A 40-year-old female was diagnosed with viral encephalitis-induced secondary brain death on September 11, 2019, based on the American Academy of Neurology (AAN) criteria for the determination of brain death in adults. Her clinical manifestations presented as comatose, lack of brainstem reflexes, and cannot breathe spontaneously. The head CT showed diffuse edema of brain tissue and gray matter with white matter structure blurred (Figure 1A). The electroencephalogram (EEG) indicated resting-state brain electrical activity. Her family finally decided to transfer to the Hang Zhou Integrative Medicine Hospital. She received mechanical ventilation and rehabilitation exercise during hospitalization lasting for almost 3 years. The patient had a high fever on September 12, 2022. Physical examination revealed intense swelling of her right occipital region and the abscess was approximately four centimeters in diameter. The brain computed tomography (CT) imaging showed the right temporoparietal cerebral hemorrhage and occipital defect with a subcutaneous abscess in Figure 1B, and laboratory workup showed white blood cell, 9.0x109/L; neutrophils, 87.8%; lymphocytes, 9.1%; red blood cell, 2.84x1012/L; hemoglobin, 86 g/L; platelet, 183x109/L; C-reactive protein, 100.2 mg/L; procalcitonin, <0.25 ug/L. The sampling of abscess fluid was conducted, and bloody pus was obtained (Figure 2). The pus's direct smear examination and culture showed B. cepacia. The colony was susceptible to cefoperazone-sulbactam, meropenem, ceftazidime, minocycline, and TMP-SMX (Table 1). To confirm the result, we further conducted metagenomic next-generation sequencing (NGS) of the abscess aspiration and revealed B. cepacia (Table 2). We analyzed its virulence genes and the major virulence factors focusing on the function of motility, such as fliM, flhA, motA, fliA, flgG, and flgI. We further found that the drug-resistant genes of this strain were mphL, satA_Ba, BcII, and bla1 via the second-generation sequencing of the whole genome.   
The cerebrospinal fluid examination (CSF) was performed to rule out intracranial infection, and no positive results were seen in the CSF, including CSF routine, culture, Cryptococcus neoformans, Mycobacterium tuberculosis and NGS. She was then treated with Cefoperazone-sulbactam 2.0g q8h for 5 days depending on the result of the antimicrobial susceptibility testing for B. cepacia. By this series of treatments, she had no fever, and the inflammation presented white blood cells, 5.5x109/L; neutrophils, 79.6%; lymphocytes, 17.4%; red blood cells, 3.0x1012/L; hemoglobin, 89 g/L; platelet, 135x109/L; C-reactive protein, 40 mg/L; procalcitonin, <0.25 ug/L. The inflammatory markers were significantly lower than before with no apparent swollen sign of the right occipital area in several days. Worth mentioning is that the patient neither reviewed for the CT nor got enough treatment courses to objectively evaluate the therapeutic effect of the soft tissue abscess with a bone fracture because family members decided to abandon treatments.