BACKGROUND: Infective endocarditis (IE) in intravenous drug users has been increasing in incidence. The major pathogen used to be methicillin-susceptible Staphylococcus aureus, but resistant isolates have also been increasing. This study aimed to investigate the clinical characteristics of IE in intravenous drug users and to evaluate the molecular patterns of methicillin-resistant S. aureus (MRSA) that cause IE in these drug users. METHODS: A total of 37 episodes of IE in intravenous drug users hospitalized from 1980 to 2006 at a 1,250-bed teaching hospital in Southern Taiwan were evaluated retrospectively. The genetic relatedness of S. aureus strains was assessed using pulsed-field gel electrophoresis. Polymerase chain reaction was used to detect Panton-Valentine leukocidin (PVL) and staphylococcal gamma-hemolysin (Hlg), and to determine the staphylococcal chromosomal cassette carrying the mecA methicillin-resistant gene (SCCmec) type. RESULTS: The patients had a mean +/- standard deviation age of 31.5 +/- 9.25 years, with a male predominance of 76%. Hepatitis C was present in all patients. Methicillin-susceptible S. aureus accounted for 76% of infections, and the most common clinical symptoms were fever (97%) and embolic phenomenon (68%). There were 4 MRSA isolates, 3 of which were SCCmec type III. PVL and Hlg genes were found in 2 and 3 MRSA isolates, respectively. Eighty percent similarity was found among the MRSA isolates by pulsed-field gel electrophoresis. CONCLUSION: Our results suggest that coinfection with hepatitis C was common in intravenous drug users with IE, and that molecular patterns of MRSA isolates had high similarity. SCCmec type III, which is usually hospital-acquired, could have caused the community-associated MRSA endocarditis in our patients.
BACKGROUND:Infective endocarditis (IE) in intravenous drug users has been increasing in incidence. The major pathogen used to be methicillin-susceptible Staphylococcus aureus, but resistant isolates have also been increasing. This study aimed to investigate the clinical characteristics of IE in intravenous drug users and to evaluate the molecular patterns of methicillin-resistant S. aureus (MRSA) that cause IE in these drug users. METHODS: A total of 37 episodes of IE in intravenous drug users hospitalized from 1980 to 2006 at a 1,250-bed teaching hospital in Southern Taiwan were evaluated retrospectively. The genetic relatedness of S. aureus strains was assessed using pulsed-field gel electrophoresis. Polymerase chain reaction was used to detect Panton-Valentine leukocidin (PVL) and staphylococcal gamma-hemolysin (Hlg), and to determine the staphylococcal chromosomal cassette carrying the mecA methicillin-resistant gene (SCCmec) type. RESULTS: The patients had a mean +/- standard deviation age of 31.5 +/- 9.25 years, with a male predominance of 76%. Hepatitis C was present in all patients. Methicillin-susceptible S. aureus accounted for 76% of infections, and the most common clinical symptoms were fever (97%) and embolic phenomenon (68%). There were 4 MRSA isolates, 3 of which were SCCmec type III. PVL and Hlg genes were found in 2 and 3 MRSA isolates, respectively. Eighty percent similarity was found among the MRSA isolates by pulsed-field gel electrophoresis. CONCLUSION: Our results suggest that coinfection with hepatitis C was common in intravenous drug users with IE, and that molecular patterns of MRSA isolates had high similarity. SCCmec type III, which is usually hospital-acquired, could have caused the community-associated MRSA endocarditis in our patients.