Pediatric Syphilis

Pediatric Syphilis

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Syphilis is an infectious disease caused by Treponema pallidum, which belongs to the Spirochaetaceae family. The genus name, Treponema, is derived from the Greek term for “turning thread.” Pathogenic members of this genus include T pallidum, T pertenue, and T carateum.

Between 1905 and 1910, Schaudinn and Hoffman identified T pallidum as the cause of syphilis, and Wasserman described a diagnostic test for the long-recognized infection. Pathogenic treponemes are associated with the following 4 diseases:

Venereal syphilis, caused by T pallidum pallidum

Yaws, caused by T pallidum pertenue

Endemic syphilis (bejel), caused by T pallidum endemicum (Go to Endemic Syphilis for more complete information on this topic.)

Pinta, caused by T carateum

The treponemes responsible for these diseases cannot be distinguished serologically, morphologically, or by genome analysis, and they have not been successfully cultivated on artificial media.

Children experience 2 forms of syphilis: acquired syphilis, which is almost exclusively transmitted by sexual contact, and congenital syphilis, which results from transplacental transmission of spirochetes (see Etiology).

Syphilis-especially in its later stages-can have numerous and complex manifestations and may resemble a number of other diseases. Syphilitic manifestations are categorized as primary, secondary, and tertiary (see Clinical Presentation).

Serologic testing has the primary role in the diagnosis (see Workup).

Penicillin remains the drug of choice to treat all stages of syphilis (see Treatment and Management, as well as Medications).

Go to Syphilis for more complete information on this topic.

When left untreated, syphilis is a lifelong infection that progresses in 3 clear characteristic stages. After initial invasion through mucous membranes or skin, the organism rapidly multiplies and widely disseminates. The organism spreads through the perivascular lymphatics and then the systemic circulation before the clinical development of the primary lesion. The primary lesion, which contains infectious treponemes, arises within hours after infection and persists throughout the primary and secondary disease.

Secondary lesions develop when spirochetal invasion of tissues of ectodermal origin (eg, skin, mucous membranes, CNS) precipitates an inflammatory response. These lesions develop 6-12 weeks after infection. This stage of rapid spirochete multiplication and dissemination may bring an invasion of the entire body. Thus, tertiary syphilis may involve any organ system.

Secondary infection becomes latent within 1-2 months after onset. Relapses with secondary manifestations can be seen during the first year of latency, a period referred to as the early latent period. Early latent syphilis (ie, duration < 1 y) is when the recurrent lesions of secondary syphilis are most likely to occur. No relapses occur after the first year; what follows is late syphilis, which may be either asymptomatic (ie, late latent) or symptomatic (ie, tertiary). Late latent syphilis is associated with resistance to both reinfection and relapse.

Tertiary syphilis can manifest in various ways. Meningeal syphilis rarely occurs and presents a few years after the original infection. Late neurosyphilis may present as focal ischemia of the CNS or stroke as a result of endarteritis of small blood vessels of the brain. Meningovascular syphilis can affect any part of the CNS. The actual destruction of the nerve cells in the cerebral cortex leads to a combination of psychiatric manifestations and neurologic findings.

Congenital syphilis is caused by transplacental transmission of spirochetes; the transmission rate approaches 90% if the mother has untreated primary or secondary syphilis. Fetal infection can develop at any time during gestation. Manifestations are defined as early if they appear in the first 2 years of life and late if they develop after age 2 years. According to a Centers for Disease Control and Prevention report, untreated syphilis, especially early syphilis, during pregnancy can lead to deafness, neurologic impairment, bone deformities, stillbirth, and neonatal death. [1]  The clinical presentation of congenital neurosyphilis may be confused with a non-accidental injury. [2]

Because inflammatory changes do not occur in the fetus until after the first trimester of pregnancy, organogenesis is unaffected. Nevertheless, all organ systems may be involved. With early-onset disease, manifestations result from transplacental spirochetemia and are analogous to the secondary stage of acquired syphilis. Congenital syphilis does not have a primary stage. Late-onset disease is seen in patients older than 2 years and is not considered contagious.

Syphilis is caused by Treponema pallidum, which belongs to the Spirochaetaceae family. Syphilis transmission usually occurs transplacentally or by sexual contact. Other modes of transmission include contact with contaminated blood or infected tissues.

Children experience 2 forms of syphilis: acquired syphilis, which is almost exclusively transmitted by sexual contact, and congenital syphilis, which results from transplacental transmission of spirochetes. Vertical transmission of early syphilis during pregnancy results in a congenital infection in at least 50-80% of exposed neonates.

From 1985-1990, overall syphilis incidence in the United States increased 75%. This resurgence was primarily due to increased illegal drug use (particularly crack cocaine) that was associated with an exchange of sex for drugs. Concomitant infection with human immunodeficiency virus (HIV) is also common because HIV and syphilis affect similar patient groups.

An overall increase in syphilis incidence has been observed in the United States, and most infected individuals are men who have sex with other men; this may also lead to an increase in HIV infection and other sexually transmitted diseases (STDs). [3]

Syphilis occurs worldwide, predominantly in large cities. With the exception of the United States, syphilis is less common in developed nations.

Certain European countries have seen an increase in congenital syphilis cases, and syphilis remains a major public health problem in sub-Saharan Africa and in the developing world. The main focus in controlling syphilis is antenatal screening and treatment of mothers who are infection.

A high prevalence of syphilis and other STDs was noted in Venezuela in a recent study. [4]

Syphilis has no racial predilection. However, its incidence appears to correlate with the socioeconomic factors-often racially imbalanced-that contribute to disease prevalence among individuals with low incomes, who live in urban and overcrowded areas, in whom drug use and the exchange of sex for drugs may be more common. For example, a report of a syphilis outbreak in North Carolina described an association between crack cocaine and sex for drugs as a causative factor, in a sociosexual network comprised predominantly of blacks. [5]

Historically, men were more commonly infected than women; however, a study involving high-risk adolescents has reported 69% of cases involved young women, indicating that the sex distribution of syphilis is in flux.

Adolescent and young adults are most at risk for syphilis, due to sexual and other risk-taking behaviors (eg, drug use).

With adequate and timely treatment, the prognosis for most patients with syphilis is excellent. However, patients with HIV infection have a high rate of failed serologic response to syphilis treatment. Most patients with HIV infection show no response or inadequate response after being treated for syphilis.

Until a practical and effective vaccine is developed, syphilis prevention depends on abstinence, the use of condoms, and detection and identification of infectious cases. Education about STDs, treatment of sexual contacts, and the reporting of each case to local public health authorities are essential.

For patient education information, see the Sexually Transmitted Diseases Center and Pregnancy and Reproduction Center, as well as Sexually Transmitted Diseases, Syphilis, Birth Control Overview, and Birth Control FAQs.

Triemstra J, Reno K, Chohlas-Wood R, Nash C. A Brief Resolved Unexplained Event and Congenital Neurosyphilis. Pediatr Ann. 2017 Feb 1. 46 (2):e61-e64. [Medline].

Hérissé AL, Chiaverini C, Hubiche T, Tran A, Rondel J, Rosello O, et al. Non-accidental injury or congenital infection?. Arch Dis Child. 2017 Sep. 102 (9):852. [Medline].

Heffelfinger JD, Swint EB, Berman SM, Weinstock HS. Trends in primary and secondary syphilis among men who have sex with men in the United States. Am J Public Health. 2007 Jun. 97(6):1076-83. [Medline].

Vasquez-Manzanilla O, Dickson-Gonzalez SM, Salas JG, Rodriguez-Morales AJ, Arria M. Congenital syphilis in valera, Venezuela. J Trop Pediatr. 2007 Aug. 53(4):274-7. [Medline].

Sena AC, Muth SQ, Heffelfinger JD, et al. Factors and the sociosexual network associated with a syphilis outbreak in rural North Carolina. Sex Transm Dis. 2007 May. 34(5):280-7. [Medline].

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Gomez GB, Kamb ML, Newman LM, Mark J, Broutet N, Hawkes SJ. Untreated maternal syphilis and adverse outcomes of pregnancy: a systematic review and meta-analysis. Bull World Health Organ. 2013 Mar 1. 91 (3):217-26. [Medline].

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[Guideline] American Academy of Pediatrics, American College of Obstetricians. Guidelines for Perinatal Care. 5th ed. 2002.

[Guideline] Screening for syphilis infection in pregnancy: U.S. Preventive Services Task Force reaffirmation recommendation statement. Ann Intern Med. 2009 May 19. 150(10):705-9. [Medline].

American Academy of Pediatrics. Syphillis. Red Book: Report of the Committee on Infectious Diseases. 26th ed. 2003. 595-607.

American Academy of Pediatrics. Syphillis. Red Book: Report of the Committee on Infectious Diseases. 29th ed. 2009. 639.

Knight CS, Crum MA, Hardy RW. Evaluation of the LIAISON Treponema Assay, a Chemiluminescent Immunoassay for the Diagnosis of Syphilis. Clin Vaccine Immunol. 2007 Apr 25. [Medline].

Woznicova V, Valisova Z. Performance of CAPTIA SelectSyph-G enzyme-linked immunosorbent assay in syphilis testing of a high-risk population: analysis of discordant results. J Clin Microbiol. 2007 Jun. 45(6):1794-7. [Medline].

Kandelaki G, Kapila R, Fernandes H. Destructive osteomyelitis associated with early secondary syphilis in an HIV-positive patient diagnosed by Treponema pallidum DNA polymerase chain reaction. AIDS Patient Care STDS. 2007 Apr. 21(4):229-33. [Medline].

Wong T, Singh AE, De P. Primary syphilis: serological treatment response to doxycycline/tetracycline versus benzathine penicillin. Am J Med. October 2008. 121(10):903-908. [Medline].

Bai ZG, Yang KH, Liu YL, et al. Azithromycin vs. benzathine penicillin G for early syphilis: a meta-analysis of randomized clinical trials. Int J STD AIDS. April 2008. 19(4):217-221. [Medline].

Rac MW, Bryant SN, McIntire DD, Cantey JB, Twickler DM, Wendel GD Jr, et al. Progression of ultrasound findings of fetal syphilis after maternal treatment. Am J Obstet Gynecol. 2014 Oct. 211 (4):426.e1-6. [Medline].

Kahn JG, Jiwani A, Gomez GB, Hawkes SJ, Chesson HW, Broutet N, et al. The cost and cost-effectiveness of scaling up screening and treatment of syphilis in pregnancy: a model. PLoS One. 2014. 9 (1):e87510. [Medline].

[Guideline] Committee on Adolescence, Society for Adolescent Health and Medicine. Screening for nonviral sexually transmitted infections in adolescents and young adults. Pediatrics. 2014 Jul. 134 (1):e302-11. [Medline]. [Full Text].

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Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA Professor of Emergency Medicine in Clinical Pediatrics, Weill Cornell Medical College; Attending Physician, Departments of Emergency Medicine and Pediatrics, Lincoln Medical and Mental Health Center; Adjunct Professor of Emergency Medicine, Adjunct Professor of Pediatrics, St George’s University School of Medicine, Grenada

Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Academy of Urgent Care Medicine, American College of Emergency Physicians, American Heart Association, American Medical Association, Association of Clinical Research Professionals, Public Responsibility in Medicine and Research, Society for Academic Emergency Medicine, Society for Simulation in Healthcare

Disclosure: Nothing to disclose.

Muhammad Aslam, MD Associate Professor of Pediatrics, University of California, Irvine, School of Medicine; Neonatologist, Division of Newborn Medicine, Department of Pediatrics, UC Irvine Medical Center

Muhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Pediatric Syphilis

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