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A man had widespread, noduloulcerative syphilitic lesions that appeared, chronologically, during the "secondary" stage of syphilis. There were no systemic manifestations of the disease, except for possible periostitis. The darkfield examination and spinal fluid examinations were negative for syphilis. It is suggested that the term "malignant" syphilis should be discarded in favor of nonduloulcerative cutaneous syphilis.
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We hereby report a case presenting a rare form of secondary syphilis with an unusual nodular eruption accompanied by pruritus and generalized lymphadenopathy, bearing a striking resemblance to lymphoma. The histologic picture was also misleading and was compatible with lymphocytoma cutis. The diagnosis was eventually made after results of serologic tests for syphilis were found to be positive, with an extremely high titer of VDRL, and dark-field microscopy had demonstrated spirochetes in a nodular lesion. Secondary syphilis should thus be considered in the differential diagnosis of nodular lesions resembling lymphoreticular disease. It is also suggested that syphilis be added to the list of diagnoses belonging to the category of pseudolymphoma.
A circulating immune complex-mediated pathogenesis for lesions of secondary syphilis has been postulated. Textbook descriptions of a lymphoplasmacytic histopathologic picture have contradicted a role for circulating immune complexes in lesion pathogenesis. Four patients with early cutaneous lesions of secondary syphilis were studied. All four patients had serum Raji cell and/or Clq binding assay evidence for circulating immune complexes. Three patients showed a neutrophilic vascular reaction on histologic study of early lesions. The patients studied had immunofluorescence microscopic evidence of immunoreactant deposition in dermal blood vessels (4 hours) and/or a neutrophilic vascular reaction (24 hours) after intradermal histamine injection. Dieterle staining of lesional tissue from all patients showed the presence of treponemal organisms in dermal blood vessels. This new preliminary evidence adds some support to a circulating immune complex-mediated pathogenesis of cutaneous lesions in human secondary syphilis.
Two cases of late cutaneous syphilis are presented. After treatment for secondary syphilis in 1957 and retreatment for rising VDRL titers ten years later, one patient had developed a nodular syphilid. The other had several gummas. He had two quantitative nonreactive vDRL tests and a negative Treponema pallidum immobilization (TPI) test, but two reactive fluorescent treponemal antibody absorption (FTA-ABS) tests. Syphilis was suspected histologically and was confirmed by the specific serologic testing, the characteristic clinical presentation, and the prompt response to penicillin treatment. The clinical, serologic, histologic, therapeutic, and pathogenetic aspects of late benign syphilis of the skin are discussed.
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Strain 2 guinea pigs made T-cell deficient by thymectomy and irradiation and protected with syngeneic bone-marrow cells (TXB guinea pigs) have a surprisingly high level of resistance to cutaneous syphilis and to the dissemination of treponemes to the draining lymph node. Compared with normal euthymic controls infected with Treponema pallidum Nichols, syphilitic TXB guinea pigs developed fewer and less severe skin lesions and their lymph nodes contained lower numbers of treponemes. Associated with this evidence for enhanced innate resistance was the ability of the TXB host to produce, during each test interval of a primary infection, more antitreponemal antibodies than that of their euthymic counterparts. Similar levels of partial protection against cutaneous and disseminated syphilitic infection and elevated antibody levels occurred in challenged normal guinea pigs passively immunized with lymphocytes from T. pallidum-infected TXB donors. In contrast, the capacity of the TXB host to be protected against a lethal infection with the unrelated intracellular protozoan parasite Toxoplasma gondii was greatly impaired unless it received an intravenous infusion of normal syngeneic thymocytes. These seemingly paradoxical results are explained primarily in terms of a residual T-helper-cell population in the TXB guinea pig which is large and competent enough to generate antisyphilis, but not anti-Toxoplasma, immunity.
This article reviews the clinical manifestations of syphilis, diagnostic tests that might help to diagnose accurately the disease, and current recommendations for therapy. The association of syphilis and human immunodeficiency virus infection raises additional questions related to transmission, diagnosis, and therapy of both diseases.
To identify the characteristic features of lues in patients infected with HIV, 402 HIV-positive patients were examined for serological and clinical signs of lues. 141 patients (133 male, 8 female, mean age 36 [18-69] years) had a positive lues serology. Treatment for lues was required in 20 of the 141 cases (14%). In ten patients (one case of lues I, nine cases of lues II) dermatological signs were predominant, macular exanthemas (n = 4) and palmo-plantar syphilides (n = 3) being most frequent. Three patients had seropositive latent lues. Eight patients presented with signs of an active neurolues (lues II: n = 1; lues III: n = 6; lues IV: n = 1). In three of the eight cases the serum FTA-ABS-IgM findings were negative. In these three patients the need for a specific treatment was realized only on the basis of cerebrospinal fluid (CSF) examination in conjunction with the clinical findings and the anamnesis. This result makes it very clear that indication for CSF puncture should be more liberal in some HIV infected patients. The markedly high proportion of cases of neurolues (40% of the luetic patients requiring treatment) is possibly due to reactivation of old lues infections.
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A retrospective questionnaire survey of a sample of 173 of the 360 cases of early congenital syphilis reported in 1972 revealed serious problems with diagnostic certainty, prevention, and treatment of congenital syphilis. Only 24 (13.9%) of the reported cases could be categorized as probably or definite cases based on criteria developed from a literature review. Forty percent of the mothers received no prenatal care and an additional 19% received no prenatal care until the third trimester. Initial and followup serologic testing was inadequate in those who received care. Eighty-three different penicillin treatment schedules were used in the treatment of 128 infants. Carefully reasoned diagnostic and therapeutic decision making about the management of congenital syphilis appears to be lacking.
Partial protection against cutaneous syphilis and dissemination of treponemes to the regional lymph nodes was achievable in Treponema pallidum-infected neonatal strain 2 guinea pigs having syphilis-immune mothers. This evidence for enhanced resistance was associated with the natural transfer of antitreponemal, maternally derived immunoglobulins before parturition.
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The results of examinations of 210 infants with early congenital syphilis with emphasis on skin involvement are analyzed. An increased incidence of syphilitic pemphigus was recorded along with decreased incidence of diffuse infiltration and papular elements.
We report on 3 HIV patients showing atypical courses of syphilis. Both the history and serology of the first patient proved a recent re-infection with T. pallidum, whereas the histopathological findings corresponded to an advanced stage of the disease (S II-III). The second patient showed the clinical picture of syphilis maligna with slowly converting and slightly positive serological reactions. The third patient had a refractory syphilis and an early relapse. Our observations suggest that syphilis might take an unusual course in HIV patients. Considering our total HIV clientèle (800 patients greater than or equal to WR 2) the frequency of these atypical cases must be rated very low (0.38%).