Fatal Streptococcus agalactiae endocarditis complicated by basal ganglia hemorrhage and multiple cerebral infarcts: A case report

INTRODUCTION

Streptococcus agalactiae (Group B Streptococcus) is a commensal organism of the gastrointestinal and genitourinary tracts, but is an infrequent etiological agent of infective endocarditis (IE). Although it is well recognized as a leading cause of neonatal sepsis and post-partum infections, IE caused by S. agalactiae is rare and typically follows an aggressive clinical course with considerable morbidity and mortality. Neurological sequelae, particularly cerebrovascular complications, significantly worsen outcomes in affected patients. We describe a case of native mitral valve S. agalactiae endocarditis complicated by intracranial hemorrhage (ICH), a presentation that has not been previously reported.

CASE REPORT

A 47-year-old female presented with a 5-day history of low-grade fever, headache, and vomiting. Her medical history included diabetes mellitus, hypertension, and diabetic nephropathy. She denied weight loss, recent infections, or substance use. The patient denied any symptoms suggestive of systemic vasculitis, including rashes, oral ulcers, joint pains, or recent dental procedures or invasive dental treatments in the preceding months.

On examination, she was febrile (101°F), tachycardic, and tachypnoeic, with stable blood pressure and normal oxygen saturation on room air. There was no mucocutaneous lesions, purpura, or other stigmata of vasculitis. Neurological examination revealed mild right-sided hemiparesis (power 4/5) with an extensor plantar response. Cardiac auscultation identified a Grade 3 pansystolic murmur at the apex. Other systemic findings were unremarkable.

Laboratory evaluation showed hemoglobin of 12.7 g/dL, leukocytosis (14,500/µL) with neutrophil predominance, platelet count of 260 × 10⁹/L, and markedly elevated C-reactive protein (228 mg/L). Renal parameters revealed elevated creatinine (242 µmol/L). Urinalysis demonstrated albuminuria with mild pyuria and microscopic hematuria. Chest radiography, electrocardiography, and abdominal ultrasonography were normal.

Non-contrast computed tomography (CT) of the brain revealed a right basal ganglia hematoma measuring 20 mm × 17 mm × 12 mm with surrounding edema [Figure 1a]. On the second hospital day, the patient developed seizures and altered consciousness, necessitating intubation and mechanical ventilation. Magnetic resonance imaging (MRI) of the brain showed multiple acute embolic infarcts involving both supratentorial and infratentorial regions, including the basal ganglia, thalami, brainstem, and cerebellum, along with a subacute right basal ganglia hematoma [Figure 1b and c]. Magnetic resonance angiography did not demonstrate intracranial aneurysms. Magnetic resonance venography did not demonstrate evidence of cerebral venous sinus thrombosis.

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Figure 1: (a) Computed tomography of the head showing a right basal ganglia hematoma (red arrow). (b and c) Magnetic resonance imaging of the brain showing acute infarcts of varying sizes affecting both cerebral hemispheres, the corpus callosum, basal ganglia, thalami, brainstem, and cerebellar hemispheres, along with a subacute hematoma in the right basal ganglia (red arrow).

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Transthoracic echocardiography revealed a large (21 mm × 19 mm), mobile pedunculated mass attached to the anterior mitral leaflet with severe mitral regurgitation, consistent with infective vegetation [Figure 2]. Blood cultures grew pan-sensitive S. agalactiae. The patient was treated with intravenous ceftriaxone from admission.

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Figure 2: (a) The echocardiogram showing anterior mitral leaflet vegetation (red arrow) and (b) severe mitral regurgitation.

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Coagulation parameters, including prothrombin time/international normalized ratio and activated partial thromboplastin time, were within normal limits, during hospitalization. The patient was not receiving anticoagulant or antiplatelet therapy prior to admission. Blood pressure remained stable without hypertensive crisis.

Given the presence of a large vegetation and severe valvular dysfunction, surgical intervention was advised following multidisciplinary discussion. However, the family elected for conservative management focused on comfort. Blood cultures obtained 72 h after initiation of ceftriaxone remained positive for pan-sensitive S. agalactiae, after which subsequent follow-up cultures were sterile. The patient completed a 4-week course of intravenous ceftriaxone, without the addition of aminoglycosides due to underlying renal impairment. Despite optimal medical therapy, the patient died 40 days after admission.

DISCUSSION

IE caused by S. agalactiae is uncommon, but is associated with a particularly aggressive disease course, often involving rapid valvular destruction and a high incidence of systemic embolization.^[1] Historically, mortality rates have been high, although outcomes have improved in recent years with earlier recognition and increased utilization of surgical management.^[2]

Neurological complications are frequent in IE, occurring in approximately one-quarter to two-thirds of patients, and are associated with worse prognoses.^[3,4] Cerebral embolism is the most common neurological manifestation, but presentations may also include ICH, mycotic aneurysms, meningitis, abscesses, encephalopathy, and seizures.^[4]

ICH in IE arises from several mechanisms, including hemorrhagic transformation of ischemic infarcts, septic arteritis, and rupture of mycotic aneurysms.^[5] While ICH occurs in approximately 5% of patients with IE, confirmed ruptured mycotic aneurysms account for only a minority of cases.^[6]

A large single-center study of left-sided IE reported that 7% of patients developed ICH, with etiologies including ruptured mycotic aneurysms, hemorrhagic transformation, and cases of unclear origin.^[6] Notably, patients with ICH of undetermined cause had higher mortality rates.^[6] Stroke is a serious complication of IE that significantly worsens outcomes, and unlike typical strokes, thrombolysis is generally avoided, while early surgical evaluation is recommended when medical therapy may be insufficient.^[7] In our patient, vascular imaging excluded mycotic aneurysms, and the hemorrhage was not attributable to hemorrhagic transformation. Common alternative causes, including coagulopathy, thrombocytopenia, anticoagulant use, uncontrolled hypertension, and cerebral venous sinus thrombosis, were not identified. Although platelet function assays were not performed and uremia-related platelet dysfunction cannot be entirely excluded, there was no clinical or laboratory evidence of overt bleeding tendency. Accordingly, this case falls into the rare category of ICH of undetermined etiology in the setting of IE.

On admission, non-contrast CT brain revealed a right basal ganglia hematoma with surrounding edema. No ischemic infarcts were identified on the initial CT. On hospital day 2, after clinical deterioration with seizures and altered consciousness, MRI brain demonstrated multiple acute embolic infarcts in both supratentorial and infratentorial regions, in addition to the previously identified subacute basal ganglia hematoma. Imaging findings indicated that the basal ganglia hematoma preceded the multifocal embolic infarcts, and its location and characteristics were not consistent with hemorrhagic transformation, supporting a primary ICH, rather than secondary hemorrhage from ischemic stroke.

Comprehensive Indian data on S. agalactiae IE are extremely limited, with a single well-documented case report.^[8] Broader surveillance studies from South India indicate an increasing burden of invasive Group B Streptococcal infections among non-pregnant adults, particularly middle-aged and older individuals with diabetes and other comorbidities, with high susceptibility to beta-lactams.^[9] The previously reported Indian IE case involved a young adult male who responded to medical therapy and did not describe concomitant ICH or extensive embolic phenomena.^[8] Internationally, GBS endocarditis is characterized by large vegetations, frequent embolic complications, and the need for prolonged beta-lactam therapy, with surgery often required in severe cases.^[9]

Early identification of neurological complications with prompt, organism-directed antimicrobial therapy and careful risk stratification are essential to reduce further embolic events, while timely surgical intervention should be considered in patients with large vegetations, severe valvular dysfunction, or recurrent embolization. Despite advances in management, major neurological complications remain associated with significantly increased mortality, as highlighted in a recent systematic review and meta-analysis, underscoring the importance of rapid multidisciplinary evaluation and individualized treatment strategies.

We conducted a structured literature search (PubMed/MEDLINE, Scopus, and Google Scholar; 1980–2025) using predefined keywords related to Streptococcus agalactiae, infective endocarditis, intracranial hemorrhage, embolic stroke, and mycotic aneurysm. No comparable case describing this specific constellation of findings was identified. To the best of our knowledge, based on available literature, such a combination has not been previously reported in S. agalactiae native valve endocarditis.

CONCLUSION

S. agalactiae is a rare but highly virulent cause of IE, often complicated by extensive embolic phenomena and poor outcomes. This case is unique as it demonstrates native mitral valve S. agalactiae IE presenting with both ICH and multiple embolic infarcts. Vascular imaging excluded mycotic aneurysms, and the hemorrhage was not due to hemorrhagic transformation, placing this in the rare category of ICH with undetermined etiology. Such a combination has not been previously reported.