The prevalence of toxigenic Clostridium difficile in Korea has been reported to be approximately 60–80 %. Although the prevalence of the tcdA−tcdB+ C. difficile strain was less then 5 % prior to the year 2000, it has become an emerging nosocomial pathogen in Korea. Therefore, we have attempted to determine the multicentre nationwide prevalence of tcdA+tcdB+ and tcdA−tcdB+ C. difficile for epidemiological purposes. C. difficile strains (n=724, 30 from 2000, 80 from 2001, 74 from 2002, 76 from 2003, 179 from 2004, 285 from 2005) were obtained retrospectively from January 2000 to December 2005 from in-patients at 6 hospitals, all of whom were suspected of having C. difficile-associated disease (CDAD), colitis or pseudomembranous colitis. The numbers of participating hospitals varied yearly (1 in 2000, 2 in 2001–2003, 3 in 2004, 5 in 2005). The hospitals were located in Seoul (n=4), Kyunggi Province (n=1) and Busan (n=1), Korea. PCR assays for tcdA and tcdB genes were conducted using 724 unduplicated C. difficile isolates. The mean prevalence of tcdA+tcdB+ and tcdA−tcdB+ C. difficile strains over the 6 years was 51.8 % (38.4–59.3 %) and 25.8 %(10–56.0 %), respectively. The mean prevalence of tcdA−tcdB+ C. difficile strains was less than 7 % until 2002, but began to increase in 2003 (13.2 %) and achieved a peak in 2004 (50.3 %). In 2005, the mean prevalence of tcdA+tcdB+ and tcdA−tcdB+ C. difficile strains was 47.7 % (30.9–60.3 %) and 27.0 % (17.6–54.8 %), respectively. This nationwide epidemiological study showed that tcdA−tcdB+ C. difficile strains have already spread extensively throughout Korea, and our results provide basic data regarding the controversies currently surrounding the toxigenicity of tcdA−tcdB+ C. difficile. The use of enzyme immunoassays capable of detecting both TcdA and TcdB is strongly recommended for the diagnosis of CDAD in microbiology laboratories, in order to control the spread of the tcdA−tcdB+ strains of C. difficile.

Panax ginseng (P. ginseng), one of the most valuable medicinal plants, is known for its healing and immunobooster properties and has been widely used in folk medicine against cardiovascular diseases, including stroke and heart attack. In this study, we explored the anti-platelet activity of gintonin (a recently discovered non-saponin fraction of ginseng) against agonist-induced platelet activation. In vitro effects of gintonin on agonist-induced human and rat platelet aggregation, granule secretion, integrin αβ activation, and intracellular calcium ion ([Ca]) mobilization were examined. Western blot analysis and immunoprecipitation techniques were used to estimate the expression of mitogen-activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and interaction of glycoprotein VI (GPVI) signaling pathway molecules such as Src family kinases (SFK), tyrosine kinase Syk, and PLCγ2. In vivo effects were studied using acute pulmonary thromboembolism model in mice. Gintonin remarkably inhibited collagen-induced platelet aggregation and suppressed granule secretion, [Ca] mobilization, and fibrinogen binding to integrin αβ in a dose-dependent manner and clot retraction. Gintonin attenuated the activation of MAPK molecules and PI3K/Akt pathway. It also inhibited SFK, Syk, and PLCγ2 activation and protected mice from thrombosis. Gintonin inhibited agonist-induced platelet activation and thrombus formation through impairment in GPVI signaling molecules, including activation of SFK, Syk, PLCγ2, MAPK, and PI3K/Akt; suggesting its therapeutic potential against platelet related CVD.

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Leuconostoc infections are rare and usually occur in immunocompromised patients. This report describes a case of Leuconostoc lactis bacteremia in a patient with coexisting rheumatoid arthritis and tuberculosis arthritis. A disrupted gastrointestinal barrier due to gastrointestinal amyloidosis in long-standing rheumatoid arthritis and tuberculosis arthritis could be a risk factor for Leuconostoc bacteremia. Despite aggressive antibiotic treatment, the patient progressed to septic shock and multi-organ failure. The fatal course might have been caused by rapid progression of gastrointestinal pathology, which could be a risk factor for Leuconostoc bacteremia.

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