Early secondary brain abscess formation caused by Bacteroides fragilis at the intracerebral hemorrhage site: A case report

Abstract

Background:

Brain abscess formation at the site of intracerebral hemorrhage (ICH) is extremely rare, particularly in association with anaerobic pathogens, such as Bacteroides fragilis, and its pathogenesis remains incompletely understood. Here, we report an ultimately fatal case of a brain abscess caused by this organism that developed at an ICH site.

Case Description:

An 86-year-old woman presented with right parieto-occipital ICH accompanied by systemic inflammatory signs. Abdominal computed tomography performed at admission revealed findings consistent with sigmoid diverticulitis. Despite initial conservative management, the patient developed bacterial meningitis due to B. fragilis. Sixteen days after stroke onset, she experienced rapid neurological deterioration caused by massive perilesional edema. Emergency surgery revealed purulent material within the hematoma cavity, and cultures confirmed B. fragilis, establishing a diagnosis of secondary abscess formation at the ICH site. Although surgical intervention and targeted antimicrobial therapy were initiated, the patient developed cerebritis and ventriculitis and ultimately died.

Conclusion:

This case suggests that hematogenous dissemination from an intra-abdominal infection may seed injured brain tissue in the early phase after hemorrhage. Disruption of the blood–brain barrier and the relatively avascular, anaerobic environment of a hematoma may predispose patients to abscess formation. In patients with ICH, persistent fever and progressive neurological deterioration despite antimicrobial therapy should prompt consideration of contrast-enhanced neuroimaging to evaluate possible intracranial infectious complications.

INTRODUCTION

Brain abscess is a serious intracranial infection with an estimated incidence of 0.4–1.3/100,000 population and a mortality rate of approximately 10–20%, despite advances in diagnostic imaging and antimicrobial therapy.[1,6,7] It may develop directly following neurosurgical procedures or head trauma or through contiguous spread from parameningeal infectious foci. Alternatively, brain abscess may occur through hematogenous dissemination from a distant focus of infection, such as lung abscesses, bacterial endocarditis, skin infections, and intra-abdominal infections.[1]

In contrast, brain abscess formation following intracerebral hemorrhage (ICH) is extremely rare, with fewer than 30 cases reported in the literature. The pathogenesis, optimal diagnostic approach, and treatment strategy for this condition remain poorly understood. Here, we report a rare case of Bacteroides fragilis brain abscess that developed at the site of ICH and review the relevant literature, with particular emphasis on the mechanisms of abscess formation and diagnostic challenges.

CASE REPORT

On day 0, an 86-year-old woman with a history of hypertension and hyperlipidemia was transferred to our hospital with a sudden onset of mild left hemiparesis. The patient was conscious with a Glasgow Coma Scale score of 14 (E4V4M6) on admission. Brain computed tomography (CT) revealed a moderate-sized right parieto-occipital ICH with a small amount of adjacent subarachnoid hemorrhage [Figure 1a]. The patient was febrile (37.6 °C), and laboratory tests showed a white blood cell count of 20,100/µL, C-reactive protein level of 4.07 mg/dL, and procalcitonin level of 18.23 ng/mL, suggesting a concurrent systemic infection. Because no headache, vomiting, neck stiffness, or other clinical signs suggestive of meningitis or intracranial infection were present, investigations focused initially on identifying an extracranial infectious source. Chest CT revealed no evidence of pneumonia, whereas abdominal CT demonstrated thickening of the sigmoid colon wall with surrounding fat stranding, suggestive of diverticulitis. In this clinical context, contrast-enhanced CT and magnetic resonance imaging (MRI) of the brain were not performed initially. Transthoracic echocardiography revealed no structural abnormalities or ventricular dysfunction. Strict blood pressure control was initiated for conservative treatment of the ICH. Conservative management was selected for the infection because the patient was clinically stable despite having a low-grade fever. However, the patient’s fever progressively worsened, reaching 39.6°C on day 6, and she subsequently developed drowsiness. Brain CT demonstrated the expected evolution of the hematoma without evidence of deterioration [Figure 1b]. Urinalysis suggested a possible urinary tract infection, and ceftriaxone was initiated empirically. Urine culture subsequently grew Escherichia coli and group B Streptococcus, whereas blood cultures were negative. On day 9, the patient developed headache and neck stiffness, prompting cerebrospinal fluid (CSF) analysis, which revealed a polymorphonuclear cell count of 1,520 cells/µL, a glucose level of 2 mg/dL, and a protein level of 254 mg/dL, consistent with bacterial meningitis. Antibiotic therapy was changed to cefepime and vancomycin on day 10. CSF culture grew B. fragilis, and antibiotic therapy was adjusted to metronidazole and ceftriaxone on day 13 based on susceptibility testing. On day 16, the patient became comatose and developed Cheyne-Stokes respiration and anisocoria. Emergency brain CT revealed a critical midline shift caused by massive edema surrounding the hematoma cavity [Figure 1c], and emergency surgery was performed. Following a large craniotomy, viscous, turbid fluid was aspirated from the hematoma cavity, and the cavity wall was excised. The aspirated fluid culture grew B. fragilis, which was identical to the pathogen isolated from the CSF. Pathological examination revealed hemorrhagic brain tissue and an abscess wall, without evidence of amyloid angiopathy. Continuous norepinephrine infusion was required for postoperative septic shock. Meropenem was subsequently administered as a monotherapy based on susceptibility testing. Meropenem was discontinued on day 30 because of liver dysfunction, after systemic inflammatory markers had improved. MRI performed on day 38 revealed a residual cystic lesion at the ICH site with massive perilesional edema [Figure 2a]. Diffusion-weighted imaging revealed a hyperintense lesion within the cyst [Figure 2b], and the wall showed contrast enhancement [Figure 2c and d]. The cerebral surface and both ventricular walls were also enhanced, indicating concomitant cerebritis and ventriculitis [Figure 2e and 2f]. Magnetic resonance angiography performed on day 44 showed no evidence of an infectious aneurysm. She remained comatose and had a poor prognosis. Therefore, the patient’s family declined further surgical intervention. Despite prolonged treatment, she died on day 99. The chronological clinical course is summarized in Table 1.

Figure 1:

Noncontrast computed tomography (CT) images of the brain. (a) CT on day 0 shows an irregularly shaped right intracerebral hemorrhage. (b) CT on day 6 shows the expected evolution of the hematoma with minimal perilesional edema. (c) CT on day 16 reveals marked perilesional brain edema with a critical midline shift.”

Figure 2:

Postsurgical magnetic resonance imaging (MRI) of the brain performed on day 38. (a) A cystic lesion with marked perilesional edema persists at the site of the intracerebral hemorrhage. (b) The cyst contents demonstrate heterogeneous high signal intensity on diffusion-weighted imaging. (c and d) Gadolinium-enhanced MRI reveals a ring-enhancing cyst (arrow in d). (e) Contrast enhancement is observed along the cerebral surface (arrows). (f) Contrast enhancement is observed along the bilateral ventricular walls (arrows).

Table 1:

Chronological clinical course.

DISCUSSION

Brain abscess developing at the site of ICH is extremely rare, with fewer than 30 cases reported in the literature.[2-5,8-11,13-15,18-29] Because the available evidence is limited to sporadic case reports, conclusions regarding its pathogenesis should be drawn with caution. In the literature, the interval between ICH onset and abscess diagnosis varies widely. Notably, the shortest reported interval was 14 days, which was observed in patients who presented with high fever at stroke onset.[4,29] Histopathological studies have demonstrated that abscess capsule formation is generally established approximately 14 days after parenchymal infection.[1,17] Therefore, cases diagnosed within this timeframe may represent early-onset abscess formation resulting from bacteremia occurring at the time of hemorrhage. Our patient exhibited systemic inflammatory signs at presentation and was diagnosed with a brain abscess 16 days after ICH onset, although the abscess had likely already formed earlier. These findings suggest that hematogenous seeding of injured brain tissue may occur during the acute phase of hemorrhage. Although no direct evidence of bacteremia was obtained, the temporal relationship between systemic infection and abscess formation supports this hypothesis. In contrast, other reported cases demonstrated a longer latency of 21–114 days and were not accompanied by infectious signs at stroke onset.[2,3,5,8-11,13-15,18-28] In such delayed-onset cases, fever developed 3–55 days later. Experimental and clinical studies have shown that blood– brain barrier permeability increases following ICH because of inflammatory responses.[16] This disruption may facilitate bacterial entry into the previously injured brain parenchyma. Furthermore, the hematoma cavity is relatively avascular and hypoxic, potentially providing a favorable microenvironment for anaerobic bacteria.

Staphylococcus aureus has been most frequently reported as a causative organism in abscesses complicating ICH,[3,4,13,18,24,25] whereas B. fragilis has rarely been identified. To the best of our knowledge, only one previous case of B. fragilis brain abscess developing at the site of ICH has been reported.[15] B. fragilis is an obligate anaerobe and a major component of the normal intestinal microbiota.[30] Disruption of mucosal integrity, such as in diverticulitis, may permit translocation into the bloodstream and subsequent abscess formation. Abdominal CT on admission revealed findings consistent with sigmoid diverticulitis, suggesting that this was the most plausible primary infectious focus. Given its preference for anaerobic, heme-rich environments, B. fragilis may be particularly suited to proliferate in an intracerebral hematoma.

Diagnosing secondary abscess formation after ICH is challenging. CSF examination may demonstrate meningitis, but cannot confirm a focal abscess, and lumbar puncture may be contraindicated in the presence of elevated intracranial pressure.[1] Blood cultures are frequently negative.[6] On CT, early abscess formation may be difficult to distinguish from the expected subacute evolution of ICH, because both conditions can show heterogeneous attenuation within the cystic lesion, progressive perihematomal edema, and mass effect. MRI may provide additional diagnostic information, particularly when diffusion-weighted imaging and contrast-enhanced sequences are combined. Restricted diffusion within a cystic lesion supports abscess formation by reflecting viscous purulent material, whereas ring enhancement suggests capsule formation. However, neither finding is pathognomonic, as diffusion abnormalities and peripheral enhancement may also be observed in an organizing hematoma.[12] Progressive or disproportionate perilesional edema during the subacute phase of ICH may serve as a clinical clue;[14,22,27] however, definitive diagnosis often requires surgical exploration and microbiological confirmation.

Antimicrobial therapy was modified according to the evolving clinical information and microbiological results. Persistent fever and altered consciousness were initially attributed to systemic infection, which is reasonable in patients with sepsis. However, this case highlights a critical pitfall: intracranial infectious complications, such as brain abscesses, may progress despite seemingly appropriate systemic management and may be clinically indistinguishable from sepsis-associated encephalopathy in the early phase. The optimal timing for contrast-enhanced neuroimaging in such cases remains challenging. This case suggests that earlier contrast-enhanced neuroimaging may be warranted when persistent high fever and progressive neurological deterioration occur despite appropriate antimicrobial therapy. These findings may serve as clinical clues to prompt earlier investigations of intracranial complications.

Surgical management of brain abscess should be individualized according to neurological status, age, comorbidities, abscess size and location, mass effect, and the need for microbiological diagnosis. Burr-hole or stereotactic aspiration is generally preferred because it enables decompression and pathogen identification while minimizing additional surgical injury. Endoscopic evacuation may also be useful for selected cystic or intraventricular lesions, particularly when direct visualization and irrigation are advantageous. In contrast, craniotomy is usually reserved for cases with severe mass effect, impending herniation, multiloculated or organized lesions, diagnostic uncertainty, or failure of less invasive treatment. In the present case, craniotomy was chosen despite the patient’s advanced age because she had been independent before onset and remained ambulatory until day 5, indicating relatively preserved baseline function. Moreover, rapid neurological deterioration with massive cerebral edema and critical midline shift suggested impending brain herniation, and surgical decompression might have been required depending on the intraoperative findings. Because the diagnosis was not definitive preoperatively and neoplastic lesions could not be completely excluded, craniotomy allowed direct inspection of the lesion, sufficient decompression, removal of purulent and organized material, and collection of specimens for microbiological and pathological evaluation. Surgical evacuation, therefore, allowed not only identification of the causative pathogen but also reduced the mass effect and bacterial burden.[1,6,7,17] Although earlier diagnosis might have allowed earlier intervention, it remains uncertain whether this would have altered the outcome, given the patient’s advanced age and the severity of the subsequent systemic infection.

CONCLUSION

This case illustrates a rare instance of B. fragilis abscess formation within an intracerebral hematoma, likely secondary to an intestinal infection. Recognizing that injured hemorrhagic brain tissue may serve as a site for hematogenous seeding is crucial for timely diagnosis and intervention. In patients with ICH, persistent fever and progressive neurological deterioration despite antimicrobial therapy should prompt consideration of contrast-enhanced neuroimaging to evaluate possible intracranial infectious complications.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that verbal informed consent for publication of the clinical information and images was obtained from the deceased patient's daughter. Every effort has been made to protect the patient's identity, although complete anonymity cannot be guaranteed

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was use of artificial intelligence (AI)-assisted technology. ChatGPT was used for language assistance.

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