A 56‐year‐old HIV+ male presented with malaise and headache for the past 3 days. His CD4 count was 487 and HIV viral load 612,718 copies/mL, and he was not on HAART. He was taking dapsone and fluconazole. Social history was unremarkable. PPD skin test was negative 4 months prior. On exam, he was afebrile with stable vital signs. Physical exam was notable for a desquamating, maculopapular rash involving his abdomen and palms; and neurological examination was significant for unsteady gait. Initial labs showed a WBC count of 12.5 × 103 cells/mm3. Chest x‐ray and EKG were unremarkable. Trie patient was admitted for suspected drug‐induced rash, for which dapsone was discontinued. Over the next several days, there was no improvement of the rash. On hospital day 3, further testing revealed a positive RPR. Additional investigation into his medical record demonstrated a negative RPR 6 months prior. When asked, he admitted to unprotected sex over the last few months. He denied recently noticing any genital lesions. He was started on intravenous penicillin G. The serum FTA‐ABS was reactive. Because of possible neurologic involvement, a lumbar puncture was conducted, which revealed hazy CSF, protein 95 mg/dL, glucose 72 mg/dL (serum level, 158), and WBC count 2/mm3. Gram. AFB, and India ink stains of the CSF were negative. Intravenous penicillin was continued. The CSF VDRL was reported reactive. On hospital day 12, he was discharged with an indwelling catheter on intravenous penicillin G.
Although the patient presented with signs of secondary syphilis, he had CSF evidence of neurosyphilis, as supported by the positive CSF VDRL. The development of neurosyphilis from early syphilis can be more frequent and rapid among HIV‐infected patients. As immunosuppression due to chronic HIV worsens, it is reasonable that neurosyphilis, similar to opportunistic neurologic infections, can arise. This suggests that the clinical expression of neurosyphilis seems to depend on a level of severe immunodepletion and emphasizes the role of cellular immunity to the mechanism of the disease process.
The diagnosis of neurosyphilis in HIV‐infected patients is important because of the predilection of T. pallidum to invade the CNS early during the course of infection and the danger of treatment failure and reactivation due to immunodeficiency and because standard treatment with intramuscular penicillin does not achieve bactericidal levels in the CSF, Underlying Treponemal CNS infection may present with neurosyphilis much eadier in those with retroviral disease. A high index of suspicion should be maintained for neurosyphilis in HIV‐coinfected patients to reduce delayed diagnosis and late complications.
N. Parikh, none; A. Kushawaha, none; K. Dahal, none; A. Adedeji, none; N. Mobarakai, none; J. Tolia, none; E. Rivera, none; P. Singh, none.
To cite this abstract:Parikh N, Kushawaha A, Dahal K, Adedeji A, Mobarakai N, Tolia J, Rivera E, Singh P. Coinfection with Human Immunodeficiency Virus (HIV) and Neurosyphilis: A Dangerous Duo. Abstract published at Hospital Medicine 2010, April 8-11, Washington, D.C. Abstract 325. Journal of Hospital Medicine. 2010; 5 (suppl 1). https://www.shmabstracts.com/abstract/coinfection-with-human-immunodeficiency-virus-hiv-and-neurosyphilis-a-dangerous-duo/. Accessed August 24, 2019.