Machine Learning Study in Caries Markers in Oral Microbiota from Monozygotic Twin Children.

In recent years, the etiology of caries has evolved from a simplistic infectious perspective based on and/or activity, to a multifactorial disease involving a complex oral microbiota, the human genetic background and the environment. The aim of this work was to identify bacterial markers associated with early caries using massive 16S rDNA. To minimize the other factors, the composition of the oral microbiota of twins in which only one of them had caries was compared with their healthy sibling.

Epidemiology of the colonization and acquisition of methicillin-resistant staphylococci and vancomycin-resistant enterococci in dogs hospitalized in a clinic veterinary hospital in Spain.

Antibiotic resistance is one of the biggest threats to human and animal health. Methicillin-resistant Staphylococcus spp. (MRS) and vancomycin-resistant Enterococcus spp.

Microcins in : Peptide Antimicrobials in the Eco-Active Intestinal Chemosphere.

Microcins are low-molecular-weight, ribosomally produced, highly stable, bacterial-inhibitory molecules involved in competitive, and amensalistic interactions between in the intestine. These interactions take place in a highly complex chemical landscape, the intestinal eco-active chemosphere, composed of chemical substances that positively or negatively influence bacterial growth, including those originated from nutrient uptake, and those produced by the action of the human or animal host and the intestinal microbiome. The contribution of bacteria results from their effect on the host generated molecules, on food and digested food, and organic substances from microbial origin, including from bacterial degradation.

Recombination blurs phylogenetic groups routine assignment in Escherichia coli: setting the record straight.

The characterization of population structures plays a main role for understanding outbreaks and the dynamics of bacterial spreading. In Escherichia coli, the widely used combination of multiplex-PCR scheme together with goeBURST has some limitations. The purpose of this study is to show that the combination of different phylogenetic approaches based on concatenated sequences of MLST genes results in a more precise assignment of E.

Normal mutation rate variants arise in a Mutator (Mut S) Escherichia coli population.

The rate at which mutations are generated is central to the pace of evolution. Although this rate is remarkably similar amongst all cellular organisms, bacterial strains with mutation rates 100 fold greater than the modal rates of their species are commonly isolated from natural sources and emerge in experimental populations. Theoretical studies postulate and empirical studies teort the hypotheses that these "mutator" strains evolved in response to selection for elevated rates of generation of inherited variation that enable bacteria to adapt to novel and/or rapidly changing environments.

Polymorphic mutation frequencies of clinical and environmental Stenotrophomonas maltophilia populations.

Mutation frequencies were studied in 174 Stenotrophomonas maltophilia isolates from clinical and nonclinical environments by detecting spontaneous rifampin-resistant mutants in otherwise-susceptible populations. The distribution of mutation frequencies followed a pattern similar to that found for other bacterial species, with a modal value of 1 x 10(-8). Nevertheless, the proportion of isolates showing mutation frequencies below the modal value (hypomutators) was significantly higher for S.

The evolution of contact-dependent inhibition in non-growing populations of Escherichia coli.

In the course of liquid culture, serial passage experiments with Escherichia coli K-12 bearing a mutator gene deletion (DeltamutS) we observed the evolution of strains that appeared to kill or inhibit the growth of the bacteria from where they were derived, their ancestors. We demonstrate that this inhibition occurs after the cells stop growing and requires physical contact between the evolved and ancestral bacteria. Thereby, it is referred to as stationary phase contact-dependent inhibition (SCDI).

Mutation rate is reduced by increased dosage of mutL gene in Escherichia coli K-12.

A variable but substantial proportion of wild Escherichia coli isolates present consistently lower mutation frequencies than that found in the ensemble of strains. The genetic mechanisms responsible for the hypo-mutation phenotype are much less known than those involved in hyper-mutation. Changes in E.

Increased mutation frequencies in Escherichia coli isolates harboring extended-spectrum beta-lactamases.

Hypermutable (mutation frequency [f], > or = 4 x 10(-8)) Escherichia coli strains were more frequently found (43%) in a collection of 89 extended-spectrum beta-lactamase (ESBL)-producing isolates from different patients (77 pulsed-field gel electrophoresis clones, 12 ESBL types) than in non-ESBL E. coli (26%) strains (P = 0.03).

SOS-independent induction of dinB transcription by beta-lactam-mediated inhibition of cell wall synthesis in Escherichia coli.

Transcription of the dinB gene, encoding DNA polymerase IV, is induced by the inhibition of cell wall synthesis at different levels. Using the beta-lactam antibiotic ceftazidime, a PBP3 inhibitor, as a model, we have shown that this induction is independent of the LexA/RecA regulatory system. Induction of dinB transcription mediated by ceftazidime produces an increase in the reversion of a +1 Lac frameshift mutation.

Fosfomycin and rifampin disk diffusion tests for detection of Escherichia coli mutator strains.

A simple method, using commercial disks to detect Escherichia coli mutator strains, is proposed. The breakpoint for detecting strains with a mutation frequency >/=5 x 10(-7) was established at >/=70 and >/=20 colonies in the inhibition zone of fosfomycin and rifampin disks, respectively, after seeding 100 microl of an overnight culture. Strains with <30 and <10 colonies in fosfomycin and rifampin inhibition zones are presumptively non-mutators.

Polymorphic mutation frequencies in Escherichia coli: emergence of weak mutators in clinical isolates.

Polymorphisms in the rifampin resistance mutation frequency (f) were studied in 696 Escherichia coli strains from Spain, Sweden, and Denmark. Of the 696 strains, 23% were weakly hypermutable (4 x 10(-8) < or = f < 4 x 10(-7)), and 0.7% were strongly hypermutable (f > or = 4 x 10(-7)).

Haemophilus influenzae bla(ROB-1) mutations in hypermutagenic deltaampC Escherichia coli conferring resistance to cefotaxime and beta-lactamase inhibitors and increased susceptibility to cefaclor.

The clinical use of cefaclor has been shown to enrich Haemophilus influenzae populations harboring cefaclor-hydrolyzing ROB-1 beta-lactamase. Such a selective process may lead to the increased use of extended-spectrum cephalosporins or beta-lactams plus beta-lactamase inhibitors and, eventually, resistance to these agents, which has not previously been observed in H. influenzae.

Frequency of mutation to rifampin resistance in Streptococcus pneumoniae clinical strains: hexA and hexB polymorphisms do not account for hypermutation.

The frequency of mutation to rifampin resistance of 200 clinical Streptococcus pneumoniae isolates was examined. Two peaks were observed in the distribution, with mode frequencies of 2.5 x 10(-7) (20% of isolates) and 2.

The regulation of microcin B, C and J operons.

Microcins are ribosomally encoded small peptide antibiotics produced by Gram(-) enterobacteria. Microcin production-biosynthesis, maturation and secretion to the medium-is encoded by gene clusters organized in operons. Production of the best known plasmid-encoded microcins (MccB, MccC and MccJ) switches on when cells reach the stationary growth phase.

Very low cefotaxime concentrations select for hypermutable Streptococcus pneumoniae populations.

A mixed culture of an hypermutable hexA Streptococcus pneumoniae mutant strain and its hexA(+) isogenic ancestor was challenged with low cefotaxime concentrations. Despite identical original cefotaxime MICs, the hexA mutant population was significantly selected at very low concentrations, and all of the tested selected variants harbored the Thr550-->Ala mutation in pbp2x. Since cefotaxime selects hypermutators, the risk of secondary acquisition of antibiotic resistance is increased; as expected, the cefotaxime-resistant mutants had a mutation frequency 10 times higher in response to to ciprofloxacin.