Virulence-associated genes in bacteria are often located on chromosomal regions, termed pathogenicity islands (PAIs). Several PAIs are found in Escherichia coli strains that cause extraintestinal infections, but their role in commensal bowel colonization is unknown. Resident strains are enriched in adhesins (P fimbriae and type 1 fimbriae), capsular antigens (K1 and K5), hemolysin, and aerobactin and mostly belong to phylogenetic group B2. Here, we investigated whether six pathogenicity islands and the virulence determinants malX and usp are associated with fitness of E. coli in the infant bowel microbiota. E. coli strains isolated from stools of 130 Swedish infants during the first year of life were examined for their carriage of PAI markers, malX, and usp by PCR. Carriage was related to strain persistence: long-term colonizers (>12 months) carried significantly more of PAI II from strain CFT703 (II CFT703 ), IV 536, and II J96 and malX and usp than intermediate colonizers (1 to 11 months) and transient strains (<3 weeks). The accumulation of PAI markers in each individual strain correlated positively with its time of persistence in the colon. Phylogenetic group B2 accounted for 69% of long-term colonizers, 46% of intermediate colonizers and 14% of transient strains. These results support the hypothesis that some bacterial traits contributing to extraintestinal infections have in fact evolved primarily because they increase the fitness of E. coli in its natural niche, the colon; accordingly, they may be regarded as fitness islands in the gut.Escherichia coli is a normal inhabitant of the large intestine, but certain strains also cause extraintestinal infections when they spread from their primary niche. Such pathogenic E. coli strains express several virulence-associated traits that contribute to the disease process, including adhesins, certain O serotypes and capsular antigens, iron-trapping compounds (such as aerobactin), and cytolytic toxins (such as hemolysin) (17).Pathogenicity-associated islands (PAIs) are particular regions on the bacterial chromosome where virulence genes have accumulated. PAIs, and their associated virulence genes, have spread among bacterial populations by horizontal transfer (15). Several PAIs were previously identified in uropathogenic E. coli strains such as E. coli 536 , E. coli J96, and E. coli CFT073. PAIs I to IV from strain 536 (I 536 to IV 536 ) encode a range of virulence factors, including P fimbriae, P-related fimbriae, ␣-hemolysin, S fimbriae, and the yersiniabactin siderophore system. PAI I J96 and II J96 encode P fimbriae, P-related fimbriae, and ␣-hemolysin; PAI I CFT073 and II CFT073 encode P fimbriae, ␣-hemolysin, and aerobactin (42) ( Table 1). usp is prevalent among strains causing urinary tract infections (24). It enhances infectivity in a mouse ascending urinary tract infection (UTI) model (48), displays homology with S-type pyocin, and may function as a bacteriocin (34). malX codes for a phosphotransferase system enzyme II that recognizes maltose and glucose (37...

Objective To investigate the clinical performance, safety, and patient-reported outcomes of an active osseointegrated steady-state implant system that uses piezoelectric technology. Study Design A prospective, multicenter, open-label, single-arm, within-subject clinical investigation. Setting Three tertiary referral clinical centers located in Melbourne, Sydney, and Hong Kong. Patients Twenty-nine adult subjects, 24 with mixed hearing loss or conductive hearing loss and 5 with single-sided sensorineural deafness. Intervention Implantation with the Cochlear Osia 2 System. Main Outcome Measures Audiological threshold evaluation and speech recognition in quiet and in noise. Patient satisfaction and safety. Results At 6-month follow-up after surgery, a mean improvement in pure-tone average of 26.0 dB hearing level and a mean improvement of 8.8 dB signal-to-noise ratio in speech reception threshold in noise was achieved with the investigational device as compared with the unaided situation. Usability of the investigational device was rated 71.4/100 mm for sound processor retention and 81.4/100 mm for overall comfort using a visual analog scale. Conclusion These outcomes confirm the clinical safety, performance, and benefit of an innovative active transcutaneous bone conduction implant using a piezoelectric transducer design in subjects with conductive hearing loss, mixed hearing loss, or single-sided sensorineural deafness.

Escherichia coli strains of phylogenetic group B2 obtained from Western human hosts are enriched in virulence-associated genes and have a superior capacity to persist in the colonic microbiota. Here, E . coli strains from 22 infants born in Pakistan whose rectal flora was sampled regularly over the first 6 months of life were examined. B2 strains did not carry the virulence-associated genes sfaD/E, papC, neuB or hlyA more often than strains of other phylogenetic groups. B2 origin was not associated with persistence in the bowel microbiota. As compared with B2 strains from Swedish infants, Pakistani B2 strains carried significantly less often the virulence genes fimH (p 0.04), papC (p 0.02), papG class III (p 0.01), sfaD/E (p < or =0.0001), neuB (p < or =0.0001), and hlyA (p 0.005), and also the high-pathogenicity island (p < or =0.0001). A minority of Pakistani B2 strains belonged to recognized uropathogenic O-groups, which are common among 'Western' B2 strains. Thus, extra-intestinal pathogenicity may be the foremost characteristic of B2 strains colonizing Western populations.

Escherichia coli segregates into phylogenetic groups, with group B2 containing both extraintestinal pathogenic E. coli (ExPEC) and enteropathogenic E. coli (EPEC) strains. Ten main B2 subgroups (subgroups I to X)/sequence type complexes (STcs), as well as EPEC lineages, have been identified. In the current study, we characterized ExPEC and EPEC strains of E. coli B2 phylogenetic subgroups/STcs that colonize Swedish and Pakistani infants. Gut commensal E. coli B2 strains, 120 from Swedish infants (n = 87) and 19 from Pakistani infants (n = 12), were assigned to B2 subgroups. Carriage of the bundle-forming pili and intimin adhesin was examined in the EPEC lineages. The ExPEC virulence markers and the time of persistence of the strains in the microbiota were previously determined. In total, 84% of the Swedish strains and 47% of the Pakistani strains belonged to 1 of the 10 main B2 subgroups (P = 0.001). Among the Swedish strains, the most common B2 subgroups were IX/STc95 (19%), II/STc73 (17%), VI/STc12 (13%), and III/STc127 (11%), with each subgroup carrying distinctive sets of ExPEC virulence markers. EPEC lineages with few ExPEC features constituted 47% of the Pakistani B2 strains but only 7% of the Swedish B2 strains (P = 0.0001). The subgroup distribution within phylogenetic group B2 strains colonizing the gut differed between Swedish and Pakistani infants. B2 subgroups with uropathogenic characteristics dominated the gut microbiota of Swedish infants, while EPEC lineage 1 strains frequently colonized the intestines of Pakistani infants. Moreover, within the B2 subgroups, ExPEC virulence genes were more prevalent in Swedish strains than in Pakistani strains. Thus, ExPEC traits exemplify the intestinal B2 strains from Western populations. IMPORTANCE The intestinal microbiota is an important reservoir for bacteria that cause extraintestinal infections. Escherichia coli is found ubiquitously in the gut microbiota, and it also causes urinary tract infections, infantile septicemia, and meningitis. Urinary tract infections are usually caused by E. coli strains that originate in the intestinal microbiota. E. coli also causes gastrointestinal infections and is a major cause of diarrhea in infants worldwide. The abilities of certain E. coli strains to cause infections are attributed to their virulence factors, i.e., bacterial components that contribute to the development of different diseases. Our study shows that different subtypes of potentially pathogenic E. coli strains dominate in the gut microbiota of infants in different geographical areas and expands our knowledge of the interplay between bacterial commensalism and pathogenicity.

The hypothesis that probiotics improves pouch-related dysfunction was not confirmed. Faecal biomarkers could play a future role in the management of pouch patients.

Staphylococcus aureus colonizes the anterior nares, and also the gut, particularly in infants. S. aureus is divided into lineages, termed clonal complexes (CCs), which comprise closely related sequence types (STs). While CC30 and CC45 predominate among nasal commensals, their prevalence among gut-colonizing S. aureus is unknown. Here, 67 gut commensal S. aureus strains from 49 healthy Swedish infants (aged 3 days to 12 months) were subjected to multi-locus sequence typing. The STs of these strains were related to their virulence gene profiles, time of persistence in the microbiota, and fecal population counts. Three STs predominated: ST45 (22% of the strains); ST15 (21%); and ST30 (18%). In a logistic regression, ST45 strains showed higher fecal population counts than the others, independent of virulence gene carriage. The lower fecal counts of ST15 were linked to the carriage of fib genes (encoding fibrinogen-binding proteins), while those of ST30 were linked to fib and sea (enterotoxin A) carriage. While only 11% of the ST15 and ST30 strains were acquired after 2 months of age, this was true of 53% of the ST45 strains (p = 0.008), indicating that the former may be less fit for establishment in a more mature microbiota. None of the ST45 strains was transient (persisting < 3 weeks), and persistent ST45 strains colonized for significantly longer periods than persistent strains of other STs (mean, 34 vs 22 weeks, p = 0.04). Our results suggest that ST45 strains are well-adapted for commensal gut colonization in infants, reflecting yet-unidentified traits of these strains.