sesA, sesB, sesC, sesD, sesE, sesG, sesH, and embp genes are genetic markers that differentiate commensal isolates of Staphylococcus epidermidis from isolates that cause prosthetic joint infection.

OBJECTIVES: Staphylococcus epidermidis can cause prosthetic joint infections. Strategies to differentiate between healthy skin and prosthetic joint infections isolates are relatively ineffective, which makes necessary to search for new differential biomarkers. Staphylococcus epidermidis has eleven surface proteins, denoted as Ses proteins. In this work, ses genes are used as biomarkers to differentiate between prosthetic joint infections and healthy skin isolates. METHODS: All prosthetic joint infections (n = 51) and healthy skin (n = 51) isolates were genotyped by pulsed-field gel electrophoresis. icaA, embp, sesA-I, and sdrF genes were determined by PCR. The phenotypic data included biofilm production and antibiotic resistance. RESULTS: 10 pulsed-field gel electrophoresis profiles were identified: four profiles were exclusive of prosthetic joint infections isolates, three profiles presented a higher proportion in prosthetic joint infections isolates and three profiles presented a higher proportion in healthy skin isolates. sesA, sesB, sesC, sesD, sesE, sesG, and sesH genes were more prevalent in healthy skin isolates than in prosthetic joint infections isolates (p < .05). Prosthetic joint infections isolates were more resistant to oxacillin (78%), ciprofloxacin (60%), levofloxacin (60%), and moxifloxacin (57%). The principal coordinate analysis and a discriminant analysis found that prosthetic joint infections isolates had as discriminant biomarker the biofilm formation, the icaA gene, oxacillin, ciprofloxacin, levofloxacin, moxifloxacin, and gentamicin resistance. In contrast, the healthy skin isolates had as discriminant biomarkers the embp, sesA, sesB, sesC, sesD, sesE, sesG, and sesH genes. CONCLUSIONS: These data suggest that ses genes can be considered biomarkers to differentiate between S. epidermidis commensal and prosthetic joint infections clinical.

Population Structure, Genetic Diversity, and Evolutionary History of Kleinia neriifolia (Asteraceae) on the Canary Islands.

Kleinia neriifolia Haw. is an endemic species on the Canarian archipelago, this species is widespread in the coastal thicket of all the Canarian islands. In the present study, genetic diversity and population structure of K. neriifolia were investigated using chloroplast gene sequences and nuclear SSR (simple sequence repeat). The differentiation among island populations, the historical demography, and the underlying evolutionary scenarios of this species are further tested based on the genetic data. Chloroplast diversity reveals a strong genetic divergence between eastern islands (Gran Canaria, Fuerteventura, and Lanzarote) and western islands (EI Hierro, La Palma, La Gomera, Tenerife), this west-east genetic divergence may reflect a very beginning of speciation. The evolutionary scenario with highest posterior probabilities suggests Gran Canaria as oldest population with a westward colonization path to Tenerife, La Gomera, La Palma, and EI Hierro, and eastward dispersal path to Lanzarote through Fuerteventura. In the western islands, there is a slight decrease in the effective population size toward areas of recent colonization. However, in the eastern islands, the effective population size increase in Lanzarote relative to Gran Canaria and Fuerteventura. These results further our understanding of the evolution of widespread endemic plants within Canarian archipelago.

Molecular and Phenotypic Characterization of Staphylococcus epidermidis Isolates from Healthy Conjunctiva and a Comparative Analysis with Isolates from Ocular Infection.

Staphylococcus epidermidis is a common commensal of healthy conjunctiva and it can cause endophthalmitis, however its presence in conjunctivitis, keratitis and blepharitis is unknown. Molecular genotyping of S. epidermidis from healthy conjunctiva could provide information about the origin of the strains that infect the eye. In this paper two collections of S. epidermidis were used: one from ocular infection (n = 62), and another from healthy conjunctiva (n = 45). All isolates were genotyped by pulsed field gel electrophoresis (PFGE), multilocus sequence typing (MLST), staphylococcal cassette chromosome mec (SCCmec), detection of the genes icaA, icaD, IS256 and polymorphism type of agr locus. The phenotypic data included biofilm production and antibiotic resistance. The results displayed 61 PFGE types from 107 isolates and they were highly discriminatory. MLST analysis generated a total of 25 STs, of which 11 STs were distributed among the ocular infection isolates and lineage ST2 was the most frequent (48.4%), while 14 STs were present in the healthy conjunctiva isolates and lineage ST5 was the most abundant (24.4%). By means of a principal coordinates analysis (PCoA) and a discriminant analysis (DA) it was found that ocular infection isolates had as discriminant markers agr III or agr II, SCCmec V or SCCmec I, mecA gene, resistance to tobramycin, positive biofilm, and IS256+. In contrast to the healthy conjunctiva isolates, the discriminating markers were agr I, and resistance to chloramphenicol, ciprofloxacin, gatifloxacin and oxacillin. The discriminant biomarkers of ocular infection were examined in healthy conjunctiva isolates, and it was found that 3 healthy conjunctiva isolates [two with ST2 and another with ST9] (3/45, 6.66%) had similar genotypic and phenotypic characteristics to ocular infection isolates, therefore a small population from healthy conjunctiva could cause an ocular infection. These data suggest that the healthy conjunctiva isolates do not, in almost all cases, infect the eye due to their large genotypic and phenotypic difference with the ocular infection isolates.

Evolution of bacterial genes: evidences of positive Darwinian selection and fixation of base substitutions in virulence genes of Helicobacter pylori.

Gene diversity in Helicobacter pylori from different origins results in a phylogeographic differentiation, and this genetic variation among populations might be driven by random drift or by selective forces. However, only the selective forces would contribute to adaptation of the bacteria to the physiology and environment of its local host and to its association with gastroduodenal diseases. We studied evolutionary forces acting on variable regions of virulence genes cagA, babA and oipA, which present geographic differences among H. pylori strains from different human groups. Gene sequences in H. pylori strains from Asia, Europe and America were analysed using state of the art analytical methods like the Maximum Likelihood method. The rate and nature of polymorphisms in these virulence genes were also compared among populations using the AMOVA and McDonald-Kreitman tests. We found strong and significant positive selection acting on variable regions of cagA, babA and oipA. We found in cagA from Asian strains regions under positive selection, which localised in amino acid sites defining the Asian fingerprint for this gene and in sites with important biological activity. Different evolutionary forces are acting on the variable region of virulence genes; they partly explain the source of genetic diversity and the differences in risk for gastroduodenal diseases among different human populations.