This technique was then transferred to a rat model in 1978 by Santoro and Levision. Female Wistar rats, weighing 200 to 300 g were used. The animals were anesthetized by subcutaneous application of 5.75% ketamine and 0.2% xylazine. Nonbacterial thrombotic endocarditis was caused by insertion of a small plastic catheter via the right carotid artery. The artery was accessed by cu ing the neck laterally on the right side. The carotid artery could be easily exposed and ligated distally. The polyethylene catheter was introduced via a small incision of the vessel and advanced until a slight resistance indicated passage through the aortic valve. The catheter was advanced through the aortic valve into the left ventricle. Proper placement was ensured via invasive pressure measurement through the catheter��s lumen. To minimize confounding factors we focused on standardization of the catheter insertion and its positioning. Preliminary experiments without secondary bacterial colonization showed that pressure monitoring and therewith objectification of catheter positioning could minimize overly traumatic injury and ensured constant lesions. The catheter was secured in place and distally ligated. A simple running suture was used for wound Ginsenoside-Ro closure. Postoperatively the rats were returned to their cage and monitored closely. Inoculation of bacteria followed 48 h after catheter placement via injection into the tail vein. Ten rats per study group were randomly assigned to two groups, one receiving the wild-type strain 12030 wt, and the other being challenged with the deletion mutant 12030DbgsA. In a separate series groups were divided using 12030wt and 12030DbgsB respectively. Animals were sacrificed on postoperative day 6 and the correct placement of the catheter was verified. The extent of native valve endocarditis was assessed and graded macroscopically with an objective grading system as outlined in table 2. Subsequently valve vegetations were removed aseptically. After weighing of the vegetations, 500 mL TSB was added per sample and the vegetations were homogenized on ice using a tissue homogenizer. Enterococcal infections are an increasing clinical problem worldwide. While enterococci Albaspidin-AA certainly are not as virulent as other gram-positive cocci, they often exhibit broad-spectrum resistance to antimicrobials, are able to acquire antibiotic resistance traits via elaborate molecular mechanisms, and are able to resist harsh environmental conditions. Biofilm formation has been shown to play a crucial role, especially in endocarditic lesions and catheter-associated infections. A variety of biofilm-associated genes have been described in enterococci, encoding adhesins, autolysins, polysaccharides, glycolipids and other molecules, each of these causing virulence in specific se ings. The deletion mutant 12030DbgsA is characterized by a loss of the major bacterial glycolipid DGlcDAG and by an accumulation of its precursor, MGlcDAG. Mutant 12030DbgsB completely lacks glycolipids in its cell wall. In a rat model of infective endocarditis we could demonstrate that these two different enterococcal deletion mutants with their altered biofilm formation capabilities produced less endocarditic lesions when compared to the wild type.