Edit concept Question Editor Create issue ticket

Congenital Syphilis

Congenital syphilis is a potentially lethal disease caused by Treponema pallidum infections occurring during intrauterine development. Skin, mucosal and bone lesions are characteristic for congenital syphilis that may be further complicated by CNS symptoms. Children at high risk and confirmed cases should be treated with penicillin.


Presentation

About two thirds of all children suffering from CS are born without any symptoms. The disease is often detected during routine screenings.

The first symptoms may appear weeks, even a few months after birth. They include skin lesions such as blisters and copper-colored rash on palms and soles, papules in face and lower abdomen and petechiae. Children often develop a purulent rhinitis and parents frequently report their children to snuffle. Of note, nasal discharge and skin lesions are highly contagious. A clinical examination may further reveal enlargement of lymph nodes, liver and spleen. Hepatomegaly is indeed the most common finding in CS and is usually associated with altered results of serum liver enzymes. More severe symptoms such as pneumonia, hemolytic anemia, thrombocytopenia and less commonly leukocytosis may be observed. Neurological symptoms may be present and consist in hydrocephalus, meningitis, seizures and consecutive mental retardation. Alterations in cerebrospinal fluid (CSF) composition may be found. Physical development may also be retarded.

When children affected by CS reach the age of half a year, they may develop osteochondritis. It may lead to pseudoparalysis and is usually not detectable in younger children [10]. This condition mainly affects the long bones of the limbs as well as the ribs and therefore strongly impairs the child's movements. Bone lesions matching with chondroepiphysitis, ostitis or periostitis are detectable in radiographic images and are of great diagnostic value because they can indeed be found in children who show hardly any additional signs of CS [11].

Clinical symptoms are different in children developing late CS, that is who manifest symptoms after reaching the age of two. Ulcerative lesions in mucosa of nose and hard palate are common, as are periostal lesions resulting in leg and head deformations (saber shins, skull bossing). The nervous system may be affected, but symptoms are rare. Tabes dorsalis and paresis as well as progressive loss of hearing due to damage to the eighth cranial nerve may possibly be observed. The eyes may suffer from interstitial keratitis, consecutive corneal scarring, but also from optic atrophy leading to blindness. Tooth deformities such as Hutchinson incisors and mulberry molars are as characteristic for late CS as perioral fissures.

Splenomegaly
  • Compared with term neonates with CS, preterm ones were more likely to have characteristic skin rash (36.2 vs. 9.7%, p 0.001), hepatomegaly (51.7 vs. 25%, p 0.02), splenomegaly (32.8 vs. 15.4%, p 0.02), PRP titer 1:8 (96.6 vs. 70.8%, p 0.001), thrombocytopenia[ncbi.nlm.nih.gov]
  • Less common presentations include patchy alopecia, anterior uveitis, meningitis, cranial nerve palsies, hepatitis, splenomegaly, periostitis and glomerulonephritis.[patient.info]
Generalized Lymphadenopathy
  • These neonates also display significant changes in bone morphology and frequently hepatosplenomegaly along with generalized lymphadenopathy.[pathwaymedicine.org]
  • These include low-grade fever, malaise, and generalized lymphadenopathy. Some disability may result from involvement of palms and soles. Periosteitis and rarefaction are more extreme in children.[drmhijazy.com]
Fever
  • Abstract We report an unusual case of recurrent fever, inflammatory knee pain, genu varum, persistent anemia, and high erythrocyte sedimentation rate in a 28-month-old boy as late manifestations of congenital syphilis (CS).[ncbi.nlm.nih.gov]
  • One hour after the first injection, the infant developed fever (39 C), tachycardia and tachypnea without worsening of rash. Vital signs improved gradually. The rash reduced markedly at postnatal day 1, and disappeared without pigmentation at day 3.[ncbi.nlm.nih.gov]
  • If untreated, the infection may cause deafness, blindness, crippling, or death. congenital syphilis Congenital lues, fetal syphilis Neonatology Transplacental infection with Treponema pallidum Clinical Early–hepatomegaly, irritability, FTT, fever, perioral[medical-dictionary.thefreedictionary.com]
  • Three babies had none of the classic symptoms, but presented with fever as their primary symptom.[nejm.org]
  • Babies exposed in utero can have deformities, delays in development, or seizures along with many other problems such as rash, fever, an enlarged liver and spleen, anemia, and jaundice.[en.wikipedia.org]
Anemia
  • The reason for anemia and thrombocytopenia in congenital syphilis is not clear. The authors suggest that hemophagocytosis may play role in pathogenesis of cytopenia, particularly thrombocytopenia in patients with congenital syphilis.[ncbi.nlm.nih.gov]
  • An elevated MCA PSV suggested fetal anemia. Successful intrauterine cordocentesis and transfusion of packed red blood cells led to resolution of fetal hydrops.[ncbi.nlm.nih.gov]
  • Abstract We report an unusual case of recurrent fever, inflammatory knee pain, genu varum, persistent anemia, and high erythrocyte sedimentation rate in a 28-month-old boy as late manifestations of congenital syphilis (CS).[ncbi.nlm.nih.gov]
  • Our patient demonstrates the typical clinical findings of lethargy, extremity swelling and the pseudoparalysis of Parot, while laboratory evaluation showed anemia, abnormal hepatic enzymes, hypoproteinemia, and confirmatory positive neonatal VDRL and[ncbi.nlm.nih.gov]
  • In the second case, a fetus at 24 weeks' gestation was hydropic and a fetal blood sample showed anemia, thrombocytopenia, and elevated liver enzymes.[ncbi.nlm.nih.gov]
Hutchinson's Triad
  • This manuscript reports a case of late congenital syphilis presenting with Hutchinson's triad at an age of 7 years.[ncbi.nlm.nih.gov]
  • Hutchinson's triad, a set of symptoms consisting of deafness, Hutchinson's teeth (centrally notched, widely spaced peg-shaped upper central incisors), and interstitial keratitis (IK), an inflammation of the cornea which can lead to corneal scarring and[en.wikipedia.org]
  • This manuscript reports a case of late congenital syphilis presenting with Hutchinson’s triad at an age of 7 years.[casereports.bmj.com]
  • Hutchinson’s triad (Hutchinson’s teeth, interstitial keratitis, and VIIIth nerve deafness) is considered pathognomonic of late congenital syphilis.[dartmouth.edu]
  • The constellation of interstitial keratitis, cranial nerve VIII deafness, and Hutchinson teeth is called the Hutchinson triad.[aao.org]
Saddle Nose
  • Untreated early syphilis infections results in a high risk of poor pregnancy outcomes, including saddle nose, lower extremity abnormalities, miscarriages, premature births, stillbirths, or death in newborns.[en.wikipedia.org]
  • History / PE : Early manifestations Hepatosplenomegaly Cutaneous lesions on palms/soles Jaundice/anemia Rhinorrhea Late/untreated manifestations Frontal bossing Hutchinson teeth Saddle nose Perioral fissures Diagnosis : VDRL FTA-ABS Treatment : Penicillin[medlibes.com]
  • Inflammation of bone's periosteum can lead to a number of morphological changes such as sinking in of the nose, resulting in a "Saddle Nose", or bowing of the tibia, resulting in "Saber Shins".[pathwaymedicine.org]
  • nose Notched and narrowed incisors-Hutchinson’s teeth Periosteal reaction and new bone formation Especially proximal 2/3 of tibia shaft common late manifestation Saber shin Bilateral forward bowing of tibia is conclusive evidence for acquired, tertiary[learningradiology.com]
  • nose; late–Hutchinson's teeth, saber shins, neurologic impairment, deafness, blindness Lab liver enzymes, anemia, monocytosis Diagnosis Serologic tests performed at birth may be negative.[medical-dictionary.thefreedictionary.com]
Rhinorrhea
  • Case 2, an Aboriginal baby of six weeks, came with more classic symptoms and signs--rhinorrhea, rash with desquamation, irritability, anaemia, and lack of movement in an upper limb; the serological diagnosis already made.[ncbi.nlm.nih.gov]
  • Untreated infants develop symptoms such as rhinorrhea, anemia, jaundice, cutaneous lesions, hepatosplenomegaly, and pseudoparalysis within weeks or months.[ncbi.nlm.nih.gov]
  • History / PE : Early manifestations Hepatosplenomegaly Cutaneous lesions on palms/soles Jaundice/anemia Rhinorrhea Late/untreated manifestations Frontal bossing Hutchinson teeth Saddle nose Perioral fissures Diagnosis : VDRL FTA-ABS Treatment : Penicillin[medlibes.com]
  • […] petechiae. other skin rash. sabre shins. anemia. lymph node enlargement. jaundice. pseudoparalysis. snuffles, aka "syphilitic rhinitis", which appears similar to the rhinitis of the common cold, except it is more severe, lasts longer, often involves bloody rhinorrhea[en.wikipedia.org]
Failure to Thrive
  • Early signs are characteristic skin lesions, lymphadenopathy, hepatosplenomegaly, failure to thrive, blood-stained nasal discharge, perioral fissures, meningitis, choroiditis, hydrocephalus, seizures, intellectual disability, osteochondritis, and pseudoparalysis[merckmanuals.com]
  • Rhinitis with highly infectious nasal discharge, nontender generalized adenopathy, alopecia, iritis, and failure to thrive occur less frequently.[dartmouth.edu]
Hutchinson's Teeth
  • Several reports in the literature have focused on oral manifestations of congenital syphilis, mainly about Hutchinson's teeth and dysplastic molars, which are more common.[ncbi.nlm.nih.gov]
  • Hutchinson's triad, a set of symptoms consisting of deafness, Hutchinson's teeth (centrally notched, widely spaced peg-shaped upper central incisors), and interstitial keratitis (IK), an inflammation of the cornea which can lead to corneal scarring and[en.wikipedia.org]
  • One of the main aspects is observed with the triad of Hutchinson, characterised by the presence of interstitial keratitis, eighth nerve deafness and Hutchinson's teeth.[ncbi.nlm.nih.gov]
  • Later childhood signs of the infection include interstitial keratitis, deafness, and notches in the incisor teeth (called Hutchinson's teeth ).[medical-dictionary.thefreedictionary.com]
  • Hutchinson’s triad (Hutchinson’s teeth, interstitial keratitis, and VIIIth nerve deafness) is considered pathognomonic of late congenital syphilis.[dartmouth.edu]
Mulberry Molar
  • RESULTS: The observed morphology of the first molars corresponds to the typical aspect of mulberry molars, while that of the canines is characterised by hypomineralisation. Hypoplastic grooves were observed on the incisal edges of all incisors.[ncbi.nlm.nih.gov]
  • Three main dental defects are described in congenital syphilis; Hutchinson's incisors, Moon's molars or bud molars, and Fournier's molars or mulberry molars.[ncbi.nlm.nih.gov]
  • This article describes two such specimens which have recently been rediscovered, and discusses the form of the dental defects which they show (Hutchinson's incisors, Moon's molars, and mulberry molars) in relation to the developmental sequence of the[ncbi.nlm.nih.gov]
  • Dental defects such as the mulberry molar and a tapered, fang-like canine suggest a diagnosis of congenital syphilis. This is the first probable case of congenital syphilis from pre-Columbian Central Europe.[ncbi.nlm.nih.gov]
  • Keywords treponematosis • pre-columbian • enamel hypoplasia • mulberry molar • congenital syphilis • hutchinson's incisor[schweizerbart.de]
Notched Incisors
  • incisors), keratitis and deafness and occurs in 63% of cases.Treatment (with penicillin) before the development of late symptoms is essential. abnormal x-rays.[en.wikipedia.org]
  • Syphilitic vasculitis can damage developing tooth buds, leading to peg-shaped, notched incisors (Hutchinson teeth) and multicusped first molars (mulberry molars). Deciduous teeth are not affected.[clinicaladvisor.com]
Hepatosplenomegaly
  • A previously healthy male infant developed hepatosplenomegaly, severe anaemia and thrombocytopenia 5 weeks after birth. Marked haemophagocytosis was present in the bone marrow. A typical maculopapular rash suggested early congenital syphilis.[ncbi.nlm.nih.gov]
  • Common clinical features of early congenital syphilis include hepatosplenomegaly, skeletal deformities, hematologic disturbances, and mucocutaneous features such as rhinitis and maculopapular rash.[ncbi.nlm.nih.gov]
  • Hepatosplenomegaly was the most common clinical finding, although almost 60% of the cases were asymptomatic. Missed opportunities for congenital syphilis prevention through antenatal care were identified.[ncbi.nlm.nih.gov]
  • Abstract A 1-day-old male newborn was born with respiratory distress, low birth weight, hepatosplenomegaly, and bullous targetoid skin lesions over the face, back, buttocks, and extremities.[ncbi.nlm.nih.gov]
  • The dominant clinical sign was hepatosplenomegaly. Laboratory investigation upon admission revealed hyperimmunoglobulinemia and hyperchylomicronemia.[ncbi.nlm.nih.gov]
Hepatomegaly
  • Abstract We present an unusual case, in which a woman presenting with markedly decreased fetal movements at 29 weeks gestation following a recent increase in fundal height was noted sonographically to have fetal hydrops consisting of scalp edema, marked hepatomegaly[ncbi.nlm.nih.gov]
  • Compared with term neonates with CS, preterm ones were more likely to have characteristic skin rash (36.2 vs. 9.7%, p 0.001), hepatomegaly (51.7 vs. 25%, p 0.02), splenomegaly (32.8 vs. 15.4%, p 0.02), PRP titer 1:8 (96.6 vs. 70.8%, p 0.001), thrombocytopenia[ncbi.nlm.nih.gov]
  • Congenital SyphilisHydropsfetalis Nasal discharge Petechial rash Necrotizing funisitis within the matrix of the umbilical cord Hepatomegaly Rash Ostitis , Metaphysitis, P eriostitis Wimberger sign 12.[slideshare.net]
  • Case of the Week: May 6-May 13, 2005 Newborn, infant with hepatomegaly. (Click for a larger image.)[pedsradiology.com]
Saber Shin
  • Inflammation of bone's periosteum can lead to a number of morphological changes such as sinking in of the nose, resulting in a "Saddle Nose", or bowing of the tibia, resulting in "Saber Shins".[pathwaymedicine.org]
  • shin Bilateral forward bowing of tibia is conclusive evidence for acquired, tertiary syphilis although similar changes can occur with congenital form Acquired syphilis affects skull (mixed sclerosis and lysis) Clavicle and tibia[learningradiology.com]
  • shins, neurologic impairment, deafness, blindness Lab liver enzymes, anemia, monocytosis Diagnosis Serologic tests performed at birth may be negative.[medical-dictionary.thefreedictionary.com]
  • […] known as Hutchinson's teeth inflammation of the cornea known as interstitial keratitis deafness from auditory nerve disease frontal bossing (prominence of the brow ridge) saddle nose (collapse of the bony part of nose) hard palate defect swollen knees saber[en.wikipedia.org]
  • Late manifestations (age 3 or older) result from scarring during early systemic disease and include Hutchinson teeth, Mulberry molars, abnormal facies, cranial nerve VIII deafness, bony changes such as saber shins and perforations of the hard palate,[aao.org]
Skin Lesion
  • Abstract A 1-day-old male newborn was born with respiratory distress, low birth weight, hepatosplenomegaly, and bullous targetoid skin lesions over the face, back, buttocks, and extremities.[ncbi.nlm.nih.gov]
  • Using PCR detection of tmpC (TP0319) and DNA sequencing of the genes TP0136 and TP0548, DNA sequences identical to Treponema pallidum subsp. pallidum strain SS14 were detected in the infant's skin lesions, serum, and cerebrospinal fluid.[ncbi.nlm.nih.gov]
  • We present a case of early congenital syphilis showing the classical features of the disease, in which skin lesions gave the clue that led to the diagnosis.[ncbi.nlm.nih.gov]
  • Early signs are characteristic skin lesions, lymphadenopathy, hepatosplenomegaly, failure to thrive, blood-stained nasal discharge, perioral fissures, meningitis, choroiditis, hydrocephalus, seizures, intellectual disability, osteochondritis, and pseudoparalysis[merckmanuals.com]
Exanthema
  • Viral exanthema. Tertiary syphilis As the presentation is variable so the differential diagnoses are extensive but syphilis should be considered in anyone presenting with cardiac or neurological signs or symptoms.[patient.info]
Corneal Opacity
  • Eyes revealed dense corneal opacities with complete loss of vision in right eye. Left eye was normal. Patient was edentulous. VDRL test was reactive in dilution and TPHA was positive. Ultra sound showed hepatosplenomegaly with left renal cyst.[ijdvl.com]
Frontal Bossing
  • Mulberry molars (permanent first molars with multiple poorly developed cusps). frontal bossing.[en.wikipedia.org]
  • History / PE : Early manifestations Hepatosplenomegaly Cutaneous lesions on palms/soles Jaundice/anemia Rhinorrhea Late/untreated manifestations Frontal bossing Hutchinson teeth Saddle nose Perioral fissures Diagnosis : VDRL FTA-ABS Treatment : Penicillin[medlibes.com]
  • Bony changes include sclerosing lesions, saber shin, frontal bossing and gummatous or destructive lesions within long bones.[hon.ch]
  • Later develop frontal bossing, poorly developed maxillas, saddle nose, winged scapulas and sabre shins Recurrent arthropathy and painless knee effusions (Clutton’s joints) occur after two years of age Hematological abnormalities Present at birth or can[cps.ca]
Seizure
  • Early signs are characteristic skin lesions, lymphadenopathy, hepatosplenomegaly, failure to thrive, blood-stained nasal discharge, perioral fissures, meningitis, choroiditis, hydrocephalus, seizures, intellectual disability, osteochondritis, and pseudoparalysis[merckmanuals.com]
  • But if the disease goes untreated, the babies can develop cataracts, deafness or seizures, and could die, according to the CDC.[scpr.org]
  • Babies exposed in utero can have deformities, delays in development, or seizures along with many other problems such as rash, fever, an enlarged liver and spleen, anemia, and jaundice.[en.wikipedia.org]
  • Seizures are when the whole body or parts of the body move without control. Developmental delays. Developmental delays are when your child doesn’t reach developmental milestones when expected.[marchofdimes.org]

Workup

Maternal serum is routinely screened in early and late pregnancy and at delivery and positive results are generally the first indication of CS. Nontreponemal and consecutive treponemal serum tests of the neonate may further confirm suspected CS. Those serum tests should not be carried out with cord blood due to little sensitive and specific results. Positive results should definitely prompt a thorough examination of the neonate for skin and mucosal lesions. Possibly detected lesions, the umbilical cord and the placenta should be further examined by darkfield microscopy and immunohistochemically. Characteristic pathological alterations may be found in all those tissues. CS can be confirmed if spirochetes are detected in those samples [12] [13]. Negative results do not rule out CS.

Infants and children developing symptoms of CS should also be thoroughly examined. A blood screen including liver function tests should be carried out as well as CSF analysis. Further neurologic testing may be indicated and comprise neuroimaging, brain stem and ophthalmologic tests. The long bones should be checked for signs of inflammatory alterations by means of radiographic imaging.

In some cases, CS manifests more than two years after birth. In order to diagnose CS, the child's and mother's medical history have to be taken into account as well as the results of a clinical examination and serologic tests. Hutchinson incisors, interstitial keratitis and eighth cranial nerve deafness are diagnostic for CS.

Even if CS cannot be confirmed, children at high risk of infection or those developing symptoms should be treated accordingly. This especially applies to neonates who often do not show any symptoms or only unspecific signs of illness [14].

The treatment of choice is penicillin. After successful treatment, nontreponemal tests should yield negative results. Treponemal tests, however, are based on the presence of antibodies and remain positive even after elimination of the pathogen [15].

Treatment

The therapy of choice equals the treatment administered in confirmed cases and consists in i.v. administration of 50,000 units aqueous crystalline penicillin G per kg of body weight, every 12 hours during the first week of life and every 8 hours thereafter for a total of 10 days. An alternative therapy is i.m. administration of 50,000 units procaine penicillin G per kg of body weight, once a day and for 10 days. In order to eliminate all causative pathogens, continuous treatment is necessary. Thus, the whole treatment has to be repeated if more than one day is missed.

Treatment is strongly recommended for neonates at high risk of infection although they may not show CS symptoms at birth. Neonates are considered at high risk if their mother suffers from untreated syphilis, if treatment has not been appropriate or was carried out with unknown drugs. If there's a sudden increase in the maternal antibody titer, a relapse has to be suspected and the child is also considered at high risk. In case a full treatment is not an option for neonates at high risk, i.m. administration of a single dose of 50,000 units of benzathine penicillin per kg body weight may be an alternative only if the mother is clinically well, does not show any signs of infection and the child will be monitored as closely as possible. This regimen may also be applied as a precaution to neonates who are not at high risk because their mother has been adequately treated.

The treatment is slightly different for children who are diagnosed after four weeks of age or who develop late CS. While drug, single dose and time frame are equal to those applied in early CS (50,000 units of aqueous crystalline penicillin G per kg body weight over 10 days), i.v. applications have to be carried out every 4 to 6 hours. This increase in frequency of administration and therefore of overall dose is due to the risk of neurosyphilis in this group of patients [16]. A single dose of benzathine penicillin G may be administered as described above after completion of therapy. Similarly to neonates being born by adequately treated mothers, asymptomatic infants or children may be preventively treated with i.m. applications of benzathine penicillin G (50,000 units per kg of body weight, i.m., once a week for three weeks). For treatment of interstitial keratitis, an ophthalmologist should be consulted. It usually consists in corticosteroids and atropine.

Prognosis

Prognosis strongly depends on time passed between maternal infection and pregnancy. Because syphilis is considered to be much more contagious in the primary stage, a condition that is already attenuated but still present in the secondary stage, it is particularly unfavorable if the infection of the mother takes place a short time before or during pregnancy. On the other hand, longer times between maternal infection and pregnancy generally improve the outcome.

Untreated primary or secondary stage syphilis during pregnancy may lead to neonatal death (14%), stillbirth (25%) or CS (41%). The remaining 20% of infants are not infected and may be born healthy. If the infected mother did already pass these early stages of syphilis, which generally means that two years have passed since infection, these numbers reduce to 9%, 12% and 2% for neonatal death, stillbirth and CS, respectively. Three out of four children are born healthy [8]. Similar numbers have been reported elsewhere [9].

Etiology

CS is an infectious disease caused by Treponema pallidum, a spirochete bacterium transmitted transplacentally during pregnancy or possibly by contact to maternal lesions at birth [4]. It has been estimated that up to 80% of children exposed to Treponema pallidum do indeed develop CS.

Consequences for the unborn or infant presumably depend on the time of infection of the mother. Early, intrauterine infection may not even be symptomatic at birth, but can also lead to preterm birth, hydrops fetalis or still birth.

Epidemiology

According to estimations published by the World Health Organization (WHO), annually about 2,000,000 pregnant women get infected with Treponema pallidum [5]. Considering the aforementioned number of up to 80% of exposed fetuses becoming infected, one would estimate 1,600,000 children to be born with CS.

CS is a major public health problem in developing countries, particular in sub-Saharan Africa and subtropical Asia. Some studies report augmented case numbers in the Western world. Prenatal screenings and treatment of affected mothers would be desirable, may, however, not be available in all developing countries.

Sex distribution
Age distribution

Pathophysiology

The spirochete bacterium Treponema pallidum is the causative agent of CS. Particularly women with primary and to a lesser degree those with secondary syphilis are at high risk to transmit the disease to their unborn children. Transmission is possible at all times during gestation. Children generally show symptoms of CS during the first two years of their life, only in rare cases do symptoms manifest later, a condition which is termed late CS [6]. Prenatal infection with Treponema pallidum can provoke neonatal death and stillbirth or may lead to severe disabilities such as neurologic problems, deafness and bone deformities [7]. Even though embryonal organogenesis is usually unaffected by infections with Treponema pallidum, CS is accompanied with systemic complications similar to those observed in secondary stage adult syphilis. All organ systems may thus be affected by CS.

Contrary to classical CS that develops in children aged under two years, late CS is not considered contagious.

Prevention

Routine testing of pregnant mothers and, in case of positive results, consecutive treatment against Treponema pallidum often cures mother and child. The WHO does recommend such screenings to be part of the routine examinations done in the first and last trimester of pregnancy [17]. Only in a few cases that are not diagnosed and treated until late pregnancy children may still show symptoms of CS at birth.

At birth, another routine screen should be carried out. Children at risk of infection should be monitored closely. In order to identify those children at risk, improved surveillance and follow-up data would be desirable [18].

Serologic monitoring is particularly important for mothers with a medical history of syphilis. Increases in antibody titers may indicate a possible relapse and thus prompt treatment. Reinfections are also possible.

Since syphilis is a contagious infectious disease, family members of the patient should be tested clinically and serologically for signs of infection. It may be the case that the patient diagnosed with syphilis is not the pregnant woman herself but someone she had sexual intercourse with. The probability that the woman did acquire syphilis is about 25 to 50%. Thus, she should be treated.

Of note, medical personnel or other people in close contact with patients suffering from early CS may get infected. They should be examined for possible lesions two to three weeks afterwards and serologically screened at this point in time as well as three months later. They should be treated if necessary. After close, unprotected contact with the affected child before he or she was diagnosed with CS, even immediate treatment may be indicated.

Summary

Congenital syphilis (CS) results from intrauterine infection with Treponema pallidum, causative agent of syphilis. Mothers suffering from stage one or two syphilis do very likely transmit the infection to their unborn child. This may result in neonatal death, stillbirth. If a living child is born, he or she may show some signs of CS, but infants usually develop first symptoms some weeks after birth. Late CS is a rare variant of CS and affects children older than two years [1]. Symptoms comprise skin and mucosal lesions, hematological alterations and hepatomegaly, bone lesions and CNS symptoms.

Routine screens during pregnancy allow identification of infected mothers. Penicillin treatment is effective and generally cures mother and child. Despite those preventive measures, CS continues to concern health care providers and case numbers are increasing in developing and even in some developed countries [2] [3].

Patient Information

Children are at risk of developing congenital syphilis (CS) if their mother is infected with Treponema pallidum, causative agent of syphilis. She may transmit the disease to her unborn child if she is not or only inadequately treated. Increasing case numbers of CS have been observed in some industrialized countries, presumably due to lessening awareness among future parents. 

The disease may lead to stillbirth, life-threatening illness or severe disability in affected children. In order to prevent these consequences, routine screens should be performed during early and late pregnancy and at delivery. An effective treatment is available and consists in the application of antibiotics.

References

Article

  1. Larsen SA, Steiner BM, Rudolph AH. Laboratory diagnosis and interpretation of tests for syphilis. Clin Microbiol Rev. 1995;8(1):1-21.
  2. Lugo A, Sanchez S, Sanchez JL. Congenital syphilis. Paediatr Dermatol 2006, 23(2):121-123.
  3. Gurlek A, Alaybeyoglu NY, Demir CY, et al. The continuing scourge of congenital syphilis in 21st century: a case report. Int J Paediatr Otorhinolaryngol 2005, 69(8):1117-1121.
  4. Pediatrics AAo. Syphilis. Red Book: Report of the Committee on Infectious Diseases. Vol 29: American Academy of Pediatrics; 2012:690–703.
  5. South East Asia and World Health Organisation. Regional Strategy for the Elimination of Congenital Syphilis. New Delhi, India: WHO; 2009.
  6. Cremin BJ, Shaff MI. Congenital syphilis diagnosed in utero. Br J Radiol. 1975;48(575):939-941.
  7. Centers for Disease Control and Prevention. Congenital syphilis - United States, 2003-2008. MMWR Morb Mortal Wkly Rep. 2010;59(14):413-417.
  8. Ingraham NR, Jr. The value of penicillin alone in the prevention and treatment of congenital syphilis. Acta Derm Venereol Suppl (Stockh). 1950;31(Suppl. 24):60-87.
  9. Kliegman RM, Stanton BF, Schor NF, Geme III JWS, Behrman RE. Syphilis (Treponema pallidum). In: Nelson, ed. Textbook of Pediatrics. Vol 19. Philadelphia, Pa, USA: Elsevier; 2012:1264
  10. Levin EJ. Healing in congenital osseous syphilis. Am J Roentgenol Radium Ther Nucl Med. 1970;110(3):591-597.
  11. Narain S, Batra B, Abraham SN, Arya LS. Symptomatic congenital syphilis presenting at birth. Indian J Pediatr. 2001;68(9):897-899.
  12. Russell P, Altshuler G. Placental abnormalities of congenital syphilis. A neglected aid to diagnosis. Am J Dis Child. 1974;128(2):160-163.
  13. Larsen SA, Steiner BM, Rudolph AH. Laboratory diagnosis and interpretation of tests for syphilis. Clin Microbiol Rev. 1995;8(1):1-21.
  14. Saloojee H, Velaphi S, Goga Y, Afadapa N, Steen R, Lincetto O. The prevention and management of congenital syphilis: an overview and recommendations. Bulletin of the World Health Organization. 2004;82(6):424-430.
  15. Ananthnarayan, Panicker. Ananthnarayan and Panicker's Text Book of Microbiology. Vol 8: University Press; 2009.
  16. 1998 guidelines for treatment of sexually transmitted diseases. Centers for Disease Control and Prevention. MMWR Recomm Rep. 1998;47(RR-1):1-111.
  17. World Health Organization. Integrated Management of Pregnancy and Child birth (IMPAC): Prevention of Mother and Child transmission of syphilis. Geneva, Switzerland;2009:1.
  18. Martin D, Bertrand J, McKegney C, Thompson L, Belongia E, Mills W. Congenital syphilis surveillance and newborn evaluation in a low-incidence state. Arch Pediatr Adolesc Med. 2001;155(2):140-144.

Ask Question

5000 Characters left Format the text using: # Heading, **bold**, _italic_. HTML code is not allowed.
By publishing this question you agree to the TOS and Privacy policy.
• Use a precise title for your question.
• Ask a specific question and provide age, sex, symptoms, type and duration of treatment.
• Respect your own and other people's privacy, never post full names or contact information.
• Inappropriate questions will be deleted.
• In urgent cases contact a physician, visit a hospital or call an emergency service!
Last updated: 2018-06-22 04:21