Subacute bacterial endocarditis (SBE) is an infection of the heart involving damaged valves or endothelium. The most common organisms causing SBE are the viridans streptococci. Viridans streptococci differ in their propensity to cause SBE, which is related to the ability to adhere to damaged heart valves and endothelium, which is a function of extracellular matrix production. Streptococcus intermedius is a member of the S. anginosus group. S. intermedius is one of the many strains of viridans streptococci and a rare cause of SBE. SBE may result following a high-grade, sustained veridans streptococcal bacteremia in patients with predisposing cardiac lesions. Because viridans streptococci are relatively avirulent pathogens in normal hosts, they usually present as SBE. Some strains of viridans streptococci are inherently more virulent (eg, S. intermedius) and clinically resemble S. lugdunensis or S. aureus. We report a case of S. intermedius SBE in a patient with mitral valve prolapse (MVP). Throughout the patient's life, she received antibiotic prophylaxis for dental procedures and never developed SBE. Because of changes in endocarditis prophylaxis guidelines in 2007, recommending no prophylaxis for dental procedures in patients with MVP, she did not receive prophylaxis for a dental procedure 3 months before admission. The change in prophylaxis recommendations was based on the relatively low incidence of endocarditis with certain cardiac lesions. The recommendations were also based on concern for antibiotic resistance from widespread antibiotic use for antibiotic prophylaxis. There has been no appreciable increase in penicillin resistance, and antimicrobial resistance is not an important consideration among the viridans streptococci. The incidence of SBE is not high after dental procedures in patients with MVP, but if SBE occurs, it may result in serious consequence for the patient. In this case, the patient developed S. intermedius, mitral valve SBE complicated by a cerebral vascular accident, and embolic occlusion of her leg. She was given optimal antibiotic treatment with ceftriaxone 2 g (intravenously) every 24 hours plus gentamicin 120 mg (intravenously) every 24 hours (synergy dose) but failed to respond to antimicrobial therapy. Although her S. intermedius bacteremia was rapidly cleared with antimicrobial therapy, sterilization of her vegetation was not accomplished, and during therapy, the size of her cardiac vegetation actually increased in size. Because of therapeutic failure despite optimal antibiotic therapy, the increasing size of her vegetation necessitated mitral valve replacement, which the patient underwent. Reasons for apparent/real antibiotic failure include inappropriate antimicrobial therapy, inadequately dosed antimicrobial therapy, antibiotic "tolerance," or increased pathogen virulence. Her strain of S. intermedius was sensitive to all antibiotics and not due to a "tolerant strain", i.e., her minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) were the same (<0.25 microg/mL). In this case, despite optimal antimicrobial therapy, and in the absence of resistance/tolerance, therapeutic failure was best explained on the basis of S. intermedius virulence. The take-home lesson for clinicians is that it is better to err on the side of antibiotic prophylaxis even in patients with low-risk cardiac lesions. Failure to administer antibiotic prophylaxis for dental procedures may result in SBE and have disastrous consequences for the patient, which, in this case, resulted in a cerebral vascular accident, embolic occlusion of the leg, and mitral valve replacement. In terms of virulence in patients with endocarditis, S. intermedius may resemble S. lugdenesis.
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