Case Presentation:

A 44‐year‐old woman presented with 1 week of headaches and blurry vision. She complained of unsteady gait, weakness, fatigue, diarrhea, subjective fevers, rash, and lip and neck swelling. She noted a history of a similar rash diagnosed 1 year earlier as impeligo. On admission, she was noted to have periorbital swelling but no pain on extraocular movements and no changes to visual acuity. She had left‐sided submandibular lymphadenopathy, left‐sided lip swelling, and cheliosis. She had desquamating 1‐cm, hyperpigmented, nonblanching macules disseminated over her entire body, most prevalent on the palms and soles. A CT scan of Ihe head was normal, and a subsequent MRI was also within normal limits. Total protein was 10.5. albumin 3.1. WBC 3.7, and ESR 110. An HIV ELISA was obtained that was positive with an HIV viral load of 62,800; the CD4 count was 100. Her hepatitis panel was negative, and the RPR was nonreactive. The FTA‐ABS, however, was reactive. CSF WBC was 37, CSF RBC 12. CSF protein 40.3, and CSF glucose 58. The CSF‐VDRL was mildly reactive at a 1:1 dilution. She was given a new diagnosis of AIDS, with HIV confirmed by Western blot. She was also diagnosed with RPR seronegative neurosyphilis, confirmed by reactive FTA‐ABS and CSF‐VDRL in conjunction with the neurological manifestations. She was treated with penicillin G 3M units IV q4h for 14 days and started on Bactrim once daily for PCP prophylaxis.


Although the prevalence of syphilis in the United States has declined in the past 50 years, the hospitalist should be aware that with the advent of HIV, the prevalence has increased. The presence of both HIV and syphilis is an important consideration, as coinfection with HIV can lead to an accelerated progression through the syphilitic stages. Concomitant immunosuppression, reduction in cell‐mediated immunity, and meningeal inflammation are all suspected mechanisms for advanced clinical presentations. Consequently, early detection of treponemal infection in HIV patients is critical to preventing advanced disease. It is also important to recognize, as in this case, that false‐negative serological tests for syphilis can occur in HIV coinfected patients due to a reduced humoral response, with a lack of B‐cell activation to treponemal cardiolipin antigens. As a result, when clinical evidence strongly suggests the presence of syphilis and the initial serological tests for syphilis are nonreactive, testing for antibodies targeted toward the treponeme should be obtained. Alternatively, a biopsy of an available lesion can be obtained to visualize spirochetes direclly on dark field microscopy.


Where neurosyphilis is suspected, an RPR of 1:32 or neurological manifestations are sufficient indicators to warrant a lumbar puncture. In this patient, the diagnosis of syphilis infection with progression to neurosyphilis was made by obtaining a reactive FTA‐ABS and a reactive CSF‐VDRL, and proper treatment was initiated.

Author Disclosure:

M. Knudson‐Johnson, none.