Innocent Until Proven Guilty: Native Valve Staphylococcus lugdunensis Infective Endocarditis Complicated by Embolic Stroke in a Peritoneal Dialysis Patient: A Case Report

Abstract

Staphylococcus lugdunensis is a coagulase-negative staphylococcus (CoNS) with unique virulence traits that mimic Staphylococcus aureus, despite traditionally being grouped among less pathogenic skin flora. Unlike other CoNS, S. lugdunensis can infect native valves and cause aggressive infective endocarditis (IE). We present a rare and instructive case of S. lugdunensis native mitral valve endocarditis complicated by cerebral embolic infarctions and requiring surgical valve replacement in a patient on chronic peritoneal dialysis. This case underscores the diagnostic challenge of CoNS bacteremia, highlights the embolic potential of S. lugdunensis, and represents one of the few documented cases of stroke complicating S. lugdunensis IE in a dialysis-dependent patient without prosthetic devices.

1. Introduction

Coagulase-negative staphylococci (CoNS) are frequently considered contaminants in blood cultures, particularly in hospitalized or immunocompetent patients. However, Staphylococcus lugdunensis, first identified in 1988, is a notable exception due to its uniquely aggressive virulence profile.1 Unlike Staphylococcus epidermidis, a CoNS species typically associated with indolent prosthetic-device infections, S. lugdunensis behaves more like Staphylococcus aureus, with the capacity to infect native valves and cause rapidly destructive infective endocarditis (IE).1,2

Although uncommon overall, S. lugdunensis shows a marked predilection for native-valve involvement—particularly the mitral valve—and carries a higher rate of surgical intervention and mortality compared with other CoNS species.2,3 Embolic complications, particularly stroke, are rare but clinically significant; a 2018 review documented only 18 reported cases worldwide.2 Herein, we present a case of S. lugdunensis native mitral valve endocarditis in a peritoneal dialysis (PD) patient complicated by multifocal embolic strokes, representing a diagnostically challenging and extremely rare clinical presentation.

2. Case presentation

A 76-year-old woman with a history of hypertension, heart failure with preserved ejection fraction (HFpEF), end-stage renal disease (ESRD) on PD, insulin-dependent diabetes mellitus, atrial fibrillation, and peripheral arterial disease presented with one week of altered mental status. Her family reported progressive somnolence, inattentiveness, and subtle behavioral changes. She denied fever, chest pain, abdominal pain, or recent trauma.

On arrival, her temperature was 37.0 °C, heart rate 88 bpm, respiratory rate 20/min, blood pressure 120/71 mmHg, and oxygen saturation 98% on room air. She was alert and oriented but exhibited slowed responses and impaired attention. Physical examination revealed no focal neurological deficits. The abdominal exam was benign, and the PD catheter exit site was clean, without erythema, tenderness, swelling, or drainage.

Laboratory evaluation revealed hemoglobin 8.8 g/dL (11–14.5 g/dL), white blood cell counts 11,000/μL (4000–10,800/μL), and normal platelets. Sodium was 131 mmol/L (136–145 mmol/L), potassium 3.1 mmol/L (3.4–4.5 mmol/L), BUN 45 mg/dL (9–23 mg/dL), and creatinine 7.3 mg/dL (0.5–0.8 mg/dL). Random glucose was 405 mg/dL, and anion gap was 10 (5–15). High-sensitivity troponin was 2838 ng/L (0–31 ng/L). Venous pH was 7.58 (7.35–7.45) with pCO₂ 30.9 mmHg (35–45 mmHg). CRP was 67 mg/L (0–5 mg/L). SARS-CoV-2 PCR was positive. Urinalysis showed 182 white blood cell count (0–5) and positive leukocyte esterase and nitrite.

Chest X-Ray showed no consolidation. Non-contrast CT of the head demonstrated a right superior cerebellar infarct. Given the patient altered mentation in addition toESRD status, being diabetic, and having indwelling PD catheter, a septic workup was commenced to identify a potential source, including urine and blood cultures. She was empirically started on intravenous ceftriaxone for presumed urinary tract infection. Heparin infusion for presumed Non-ST-Elevation Myocardial Infarction (NSTEMI) was started after consulting neurology who thought the stroke was subacute and discussing the risk and benefits with the family. Cardiology subsequently determined the troponin elevation to represent type II myocardial injury, and heparin was discontinued.

MRI of the brain revealed multiple acute-to-subacute infarcts in bilateral frontoparietal, occipital, periventricular, cortical, subcortical, and cerebellar territories, the largest measuring 1.8 cm in the right cerebellum, consistent with embolic stroke (Fig. 1). Contrast-enhanced MRI demonstrated diffuse pachymeningeal enhancement with nodular foci concerning for septic emboli (Fig. 2).

Fig. 1.

Brain MRI without IV contrast showing right cerebellar infarct measuring 1.8 cm.

Fig. 2.

Brain MRI with IV contrast showing with small diffuse nodular intra axial enhancement suspicious for septic emboli.

Blood cultures grew gram-positive cocci in clusters in 2 sets, and antibiotic therapy was escalated to vancomycin. Initial speciation identified CoNS. Transthoracic echocardiogram (TTE) revealed dense posterior mitral leaflet calcification with a 4 × 9 mm mobile echodensity. Although the PD exit site appeared normal, peritoneal fluid contained 283 WBC/μLwith 76% polymorphonuclear leukocytes (PMNs), corresponding to an absolute PMN count of 215 cells/μL (Spontaneous bacterial peritonitis (SBP) is diagnosed when ascitic fluid analysis demonstrates a PMN count ≥250 cells/mm³), raising suspicion for PD catheter–associated infection. CT abdomen demonstrated splenic infarcts without abscess formation. The PD catheter was removed as part of source control, and the tip was sent for culture, and the patient was transitioned to hemodialysis.

Transesophageal echocardiography (TEE), performed once isolation precautions were lifted, confirmed a 1.6 × 0.3 cm hypermobile vegetation on the posterior mitral leaflet (Fig. 3). Final culture identification confirmed S. lugdunensis (Table 1), and antibiotic therapy was narrowed to cefazolin. Despite appropriate antimicrobial therapy, she developed progressive mitral regurgitation and ultimately underwent surgical mitral valve replacement, with favorable postoperative recovery.

Fig. 3.

TEE showing a 1.6 × 0.3 cm long irregular hypermobile echo density on the posterior mitral valve leaflet consistent with vegetation.

Table 1.

Staphylococcus lugdunensis blood culture sensitivity.

	Staphylococcus lugdunensis
Drug	MIC Interp	MIC Dilutn
Clindamycin	S	< = 0.5
Doxycycline	S	< = 0.5
Gentamicin	S	< = 2
Oxacillin	S	< = 0.25
Penicillin	R	1
Rifampin	S	< = 0.5
Vancomycin	S	1

3. Discussion

S. lugdunensis is an emerging, relatively uncommon member of the CoNS family. Although considered part of normal skin flora, particularly in the perineal and inguinal regions, it displays a virulence profile more closely resembling S. aureus than other CoNS species.3,4 This pathogenicity enables it to cause rapidly progressive and destructive infections, including skin and soft tissue infections, osteoarticular infections, and, most notably, IE.3,4

Our patient presented with a subacute neurocognitive decline and multifocal embolic strokes, ultimately found to be secondary to S. lugdunensis native mitral valve endocarditis. Central nervous system involvement from S. lugdunensis is rare, but septic emboli to the brain and meningitic involvement have been documented in the context of IE.2 S. lugdunensis IE has been increasingly recognized as a clinically significant cause of native-valve endocarditis, with a disproportionate predilection for the mitral valve.2,5 While accounting for less than 1% of all IE cases, S. lugdunensis represents approximately 5% of CoNS-associated IE and is associated with higher morbidity and mortality than other CoNS species.5,6 S. lugdunensisIE can be aggressive, with complications such as systemic embolization, abscess formation, and valve perforation occurring frequently. In a multicenter series, up to 70% of cases involved native valves, and aggressive surgical intervention was frequently required due to rapid valvular destruction.6 Mortality has been reported as high as 38.8%.7

Accurate identification of S. lugdunensis is essential but often delayed. Because the organism produces bound coagulase (clumping factor), up to 65% of isolates may initially be misidentified as S. aureus using older methods, and when correctly identified as a CoNS, it may be mischaracterized as a contaminant, delaying diagnosis and treatment.8,9 In our case,2 sets of blood cultures were growing CoNS which impelled us to look beyond mere contamination.

An additional notable feature of this case is the suspected PD catheter source. While S. lugdunensis peritonitis occurs in PD patients, hematogenous seeding resulting in native-valve IE appears exceedingly rare; we did not identify a peer-reviewed case directly linking S. lugdunensis PD-peritonitis to subsequent native-valve IE. Nevertheless, S. lugdunensis PD-peritonitis is well documented.2,10,11 In this patient, peritoneal fluid leukocytosis (283 WBC/μL) suggested underlying peritonitis despite peritoneal fluid and PD catheter tip cultures being negative. The absence of an alternative infectious source and the temporal association with bacteremia strongly supported PD-related seeding. Catheter removal was therefore essential for source control.

S. lugdunensis is generally susceptible to β-lactam antibiotics, and methicillin resistance mediated by mecA remains uncommon, reflecting its distinct evolutionary behavior compared with other pathogenic CoNS.8 Despite favorable pharmacologic susceptibility, medical therapy alone may be insufficient due to biofilm formation and a propensity for tissue invasion, particularly in the setting of indwelling devices such as PD catheters.8 This patient developed progression of mitral regurgitation despite targeted therapy and ultimately required valve replacement—consistent with published clinical outcome trends.5,7

This case reinforces several critical diagnostic considerations. S. lugdunensis recovered from multiple blood cultures should be treated as a true pathogen, not a contaminant. Species-level identification is essential, and early echocardiography is warranted to evaluate for IE in cases of persistent bacteremia. Current IE guidelines emphasize early surgical consultation for aggressive or complicated disease, especially when structural deterioration or embolic complications occur.12

It is imperative to understand that despite being a CoNS, S. lugdunensis behaves very differently and is clinically as relevant as other pathogenic species. Given its exceptional traits and aggressive nature, imaging including TEE, and careful clinical surveillance are warranted even after initiation of appropriate antimicrobials to look for development of periannular extension, abscess formation, and extracardiac spread of infection.6

4. Conclusion

S. lugdunensis is an aggressive CoNS capable of causing rapidly progressive native-valve IE with systemic embolization, even in the absence of prosthetic material. S. lugdunensis should not be underestimated when isolated from blood cultures, particularly when present in multiple sets. This case highlights the importance of species-level identification in dialysis patients and the need for early recognition of embolic complications even in the absence of focal deficits. Prompt echocardiographic assessment, targeted antimicrobial therapy, and timely surgical intervention are crucial to preventing irreversible complications. This report adds to the limited literature describing S. lugdunensis native-valve endocarditis complicated by stroke in a patient receiving PD.