, widely spaced notched central incisors, known
explicitly as Hutchinson’s teeth, are typical features of late CS.Mulberry molars
and perforation of the hard palate are rare but almost pathognomonic for syphilis. In
addition, perioral ssures (rhagades) can be observed [2, 3, 12, 16].
Skeletal abnormalities may involve long bones. “Saber shins” (anterior bowing of
the shins), “Clutton joints” (painless arthritis of the knees), and “Higoumenakis sign”
(enlargement of the sternoclavicular joint) are the hallmarks of physical examination.
Neuromotor development abnormalities and rare hematologic conditions such as paroxysmal nocturnal hemoglobinuria are exceptional manifestations [2, 3, 12].
10.6 Congenital Syphilis andHearing Loss
In utero, syphilis exposure is a risk indicator for developing congenital, delayedonset, or progressive hearing loss (HL) in childhood [3]. Although it is a constant
but the least common element of the Hutchinson triad described many years ago,
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there is scarce information about CS-associated HL in the literature data and leading textbooks in the eld [2, 3, 12, 15, 29]. Few contemporary studies have looked
at HL in these children. While most evidence suggests that HL occurs late in the
disease [3], typically in the absence of treatment, other more recent publications
suggest that there could be an association with hearing decits in the neonatal
period [30, 31]. Accordingly, as disease incidence is relatively low and can occur at
any time in childhood, the incidence of CS-associated HL is hard to estimate. As a
result of the plummeting incidence of this disease in children, driven by timely
diagnosis and treatment in pregnancy, estimates for the prevalence of HL in children
and adolescents with CS come from studies conducted a decade ago. One of the rst
studies to investigate HL in children with CS found a prevalence of 14% [32]. In
another study, the prevalence was higher at 38%; however, critics of this estimate
note that the diagnosis of CS remained questionable as specic serologic or clinical
criteria were not provided [33].
It has become generally accepted that hearing disturbances in the neonatal period
are rare. This belief has been primarily driven by a study by Gleich etal. [33], in
which none of the 75 children diagnosed with CS had evidence of HL during the
neonatal period, and all infants demonstrated symmetric waveforms with normal
amplitudes and latencies. While these ndings are reassuring because no frequencyspecic audiometric assessments were performed, some degree of HL could have
been missed, and perhaps more importantly, so could have progressive HL as the
study lacked reevaluation of those patients. Although contemporary studies have
cast doubt on neonatal HL as a consequence of CS, screening for HL at birth remains
part of the evaluation guidelines, as otosyphilis can present at any time during
infection.
While the incidence of HL in CS may be distributed over a much wider age
range, onset is often clustered around 8–10years [34]. In a study by Tamari etal.
[32] of 310 syphilitic patients, the onset of HL occurred in the rst two decades of
life. This nding is supported by another study which found that 12% of patients
with CS developed symptoms of hearing disturbances before the age 10 [33]. In the
case of HL attributable to CS, the presentation is often sudden and bilateral, with
loss of high frequencies preceding those found in normal conversational [15, 34,
35]. Despite the fact that most cases appear to affect both ears equally, there have
been reports of children with unilateral HL [36].
The pathogenesis of syphilis sheds light on why HL may be seen in both congenital and acquired forms. The most common form of HL involves the eighth cranial nerve, which can be affected by T. pallidum within or outside the CSF space,
the cochlea vestibular apparatus, or the temporal bone [37]. Though some clinical
differences exist, it is not always easy to distinguish CS-related late-onset HL from
adult-type syphilitic HL.In the former, vestibular symptoms usually do not accompany decits in hearing. When HL occurs in adults, it is typically asymmetric, uctuating with sudden onset of tinnitus and vertigo [38]. However, if the spirochetes
invade only the perilymph of the inner ear and the inammation is restricted to the
cochlea and vestibular system, the patient may experience HL together with vertigo
[37]. If the infection is limited to the inner ear, CSF indices will typically be within
normal limits. When spirochetes spread through the CSF and invade the perilymph
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of the inner ear via the cochlear aqueduct, CSF analysis is usually abnormal. In
these cases, abnormal auditory brainstem responses (ABRs) indicative of upper
brainstem pathways or cochlear nerve dysfunction may occur.
Cochlear degeneration and brous adhesions due to osteochondritis of the otic
capsule, osteitis, and periostitis of the temporal bone and the ossicles in the middle
ear can be observed in untreated CS or chronic adult infection [15, 37]. Histological
obliterative endarteritis appearance can cause a decrease in vascular supply contributing to bony necrosis [39]. As can be seen from the diversity in pathophysiology,
symptomatic, audiometric, and laboratory (CSF ndings), differences and therapeutic responses may be observed among patients [37].
Syphilis-related morbidity was markedly reduced after penicillin treatment.
Therefore, publications describing the otologic complications of CS often belong to
the pre-antibiotic era. However, even in these studies, data on children are limited.
When steroid treatment was being investigated as an adjuvant in treating bacterial
and tuberculous meningitis, prednisone was suggested as a potential treatment that
could potentially benet HL, especially in adults [40]. While no contemporary studies have evaluated these ndings in syphilis, a meta-analysis found that, in highincome countries, adjuvant glucocorticoid therapy reduced severe HL in bacterial
meningitis [41].
Long-term follow-up of these children is important since the true incidence and
age of onset of CS in children are not known precisely, and newborn screening tests
may be completely normal. Therefore, a repeat hearing screening should be performed later, between 2 and 3years of age, for all children with CS who have received
appropriate treatment in the neonatal period. For those, who did not get proper treatment, at least an annual audiological examination should be provided [35].
E. M. Kara et al.
10.7 Diagnostic Approach
The Centers for Disease Control and Prevention recommends that all infants born to
seropositive mothers should be evaluated with a thorough physical examination
(including the examination of the placenta and umbilical cord), laboratory tests
(complete blood count, liver transaminases, CSF pleocytosis analysis, protein level,
and VDRL) radiologic investigation (long bone radiographs, neuroimaging, HIV
test), and additionally quantitative nontreponemal tests (NTTs) as clinically indicated (Fig.10.2) [3, 12, 27, 29].
10.7.1 Laboratory Evaluation
Routine blood tests are inconclusive in CS.Complete blood count can yield hematologic abnormalities in up to 75% of symptomatic infants [29]. Approximately half
of the cases present elevated white blood cell count, prominently monocytosis [29].
Thrombocytopenia may be encountered. An increase in liver enzymes may often be
observed after the initiation of the therapy.
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Reactive Maternal RPR/VDRL
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Maternal Treponemal Test Non-reactive
False Positive:
No further evaluation.
Consider repeat testing if
pregnant
Infant PE normal;
evaluationa normal, infant
VDRL/RPR same or less
than 4 fold the maternal
VDRL/RPR titer
b
Treatment
(option 1 or 2)
Evaluate
c
Maternal Treatment:
None, or Undocumented, or
4 weeks or less before delivery, or
Nonpenicilin drug, or Maternal
evidence of reinfection/relapse
a
Infant PE abnormal;
evaluation
abnormal/incomplete; or
infant VDRL/RPR at least 4
fold greater than maternal
VDRL/RPR titer
Treatment (option 1)
a
c
Maternal Treponemal Test Reactive
Maternal Treatment:
Maternal penicillin treatment
during pregnancy AND >4 weeks
before delivery AND no evidence
of maternal reinfection/relapse
Infant VDRL/RPR 4
fold/greater than
maternal VDRL/RPR titer
Evaluationa and
treatment (option 1)
Infant PE is abnormal Infant PE is normal
c
Infant VDRL/RPR same or
less than 4 fold the
maternal VDRL/RPR titer
No evaluation;
Treatment (option 2)
Maternal Treatment:
Adequate maternal treatment
during pregnancy with stable low
titer (serofast).
RPR 1:4 or VDRL 1:2
If infant PE is
abnormal,
proceed with
evaluation
If infant PE is
normal, no
treatment, no
a
evaluation
c
Fig. 10.2 Evaluation and management of congenital syphilis*. PE indicates physical examination,
RPR rapid plasma reagin, VDRL Venereal Disease Research Laboratory. aEvaluation includes com-
plete blood cell and platelet count; cerebrospinal uid examinationfor cell count, protein, and
quantitative VDRL; other tests as clinically indicated (e.g., chest and long-bone radiographs, eye
examination, liver function tests, neuroimaging, and auditory brainstem response). bMany experts
recommend option 1. cTreatment options: Option 1: Aqueous penicillin G 50,000 units/kg, intravenous, q12h (≤1-week old), q8h (>1-week and ≤4-week old), q6h (>4-week old)×10 days, or
procaine penicillin G 50,000 units/kg, intramuscular × 10 days (≤4-week old). Option 2:
Benzathine penicillin G 50,000 units/kg, intramuscular as a single dose. (*Adapted and modied
from Refs. [3, 12, 26, 28, 42])
Cerebrospinal uid analysis may reveal pleocytosis, elevated protein level, and
reactive VDRL test, the only test approved for testing CSF [2, 3, 29]. Since the
VDRL test in the CSF may yield false-negative or false-positive results, detecting
T. pallidum by polymerase chain reaction (PCR) can be a more reliable alternative [43].
10.7.1.1 Tests forOrganism
It is difcult to culture T. pallidum in the laboratory environment; therefore, various
methods are used in clinical practice. The rst is the direct visualization of T. pal-
lidum by darkeld microscopy or uorescent antibody methods [3, 12, 29]. Thin,
delicate, corkscrew-shaped organisms with rigid, tightly spiral-shaped, typical
back-and-forth rotational motion of T. pallidum can be observed with darkeld
microscopy, which can be studied in body uids such as runny nose or samples
taken from moist skin lesions. However, spirochetes are exquisitely susceptible to
antimicrobials, so microscopic examination may be unrevealing if done after
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starting therapy [29]. Microorganisms can also be detected by staining histopathological samples or autopsy materials.
Historically, the reference test in the diagnosis of CS was the rabbit infectivity
test (RIT) which involves the serial passage of infected material such as CSF or
other body uids in the testes of rabbits to detect alive T. pallidum [38, 39]. Once
considered the gold standard for measuring infectivity, RIT is no longer suitable for
clinical use due to animal testing [44].
E. M. Kara et al.
10.7.1.2 Serological Tests
Serological tests can be evaluated under two headings: Nontropenemal tests (NTTs:
Venereal Disease Research Laboratory [VDRL] and rapid plasma reagin [RPR])
and treponemal tests (TTs: uorescent treponemal antibody absorption [FTA-ABS],
T. pallidum particle agglutination [TP-PA], enzyme immunoassay [EIA], chemiluminescence immunoassay [CIA], micro hemagglutination test for T. pallidum
[MHA-TP]) [2].
Nontropenemal tests are inexpensive, performed quickly, and have high sensitivity; however, they are not specic. They detect IgM and IgG antibodies to cellular
lipids and lecithin [29]. A false-positive NTT result (usually has a titer ≤1:4) may
occur in various clinical syndromes, including connective tissue disorders, infectious diseases (e.g., hepatitis, chickenpox, and infectious mononucleosis), and pregnancy [3, 12, 29]. A false-negative reaction called the “prozone effect” can result
from excessive antibody production inhibiting antigen–antibody interaction [2, 29].
The prozone effect should be suspected when an infant presents signs of CS but the
mother is seronegative. The prozone effect can be overcome with serial dilution of
the samples.
There are several differences between TTs and NTTs. Treponemal tests become
positive slightly earlier and stay positive for a lifetime, but they cannot reect the
infection activity [29]. False positivity mainly occurs in other spirochetal infections,
such as Lyme disease [44], and can also be seen with endemic trypanosomoses [45].
Recombinant T. pallidum antigen tests, EIA, and CIA are often used for population-
level screening, with conrmation done by a different TT, and a quantitative NTT is
referred to as reverse sequence testing [46].
10.7.2 Radiology
Radiological evaluation of long extremities is of great importance to the newborn
assessment of suspected CS, as radiographic abnormalities are common in early
syphilis [47]. Abnormalities can be detected in 95% of symptomatic infants and up
to 20% with asymptomatic disease [29, 47]. The changes are usually present at
birth, sometimes appearing in the rst weeks of life.
Symmetric localized demineralization and osseous destruction of the medial portion of the proximal tibial metaphysis, referred to as Wimberger sign, or irregular
areas of increased density and rarefaction called moth-eaten appearance can be
observed [3, 47]. Sometimes these pathological changes in the long bones cause
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pain and fractures, leading to a limitation of movement of the affected extremity.
This condition is called pseudoparalysis of Parrot [48]. Multiple layers of periosteal
new bone formation are referred to as periostitis and can be encountered [47].
Lesions in the bone often heal spontaneously within months [16]. In untreated
cases, opacication of both lungs, characteristically called pneumonia alba, may be
observed on chest radiography.
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10.8 Evaluation andManagement
All newborns born to mothers with a reactive test for syphilis at birth should be
evaluated for the possibility of CS.A negative NNT result at delivery does not rule
out the possibility of CS owing to the case of the prozone effect [42], and the decision to treat an infant according to the diagnosis of CS should be made after evaluating the clinical, serological, and epidemiological ndings together. Risk analysis of
the mother for syphilis, serological examination, adequacy of the treatment if
treated, and the possibility of reinfection or relapse should be evaluated. Case denitions for CS have been made to provide a standardized and applicable treatment
algorithm. The evaluation and management algorithm and treatment options are
summarized in Fig.10.2 and Table10.2 [3, 12, 23, 27, 29].
If a neonate has any of the following indicators, including abnormal physical
ndings compatible with CS or a reactive (≥four-fold the corresponding maternal
titer) serum NTT (VDRL or RPR), or a positive darkeld or uorescent antibody
test for T. pallidum in neonatal nasal discharge, umbilical cord or other body uids,
is dened as “proven or highly probable CS” [12, 23, 27].
“Possible CS” is the term used to dene neonates with normal physical examination who have a reactive NTT (<four-fold the maternal titer) born to untreated or
inadequately treated syphilitic mothers. These infants should be further evaluated
according to the American Academy of Pediatrics (AAP) and the CDC recommendations [12, 23, 27].
An asymptomatic neonate (normal physical examination) with a reactive NTT
(<four-fold the maternal titer) whose mother received adequate and proper treatment (for more than 4weeks before delivery) and has no evidence of relapse or
reinfection is considered as “CS less likely.” Such infants should be treated with a
single dose of intramuscular (IM) penicillin G benzathine [12, 27, 47]. However,
some experts recommend not treating neonates under close serologic follow-up provided their mothers’ NTT decreased at least four-fold after therapy or remained
stable at low titer [12, 23].
The distinction between congenital and acquired syphilis is challenging after
>1month of age. The possibility of sexual abuse must always be evaluated [27]. The
child’s examination should include CSF analysis (cell count, protein, and VDRL),
complete blood test, HIV test, and other tests (long-bone and chest radiographs,
liver function tests, abdominal ultrasonography, ophthalmologic examination, ABR,
and neuroimaging studies) as clinically indicated. Those infants should be treated
with parenteral penicillin therapy [12, 23, 27].
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E. M. Kara et al.
Table 10.2 Evaluation and treatment of infants with congenital syphilis
Case
Proven or highly
probable
congenital
syphilis
Evaluation
CSF analysis:
VDRL, cell count, and protein;
CBC and platelet count;
other tests as clinically
indicated (e.g., long-bone
radiographs, liver function tests,
Treatment
Aqueous penicillin G 50,000U/kg IV
q12h (≤1wk old),
q8h (>1wk old, ≤4wk old),
q6h (>4wk old)×10d, or
Procaine penicillin G 50,000U/kg
IM×10d (≤4wk old)
a
ophthalmologic examination,
hearing evaluation,
neuroimaging)
Possible
congenital
syphilis
CSF analysis:
VDRL, cell count, and protein;
CBC and platelet count; long
bone radiographs
If complete evaluation is normal:
(a) Benzathine penicillin G 50,000U/kg
IM×1b or
(b) Aqueous penicillin G 50,000U/kg
IV q12h (≤1wk old),
q8h (>1wk old, ≤4wk old),
q6h (>4wk old)×10days, or
(c) Procaine penicillin G 50,000U/kg
IM×10d (≤4wk old)
Congenital
syphilis less
likely
No evaluation Benzathine penicillin G 50,000U/kg
IM×1 (preferred),
or
Clinical, serologic follow-up
Congenital
syphilis unlikely
None None
or
Benzathine penicillin G 50,000U/kg
IM×1 (some experts) if follow-up is
uncertain
Congenital
syphilis in
infants aged
>28d
CSF analysis:
VDRL, cell count, protein;
CBC and differential; platelet
count
Aqueous penicillin G 50,000units/kg
q4–6h×10d
d
As clinically indicated:
radiographs of long bones, liver
function tests, neuroimaging
(cranial ultrasonography), eye
examination, hearing evaluation
CBC indicates complete blood count, CSF cerebrospinal uid, d day, h hour, IM intramuscular, IV
intravenous, q quaque (every), U unit, VDRL Venereal Disease Research Laboratory
a
Adapted and modied from Ref. [3, 12, 23, 27, 29]
b
Clinical and serologic follow-up must be certain
c
If the infant’s nontreponemal test is non-reactive, no evaluation is required, but the infant should
receive a single IM dose of benzathine penicillin G 50,000U/kg
d
Some experts prefer prolonged therapy by administering a single dose of benzathine penicillin G
after the 10-day course of IV aqueous penicillin G
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