Bartonella henselae and Demyelinating Disease: A Convergence Hypothesis with Adjuvant-Aluminum Monocytic Trafficking

Abstract Background Bartonella henselae is a gram-negative, endotheliotropic bacterium with a demonstrated capacity to activate vascular endothelium through an NF-κB-dependent pathway. Published cases of neuroinvasive bartonellosis show cerebral vasculitis with perivascular destruction of axons and myelin, and a documented diagnostic overlap with multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), and Guillain-Barré syndrome (GBS) —the latter predominantly affecting the peripheral, not the central, nervous system. Multiple aluminum-adjuvanted parenteral vaccines —from different manufacturers and antigens— include in their official product information a set of reported neurological events spanning CNS demyelinating disease (MS, ADEM, myelitis, optic neuritis), peripheral nervous system (PNS) involvement (GBS, polyradiculoneuritis, neuropathies), and encephalitis/encephalopathy —the latter not necessarily demyelinating—, generally classified as very rare and without established causality. Hypothesis We propose that, in a subset of cases, temporally close coexposure between B. henselae infection and administration of an aluminum-adjuvanted vaccine produces a demyelinating phenotype more likely or more severe than infection alone, via a cellular trafficking mechanism: aluminum-laden phagocytic cells of monocyte-macrophage lineage, generated at the injection site, are recruited —as CCR2+ monocytes— toward the compartment Bartonella has already compromised, following a CCL2 gradient elevated by the vasculitic lesion itself. B. henselae is the direct CNS-access mechanism; the vaccine supplies the cellular aluminum load, not the access route itself. Whether this moves from hypothesis to testable model turns on a single step: whether Bartonella elevates CCL2 locally in its lesion (Section 4.2). Conclusions The scenario places direct causal responsibility on B. henselae and reduces the vaccine to a transportable cellular aluminum source — a distinction that matters because it points to what would need to be measured to test the hypothesis: not the vaccine alone, but the coexposure and its temporal window (predictions 1-3, Section 7). The set of neurological events already reported across multiple aluminum-adjuvanted vaccines (Section 3) places the scenario within what pharmacovigilance can, in principle, examine.