Figure 1.
Study site and syphilis network.
The city of Cali is located in south-western Colombia (see inset). Cali is divided into 22 (numbered in the figure) distinct geographic districts called “comunas”. These are clustered within 5 administrative regions called Empresas Socials del Estado “ESEs”: Ladera (yellow), North (blue), Center (pink), South-East (purple) and East (green). Public health hospitals are strategically distributed within the “ESEs”. The syphilis patient recruitment network was comprised of 13 hospitals and health centers located throughout the city.
Figure 2.
Palmar and plantar rash of secondary syphilis.
Typical palmar and plantar rash of secondary syphilis is shown in the representative figures. Similar lesions were evident in 59.6% of all secondary syphilis subjects enrolled. These lesions consist of smooth or scaly plaques and papules, which can become hyperpigmented in dark-skinned individuals as shown in the figure.
Figure 3.
Mucosal and cutaneous lesions of secondary syphilis.
Secondary syphilis has been known as the “Great Imitator” due to the diversity of dermatologic lesions and which can be confounded with other cutaneous diseases. (A and B) Diffuse erythematous papular exanthem is shown over abdomen in A and lower extremity in B. (C and D) Multiple moist, hypopigmented, flattened plaques consistent with condyloma lata are shown on external genital areas (male and female respectively in C and D). (E) Inflammatory responses can affect hair follicles leading to “moth-eaten alopecia” as depicted in the figure. (F) Oral mucosal patches, as shown in the figure can be present during secondary syphilis. (G) Pigmentary plaques are shown over the buttocks of a dark-skinned secondary syphilis patient. (H) Psoriasiform syphilitic lesions, as shown in the representative micrograph, could easily be misdiagnosed as psoriasis.
Table 1.
Signs and symptoms associated with secondary syphilis.
Figure 4.
Secondary syphilis histopathology.
The figure shows histopathologic anomalies seen in punch biopsies obtained from four secondary syphilis patients skin lesions. Corresponding clinical appearance of the lesions are also shown. (A) Markedly inflamed hair follicle (“folliculitis”) with extension of inflammatory cell infiltrate into parafollicular blood vessel and connective tissue. Corresponding “moth-eaten” alopecia is shown in the adjacent micrograph. (B) Dark-skinned patient (pigmented basal keratinocytes); further darkening of a patch of skin in the form of a macule, as shown herein, is caused by deposition of dermal melanophages (“pigment incontinence”) (C) Skin biopsy obtained near the sole reveals a thick stratum corneum layer, epidermal reactive psoriasiform hyperplasia associated with chronic inflammation of the dermal papilla, and a superficial perivascular lymphoplasmocytic infiltrate. (D) Edge of an ulcer located in the lower extremity reveals fibrinoid exudate on the ulcer bed, surrounded by granulation tissue and reactive hyperplasia of the epidermis.
Table 2.
Histologic abnormalities observed in secondary syphilis skin lesions (n = 11).
Table 3.
Quantitation of T. pallidum DNA in whole blood (WB) samples by real-time PCR (n = 26).
Table 4.
Patients and strain type analysis using DNA obtained from skin lesions.