Talks
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Resident
Academic Level (Author 1)
Resident
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Internal Medicine
Academic Level (Author 2)
Resident
Discipline/Specialty (Author 2)
Internal Medicine
Academic Level (Author 3)
Resident
Discipline/Specialty (Author 3)
Internal Medicine
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Resident
Discipline/Specialty (Author 4)
Internal Medicine
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Medical Student
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Oral Presentation
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Clinical Science
Abstract Type
Case Report
Abstract
Background: Infective endocarditis (IE) results from bacterial adhesion to endocardial tissue and valvular apparatus. While viridans group streptococci and Enterococcus species are associated with subacute disease, Staphylococcus aureus, including methicillin-resistant strains (MRSA), is a leading cause of more acutely destructive presentations. The entry of these pathogens can occur through surgical and dental procedures, intravenous drug use, or less apparent etiology. Classic peripheral stigmata (Osler nodes, Janeway lesions, splinter hemorrhages, Roth spots) are now uncommon but clinically meaningful. Current guidelines emphasize rapid multimodality imaging to detect cerebral and systemic emboli in symptomatic IE. We present a 50-year-old man with S. aureus IE, acute ischemic stroke, and striking peripheral stigmata.
Case Presentation: A 50-year-old man with a history of hypertension, obesity, chronic low back pain, and gout presented to the emergency department with new-onset right leg weakness, fever episodes over the past week, chills, and painful, violaceous nodular lesions on some fingers, as well as, nontender erythematous macules on palms. He had recently received an epidural glucocorticoid injection in Mexico to treat his low back pain. A CT scan of the head revealed an acute ischemic stroke in the left anterior cerebral artery territory, leading to an echocardiogram, which showed a 9mm mitral valve vegetation suspicious for infective endocarditis. Blood cultures confirmed Staphylococcus aureus (MRSA) bacteremia. Initial intravenous vancomycin therapy failed to clear the bacteremia, and subsequent chest and abdomen CT scans revealed a splenic infarct consistent with septic embolization. Antimicrobial treatment was escalated to daptomycin and ceftaroline, resulting in microbiological clearance within 24 hours. Pain was managed with opioids; he started physical therapy and remained hemodynamically stable upon discharge. He required prolonged IV antibiotic coverage as recommended by the Infectious Disease specialist.
Conclusions: Classic peripheral stigmata are now infrequently encountered in infective endocarditis, yet their presence remains clinically meaningful. When Osler nodes and Janeway lesions coexist, they often reflect larger vegetations and a heightened embolic burden, including cerebral involvement. This is particularly relevant in Staphylococcus aureus endocarditis, a pathogen strongly associated with neurological complications and systemic embolization. In such settings, bedside findings should act as an early severity signal, prompting immediate neurovascular and whole-body imaging to identify overt and silent embolic events. Stroke complicates a substantial proportion of IE cases and frequently occurs alongside extracerebral emboli, reinforcing the need for a systematic approach. Contemporary guidance discourages intravenous thrombolysis in IE-related ischemic stroke while supporting consideration of mechanical thrombectomy when feasible. This case underscores that careful physical examination, paired with guideline-driven imaging and early multidisciplinary involvement, can meaningfully influence diagnostic pathways and management decisions. Even in the era of advanced imaging, classic stigmata remain powerful clinical clues that can shape outcomes in high-risk S. aureus endocarditis.
Recommended Citation
Loayza Pintado, Jose J.; Aboytes Trevino, Jorge; Galindo, Julian; Aqeel, Mohammad; Cauba, John; Nwose, Joshua; and Suarez Parraga, Andres, "From Skin to Spleen to Brain: Full-Spectrum Embolic Complications in Staphylococcus aureus Endocarditis" (2026). Research Symposium. 8.
https://scholarworks.utrgv.edu/somrs/2026/talks/8
Included in
From Skin to Spleen to Brain: Full-Spectrum Embolic Complications in Staphylococcus aureus Endocarditis
Background: Infective endocarditis (IE) results from bacterial adhesion to endocardial tissue and valvular apparatus. While viridans group streptococci and Enterococcus species are associated with subacute disease, Staphylococcus aureus, including methicillin-resistant strains (MRSA), is a leading cause of more acutely destructive presentations. The entry of these pathogens can occur through surgical and dental procedures, intravenous drug use, or less apparent etiology. Classic peripheral stigmata (Osler nodes, Janeway lesions, splinter hemorrhages, Roth spots) are now uncommon but clinically meaningful. Current guidelines emphasize rapid multimodality imaging to detect cerebral and systemic emboli in symptomatic IE. We present a 50-year-old man with S. aureus IE, acute ischemic stroke, and striking peripheral stigmata.
Case Presentation: A 50-year-old man with a history of hypertension, obesity, chronic low back pain, and gout presented to the emergency department with new-onset right leg weakness, fever episodes over the past week, chills, and painful, violaceous nodular lesions on some fingers, as well as, nontender erythematous macules on palms. He had recently received an epidural glucocorticoid injection in Mexico to treat his low back pain. A CT scan of the head revealed an acute ischemic stroke in the left anterior cerebral artery territory, leading to an echocardiogram, which showed a 9mm mitral valve vegetation suspicious for infective endocarditis. Blood cultures confirmed Staphylococcus aureus (MRSA) bacteremia. Initial intravenous vancomycin therapy failed to clear the bacteremia, and subsequent chest and abdomen CT scans revealed a splenic infarct consistent with septic embolization. Antimicrobial treatment was escalated to daptomycin and ceftaroline, resulting in microbiological clearance within 24 hours. Pain was managed with opioids; he started physical therapy and remained hemodynamically stable upon discharge. He required prolonged IV antibiotic coverage as recommended by the Infectious Disease specialist.
Conclusions: Classic peripheral stigmata are now infrequently encountered in infective endocarditis, yet their presence remains clinically meaningful. When Osler nodes and Janeway lesions coexist, they often reflect larger vegetations and a heightened embolic burden, including cerebral involvement. This is particularly relevant in Staphylococcus aureus endocarditis, a pathogen strongly associated with neurological complications and systemic embolization. In such settings, bedside findings should act as an early severity signal, prompting immediate neurovascular and whole-body imaging to identify overt and silent embolic events. Stroke complicates a substantial proportion of IE cases and frequently occurs alongside extracerebral emboli, reinforcing the need for a systematic approach. Contemporary guidance discourages intravenous thrombolysis in IE-related ischemic stroke while supporting consideration of mechanical thrombectomy when feasible. This case underscores that careful physical examination, paired with guideline-driven imaging and early multidisciplinary involvement, can meaningfully influence diagnostic pathways and management decisions. Even in the era of advanced imaging, classic stigmata remain powerful clinical clues that can shape outcomes in high-risk S. aureus endocarditis.
