Legalomics: why microbiology matters to the promotion of just societies.

Herpes simplex virus (HSV) is the most common cause of sporadic viral encephalitis in immunocompetent adults, with an incidence of 2–4 cases per 1 million persons annually. While HSV-1 classically causes orolabial disease and HSV-2 predominantly causes genital infection, both viruses establish lifelong latency in sensory ganglia with the potential for reactivation throughout the host’s lifetime. Despite the availability of acyclovir, HSV encephalitis (HSVE) remains associated with significant morbidity and mortality, with case fatality rates of 15%–28% and neurological sequelae in up to 50% of survivors. Poor outcomes are strongly associated with delaying acyclovir treatment more than 2 days from hospital admission, and each additional day of delay increases the 6-month mortality risk. HSVE following neurosurgical intervention is rarely documented and is most commonly reported after epilepsy surgery, tumor resection, spinal surgery, and craniocervical decompression. Proposed mechanisms include direct manipulation of neural structures harboring latent virus and perioperative immunosuppression from corticosteroid administration. Reactivation in the ganglia may then lead to axonal spread along the trigeminal or olfactory pathways or hematogenous dissemination. Similarly, brain injury induces systemic immunosuppression, predisposing the patient to HSV reactivation. Traumatic brain injury (TBI) activates the sympathetic nervous system, resulting in a catecholamine surge that upregulates PD-1 expression on T lymphocytes and impairs CD4+ and CD8+ T-cell function. This immunosuppression is characterized by lymphopenia, reduced interferon-γ production, and aberrant monocyte polarization—alterations that compromise antiviral immunity. In a prospective cohort study of 344 patients with severe brain injury, HSV reactivation, detected in tracheal aspirates, occurred in 39% of HSV-seropositive patients and was independently associated with poor neurological recovery at 6 months. However, prior studies have primarily characterized respiratory HSV shedding in critically ill patients rather than CSF-confirmed HSVE, a qualitatively distinct and more severe clinical entity. Whether brain injury– and critical illness–associated immunosuppression is associated with clinically apparent HSVE remains poorly characterized. We present a case series of 3 adults (2 men, 1 woman) who developed HSVE following spontaneous thalamic intracranial hemorrhage (ICH), traumatic subdural hematoma, and nonaneurysmal subarachnoid hemorrhage (SAH), highlighting the diagnostic challenges and the critical importance of early recognition and treatment in this patient population. In all 3 cases, empiric acyclovir therapy was initiated when clinical or radiographic findings raised concern for concurrent HSVE. CSF testing was performed promptly using the BioFire FilmArray Meningitis/Encephalitis Panel (MEP; bioMérieux), a multiplex polymerase chain reaction (PCR) assay. None of the 3 patients had a previous immunosuppressive history. Key demographic, clinical, diagnostic, treatment, and outcome features for the 3 cases are summarized in .