Yaws‑Like Lesions in HIV Patients – A Comprehensive Guide

Overview

Yaws‑like lesions refer to skin and soft‑tissue lesions that resemble those caused by Treponema pallidum pertenue (the bacterium that causes yaws) but occur in people living with human immunodeficiency virus (HIV). These lesions are not true yaws; they are often a manifestation of opportunistic infections, co‑infections, or immune‑reconstitution phenomena unique to the HIV‑infected population.

Although classic yaws is endemic in tropical regions of Africa, Asia, and the Pacific, yaws‑like lesions have been reported worldwide among individuals with advanced or untreated HIV infection. In the United States, a 2022 review of dermatologic manifestations in HIV patients identified yaws‑like or “syphilitic‑like” lesions in 2–4 % of individuals with CD4 counts <200 cells/µL [1].

Key points:

• Who it affects: Primarily adults with moderate‑to‑severe immunosuppression (CD4 < 350 cells/µL), but cases in children and adolescents have been described.
• Prevalence: Exact global prevalence is unknown because lesions are often misdiagnosed as syphilis, herpes, or other dermatoses. Reporting from dermatology clinics in sub‑Saharan Africa suggests an incidence of < 0.5 % among all HIV‑positive patients, rising to > 5 % in those with CD4 < 100 cells/µL [2].
• Geography: More common in regions where yaws is endemic and where HIV prevalence is high (e.g., East Africa, Southeast Asia). Cases also occur in non‑endemic, high‑income countries among travelers or migrants.

Symptoms

The clinical picture can vary, but most patients present with one or more of the following:

• Papules or nodules: Small, raised, often painless lesions that may be erythematous or skin‑colored.
• Painless ulcers (chancre‑like): Rounded or oval ulcers with a clean base and indurated borders, similar to primary syphilis.
• Hyperkeratotic plaques: Thickened, scaly patches that may resemble yaws’s “bulky” lesions.
• Multiple lesions: Frequently disseminated on the extremities, trunk, and face; may coalesce into larger ulcerated areas.
• Hepatosplenomegaly: Enlargement of liver and spleen can accompany late‑stage disease, suggesting systemic spread.
• Systemic symptoms: Low‑grade fever, malaise, weight loss, and night sweats—especially when lesions are part of a broader opportunistic infection.
• Neurologic signs (rare): If the infection spreads to the nervous system, patients may experience headache, meningismus, or focal deficits.

Because these lesions mimic syphilis, secondary infections (e.g., Staphylococcus aureus) are common, leading to increased pain, purulent discharge, and delayed healing.

Causes and Risk Factors

Yaws‑like lesions are not caused by T. pallidum pertenue itself. The most widely accepted mechanisms are:

1. Co‑infection with Treponema pallidum (syphilis) or related spirochetes: In immunocompromised hosts, syphilis may adopt an atypical, “yaws‑like” morphology.
2. Immune reconstitution inflammatory syndrome (IRIS): After initiation of antiretroviral therapy (ART), recovering immunity can trigger an exaggerated inflammatory response to latent treponemal antigens, producing yaws‑like lesions.
3. Other bacterial or fungal infections: Species such as Haemophilus ducreyi (the causative agent of chancroid) or atypical mycobacteria can create similar ulcerative lesions in HIV patients.
4. Direct HIV‑related skin changes: HIV can cause vasculitis and dysregulated wound healing, predisposing the skin to ulcerative lesions.

Risk factors include:

• CD4 count < 350 cells/µL, especially < 100 cells/µL.
• Untreated or late‑stage HIV infection.
• Recent initiation of ART (within the first 3–6 months).
• History of syphilis, chancroid, or other sexually transmitted infections (STIs).
• Poor access to condoms and safe‑sex education.
• Living in or traveling to yaws‑endemic regions.

Diagnosis

Correct diagnosis hinges on a combination of clinical suspicion, laboratory testing, and sometimes histopathology.

1. Clinical Evaluation

• Detailed history: HIV status, CD4 count, recent ART changes, sexual history, travel.
• Physical exam: Distribution, number, and morphology of lesions; check for mucosal involvement.

2. Laboratory Tests

• Serologic testing for syphilis: Rapid plasma reagin (RPR) or venereal disease research laboratory (VDRL) test plus treponemal confirmatory test (e.g., FTA‑ABS, TP‑PA). A positive treponemal test with a low or non‑reactive non‑treponemal test may suggest atypical disease.
• PCR assays: When available, PCR on ulcer exudate can identify T. pallidum, H. ducreyi, or other pathogens.
• HIV labs: CD4 count, HIV viral load, and ART regimen review.
• Complete blood count & liver function tests: To assess systemic involvement.

3. Skin Biopsy

Indicated when the diagnosis remains unclear after serology. Histology may show:

• Perivascular infiltrates of lymphocytes and plasma cells.
• Endarteritis obliterans (typical of treponemal infection).
• Special stains (Warthin‑Starry) can highlight spirochetes.

4. Imaging (rare)

If systemic spread is suspected, chest X‑ray, abdominal ultrasound, or MRI of the brain may be ordered.

Treatment Options

The cornerstone of therapy is addressing the underlying infection and optimizing HIV management.

1. Antimicrobial Therapy

• Penicillin G: First‑line for treponemal infection. Recommended dose for secondary syphilis (often the model for yaws‑like lesions) is 2.4 million units IM once weekly for 3 weeks. For neurosyphilis, IV aqueous penicillin G 18‑24 million units/day for 10–14 days.
• Doxycycline 100 mg PO twice daily for 14 days is an alternative for patients allergic to penicillin.
• Azithromycin 2 g PO single dose may be considered where compliance is an issue, but resistance is rising.
• If PCR identifies H. ducreyi or atypical mycobacteria, appropriate antibiotics (e.g., ciprofloxacin, clarithromycin) are added.