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Abstract: Background: Staphylococcus aureus (S aureus) is the major cause of skin and soft tissue infections (SSTIs). Increased methicillin-resistant strains have attracted a global concern. The aim of this study is to evaluate the prevalence of methicillin-resistant S aureus (MRSA) SSTIs in dermatologic settings and evaluate their susceptibility results. Methods: A retrospective chart analysis of patients diagnosed with SSTIs in the Department of Dermatology, Buddhist Tzu Chi General Hospital in Hualien, Taiwan from November 2003 to July 2007 was conducted. Wound or pus bacterial culture results from a wound site were collected. The epidemiology, microbiology, and antibiotic susceptibility were assessed. Minocycline treatment experience in 15 MRSA SSTIs inpatients was presented. Results: Of the 443 SSTI episodes included, 59.6% were males and 40.4% were females. S aureus was the leading cause (53.3%), and among them 53.0% were MRSA. Minocycline (94.4%), trimethoprim/sulfamethoxazole (95.2%), levofloxacin (95.7%), and fusidic acid (98.9%) were the major susceptible antimicrobial agents to MRSA. Only 14.4% was susceptible to clindamycin. In the MRSA infected inpatients, 75.6% were community-associated. In our clinical experience, 15 inpatients with poor clinical response to beta-lactam empirical antimicrobial therapy received minocycline as combination therapy based on the susceptibility results, all of which obtained satisfied clinical remission. Conclusions: S aureus is still the leading causative bacterial organism for SSTIs in the dermatologic settings in eastern Taiwan. Methicillin-resistant strains are increasing and among which most are community-associated in eastern Taiwan. MRSA strains are still susceptible to other non-beta lactam antibiotics, such as minocycline, trimethoprim/sulfamethoxazole, levofloxacin, and fusidic acid in dermatological settings, of which minocycline is an alternative choice in our clinical experience. [Copyright &y& Elsevier]

This study investigated the protective effects of the administration of steroids on optic nerves (ON) and retinal ganglion cells (RGCs) in a rodent model of non-arteritic anterior ischemic optic neuropathy (rAION). We induced rAION using rose bengal and argon laser irradiation in a photodynamic procedure on the optic discs of rats. The treated groups received methylprednisolone (MP) via peritoneal injection for 2 weeks. The control group received intraperitoneal injections of phosphate-buffered saline (PBS) post-rAION. At the 4th week post-infarct, MP treatments significantly rescued the RGCs (mm 2 ) in the central retinas (1920 ± 210, p < 0.001) and mid-peripheral retinas (950 ± 240, respectively, p = 0.018) compared with those of the PBS-treated rats (central: 900 ± 210 and mid-peripheral: 440 ± 180). Functional assessment with flash visual-evoked potentials demonstrated that P1 latency (ms) was shortened in the MP group compared to the PBS group (108 ± 14 and 147 ± 9, respectively, p < 0.001). In addition, the P1 amplitude (uV) was enhanced in the MP group compared to the PBS group (55 ± 12 and 41 ± 13, respectively, p < 0.05). TUNEL assays showed a decrease in the number of apoptotic cells in the RGC layers of MP-treated retinas compared to the PBS-treated group (p < 0.05). ED1 positive cells (/HPF) were significantly decreased in the ONs of the MP group compared to the PBS group (p < 0.001). In conclusion, systemic administration of MP had neuroprotective effects on RGC survival and ON function in the rAION animal model. [ABSTRACT FROM AUTHOR]