Sequence-type 5 (ST5) of methicillin-resistant Staphylococcus aureus (MRSA), harboring the staphylococcal chromosomal cassette mec type IV (SCCmecIV), was first detected in Portugal. It emerged as a significant cause of healthcare-associated (HA) infection in pediatric units and was hence named the pediatric clone. Another ST5 lineage, which carries SCCmecII, also prevailed in the USA and Japan for multiple years. More recently, another MRSA lineage, ST105-SCCmecII, part of the evolution of clonal complex 5 (CC5) MRSA, has emerged as the cause of hospital-acquired bloodstream infection outbreaks in countries including Portugal, the USA, and Brazil. This article reviews studies on the epidemiology and evolution of these newly emerging pathogens. To this end, a search of PUBMED from inception to 2024 was performed to find articles reporting the occurrence of ST105 MRSA in epidemiologic studies. A second search was performed to find studies on MRSA, CC5, ST5, and SCCmecII. A search of PUBMED from 1999 to 2024 was also performed to identify studies on the genomics and evolution of ST5, CC5, and ST105 MRSA. Further studies were identified by analyzing the references of the previously selected articles from PUBMED. Most articles on ST105 MRSA were included in this review. Only articles written in English were included. Furthermore, only studies that used a reliable genotyping method (e.g., whole genome sequencing, or MLST) to classify the CC5 lineages were selected. The quality and selection of articles were based on the consensus assessment of the three authors in independent evaluations. In conclusion, ST105-SCCmecII is an emerging MRSA in several countries, being the second/third most important CC5 lineage, with a relatively high frequency in bloodstream infections. Of concern is the increased mortality from BSI in patients older than 15 years and the higher prevalence of ST105-SCCmecII in the blood of patients older than 60 years reported in some studies.

Staphylococcus aureus is a pathogen commonly resistant to antibiotics. Biofilm formation is one of the important factors related to its virulence. Non-antibiotics drugs, such as nonsteroidal anti-inflammatory agents (NSAIDs), have been studied as an alternative for treating infections by multiresistant pathogens and biofilm-associated infections. In this study, the effects of NSAID sodium diclofenac on growth inhibition and biofilm formation of S. aureus were evaluated. The minimum inhibitory concentration (MIC) of diclofenac for fifty isolates ranged from 200 to 400μg/mL. Diclofenac sub-MICs induced biofilm in 32.3 of biofilm-negative strains in tryptic soy broth. All biofilms induced by the drug showed a PIA- (polysaccharide intercellular adhesion-) independent composition, and the scanning electron microscopy showed that the induced biofilm presented a very discrete matrix. The combination of diclofenac with rifampicin sub-MICs induced strong production of PIA-dependent biofilm in three of four strains, while combination of NSAID with NaCl induced the formation of partially polysaccharide biofilm in two strains and PIA-independent biofilm in another strain. The combination of NSAID with glucose resulted in PIA-independent biofilms in all four strains tested. The results showed that diclofenac can commonly induce biofilm production by a PIA-independent pathway. However, when this NSAID is combined with other types of inducing agents, the composition of the biofilm produced may vary.

Streptococcus pyogenes is known to be associated with a variety of infections, from pharyngitis to necrotizing fasciitis (flesh-eating disease). S. pyogenes of the ST62/emm87 lineage is recognized as one of the most frequently isolated lineages of invasive infections caused by this bacterium, which may be involved in hospital outbreaks and cluster infections. Despite this, comparative genomic and phylogenomic studies have not yet been carried out for this lineage. Thus, its virulence and antimicrobial susceptibility profiles are mostly unknown, as are the genetic relationships and evolutionary traits involving this lineage. Previously, a strain of S. pyogenes ST62/emm87 (37–97) was characterized in our lab for its ability to generate antibiotic-persistent cells, and therapeutic failure in severe invasive infections caused by this bacterial species is well-reported in the scientific literature. In this work, we analyzed genomic and phylogenomic characteristics and evaluated the virulence and resistance profiles of ST62/emm87 S. pyogenes from Brazil and international sources. Here we show that strains that form this lineage (ST62/emm87) are internationally spread, involved in invasive outbreaks, and share important virulence profiles with the most common emm types of S. pyogenes, such as emm1, emm3, emm12, and emm69, which are associated with most invasive infections caused by this bacterial species in the USA and Europe. Accordingly, the continued increase of ST62/emm87 in severe S. pyogenes diseases should not be underestimated.

Small regulatory RNAs (sRNAs) are fast-acting non-coding RNAs (ncRNAs), stress-responsive regulators that fine-tune bacterial gene expression, shaping virulence, antimicrobial resistance, metabolism, and biofilm development. At the post-transcriptional level, sRNAs pair with target mRNAs to block or enhance translation, remodel secondary structures, adjust transcript stability, and act as molecular sponges for other sRNAs. Staphylococcus aureus , a leading cause of hospital-acquired infections, relies on a multiple-layered regulatory network, including post-transcriptional mechanisms, to transition between planktonic and biofilm lifestyles. Here, we expand the cross-lineage sRNA repertoire of S. aureus by integrating newly generated RNA-seq data from the Brazilian ST239 Bmb9393 strain with public datasets from five USA-lineage strains previously uncharacterized for sRNAs. Using sequence homology and covariance models, we predicted and annotated candidate sRNA loci across all analyzed genomes, quantified their expression under planktonic and biofilm conditions, and assigned genomic context. Integration of differential-expression (DE) profiles with weighted gene co-expression network analysis (WGCNA) identified sRNAs associated with biofilm and virulence, in modules that include well-known regulators ( sarA , mgrA , RNAIII) and the adhesin clfA . To prioritize functional target interactions, we combined DEG concordance, network features, and interaction-energy thresholds, depleting millions of initial predictions to thousands of high-confidence sRNA-mRNA pairs. Our integrative bioinformatics framework provides additional insights into sRNA-mediated regulation in S. aureus , highlighting biofilm- and resistance-linked candidates, and yields a ranked, reusable set of sRNA-mRNA interactions to guide hypothesis-driven experiments across diverse genetic backgrounds.

The study includes an epidemiological panel of the prevalence of mastitis - both clinical and subclinical - on farms in Ethiopia, and interestingly provides information on the odds ratio of variables such as the animals' age, frequency of hygienic...

Staphylococcus aureus is a pathogen commonly involved in the etiology of nosocomial and community-acquired infections. This microorganism adheres and forms biofilm on biotic and abiotic surfaces, which is a significant complication for infection control. More recently, non-antibiotic medications, such as nonsteroidal anti-inflammatory agents (NSAIDs), have been studied as an alternative for treating infections caused by multidrug-resistant pathogens and infections associated with biofilms. This study assessed the effects of prolonged exposure of S. aureus strains to the NSAID diclofenac sodium regarding biofilm production, direct adhesion, hydrophobicity, susceptibility to antimicrobials, hemolysis, and biochemical profile. Some strains exposed to diclofenac showed increased direct adhesion to hydrophobic and hydrophilic surfaces and increased cell surface hydrophobicity. Two strains, one reference and one clinical, were subjected to repeated and prolonged passages in a culture medium with a diclofenac gradient. In one of them, the drug suppressed biofilm production in the assay with and without subinhibitory concentrations (sub-MICs) from NSAID. Additional repeated passages of this strain in a medium without diclofenac partially recovered the original biofilm-positive phenotype, but only in culture with sub-MICs of the drug. The original characteristics of the strains regarding susceptibility or resistance to antimicrobials and biochemical profile were not affected by prolonged exposure to diclofenac. However, the clinical isolate showed suppressed hemolytic activity.