Clinical study

Syphilis and neurosyphilis in a human immunodeficiency virus type-1 seropositive population: Evidence for frequent serologic relapse after therapy☆

Les vascularites cérébrales sont un groupe hétérogène d'affections neurologiques de diagnostic difficile. Elles peuvent être primitives ou associées à une autre affection neurologique ou multi-systémique, principalement auto-immune ou infectieuse. Les causes infectieuses sont fréquentes et de mécanismes physiopathologiques variés : (1) liées à un agent pathogène angiotrope (varicelles, syphilis, aspergillus) ; (2) compliquant une infection méningée généralement sous arachnoïdienne (pneumocoque, méningocoque, tuberculose, cysticercose) ; (3) survenant par contiguïté d'un foyer infectieux sinusien ou orbitaire (aspergillose, mucormycose) ; et (4) compliquant une infection chronique responsable de manifestations immunologiques (hépatite B, hépatite C, virus de l'immunodéficience humaine). Devant une vascularite cérébrale, les causes infectieuses doivent donc être systématiquement envisagées, et l'enquête diagnostique doit être individualisée selon le contexte clinique du patient. Inversement, les vascularites cérébrales doivent être connues et identifiées devant des symptômes neurologiques survenant au cours d'une infection bactérienne, virale, fongique ou parasitaire. Nous proposons ici une mise au point sur les causes infectieuses de vascularites cérébrales, et sur leurs aspects diagnostiques et thérapeutiques.

Infections are a frequent cause of cerebral vasculitis, important to diagnose because a specific treatment may be required. Infection-associated vasculitis can be caused by angiotropic pathogens (varicella zoster virus, syphilis, aspergillus). They can be associated with subarachnoidal meningitis (tuberculosis, pyogenic meningitis, cysticercosis). They can appear contiguously to sinuses or orbital infection (aspergillosis, mucormycosis). Finally, they also may be due to an immune mechanism in the context of chronic infections (hepatitis B virus, hepatitis C virus, human immunodeficiency virus). Cerebral vasculitis are severe conditions and their prognosis is directly linked to early recognition and diagnosis. Infectious causes must therefore be systematically considered ahead of cerebral vasculitis, and the appropriate investigations must be determined according to the patient's clinical context. We propose here an update on the infectious causes of cerebral vasculitis, their diagnosis modalities, and therapeutic options.

The epidemiology of spinal cord disease in human immunodeficiency virus (HIV) infection is largely unknown due to a paucity of data since combination antiretroviral therapy (cART). HIV mediates spinal cord injury indirectly, by immune modulation, degeneration, or associated infections and neoplasms. The pathologies vary and range from cytotoxic necrosis to demyelination and vasculitis. Control of HIV determines the differential for all neurologic presentations in infected individuals. Primary HIV-associated acute transverse myelitis, an acute inflammatory condition with pathologic similarities to HIV encephalitis, arises in early infection and at seroconversion. In contrast, HIV vacuolar myelopathy and opportunistic infections predominate in uncontrolled disease. There is systemic immune dysregulation as early as primary infection due to initial depletion of gut-associated lymphoid tissue CD4 cells and allowance of microbial translocation across the gut that never fully recovers throughout the course of HIV infection, regardless of how well controlled. The subsequent proinflammatory state may contribute to spinal cord diseases observed even after cART initiation. This chapter will highlight an array of spinal cord pathologies classified by stage of HIV infection and immune status.

No portion of the central nervous system is immune to the ravages of syphilis. Infection by Treponema pallidum can affect the meninges, brain, brainstem, spinal cord, nerve roots, and cerebral and spinal blood vessels. As a consequence, the disease may present in diverse and, at times, diagnostically challenging fashions. Neurologic manifestations of syphilis may develop within months of the initial infection or, alternatively, take decades to appear. Although approximately one-third of individuals infected by T. pallidum display cerebrospinal fluid abnormalities suggestive of invasion of the central nervous system by the organism, only a fraction of these develop clinically significant neurologic manifestations. The features of neurosyphilis may be modified by the concomitant presence of immunosuppressive agents or conditions such as HIV/AIDS. The epidemiology of neurosyphilis has largely paralleled that of syphilis in general. A dramatic decline occurred by the early 1950s as a consequence of public health measures and the widespread use of antibiotics. The incidence had increased by the onset of the AIDS pandemic and has since corresponded with the adoption of safe sex practices. The CSF Venereal Disease Research Laboratory (VDRL) test remains the “gold standard” for diagnosis, but is not invariably positive. Penicillin remains the most effective and recommended therapy.