ACRT Journal

Introduction

Methicillin-resistant Staphylococcus aureus (MRSA) bacteremia is a severe bloodstream infection associated with high morbidity and mortality. It can lead to metastatic complications such as infective endocarditis, osteomyelitis, and sepsis, and is frequently associated with healthcare exposures, indwelling devices, and immunocompromised states [1].

In patients with cardiac implantable electronic devices (CIEDs), the risk of endocarditis or device-related infection is significantly increased. As a result, echocardiographic evaluation preferably transesophageal is recommended in all cases of S. aureus bacteremia [2]. However, the absence of vegetations or device involvement on imaging does not exclude metastatic foci, which can be clinically silent and poses diagnostic challenges, especially in elderly or neuropathic individuals [3].

Here, we present a case of persistent MRSA bacteremia in a patient with a pacemaker and no imaging evidence of device infection, ultimately diagnosed with vertebral spondylodiscitis and chronic osteomyelitis of the foot. This case underscores the diagnostic challenges of metastatic MRSA infection in the absence of apparent cardiac involvement. It highlights the role of advanced imaging and combination antimicrobial therapy in successful management.

Case Presentation

A 67-year-old male presented to the emergency room with fever, abdominal pain, diarrhea, and vomiting that had been ongoing for more than 72 hours. His medical history was notable for type 2 diabetes mellitus treated with insulin, complicated by diabetic retinopathy, peripheral neuropathy, and Charcot foot deformity. He also had a history of recurrent soft tissue abscesses and chronic osteomyelitis involving the right foot, which had previously required amputation of the first and third metatarsals. Other comorbidities included first-stage obesity, mixed dyslipidemia, stage 3 chronic kidney disease (KDOQI classification), and chronic heart failure with preserved ejection fraction (HFpEF), likely secondary to hypertensive cardiomyopathy. Additionally, he had a history of thrombosis of the right small saphenous vein, for which he had been on oral anticoagulation since February 2025, and a dual-chamber pacemaker was implanted the same month due to complete atrioventricular block.

At admission to our Geriatrics department, the patient was alert, oriented, and cooperative. He had no facial dysmorphisms, rash, or peripheral edema. Oxygen saturation was 95% on room air. Heart rate was regular at 76 bpm, and blood pressure was 100/50 mmHg. Auscultation of the lungs revealed diffusely decreased breath sounds. The abdomen was notably distended due to adiposity but remained soft, non-tender, with hypoactive bowel sounds. The right foot exhibited structural deformity consistent with known Charcot arthropathy and was warm to the touch, without erythema, overt signs of cellulitis, or visible ulceration.

Initial bloodwork revealed marked leukocytosis (WBC 13.93 × 10⁹/L), severe hyperglycemia (glucose 498 mg/dL), hyponatremia (Na⁺ 121 mmol/L), acute renal failure (serum creatinine 3.93mg/dl and eGFR 25 mL/min/1.73m²) and elevated inflammatory markers, including C-reactive protein (CRP) 26.63 mg/dL (n.v. <0.50mg/dL) and procalcitonin (PCT) 31.77 ng/ mL (n.v. 0.05 ng/mL). Blood cultures drawn on days 1, 2, 6, 7, 10, 12, and 15, and partially on day 19 yielded methicillin-resistant Staphylococcus aureus (MRSA), confirming sustained MRSA bacteremia.

Given the presence of an intracardiac device and persistent MRSA bacteremia, both transthoracic and transesophageal echocardiography (TTE and TEE) were promptly performed. These showed no evidence of valvular vegetations or leadassociated infection. Nevertheless, the ongoing positivity of blood cultures raised concern for disseminated opportunistic infections. A contrast-enhanced full-body CT scan revealed multiple bilateral pulmonary nodules consistent with septic emboli (Figure 1), as well as a chronic right subdural hematoma and a hyperdense focus in the right frontal region. Whole-body 18F-FDG PET/CT (Figures 2,3) demonstrated no abnormal uptake at the pacemaker pocket or along the leads, but revealed increased metabolic activity in the D11 vertebral body (SUV max 12.9), and in the right talus, tarsal bones, and surrounding soft tissues of the lateral malleolus (SUV 7.8) findings suggestive of vertebral osteomyelitis (spondylodiscitis) and chronic osteomyelitis, respectively. Additionally, a reversed liver-to-spleen metabolic gradient (spleen SUV 5.4) was observed, likely reflecting reactive inflammatory changes.

Figure 1: CT scan revealed multiple subcentimeter-sized pseudonodular formations in the expanded lung parenchyma, some of which are triangular, suspicious for septic emboli.

Figure 2: MRI of the thoracolumbar spine (T10-T11) showing vertebral signal abnormalities with T1 hypointensity, long-TR hyperintensity, and post-contrast enhancement involving the adjacent disc consistent with spondylodiscitis. A thin enhancing epidural collection (~3 mm thick, ~26 mm long) is seen in the anterior spinal canal, extending into the neural foramina. Bilateral paravertebral soft tissue enhancement, more evident on the left, shows a small fluid collection (~20 × 4 mm) suggestive of early abscess formation.

Figure 3: Coronal fused 18F-FDG PET/CT image showing intense hypermetabolic activity at the D11 vertebral body (SUV max 12.9), consistent with spondylodiscitis. Notably, the spleen shows increased uptake relative to the liver (inverted liverspleen gradient), suggestive of reactive/inflammatory splenic hypermetabolism.

The differential diagnosis initially prioritized infective endocarditis (IE), given the presence of a cardiac implantable electronic device (CIED) and sustained MRSA bacteremia. According to the modified Duke criteria [4], a definite diagnosis of IE requires either two major criteria, one major and three minor criteria, or five minor criteria. In our case, persistent bacteremia constituted one major criterion; however, there was no evidence of valvular vegetation or pacemaker lead involvement on imaging studies. Furthermore, PET/CT imaging revealed no abnormal metabolic uptake around the pacemaker generator or leads, making CIEDrelated endocarditis unlikely. Given the absence of a second major criterion and insufficient minor criteria, the diagnosis of IE was not supported. As a result, attention shifted toward alternative sources of infection. The primary diagnostic challenge laid in the discordance between persistent MRSA bacteremia and the absence of device-related infection, which delayed identification of the actual infectious burden.

Ultimately, advanced imaging studies including MRI of the thoracolumbar spine (Figure 4), plain radiography of the right foot, and whole-body 18F-FDG PET/CT revealed two likely sources contributing to the persistent bacteremia: spondylodiscitis at the D10–D11 levels with associated epidural and paravertebral abscesses, and chronic osteomyelitic changes in the right foot. The spinal infection was characterized by vertebral involvement with adjacent epidural enhancement and paravertebral soft tissue abscesses, consistent with hematogenous seeding. The right foot, previously affected by Charcot neuroarthropathy and prior partial amputation, showed progression of osteolysis involving the remaining tarsal structures.

Figure 4: Axial fused 18F-FDG PET/CT image at the thoracolumbar level showing increased FDG uptake at D11 vertebral body, consistent with spondylodiscitis. Inferiorly, partial visualization of the right ankle reveals focal hypermetabolic activity involving bone and soft tissue, suggestive of distal osteomyelitis.

At the time of presentation (day 1), the patient exhibited highgrade fever, gastrointestinal symptoms, and markedly elevated inflammatory markers (CRP >30 mg/dL, PCT >30 ng/mL), raising suspicion for sepsis of unknown origin. Given his diabetic status, chronic osteomyelitis, and renal impairment, empiric broadspectrum coverage was started with meropenem, adjusted for stage IV chronic kidney disease. This was intended to provide coverage for multidrug-resistant Gram-negative bacilli, anaerobes, and enteric pathogens, particularly given the abdominal complaints. At this stage, no Gram-positive coverage was included beyond meropenem’s limited spectrum. Blood cultures on days 1-2 resulted positive for MRSA (Table 1), prompting a switch from meropenem to teicoplanin on day 3 along with ceftriaxone, which was chosen for its MRSA coverage and safety in renal impairment. Despite dual therapy, blood cultures remained positive between days 6 and 15, with only partial improvement in CRP and PCT. Persistent bacteremia and concern for deep-seated infection prompted escalation on day 14 to linezolid, with discontinuation