Bacterial neurotoxins: The snake venoms of the microbial world-a clinical and bioengineering approach.

Bacterial meningitis remains a critical global health concern, with mortality rates reported as high as 54% [-]. In the management of central nervous system (CNS) infections, the primary objective is the rapid differentiation between bacterial and viral etiologies. remains the predominant causative pathogen, accounting for approximately 60% of cases [,], with antimicrobial non-susceptibility identified in 42.2% of isolates []. Although the incidence fluctuated during the COVID-19 pandemic, an 87% resurgence in pneumococcal meningitis was observed during 2022-2023, emphasizing the ongoing need for rapid identification and treatment of this pathogen []. While clinical diagnostic frameworks are typically designed to identify a single primary etiology, the simultaneous occurrence of bacterial and viral pathogens presents a significant diagnostic challenge. Such co-infections account for approximately 2.8%-4.8% of culture-positive meningitis cases in the pediatric population [], although comparable data in adults remain limited. This phenomenon represents a complex clinical scenario in which multiple diagnostic categories must be considered simultaneously. Among viral etiologies, reactivation of varicella-zoster virus (VZV) predominantly affects older adults and immunocompromised individuals []. We present the case of a 61-year-old woman who developed acute metabolic encephalopathy precipitated by systemic sepsis secondary to meningitis caused by concurrent infection with and VZV. A 61-year-old woman with a history of hypertension presented with an acute stroke activation after being found down at her residence. According to the patient’s daughter, the patient was at her baseline state of health the evening prior to admission, at which time she developed acute encephalopathy characterized by severe agitation and aphasia. Upon arrival at the emergency department, the patient was in severe respiratory distress, with tachypnea (40 breaths/minute) and hypoxia, with an oxygen saturation of 87% on room air. She required immediate stabilization with non-invasive positive pressure ventilation (BiPAP) and intravenous sedation. On physical examination, the patient was obese, non-verbal, and responded only to noxious stimuli. Cutaneous examination was notable for facial erythema accompanied by retiform purpura, likely due to vasculitis. On detailed neurological examination, the patient was awake and alert and appeared to visually track and regard the examiner; however, she did not answer orientation questions, follow commands, or demonstrate any usable speech. She was unable to name, repeat, pantomime, or otherwise participate meaningfully in language testing. Cranial nerve examination revealed pupils measuring 4 mm that were round and equal, with minimal reactivity to light. Extraocular movements were intact without nystagmus, and the patient appeared to track the examiner appropriately. Blink-to-threat was present bilaterally. Jaw movements were intact. There was no facial asymmetry at rest or with spontaneous movement. Palatal elevation was symmetric. The tongue protruded in the midline with normal side-to-side movement, without evidence of atrophy or fasciculations. Head rotation and shoulder shrug were intact and symmetric (5/5 bilaterally). Motor examination demonstrated normal muscle bulk and tone throughout. The patient moved both upper extremities spontaneously against gravity. In the lower extremities, the legs fell to the bed when lifted; however, the patient demonstrated equal flexion bilaterally. There was no obvious asymmetry in spontaneous motor activity. Sensory examination demonstrated localization and withdrawal to painful stimuli in all four extremities. Coordination testing could not be performed because the patient was unable to understand or follow commands. The patient was noted to be using accessory muscles of respiration and appeared to be in respiratory distress. Initial laboratory evaluation revealed profound leukocytosis, with a white blood cell count of 18,200/µL, and severe high-anion-gap metabolic acidosis secondary to hyperlactatemia. Laboratory values on admission, day 1, and day 14 are listed in Table .