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Anthrax is a rare but potentially fatal zoonotic disease caused by Bacillus anthracis [1]. While cutaneous anthrax is the most common form, systemic dissemination can lead to severe complications, including meningoencephalitis, septic shock, and neurogenic shock [2]. We herein report a fatal case of anthrax with rapid neurological deterioration, cerebral herniation, and neurogenic shock, highlighting the critical importance of early recognition and aggressive management. A 45-year-old male was admitted to our emergency department with a 10-day history of untreated left-hand trauma, followed by fever, blackened swelling of the fingers, and progressive neurological symptoms. The patient had engaged in fishing activities post-injury, likely facilitating bacterial entry. Initial symptoms included high-grade fever (39°C), cough, black eschar on the hand, and generalized myalgia. Despite empirical antibiotic therapy at a local clinic, his condition deteriorated rapidly, culminating in altered consciousness and respiratory distress. On admission, the patient presented with persistent fever, headache, vomiting, and coma. Cranial computed tomography (CT) revealed increased density in the falx cerebri and bilateral tentorium cerebelli, suggestive of subarachnoid hemorrhage or meningeal inflammation. White Blood Cell Count: 16.65 × 109/L↑, Absolute Neutrophil Count: 15.23 × 109/L↑, C-Reactive Protein (CRP): 37.48 mg/L↑; Myoglobin: 1065.00 ng/mL↑; Procalcitonin (PCT): 0.40 ng/mL↑; Cerebrospinal Fluid (CSF) Findings: Appearance: Light yellow, slightly turbid, Nucleated Cell Count: 670 × 106/L, Mononuclear Cells: 19.7%, Polynuclear Cells: 80.3%, Red Blood Cell Count: 1000 × 106/L, Pandy Test: 3 +, Biochemistry:ADA: 8.49 U/L, GLU: 2.08 mmol/L, CL: 111 mmol/L, PR: 12.38 g/L. Initial assessments of the CSF and blood cultures did not yield definitive results. However, next-generation sequencing (NGS) of the CSF provided conclusive evidence, confirming the presence of Bacillus anthracis and establishing a diagnosis of anthrax meningoencephalitis. Despite negative blood and wound cultures, clinical manifestations and molecular confirmation strongly indicated systemic anthrax infection. Microscopic examination of Wright's stained CSF cytology smears revealed numerous neutrophils with segmented nuclei and phagocytic cells containing anthrax bacilli (Figure 1A–D). These findings indicate the body's immune response to bacterial invasion and provide a direct visual link to the pathogenic process in anthrax meningoencephalitis. Identifying these cellular elements in the CSF is crucial for understanding disease progression and guiding treatment decisions (Figure 1). Initially diagnosed with meningitis, the patient received empirical antibiotic therapy with ceftriaxone and ganciclovir. Due to persistent high fever, vancomycin was added. Subsequent NGS results confirmed anthrax infection, prompting a switch to levofloxacin, linezolid, and meropenem. Supportive care included sedation, anti-inflammatory medications, diuretics, and neuroprotective agents. However, the patient's condition worsened. His left hand showed signs of necrosis and purpura, indicating severe skin and soft tissue infection. Despite negative skin secretion and blood cultures, anthrax was considered the primary cause of neurological and systemic complications. The patient developed respiratory failure due to poor coughing ability and was intubated. He later developed central respiratory failure, low blood pressure requiring norepinephrine, and unresponsiveness to pain stimuli with dilated pupils and absent pupillary light reflexes, indicating brain herniation. Neurosurgery consultation deemed surgical intervention inappropriate. Despite mannitol for cerebral edema, his condition did not improve. Progressive hypotension and bradycardia led to his death. The patient's death was attributed to cerebral herniation caused by anthrax infection. The final diagnosis included cerebral herniation, meningitis, neurogenic shock, septic shock, skin and soft tissue infection, and acute kidney injury. This case highlights the rapid progression of anthrax to severe neurological and systemic complications and the challenges in managing such cases. Anthrax, a rare but critical infectious disease caused by Bacillus anthracis, can present in various forms, including cutaneous, gastrointestinal, and pulmonary anthrax [3]. This case highlights how an initial hand injury and subsequent water exposure can lead to systemic anthrax infection. The rapid progression to severe complications underscores the virulence of the anthrax bacillus and the urgency of early diagnosis and treatment. The ineffectiveness of initial empirical antibiotic therapy against anthrax emphasizes the importance of prompt pathogen identification through advanced diagnostics like NGS. Microscopic examination of Wright's stained CSF cytology smears revealed a significant neutrophilic response and phagocytic cells containing anthrax bacilli (Figure 1), providing a direct visual link to the pathogenic process in anthrax meningoencephalitis. This cellular response is crucial for understanding disease progression and guiding treatment decisions. The development of cerebral herniation and neurogenic shock illustrates the severe neurological and systemic complications that can arise from anthrax infection. Cerebral herniation is a life-threatening condition requiring immediate intervention to reduce intracranial pressure and stabilize neurological status [4]. Neurogenic shock, resulting from nervous system damage leading to vasodilation and hypotension [5], necessitates a comprehensive management approach including fluid resuscitation, vasopressor therapy, and addressing the underlying cause. This case underscores the necessity of a high index of suspicion for anthrax in patients with necrotizing skin lesions and progressive neurological symptoms. Early use of advanced diagnostics and prompt initiation of targeted antimicrobial therapy are crucial. The identification of neutrophils with segmented nuclei and phagocytosed anthrax bacilli within phagocytic cells in Wright's stained CSF cytology smears is a critical finding that supports the diagnosis and aids in understanding the disease's pathogenesis. Public health awareness and clinician education remain essential to prevent similar outcomes and to ensure timely and appropriate management of anthrax infections. All authors contributed to the conception and drafting of the manuscript. All authors read and approved the final manuscript. The authors thank the medical and nursing staff involved in the care of the patient. The authors have nothing to report. This case received approval from the Ethics Committee for Biomedical Research Involving Humans at Shandong Provincial Hospital Affiliated to Shandong First Medical University (Ethical Approval No. (SWYX: NO. 2025-755)). All procedures were conducted in strict compliance with both local legislative requirements and institutional governance frameworks. Written informed consent was obtained from the patient prior to their inclusion in this investigation. Furthermore, explicit authorization for the publication of potentially identifiable visual materials or personal data was separately acquired through supplementary consent documentation. The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.