Staphylococcus aureus is an opportunistic pathogen and the major causative agent of numerous hospital- and community-acquired infections. Multilocus sequence typing reveals a highly clonal structure for S. aureus. Although infrequently occurring across clonal complexes, homologous recombination still contributed to the evolution of this species over the long term. agr-mediated bacterial interference has divided S. aureus into four groups, which are independent of clonality and provide another view on S. aureus evolution. Genome sequencing of nine S. aureus strains has helped identify a number of virulence factors, but the key determinants for infection are still unknown. Comparison of commensal and pathogenic strains shows no difference in diversity or clonal assignments. Thus, phage dynamics and global transcriptome shifts are considered to be responsible for the pathogenicity. Community-acquired methicillin-resistant S. aureus (C-MRSA) is characterized by a short SCCmec and the presence of a Panton-Valentine leukocidin locus, but no studies have proven their exact biologic roles in C-MRSA infection, indicating the existence of other mechanisms for the genesis of C-MRSA.

For critical patients with A. baumannii complex infection, ventilator-associated pneumonia in particular, the selective pressure from prior use of broad-spectrum antibiotics for 5 days or more increased risk of subsequent imipenem-resistant A. baumannii complex bacteremia. To reduce mortality, rapid identification of imipenem-resistant A. baumannii complex and early initiation of appropriate antimicrobial therapy in these high-risk patients are crucial.

Cancer is a genetic disease caused by somatic mutations; however, the understanding of the causative biological processes generating these mutations is limited. A cancer genome bears the cumulative effects of mutational processes during tumor development. Deciphering mutational signatures in cancer is a new topic in cancer research. The Wellcome Trust Sanger Institute (WTSI) has categorized 30 reference signatures in the COSMIC database based on the analyses of ∼10 000 sequencing datasets from TCGA and ICGC. Large cohorts and bioinformatics skills are required to perform the same analysis as WTSI. The quantification of known signatures in custom cohorts is not possible under the current framework of the COSMIC database, which motivates us to construct a database for mutational signatures in cancers and make such analyses more accessible to general researchers. mSignatureDB (http://tardis.cgu.edu.tw/msignaturedb) integrates R packages and in-house scripts to determine the contributions of the published signatures in 15 780 individual tumors from 73 TCGA/ICGC cancer projects, making comparison of signature patterns within and between projects become possible. mSignatureDB also allows users to perform signature analysis on their own datasets, quantifying contributions of signatures at sample resolution, which is a unique feature of mSignatureDB not available in other related databases.

In recent years a significant increase in the incidence of Serratia marcescens infections was noted at the Chang Gung Memorial Hospital, Taoyuan

Background: Acute diarrhea is a major cause of childhood morbidity and an economic burden for families. The aim of this study is to explore the effect of probiotics on clinical symptoms, intestinal microbiota, and inflammatory markers during childhood diarrhea. Methods: Children (n = 81) aged six months to six years (mean age 2.31 years) hospitalized for acute diarrhea were randomized to receive probiotics (Lactobacillus casei variety rhamnosus; n = 42) or no probiotics (n = 39) orally twice daily for seven days. Feces samples were also collected to evaluate microbial content using a traditional agar plate and next-generation sequencing. Immunoglobulin A (IgA), lactoferrin, and calprotectin were determined by enzyme-linked immunosorbent assay (ELISA) and compared in different groups. Other clinical symptoms or signs, including fever, vomiting, diarrhea, abdominal pain, bloated abdomen, daily intake, appetite, and body weight were also assessed. Results: Data were collected from 81 individuals across three different time points. Total fecal IgA levels in fecal extracts of the probiotics group were higher than those in the control group, reaching statistical significance (p < 0.05). Concentrations of fecal lactoferrin and calprotectin were significantly downregulated in patients with probiotic Lactobacillus casei variety rhamnosus (Lc) consumption compared to those of the control (p < 0.05). Probiotic Lc administration may be beneficial for gut-microbiota modulation, as shown by the data collected at one week after enrollment. Counts of Bifidobacteria and Lactobacillus species were elevated in stool culture of the probiotic group. Appetite and oral intake, body-weight gain, abdominal pain, bloating, as well as bowel habits (diarrhea) were much better in children receiving probiotics compared with those in the control group. Conclusion: Fecal IgA increased during acute diarrhea under Lc treatment; in contrast, fecal lactoferrin and calprotectin were downregulated during acute diarrhea under Lc treatment. Probiotic Lc may be a useful supplement for application in children during acute diarrhea to reduce clinical severity and intestinal inflammatory reaction.

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Introduction Mycobacterium marinum causes skin and soft tissue, bone and joint, and rare disseminated infections. In this study, we aimed to investigate the relationship between treatment outcome and antimicrobial susceptibility patterns. A total of 27 patients with M. marinum infections were enrolled. Methods Data on clinical characteristics and therapeutic methods were collected and analyzed. We also determined the minimum inhibitory concentrations of 7 antibiotics against 30 isolates from these patients. Results Twenty-seven patients received antimycobacterial agents with or without surgical debridement. Eighteen patients were cured, 8 failed to respond to treatment, and one was lost to follow-up. The duration of clarithromycin (147 vs. 28; p = 0.0297), and rifampicin (201 vs. 91; p = 0.0266) treatment in the cured patients was longer than that in the others. Surgical debridement was performed in 10 out of the 18 cured patients, and in 1 of another group ( p = 0.0417). All the 30 isolates were susceptible to clarithromycin, amikacin, and linezolid; 29 (96.7%) were susceptible to ethambutol; 28 (93.3%) were susceptible to sulfamethoxazole; and 26 (86.7%) were susceptible to rifampicin. However, only 1 (3.3%) isolate was susceptible to doxycycline. Discussion Early diagnosis of the infection and appropriate antimicrobial therapy with surgical debridement are the mainstays of successful treatment. Clarithromycin and rifampin are supposed to be more effective agents.

Streptococcus pneumoniae infection is a leading cause of morbidity and mortality worldwide. One of the most severe complications of invasive pneumococcal disease (IPD) is haemolytic uraemic syndrome (HUS). This study was undertaken to determine the risk factors and role of pneumococcal neuraminidases in HUS in children with IPD. Eighteen cases of HUS and 54 patients with IPD without HUS were identified. The controls were patients with culture-confirmed IPD without HUS. Clinical and laboratory characteristics of the two groups of patients were compared. Bacterial isolates from both groups were serotyped, sequence typed and examined for their carriage of three neuraminidase genes. Necrotizing pneumonia and serotype 3 infection were significantly associated with HUS in children with IPD, suggesting that a severe pulmonary suppurating disease increase the risk of HUS. Serotype 14 was associated with necrotizing pneumonia but not HUS. Children with HUS were more likely to require surgery and had a longer duration of hospitalization. The study identified a significantly higher carriage of a neuraminidase gene, nanC, in the causative pneumococcal isolates from patients with HUS (89% versus 41%, p 0.001). The sensitivity and specificity of nanC to predict HUS were 89% and 59%, respectively. In conclusion, necrotizing pneumonia, serotype 3 infection and neuraminidase gene nanC were associated with HUS in children with IPD. The result suggests that NanC could provide an additive effect to NanA and NanB in the overall activity of pneumococcal neuraminidases to expose Thomsen-Friedenreich antigen on various cells in patients with HUS.