Human Infective Endocarditis Caused by Streptococcus suis Serotype 2

An otherwise healthy 43-year-old male complained of malaise, fever, dyspnea, and upper back pain. He was treated with nonsteroidal drugs. Twelve days later, he was found to have severe orthopnea. Electrocardiography revealed sinus tachycardia and a complete left bundle branch block. Finally, due to acute respiratory insufficiency, the patient was admitted to the hospital of the Justus-Liebig University Giessen, Giessen, Germany, after emergency intubation. Transesophageal echocardiography revealed severe aortic regurgitation, huge aortic valve vegetations, and a ventricular septal defect located immediately left of the membranous septum. Blood cultures were taken, and intravenous antibiotic treatment with ceftazidime (two doses of 2 g each), rifampin (one dose of 600 mg), and vancomycin (two doses of 1 g each) was initiated (leukocytes/ l, 43,800; C-reactive protein, 189.7 mg/liter; body temperature, 38.5°C). The patient subsequently underwent emergency surgery consisting of aortic root debridement, aortic valve replacement with a 23-mm mechanical heart valve, and sealing of the ventricular septal defect by use of autologous pericardium. The perioperative and postoperative courses were uneventful. The patient was extubated 6 h after surgery, discharged home 10 days later, and prescribed a 6-week ambulatory intravenous antibiotic treatment. The 15-month follow-up was without complications: neither reinfectionnor valve-related events were noted, and clinical parameters were within normal ranges (leukocytes/ l, 8,300; C-reactive protein, 4 mg/liter; body temperature, 37°C). The patient resumed his job without restriction. Both the inoculated blood cultures and the aortic valve revealed a pure culture of viridans streptococci after 24 h of cultivation on sheep blood agar plates in an atmosphere of 5% CO2. At 48 h, the bacterial colonies showed a very small zone of beta-hemolysis (Fig. 1). A commercial system for the phenotypic identification of gram-positive bacteria, the BBL Crystal gram-positive ID kit (Becton-Dickinson, Heidelberg, Germany), revealed Streptococcus bovis, which is a non-betahemolytic bacterium. To achieve taxonomic certainty, we amplified the 16S rRNA gene of this isolate with primers 63F (5 -CAG GCC TAA CAC ATG CAA GTC-3 ) and 1220R (5 -TTG TAG CAC GTG TGT AGC CC-3 ), and the nucleic acid sequence of the amplicon was determined with the DNA sequencing system MegaBACE 1000 (Molecular Dynamics, GE Healthcare, Uppsala, Sweden) by using the same primers. Sequence comparisons (GenBank database, National Center for Biotechnology Information, Bethesda, Md.) revealed the strain to be the closely related species Streptococcus suis, which was further confirmed by suilysinand capsule-specific PCR (12, 20). Unfortunately, the BBL Crystal gram-positive ID kit did not identify S. suis, since this animal pathogen, apart from S. bovis, was not represented in its database, which is dominated by human pathogens (identification scheme manual; Becton-Dickinson). The MICs of the S. suis isolate for ceftazidime (0.25 g/ml), rifampin (0.016 g/ml), and vancomycin (0.75 g/ml) were determined by using a commercially available epsilometer test (Etest; AB Biodisk, Solna, Sweden) as recommended by the vendor. The rapid and destructive progression of the disease was obviously caused by a highly virulent strain of S. suis. A serotype-specific PCR indicated that the isolate was either an S. suis serotype 2 or an S. suis serotype 1/2 strain. This finding was achieved by detecting the capsular gene cps2J present in the capsular biosynthesis locus of S. suis serotypes 2 and 1/2 (20). To verify this data, serotyping of the S. suis isolate was also performed using a slide agglutination test method with rabbit antiserum, raised against the reference strains of S. suis (29). Agglutination identified the isolate clearly as belonging to serotype 2.