Abstract Serratia marcescens is an opportunistic gram-negative bacteria rarely associated with infective endocarditis (IE) in people who inject drugs (PWID). Pulmonary involvement with cavitary lesions is more rare. We present a significant case of a patient with S. marcescens IE complicated by cavitary lung lesion and beta-lactamase resistance. 27-year-old female PWID developed generalized malaise, fatigue, abdominal pain, and dyspnea. D-dimer was elevated. Computed Tomography (CT) angiography chest revealed multifocal thick-walled cavitary lesions concerning for septic emboli without pulmonary embolism. Broad spectrum antibiotics were started. The patient was diagnosed with Hepatitis C; human immunodeficiency virus testing was negative. Initial blood cultures grew S. marcescens resistant to amoxicillin-clavulanate and cefazolin, but sensitive to ceftriaxone. Transesophageal echocardiogram demonstrated several right ventricle vegetations, with a 5.28cm vegetation on the tricuspid valve. Dyspnea and fevers persisted for a week. A repeat CT chest demonstrated increased cavitation and new bilateral pleural effusions with loculations. Bilateral chest tubes were placed and pleural fluid studies revealed exudative effusions with negative cultures. Given the breakthrough fevers and imaging findings, antibiotic treatment was broadened to meropenem from vancomycin and cefepime. After 3 days of successful treatment, antibiotics were de-escalated to ceftriaxone. Cardiothoracic Surgery performed bioprosthetic tricuspid valve replacement. Repeat blood cultures grew S. marcescens resistant to ceftriaxone, amoxicillin-clavulanate, and cefazolin after several weeks of negative blood cultures. Because of the new sensitivity profile, antibiotics were transitioned to ertapenem and she was discharged on 6 weeks of therapy. She presented to the hospital with cardiac arrest several days later and died before outpatient follow-up. S. marcescens is a gram-negative rod causing 1-2% of nosocomial infections with an estimated yearly incidence of 1.3 persons per 100,000. Pulmonary cavitary lesions typical result from septic emboli in IE, but S. marcescens is a rare source. Literature review shows multiple cases with cavitary lesions from Serratia in immunocompromised individuals or PWID. S. marcescens has inducible AmpC and can acquire extended-spectrum beta-lactamase resistance. Literature review and IDSA guidelines emphasize the low rate of expression of clinically significant AmpC, suggesting carbapenem-sparing regimens is reasonable. Breakthrough resistance during therapy, as in our patient, highlights the need for serial cultures when clinically appropriate. Given the aggressive course and high mortality associated with cavitary Serratia IE, early recognition, multidisciplinary management, and consideration of carbapenem coverage are warranted. Clinicians should include Serratia in the differential diagnosis of cavitary lung lesions in PWID with right-sided IE, even when more common pathogens are suspected. This abstract is funded by: None
Kong et al. (Fri,) studied this question.