Dermatologic Manifestations of Yaws Clinical Presentation

  • Author: Caroline L Levine, MD; Chief Editor: William D James, MD   more...
 
Updated: Jan 31, 2012
 

History

The typical yaws patient is young and from an endemic area and has been exposed to infected persons with active disease.[4, 5]

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Physical

Yaws has 3 clinical stages: primary, secondary, and tertiary. Stages are interspersed with asymptomatic latent periods.

  • Primary stage of yaws
    • After an incubation period of 9-90 days (with an average of 3 wks), the primary lesion, or the mother yaw, develops at the site of inoculation after a scratch, a bite, or an abrasion of exposed skin, most commonly on the legs, the feet, or the buttocks.
    • The lesion is a reddish, nontender, and, occasionally, pruritic papulonodule.
    • The mother yaw ulcer develops a honey-brown crust and enlarges horizontally to 1-5 cm in diameter, sometimes coalescing with satellite lesions. The crust frequently sloughs off and reveals a raspberrylike base (hence the synonym frambesia).
    • On rare occasions, a primary lesion is not seen.
    • Because the exudate of the raspberrylike ulcer is teeming with treponemes, these lesions are considered highly infectious.
    • Lymphadenopathy, fever, and joint pain may accompany this stage.
    • The mother yaw resolves spontaneously in 2-9 months, leaving an atrophic scar with central hypopigmentation and peripheral hyperpigmentation.
  • Secondary stage of yaws
    • Following a period of latency (about 6-16 wk after the primary stage), an eruption of disseminated skin lesions, bone lesions, and constitutional symptoms appears.
    • The cutaneous lesions, or the daughter yaws, resemble the mother yaw but are smaller (up to 2 cm in diameter) and are frequently located adjacent to body orifices, particularly the mouth and the nose.
    • The daughter yaws expand, ulcerate, and exude a fibrinous fluid teeming with treponemes, which dries into a crust. The exudate attracts flies, which are bothersome to the person who is affected.
    • Occasionally, central resolution yields circinate or annular scaly lesions resembling fungal infections. These lesions are referred to as tinea yaws.
    • Papulosquamous patches and plaques that resemble syphilis may be noted on any part of the body.
    • Lesions in the axillae or the groin resemble condylomata lata; lesions on the mucous membranes resemble hypertrophic mucous patches.
    • Piannic onychia is a paronychia caused by papillomas in the nail fold.
    • Papillomas on the plantar surfaces can form thick, hyperkeratotic plaques that may become fissured or eroded. Lesions are painful and cause a deliberate crablike gait (crab yaws). Macular and hyperkeratotic lesions on the palms and the soles resembling syphilis may also be present.
    • Skeletal involvement includes painful osteoperiostitis and fusiform soft tissue swelling of the metatarsals and the metacarpals. Some of the early bone changes can be seen on radiographs. Periosteal thickening can often be palpable.[6]
    • Secondary-stage manifestations are generally nonscarring and reversible, subsiding in weeks to months.
    • Patients may develop relapses at intervals up to 5 years after infection. Relapsing lesions tend to occur in the perioral, perianal, and periaxillary areas. The disease then enters a noninfectious latent period, and patients do not exhibit any signs or symptoms.
  • Tertiary stage of yaws
    • In about 10% of cases, after 5-15 years of latency, a late stage develops, characterized by destructive skin lesions, bone lesions, and possible neurologic and ophthalmologic involvement.
    • Progressively enlarging, painless, subcutaneous nodules develop, which undergo abscess formation, necrosis, and ulceration. Lesions have well-defined edges and an indurated base with granulation tissue and yellowish slough.
    • Ulcers may become infected, causing destruction of underlying structures. They may also coalesce, forming serpiginous tracts that heal with keloid formation, which leads to crippling deformities and contractures.
    • Hyperkeratosis and keratoderma of the palms and the soles as well as juxta-articular ulcerated gummatous nodules may accompany lesions.
    • Late skeletal lesions consist of hypertrophic periostitis, gummatous periostitis, osteitis, and osteomyelitis. Chronic osteitis of the tibia can lead to saber shins. In about 1% of patients, bilateral hypertrophic osteitis of the external aspects of the nasal processes of the maxillae with persistent swelling occurs. This condition is referred to as goundou, which slowly progresses over 5-20 years and eventually may lead to massive destruction and perforation of the nose and the palate (gangosa).
    • Neurologic and ophthalmologic involvement is debated in the literature. Some reports suggest that disc atrophy, optic atrophy, and myeloneuropathies may occur.
  • Attenuated yaws
    • Some reports describe an attenuated, less contagious form of yaws in areas of low disease prevalence.
    • A solitary patch or a few, dry, flat, gray patches confined to the skin folds characterize attenuated yaws.
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Causes

Yaws is caused by T pallidum subsp pertenue, a slender spirochete, which is serologically indistinguishable from the spirochete that causes syphilis (T pallidum). Like the other nonvenereal treponematoses, yaws is not found in urban centers, it is not sexually transmitted, and it is not congenitally acquired. Children serve as the primary reservoir for yaws, spreading the disease via skin-to-skin and skin-to-mucous membrane contact.

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Contributor Information and Disclosures
Author

Caroline L Levine, MD  Staff Physician, Department of Dermatology, Emerson Hospital, Mt Aburn Hospital

Caroline L Levine, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Donald Belsito, MD  Professor of Clinical Dermatology, Department of Dermatology, Columbia University Medical Center

Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, New York County Medical Society, New York Dermatological Society, Noah Worcester Dermatological Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

References
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  3. Guerrier G, Marcon S, Garnotel L, Deltour R, Schinas S, Mathelin JP, et al. Yaws in Polynesia's Wallis and Futuna Islands: a seroprevalence survey. N Z Med J. Apr 29 2011;124(1333):29-31. [Medline].

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  9. Backhouse JL, Hudson BJ, Hamilton PA, Nesteroff SI. Failure of penicillin treatment of yaws on Karkar Island, Papua New Guinea. Am J Trop Med Hyg. Sep 1998;59(3):388-92. [Medline].

  10. Manirakiza A, Boas SV, Beyam NE, Zadanga G, Konamna FX, Njuimo SP, et al. Clinical outcome of skin yaws lesions after treatment with benzathinebenzylpenicillin in a pygmy population in Lobaye, Central African Republic. BMC Res Notes. Dec 15 2011;4(1):543. [Medline].

  11. Agmon-Levin N, Bat-sheva PK, Barzilai O, et al. Antitreponemal antibodies leading to autoantibody production and protection from atherosclerosis in Kitavans from Papua New Guinea. Ann N Y Acad Sci. Sep 2009;1173:675-82. [Medline].

  12. Engelkens HJ, ten Kate FJ, Judanarso J, et al. The localisation of treponemes and characterisation of the inflammatory infiltrate in skin biopsies from patients with primary or secondary syphilis, or early infectious yaws. Genitourin Med. Apr 1993;69(2):102-7. [Medline].

  13. Koff AB, Rosen T. Nonvenereal treponematoses: yaws, endemic syphilis, and pinta. J Am Acad Dermatol. Oct 1993;29(4):519-35; quiz 536-8. [Medline].

  14. Sanchez MR. Endemic (Nonvenereal) Treponematoses. In: Freedberg IM, Eisen AZ, Wolff K, Austen F, Goldsmith LA, Katz S, eds. Fitzpatrick's Dermatology in General Medicine. 6th ed. New York, NY: McGraw-Hill; 2003.

  15. Sehgal VN, Jain S, Bhattacharya SN, Thappa DM. Yaws control/eradication. Int J Dermatol. Jan 1994;33(1):16-20. [Medline].

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