Endovascular
infections, including
endocarditis, are life-threatening infectious syndromes. Staphylococcus aureus is the most common world-wide cause of such syndromes with unacceptably high morbidity and mortality even with appropriate
antimicrobial agent treatments. The increase in
infections due to methicillin-resistant S. aureus (MRSA), the high rates of
vancomycin clinical treatment failures and growing problems of
linezolid and
daptomycin resistance have all further complicated the management of patients with such
infections, and led to high healthcare costs. In addition, it should be emphasized that most recent studies with
antibiotic treatment outcomes have been based in clinical settings, and thus might well be influenced by host factors varying from patient-to-patient. Therefore, a relevant animal model of endovascular
infection in which host factors are similar from animal-to-animal is more crucial to investigate microbial pathogenesis, as well as the efficacy of novel
antimicrobial agents.
Endocarditis in rat is a well-established experimental animal model that closely approximates human native valve
endocarditis. This model has been used to examine the role of particular staphylococcal
virulence factors and the efficacy of
antibiotic treatment regimens for staphylococcal
endocarditis. In this report, we describe the experimental
endocarditis model due to MRSA that could be used to investigate bacterial pathogenesis and response to
antibiotic treatment.