Skip to main content
eScholarship
Open Access Publications from the University of California

Dermatology Online Journal

Dermatology Online Journal bannerUC Davis

Benign nodular tertiary syphilis: A rare presenting manifestation of HIV infection

Main Content

Benign nodular tertiary syphilis: A rare presenting manifestation of HIV infection
TN Revathi1 MD, Shilpa Bhat2 MBBS, GS Asha1 MD
Dermatology Online Journal 17 (2): 5

1. Assistant Professor, Dept of Skin and STD, Victoria Hospital, Bangalore Medical College and Research Institute, Bengaluru. India
2. Postgraduate, Dept of Skin and STD, Victoria Hospital, Bangalore Medical College and Research Institute, Bengaluru. India. docshilpabhatholla@gmail.com


Abstract

Late cutaneous syphilis has become a rarity as a result of the effective treatment of early and latent syphilis with antibiotics. We report a heterosexual male who presented with multiple large annular plaques of two years duration. Skin biopsy revealed endarteritis and non-caseating granulomas in the dermis along with plasma cells. VDRL and TPHA were reactive. ELISA for HIV-1 antibodies was reactive. This is the first report of nodular tertiary syphilis as the presenting manifestation of HIV.



Introduction

Syphilis is a sexually transmitted infectious disease caused by Treponema pallidum. Acquired syphilis can be divided into primary, secondary, latent, and tertiary stages. Tertiary cutaneous syphilis can occur 3 to 5 years after primary infection. About one third of people with untreated primary syphilis eventually develop manifestations of tertiary syphilis. In the last decade there was a rise in the incidence of syphilis in the Indian subcontinent as in the various parts of the world, attributed to widespread coinfection with HIV.

It is extremely rare to find tertiary syphilis in this era of antibiotics. Here we describe a heterosexual male patient who presented with this rarest form of syphilis as a presenting manifestation of HIV.


Case report

A 28-year-old married man presented with a 2 year history of persistant, multiple raised cutaneous plaques with central clearing that formed annular and serpiginous patterns. There was a history of an evening rise in temperature for the last 3 months, associated with increased fatiguability and significant weight loss. He denied premarital or extramarital sexual exposure. He also denied any symptoms or signs of primary, secondary, or relapsing stages of syphilis. There was no history of intravenous drug use, blood transfusions, or seizures.


Figure 1Figure 2

Figure 3

Cutaneous examination showed multiple, large, annular plaques with raised, nodular and ulcerated, crusted borders. The lesions showed atrophic tissue paper like scar with hypopigmented centers and these hyperpigmented peripheries. Two such bilaterally symmetrical lesions were present over the abdomen and upper back. Another lesion was on the outer aspect of the right arm (Figures 1, 2, and 3). A few crusted nodular lesions were seen in the V area of the neck, right upper chest, angle of the left mandible, and near the left eyebrow. A crusted plaque with an atrophic center and a punched out ulcer of 2 x 2 cm were present over the scrotum. There were three firm, nontender, inguinal nodes palpable on the right. There were no mucosal lesions, alopecia, or involvement of palms and soles. There was no generalized lymphadenopathy. Systemic examination did not reveal any abnormality. The significant laboratory investigations included hemoglobin 10.2 g percent, total leukocyte count 7,700 cells/mm³, (P-56%, L-38%, E-6%). ESR was elevated at 137 mm/hr. The peripheral blood smear showed microcytic hypochromic anemia. The VDRL test was reactive at a titer of 1:32; TPHA test was also reactive. ELISA for HIV-1 antibodies was positive and CD4 count was 517 (normal: 500-1600). Montoux test was negative and the chest roentgenogram was normal. Dark field microscopy from the lesions and FNAC of the lymph node did not demonstrate spirochetes. CSF examination of the patient was normal. Ultrasound evaluation of the aorta was normal.


Figure 4Figure 5

Figure 6

Skin biopsy of a representative lesion revealed non-caseating epithelioid granulomas and Langhan giant cells in the dermis on H and E staining (Figure 4). Endothelial cell proliferation and perivascular cuffing by lymphocytes and plasma cells were seen in the dermis (Figures 5 and 6). Silver stain did not detect the presence of spirochetes. The absence of spirochetes both under dark field microscopy as well as in histopathologic examination using silver stains favored the diagnosis of benign nodular tertiary syphilis. Because the above tests would be positive in Lues maligna, the possibility of the later was ruled out.

The patient was given 2.4 M units of benzathene penicillin at weekly intervals for 3 weeks. The patient showed significant improvement by the end of three weeks, but never returned for further follow up.


Discussion

Tertiary syphilis appears in two types: The superficial or nodular syphilid and a deeper gummatous syphilid. The nodular syphilid, as in this case, consists of painless, indurated, dull red nodules of varying size that may occur on any part of the body. They may remain discrete or coalesce to form plaques. Multiple nodules can be distributed in an arciform pattern with a predilection for the face, the scapular and interscapular areas, and the extremities [1]. About 35 percent of individuals with late latent syphilis will develop the manifestations of tertiary syphilis [2]. These lesions should be differentiated from sarcoidosis, leprosy, lupus vulgaris, granuloma annulare, tuberculosis, deep mycosis, and leishmaniasis [3].

Most of our knowledge of tertiary syphilis is derived from the Oslo study, in which 2,181 early syphilis cases were untreated. Rare recent reports of tertiary syphilis in the literature were described in African patients [4] and 2 cases of tertiary syphilis were reported from Europe in the year 1999 [5]. Another case was reported from India by Sule and Deshpande [3]. Nodulo-ulcerative tertiary syphilis of the face, misdiagnosed as discoid lupus erythematosus, was reported by Chung, Kantor, and Whipple [6]. All those cases were HIV negative. Three more cases were reported in 2007 by Pereira T, Fernandes JK, Vieira AP, et al, all of which were HIV negative [7].

Studies have reported that HIV infection is 8 to 12 times more common in patients who have positive serology for syphilis [8]. The clinical presentation of syphilis in HIV positive patients is commonly the same as in HIV negative patients. However, unusual and atypical features may be seen. HIV positive patients are at increased risk of developing Lues maligna. In contrast to tertiary syphilis, the lesions of lues maligna are multiple and have a round or oval configuration. There is no tendency to central healing and the plaques and nodules exhibit a lamellated, brown-black rupioid crust. Moreover, the early onset of necrotic ulcers in the disease is in contrast to the later occurring gummas of tertiary syphilis [9]. HIV positive patients are more likely to progress to clinical neurosyphilis than those without HIV infection [10]. A detailed neurological evaluation including CSF examination is required in this group of patients.

Currently, tertiary syphilis is rarely seen. However, this case emphasizes that it still exists and must be considered in the differential diagnosis of nodulo-ulcerative plaques.


Conclusion

Late syphilis can be a presenting manifestation of HIV. Our case demonstrates the need for dermatologists and dermatopathologists to maintain a high index of suspicion for tertiary syphilis in non-healing annular lesions of long duration, especially when there is a co-infection with HIV.


We heartily acknowledge the support of:
Dr M Mallikarjun, Professor and Head, Dept. of Skin and STD, Victoria Hospital, Bangalore
Dr HV Nataraja, Professor, Dept of Skin and STD, Victoria Hospital, Bangalore
Dr S Sacchidanad, Professor, Dept of Skin and STD, Victoria Hospital, Bangalore
Dr Dayanand, Assistant Professor, Dept of Pathology, Victoria Hospital, Bangalore

References

1. The late R.S Morton, G. R Kinghorn and F. Kerdel-Vegas. In, Champion RH, Burton JL, Ebling FJG(ed). Rook's Textbook of Dermatology.5th edition.London,Blackwell publishers,1992;2533-2638.

2. Gjestland T. The Oslo study of untreated syphilis: an epidemiologic investigation of the natural course of the syphilitic infection based upon a re-study of the Boeck-Bruusgard material. Acta Derm Venereol 1955; 35(suppl 34):1

3. Sule RR, Deshpande SG, Dharmadhikari NJ, Joshi VR. Late cutaneous syphilis. Cutis. 1997Mar;59(03):135-37. [PubMed]

4. Sekkat A, Sedrati O, Derdabi D. La syphilis tertiaire cutanéo-muqueuse. Ann Dermatol Venereol 1994; 121: 146-51.

5. Varela P, Alves R, Velho G, Santos C, Massa A, Sanches M. Two recent cases of tertiary syphilis. Eur J Dermatol.1999; 9: 371-3. [PubMed]

6. Chung G, Kantor GR, Whipple S. Tertiary syphilis of the face. J Am Acad Dermatol 1991; 24: 832-5. [PubMed]

7. Pereira T, Fernandes JK, Vieira AP, et al. Tertiary syphilis. Int J Dermatol 2007; 46:1192-1195. [PubMed]

8. Don PC, Rubinstein R, Christie S. Malignant syphilis (lues maligna) and concurrent infection with HIV. Int J Dermatol. 1995; 34(6):403-7. [PubMed]

9. Fisher DA, Chang LW, Tuffanelli DL. Lues maligna. Presentation of a case and a review of the literature. Arch Dermatol. 1969; 99: 70-73.

10. Hook EW. Syphilis and HIV Infection. J Infect Dis.1989; 160: 530-34. [PubMed]

© 2011 Dermatology Online Journal