Introduction

Syphilis is an infectious disease caused by the spirochete Treponema pallidum¹. It is a systemic disease that affects the skin, adnexa, and mucous membranes. It is transmitted through direct contact with infected mucous membranes during sexual intercourse, most commonly in men who have sex with men (MSM)¹,². The course of the disease is usually classified as early or late syphilis. The first group (early syphilis) includes primary (chancre stage) and secondary (disseminated stage) disease. Late syphilis includes late latent syphilis, latent syphilis of unknown duration, and tertiary syphilis characterized by cardiovascular, neurologic, and gummy lesions.¹ In some cases, primary and secondary stages may occur concurrently, which is referred to as simultaneous primary and secondary syphilis (sPSS)³-⁹. However, it is often associated with immunocompromised (human immunodeficiency virus [HIV]-positive) patients and also affects immunocompetent patients¹⁰,¹¹. We report the case of an immunocompetent patient with sPSS and review cases in the literature.

Case report

A 23-year-old man presented with genital ulcers that had been present for four weeks and had been previously treated with a class 1 steroid (clobetasol propionate) for two weeks. Physical examination revealed multiple ulcers with indurated bases involving the penile body (Fig. 1A). He also had multiple erythematous, papular, and scaly plaques on the palms (Fig. 1B) and soles, and bilateral non-painful inguinal lymphadenopathy.

Figure 1 A: multiple indurated penile ulcers. B: palmar manifestation of papulosquamous syphilis. 

Laboratory tests were positive for syphilis (FTA-ABS), and Venereal Disease Research Laboratory (VDRL) tests were reactive and high (VDRL titer 1:320). Serologic testing for HIV and hepatitis was negative. Histologic findings of penile ulceration and palm plaque included ulceration and psoriasiform hyperplasia, respectively, with abundant plasmatic CD79A+ cells. Spirochetes were not found. The patient was treated with a single dose of 2.4 million IU penicillin G benzathine without relapse.

We performed a literature review of cases of sPSS. Of the 24 patients (including the present case), 23 were male and only one was female, with a mean age of 39.6 ± 9.41 years (Table 1). The main risk factors described were multiple sexual partners, unprotected sexual contact, and MSM. Regarding immunological status, 13 (54%) patients were immunocompetent at the time of syphilis diagnosis, which excluded HIV infection; 11 patients were immunosuppressed (45%) and 16 (66%) cases had comorbidities, mainly HIV infection (11 cases, 68%). Most patients were MSM (7 cases, 29%); however, this information was not reported in 8 (33%) cases. Multiple chancres occurred in 9 (37%) patients, and the time of development of sPSS ranged from 3 days to 3 months.

Discussion

sPSS is considered a relatively common disease in immunocompromised patients, associated with HIV infection in at least 25% of cases¹². This is due to the alterations in innate and humoral immunity caused by HIV infection, which favor the spread of the pathogen through the bloodstream and promote the rapid appearance of secondary lesions and atypical disease features; these atypical presentations are often observed in patients with high viral loads and low CD4+ T-lymphocyte counts¹³.

The simultaneous occurrence of primary and secondary lesions in immunocompetent patients is rare but possible¹⁴,¹⁵. The mechanism by which immunocompetent patients without comorbidities⁹, as in our case, present simultaneously with chancre and secondary manifestations is not well understood. However, some theories have been proposed. One is that there is a window period for detection of HIV with a negative test but coinfection with both sexually transmitted diseases¹,³,⁴. Another theory is that primary chancre, which consists of a local tissue reaction associated with inoculation, occurs three weeks to 90 days after sexual contact and usually resolves six weeks before secondary manifestations, representing hematogenous dissemination of spirochetes¹,⁵. This rapid dissemination results in secondary features developing before the primary lesion disappears⁵. Other theories suggest that multiple sexual contacts may cause re-infection without adequate protection or that autoinoculation may be a possible explanation³.

Regardless of immunologic status and clinical presentation, all patients, including our case, were successfully treated with penicillin G benzathine (single or multiple doses) without relapse.

Although sPSS is mainly associated with immunocompromised patients, it is not an exclusive feature and affects immunocompetent patients¹⁶,¹⁷. At the time of syphilis diagnosis, whether typical or atypical, HIV infection must be excluded because both diseases share the same risk factors. Immunocompetent patients with sPSS and a seronegative result at the time of diagnosis need to be followed up because they may be in a window period¹,⁸. It is essentially an appropriate treatment to prevent relapse and long-term complications.