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653. To Treat or Not to Treat Corynebacterium striatum? That is the Question

Abstract Background As part of normal skin flora, Corynebacterium striatum (CS) can be isolated in clinical specimens and dismissed as a contaminant or colonizer. However, this organism is an emerging multi-drug-resistant opportunistic pathogen that causes serious infections and demonstrates worrisome resistance to antimicrobials. CS has been implicated in both osteomyelitis (OM) and septic arthritis (including prosthetic joint infections (PJI)), for which aggressive source control and antibiotics are needed. Because there is no accepted treatment standard when CS is found, we performed a retrospective analysis of patients with CS isolated from orthopedic sites. Methods We retrospectively analyzed cultures in which CS was isolated from 2015 to 2017. We restricted this analysis to patients with orthopedic cultures, bone and PJI. Charts were reviewed for clinical and microbiological data. Duration of follow-up was calculated to the last follow-up visit in our system for the patient after treatment of the infection. “Targeted” treatment was defined as treatment based on antimicrobial susceptibilities of the CS. Results We identified 20 cases of OM and 6 PJI with CS identified in culture. 17/26 (65%) were multi-drug resistant. CS was the only organism (monomicrobial) in 46% (12/26) of cultures (8/20 OM, 4/6 PJI). All monomicrobial OM and PJI received targeted treatment and were cured clinically at the last follow-up (average 201 days OM and 124 days PJI). Of 12 polymicrobial OM infections, all improved clinically by last follow-up; 75% (9/12) were treated with targeted treatment for CS and 25% (3/12) without targeted treatment. All polymicrobial PJI (2/2, 100%) improved without targeted treatment. Conclusion Our review suggests that CS can cause OM and PJI, with a high rate of drug resistance. Cure rates are excellent in monomicrobial infections when therapy is targeted to susceptibility. The role of targeted therapy for polymicrobial infections in which another more likely pathogen is found is not clear, particularly in the setting of effective surgical source control. Further prospective research is necessary to clarify the prevalence and factors associated with CS infections, and the importance of treatment of this organism in orthopedic infections. Disclosures All authors: No reported disclosures.

Background. As part of normal skin flora, Corynebacterium striatum (CS) can be isolated in clinical specimens and dismissed as a contaminant or colonizer. However, this organism is an emerging multi-drug-resistant opportunistic pathogen that causes serious infections and demonstrates worrisome resistance to antimicrobials. CS has been implicated in both osteomyelitis (OM) and septic arthritis (including prosthetic joint infections (PJI)), for which aggressive source control and antibiotics are needed. Because there is no accepted treatment standard when CS is found, we performed a retrospective analysis of patients with CS isolated from orthopedic sites.
Methods. We retrospectively analyzed cultures in which CS was isolated from 2015 to 2017. We restricted this analysis to patients with orthopedic cultures, bone and PJI. Charts were reviewed for clinical and microbiological data. Duration of follow-up was calculated to the last follow-up visit in our system for the patient after treatment of the infection. "Targeted" treatment was defined as treatment based on antimicrobial susceptibilities of the CS.
Conclusion. Our review suggests that CS can cause OM and PJI, with a high rate of drug resistance. Cure rates are excellent in monomicrobial infections when therapy is targeted to susceptibility. The role of targeted therapy for polymicrobial infections in which another more likely pathogen is found is not clear, particularly in the setting of effective surgical source control. Further prospective research is necessary to clarify the prevalence and factors associated with CS infections, and the importance of treatment of this organism in orthopedic infections.
Disclosures. All authors: No reported disclosures. 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.

Biofilm Forming Methicillin-Resistant
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.