Thymidine Auxotrophic Staphylococcus aureus Small-Colony Variant Endocarditis and Left Ventricular Assist Device Infection

Abstract

We describe a thymidine-dependent small-colony variant of Staphylococcus aureus associated with left ventricular assist device infection and prosthetic valve and pacemaker endocarditis. CASE REPORTT he patient was a 34-year-old woman who 3 years prior had suffered an anterior wall myocardial infarction resulting in ischemic cardiomyopathy, which necessitated placement of a pacemaker biventricular defibrillator. Subsequently, there was progressive deterioration of cardiac function. A left ventricular assist device (LVAD) was placed as a bridge to heart transplantation. During the same surgery, her native tricuspid valve was replaced with a pericardial tissue valve on account of tricuspid regurgitation. One month after surgery, she developed fever and chills, and blood cultures grew methicillin-resistant Staphylococcus aureus (MRSA) which was susceptible to gentamicin, rifampin, linezolid, trimethoprim-sulfamethoxazole (TMP-SMX), and vancomycin (MIC, 2 g/ml) and resistant to erythromycin and levofloxacin. Trans-esophageal echocardiography (TEE) showed no evidence of endocarditis. She was treated with 6 weeks of vancomycin and rifampin, with gentamicin administered during the first 2 weeks of therapy. Five days after completing antimicrobial therapy, she developed recurrent fevers, and blood cultures again grew MRSA which was susceptible to gentamicin, linezolid, TMP-SMX, vancomycin (MIC, 1 g/ml), and daptomycin and resistant to rifampin, erythromycin, and levofloxacin. A TEE demonstrated vegetations on the pacemaker leads and the prosthetic tricuspid valve. She was treated with daptomycin, gentamicin, and (until the isolate was known to be resistant to rifampin) rifampin. A follow-up TEE after 2 months of antimicrobial therapy showed reduction in the size of the vegetations. She received 5 months of daptomycin and gentamicin; TEE at the end of therapy showed old and healed vegetations. However, over the ensuing year, she had recurrent MRSA bacteremia and soft tissue infection surrounding her LVAD generator site. As a result, from December 2008 through March 2010, she received continuous antimicrobial therapy with various combinations of vancomycin, rifampin, daptomycin, gentamicin, quinupristin-dalfopristin, and TMP-SMX (Fig. 1). During this time, only one isolate (of several) was identifiable, and susceptibility testing was reportable using the BD Phoenix automated microbiology system (BD Diagnostic Systems, Franklin Lakes, NJ). That isolate, recovered from an umbilical driveline aspirate, was reported as susceptible to gentamicin, linezolid, TMP-SMX, and vancomycin (MIC, 2 g/ml), resistant to rifampin, erythromycin, and levofloxacin, and nonsusceptible to daptomycin (MIC, 4 g/ml). Because of inadequate growth in the test medium, other isolates, including bloodstream isolates and another umbilical driveline aspirate, were not identifiable, and susceptibility testing was not reportable using the BD Phoenix automated microbiology system.Despite ongoing combination antimicrobial therapy and incision and drainage of ...

The novel speciesStreptococcus tigurinusand its association with oral infection

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Clinical Significance and Pathogenesis of Staphylococcal Small Colony Variants in Persistent Infections

“…Maduka-Ezeh et al described the case of a 34-year-old woman who received a left ventricular assist device (LVAD) as a bridge until transplantation after an anterior wall myocardial infarction (38). Her tricuspid valve was replaced at the same time.…”

Evolution of Staphylococcus aureus under Vancomycin Selective Pressure: the Role of the Small-Colony Variant Phenotype

“…Although SCVs have been isolated from persistent infections and subsequently analyzed, the population dynamics of S. aureus have yet to be characterized in severe infections, such as endocarditis (17)(18)(19). In lieu of in vivo data revealing the interplay between S. aureus phenotypes during antibiotic treatment, our observations suggest that vancomycin will preferentially select for the amplification of SCV subpopulations.…”