Nivolumab Patient Develops Rare Brain-to-Blood Bacterial Spread from Oral Microbe
A cancer patient on nivolumab developed Eikenella corrodens bacteremia after CNS infection, revealing how immune checkpoint therapy may enable dangerous microbial dissemination.
Summary
A 50-year-old man with advanced nasopharyngeal carcinoma on nivolumab immunotherapy developed a rare secondary bloodstream infection caused by Eikenella corrodens, an oral commensal bacterium, following left temporal cerebritis and subdural empyema. Blood cultures turned positive after 28 hours and the organism was confirmed by MALDI-TOF mass spectrometry and 16S rRNA gene sequencing. The case illustrates how immune checkpoint inhibitors may disrupt immune homeostasis, compromise blood-brain barrier integrity, and alter mucosal microbiota in ways that allow normally harmless oral bacteria to invade the CNS and then disseminate into the bloodstream. A literature review of similar E. corrodens CNS and head-and-neck infections is included. The patient was transitioned to palliative care given advanced disease.
Detailed Summary
Eikenella corrodens is a fastidious, facultative anaerobic Gram-negative bacillus that normally resides in the oropharyngeal, gastrointestinal, and genitourinary mucosa. It belongs to the HACEK group of organisms historically associated with culture-negative endocarditis and polymicrobial head-and-neck infections. While it rarely causes isolated bacteremia, this case report and accompanying literature review document a clinically significant pathway: progression from localized CNS infection to secondary bloodstream invasion, particularly in immunologically compromised oncology patients.
The index patient was a 50-year-old Caucasian man with EBV-positive, non-keratinizing undifferentiated squamous cell carcinoma of the nasopharynx (staged cT4N1M0, Stage IVa), diagnosed in April 2023. His oncologic history included concurrent chemoradiotherapy (70–63–56 Gy over 35 fractions) plus cisplatin (cumulative 185 mg/m²), surgical resection, adjuvant brachytherapy (3000 cGy), and subsequent cisplatin-gemcitabine chemotherapy. By March 2025, he had initiated nivolumab (240 mg IV every two weeks) for leptomeningeal progression. Three days after his most recent nivolumab dose, he presented with high-grade fever (39°C), altered mental status, severe aphasia, right oculomotor nerve palsy, and right-sided hemiparesis.
On admission, laboratory findings revealed neutrophilic leukocytosis (WBC 13.49 × 10⁹/L; neutrophils 12.54 × 10⁹/L) and normocytic anemia (hemoglobin 10.7 g/dL). Brain CT showed left temporal hypodensity with hemispheric swelling and midline shift, plus extensive edema of the sphenoidal sinuses and ethmoidal labyrinths. Subsequent MRI confirmed left temporal cerebritis with ipsilateral subdural empyema, consistent with contiguous spread from adjacent sinonasal structures. Blood cultures collected from both peripheral and central venous catheter sites turned positive at 28 hours. Identification by MALDI-TOF MS (Bruker Biotyper, score ≥2.0 for species-level identification) and confirmatory 16S rRNA gene sequencing (BLASTn against NCBI database) established E. corrodens as the causative organism.
Antimicrobial susceptibility was assessed by E-test on Mueller-Hinton agar supplemented with 5% sheep blood and β-NAD, with MICs reported descriptively given the absence of EUCAST or CLSI species-specific breakpoints for E. corrodens. Initial empiric piperacillin-tazobactam (18 g/day IV) was escalated to ceftriaxone (2 g once daily IV) upon definitive identification. The patient defervesced within 48 hours, leukocyte counts normalized, and follow-up blood cultures at 48 and 72 hours post-ceftriaxone initiation were negative, confirming microbiological clearance.
The authors propose four mechanistic pathways by which nivolumab and the underlying malignancy may have facilitated this unusual infection: (1) nonspecific T-cell activation disrupting immune homeostasis and pathogen surveillance; (2) neuroinflammatory effects compromising blood-brain barrier integrity; (3) corticosteroid use for immune-related adverse events adding immunosuppressive burden; and (4) ICI-mediated alterations in mucosal immunity and microbiota composition promoting E. corrodens overgrowth and translocation. The accompanying literature review synthesizes published cases of E. corrodens bacteremia secondary to CNS and head-and-neck infections, contextualizing this case within a rare but growing body of evidence. Given advanced disease, neurosurgical drainage was deemed inappropriate, and the patient was transitioned to palliative hospice care.
Key Findings
- Blood cultures turned positive at 28 hours; E. corrodens confirmed by MALDI-TOF MS (score ≥2.0, species-level) and 16S rRNA gene sequencing via BLASTn
- Microbiological clearance achieved: follow-up blood cultures at 48 and 72 hours post-ceftriaxone (2 g once daily IV) were both negative
- Patient defervesced within 48 hours and leukocyte counts normalized after antibiotic escalation from piperacillin-tazobactam to ceftriaxone
- Nivolumab dose (240 mg IV) was administered just 3 days before symptom onset, temporally linking ICI therapy to the infectious event
- Imaging confirmed contiguous spread: left temporal cerebritis and subdural empyema arising from sphenoidal sinus and ethmoidal labyrinth infection
- No EUCAST or CLSI species-specific breakpoints exist for E. corrodens, requiring descriptive MIC reporting without categorical susceptibility interpretation
- Literature review spanning 1958–June 2025 identified E. corrodens bacteremia secondary to CNS and head-and-neck infections as a rare but clinically significant pattern in immunocompromised hosts
Methodology
This is a single case report combined with a systematic literature review (Cochrane, MEDLINE, Embase, and other databases, 1958–June 2025) of E. corrodens bacteremia secondary to CNS and head-and-neck infections. Microbiological identification used MALDI-TOF MS (Bruker Biotyper, MBT Compass 4.1) with standard score thresholds (≥2.0 species-level) and confirmatory partial 16S rRNA gene sequencing with BLASTn analysis. Antimicrobial susceptibility was determined by E-test gradient diffusion on supplemented Mueller-Hinton agar; no formal statistical analysis was performed given the case-report design.
Study Limitations
This is a single case report, precluding any generalizable conclusions about incidence, causality, or treatment efficacy. The causal role of nivolumab in facilitating BBB compromise and E. corrodens dissemination is mechanistically plausible but unproven. No external funding was received, and no conflicts of interest were declared by the authors.
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