654. Biofilm Forming Methicillin-Resistant Staphylococcus aureus Induces Renal Deterioration and Severe Virulence in a Mouse Bacteraemic Model

BACKGROUND: Methicillin-resistant S. aureus (MRSA), a responsible bacterium to nosocomial infection, induces biofilm (BF) infection. We previously indicated that individual MRSA manifests a various BF forming ability, and high BF formers infused in the blood can survive even after phagocytosis by Kupffer cells. In this study, we advance the research to examine the development of BF formation in tissues during 96 h after infusion. METHODS: Out of 172 clinical isolates of MRSA, highest BF former (H-BF) and lowest BF former (L-BF) were used. Bacteria were infused via tail vain. Mice were checked for general status and bacterial distribution in the organs (liver, lung, spleen and kidney) at histological and bacteriological levels. BF was also histologically detected by stains for polysaccharides. RESULTS: After MRSA infusion, general status in L-BF maintained in normal range during the study, H-BF however revealed poor status, which was aggravated in accordance with time. After infusion, bacteria started to reappear in the blood after 24 h of the study, and, on 96 hour, H-BF exhibited an eight times greater extent than L-BF. Bacterial colonies were formed in the kidney in both of the groups, and colonies in the liver were only noted in H-BF. In the kidney, CFU in both of the groups increased by time, and its number on 96 h was significant greater in H-BF than L-BF. In H-BF, bacterial embolism accompanied with BF was histologically found in medullary capillaries in the kidney on 24 hours. Growing BF aggressively penetrated into the stroma and tubular lumen forming a wedge-like renal necrosis. CONCLUSION: These results indicate that BF forming MRSA in the blood preferably settle and form BF in the kidney in mice, which leads to a biofilm infection and a severe deterioration. Although the mechanisms of kidney specific lesions formed by MRSA are still unclear, BF forming ability in MRSA might be crucially important for bacterial virulence in vivo. DISCLOSURES: All authors: No reported disclosures.