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Pseudomonas aeruginosa is not a common enteric pathogen. The association between human histo-blood group antigens (HBGAs) and P. aeruginosa enteric infection has not yet been studied.We collected stool samples from healthy children under 2 years of age for P. aeruginosa gut colonization rate. Saliva samples were collected from patients with P. aeruginosa-associated diarrheal diseases and normal healthy children. Genomic DNA was extracted from saliva samples for ABO blood group typing and FUT2 genotyping. Lewis phenotype was detected using ELISA assay.A total of 85 patients with P. aeruginosa-associated diarrheal diseases and 105 healthy children were enrolled for collecting saliva specimens. The stool colonization rate was 5/101 (5%) in healthy children, 4/58 (6.9%) in infants, and 1/43 (2.3%) in children 1-2 years old, respectively. Blood group A was more frequent in patients with P. aeruginosa-associated diarrheal diseases 24/77 (31.2%) than in healthy children 18/102 (17.6%) (P = 0.035). All patients and healthy children were secretor positive. The distribution of weak-secretor genotype SeInfants had a higher gut P. aeruginosa colonization rate than children. Children with blood group A and Le

The genogroups GI and GII of norovirus (NoV) ribonucleic acid (RNA) genetic variants are the most prevalent cause of acute gastroenteritis outbreaks, especially in children, worldwide. A fast, accurate and convenient tool for diagnosis of NoV may be preferable to the more complicated performance of real-time reverse transcription-polymerase chain reaction (RT-PCR).In this study, we developed and evaluated a tool using insulated isothermal PCR (iiPCR)-mediated POCKIT Central NoV GI and NoV GII assay systems for diagnosis of NoV infection in pediatric patients suspected with gastroenteritis.Performance of POCKIT Central Norovirus GI and GII assays using RT-iiPCR, compared to regular real-time RT-PCR showed the same diagnosis rate to NoV GI (100% of total percent agreement and 1.0 of Cohen's kappa value) and a similar detection rate to norovirus GII (96.3% of total percent agreement and 0.92 of Cohen's kappa value). In exclusivity tests, the POCKIT Central NoV GI and GII assays showed negative results to other viruses, indicating that the assays may be a NoV-specific detection tool.POCKIT Central NoV GI and GII Assay systems can provide a simple, rapid, sensitive, and specific point-of-need diagnostic tool for the detection of NoV GI and GII RNAs in clinical specimens from children with acute gastroenteritis.

FliA is known to be a sigma factor that regulates bacterial flagella gene expression. Accumulating evidence suggests that FliA is involved in bacterial behavior other than motility. To elucidate the contribution of FliA to Pseudomonas aeruginosa pathophysiology, we analyzed the biological properties and gene expression profiles of a ΔfliA mutant. Transcriptome analysis results demonstrated that the expression levels of flagella biogenesis genes decreased dramatically in the mutant; consequently, the Δ fliA mutant failed to synthesize flagella and exhibited reduced motility. The ΔfliA mutant displayed stronger hemolytic and caseinolytic activities, as well as pyocyanin production. The expression of type 6 secretion system-II genes and interbacterial competition activity was decreased in the ΔfliA mutant. Direct evidence of fliA participation in virulence was obtained from analysis of hypervirulent strain B136-33. Adhesion to and cytotoxicity toward mammalian cells and penetration through cell layers were noted; furthermore, the colonization ability of the fliA::Tn5 mutant in the intestines of laboratory mice was compromised. Notably, the fliA-overexpressing strain displayed phenotypes similar to that of the fliA -defective strain, indicating that optimal FliA levels are critical to bacterial physiology . Our findings indicate that FliA plays diverse roles in P. aeruginosa , not only in flagella biosynthesis, but also in pathophysiology.

Objectives Mycoplasma pneumoniae is currently the most commonly detected bacterial cause of childhood community-acquired pneumonia in several countries. Of note, clonal expansion of macrolide-resistant ST3 occurred in Japan and South Korea. An alarming surge in macrolide resistance complicates the treatment of pneumonia. We aimed to evaluate the clinical manifestation and clonal relatedness of M. pneumoniae circulating among children in Taiwan. Methods We prospectively enrolled 626 children with radiologically confirmed pneumonia between 2017 and 2019. An M. pneumoniae infection was suspected on clinical grounds, and tested by real-time PCR and oropharyngeal swab cultures. We used multilocus sequence typing and whole-genome sequencing to characterize the genetic features of M. pneumoniae. Results A total of 226 children with M. pneumoniae pneumonia were enrolled. Macrolide resistance was found in 77% (174/226) of patients. Multi-locus sequence typing revealed that ST3 (n = 93) and its single-locus variant ST17 (n = 84) were the predominant clones among macrolide-resistant strains. ST17 presented clinical characteristics comparable to its ancestor ST3. On multivariate analysis, macrolide resistance (OR 3.5; 95% CI 1.4–8.5; p 0.007) was independently associated with fever >72 hours after macrolide treatment. By whole-genome sequencing, prediction analysis of recombination sites revealed one recombination site in ST3 and ST17 compared with M29 (a macrolide-sensitive ST3 strain isolated from China in 2005) containing cytadhesin MgpC-like protein, RepMP4 and RepMP5. ST17 had another recombination site containing an adhesin and RepMP2/3. Conclusions In addition to macrolide resistance, ST3 and its ST17 variant might evolve through recombination between repetitive sequences and non-P1 cytadhesins for persistent circulation in Taiwan.

Carbapenem resistance in Acinetobacter baumannii is a global problem. The purpose of this study was to elucidate current resistance mechanisms of imipenem-resistant A. baumannii (IRAB) in Taiwan and their correlation with patient outcomes. Acinetobacter baumannii clinical isolates from two teaching hospitals in Taiwan were collected in 2009 and were examined by Etest for determination of the minimum inhibitory concentrations (MICs) of imipenem, ceftazidime and ceftriaxone. Primers specific for carbapenemase genes and upstream regions were designed for PCR amplification. Bacterial isolates were genotyped by pulsed-field gel electrophoresis (PFGE). Clinical presentations of patients were analysed retrospectively. Upstream insertion sequence ISAba1 was found in 34 isolates that carried bla(OXA-23), including 28 with transposon Tn2006 (ISAba1-bla(OXA-23)-ISAba1) in an AbaR4-type resistance island and 6 with Tn2008 (ISAba1-bla(OXA-23)), as well as in 8 isolates carrying ISAba1-bla(OXA-51-like). All of these isolates expressed full resistance to imipenem (MIC>32 mg/L). Forty-one different PFGE genotypes were found among 62 isolates. Tn2006 was found in 19 genotypes (46.3%), which is more common than ISAba1-bla(OXA-51-like) (12.2%) (P=0.001). Prior use of carbapenems or extended-spectrum cephalosporins for ≥5 days was the only independent risk factor significantly associated with IRAB infection (odds ratio=361.175). Higher mortality was significantly associated with infection caused by IRAB and ISAba1-bla(OXA-23)-carrying strains compared with infection caused by imipenem-susceptible A. baumannii and ISAba1-bla(OXA-51-like)-carrying strains (P=0.009 and 0.027, respectively). Tn2006 is currently the most common imipenem resistance determinant, which showed a higher ability to spread among A. baumannii and was associated with a higher mortality in IRAB-infected patients.

The optimal age for administration of recently approved prophylactic human papillomavirus (HPV) vaccines remains undetermined.The aim of the study was to explore the age-specific seroprevalence of HPV 16 and 18 in the general population to design an HPV vaccination campaign for Taiwan.HPV seroprevalence was assessed by virus-like particle (VLP)-based ELISA in 1702 plasma samples collected in 1999.The sample population consisted of 1000 (58.8%) females and 702 (41.2%) males; age ranged from 17 days to 86 years. The age-specific distributions reveal a significant rise in HPV 16 seropositivity commencing at 19-25 years of age and peaking at60 years. The trend of seropositivity increase with age was also highly significant for HPV 18 (P(Trend)0.0001). Males had lower overall seroprevalence in gender comparison (7.6% versus 3.85% for HPV 16, 3.9% versus 2.71% for HPV 18), were older at seroconversion (19-25 years versus 26-30 years) with a more obvious seropositivity nadir in middle age.The age-specific seroprevalence of HPV 16 and 18 increases in young adults after the age of 18 years, with gender distribution varying. We conclude that the optimal age for universal HPV vaccination in Taiwan is 15 years or below.

1Division of Pediatric Gastroenterology, Department of Pediatrics, Chang Gung Children’s Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan 2Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Taoyuan, Taiwan 3St Paul’s Hospital, Taoyuan, Taiwan 4Division of Pediatric Infectious Diseases, Department of Pediatrics, Chang Gung Children’s Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan