Staphylococcus aureus is a common human pathogen with a variety of virulence factors, which can cause multiple infectious diseases. In recent decades, due to the constant evolution and the abuse of antibiotics, Staphylococcus aureus was becoming more resistant, the infection rate of MRSA remained high, and clinical treatment of MRSA became more difficult. The genetic diversity of MRSA was mainly represented by the continuous emergence of epidemic strains, resulting in the constant changes of epidemic clones. Different classes of MRSA resulted in different epidemics and resistance characteristics, which could affect the clinical symptoms and treatments. MRSA had also spread from traditional hospitals to community and livestock environments, and the new clones established a relationship between animals and humans, promoting further evolution of MRSA. Since the resistance mechanism of MRSA is very complex, it is important to clarify these resistance mechanisms at the molecular level for the treatment of infectious diseases. We firstly described the diversity of SCCmec elements, and discussed the types of SCCmec, its drug resistance mechanisms and expression regulations. Then, we described how the vanA operon makes Staphylococcus aureus resistant to vancomycin and its expression regulation. Finally, a brief introduction was given to the drug resistance mechanisms of biofilms and efflux pump systems. Analyzing the resistance mechanism of MRSA can help study new anti-infective drugs and alleviate the evolution of MRSA. At the end of the review, we summarized the treatment strategies for MRSA infection, including antibiotics, anti-biofilm agents and efflux pump inhibitors. To sum up, here we reviewed the epidemic characteristics of Staphylococcus aureus, summarized its classifications, drug resistance mechanisms of MRSA (SCCmec element, vanA operon, biofilm and active efflux pump system) and novel therapy strategies, so as to provide a theoretical basis for the treatment of MRSA infection. 

https://www.dovepress.com/getfile.php?fileID=89948

Progress in the Prevalence, Classification and Drug Resistance Mechanisms of Methicillin-Resistant Staphylococcus aureus

Staphylococcus aureus is a successful pathogen that produces a wide range of virulence factors that it uses to subvert and suppress the immune system. These include the bicomponent pore-forming leukocidins. ABSTRACT Staphylococcus aureus is a successful pathogen that produces a wide range of virulence factors that it uses to subvert and suppress the immune system. These include the bicomponent pore-forming leukocidins. How the expression of these toxins is regulated is not completely understood. Here, we describe a screen to identify transcription factors involved in the regulation of leukocidins. The most prominent discovery from this screen is that SarS, a known transcription factor which had previously been described as a repressor of alpha-toxin expression, was found to be a potent repressor of leukocidins LukED and LukSF-PV. We found that inactivating sarS resulted in increased virulence both in an ex vivo model using primary human neutrophils and in an in vivo infection model in mice. Further experimentation revealed that SarS represses leukocidins by serving as an activator of Rot, a critical repressor of toxins, as well as by directly binding and repressing the leukocidin promoters. By studying contemporary clinical isolates, we identified naturally occurring mutations in the sarS promoter that resulted in overexpression of sarS and increased repression of leukocidins in USA300 bloodstream clinical isolates. Overall, these data establish SarS as an important repressor of leukocidins and expand our understanding of how these virulence factors are being regulated in vitro and in vivo by S. aureus.

SarS Is a Repressor of Staphylococcus aureus Bicomponent Pore-Forming Leukocidins

Methicillin-resistant Staphylococcus aureus (MRSA) is a frequent cause of nosocomial and community infections, in some cases severe and difficult to treat. In addition, there are strains of MRSA that are specifically associated with food-producing animals. For this reason, in recent years special attention has been paid to the role played by foodstuffs of animal origin in infections by this microorganism. With the aim of gaining knowledge on the prevalence and types of MRSA in meat and meat products, a review was undertaken of work published on this topic since 2001, a total of 259 publications, 185 relating to meat samples from retail outlets and 74 to samples of animal origin collected in farms, slaughterhouses and meat processing facilities. Strains of MRSA were detected in 84.3% reports (156 out of 185) from retail outlets and 86.5% reports (64 out of 74) from farms, slaughterhouses and meat processing facilities, although in most of the research this microorganism was detected in under 20% of samples from retail outlets, and under 10% in those from farms, slaughterhouses and meat processing facilities. The meat and meat products most often contaminated with MRSA were pork and chicken. In addition to the mecA gene, it is crucial to take into consideration the mecB and mecC genes, so as to avoid misidentification of strains as MSSA (methicillin-susceptible Staphylococcus aureus). The great variety of methods used for the determination of MRSA highlights the need to develop a standardized protocol for the study of this microorganism in foods. 

Prevalence and types of methicillin-resistant Staphylococcus aureus (MRSA) in meat and meat products from retail outlets and in samples of animal origin collected in farms, slaughterhouses and meat processing facilities. A review

Bacterial pathogens adapt to host niches because of within-host selective pressures, and this evolutionary process provides valuable insights into host-pathogen interactions. However, genetic changes underlying adaptive phenotypes are difficult to identify from data generated by genome-wide association studies of unrelated bacterial clones. Here, we followed the evolution of a single Klebsiella pneumoniae clone in 110 patients during a 5-year nosocomial outbreak by combining comparative genomics with phenotypic characterization. Strong positive within-patient selection targeted key virulence factors in isolates from infection sites. The clone repeatedly lost acute virulence primarily via alterations in capsule and lipopolysaccharide, changed regulation of iron uptake, and increased biofilm formation. These phenotypes represent likely niche adaptations, mainly to the urinary tract, and some were associated with trade-offs during gastrointestinal colonization. The substantial convergent evolution reflects the trajectories undertaken by high-risk clones of K. pneumoniae and other pathogens adapting during acute and chronic infections.

Convergent within-host evolution alters key virulence factors in a Klebsiella pneumoniae clone during a large hospital outbreak

ABSTRACT Severe COVID-19 has been associated with coinfections with bacterial and fungal pathogens. Notably, patients with COVID-19 who develop Staphylococcus aureus bacteremia exhibit higher rates of mortality than those infected with either pathogen alone. To understand this clinical scenario, we collected and examined S. aureus blood and respiratory isolates from a hospital in New York City during the early phase of the pandemic from both SARS-CoV-2+ and SARS-CoV-2− patients. Whole genome sequencing of these S. aureus isolates revealed broad phylogenetic diversity in both patient groups, suggesting that SARS-CoV-2 coinfection was not associated with a particular S. aureus lineage. Phenotypic characterization of the contemporary collection of S. aureus isolates from SARS-CoV-2+ and SARS-CoV-2− patients revealed no notable differences in several virulence traits examined. However, we noted a trend toward overrepresentation of S. aureus bloodstream strains with low cytotoxicity in the SARS-CoV-2+ group. We observed that patients coinfected with SARS-CoV-2 and S. aureus were more likely to die during the acute phase of infection when the coinfecting S. aureus strain exhibited high or low cytotoxicity. To further investigate the relationship between SARS-CoV-2 and S. aureus infections, we developed a murine coinfection model. These studies revealed that infection with SARS-CoV-2 renders mice susceptible to subsequent superinfection with low cytotoxicity S. aureus . Thus, SARS-CoV-2 infection sensitizes the host to coinfections, including S. aureus isolates with low intrinsic virulence. IMPORTANCE The COVID-19 pandemic has had an enormous impact on healthcare across the globe. Patients who were severely infected with SARS-CoV-2, the virus causing COVID-19, sometimes became infected with other pathogens, which is termed coinfection. If the coinfecting pathogen is the bacterium Staphylococcus aureus , there is an increased risk of patient death. We collected S. aureus strains that coinfected patients with SARS-CoV-2 to study the disease outcome caused by the interaction of these two important pathogens. We found that both in patients and in mice, coinfection with an S. aureus strain lacking toxicity resulted in more severe disease during the early phase of infection, compared with infection with either pathogen alone. Thus, SARS-CoV-2 infection can directly increase the severity of S. aureus infection. 

SARS-CoV-2 infection predisposes patients to coinfection with Staphylococcus aureus

http://www.cell.com/article/S1931312822005753/pdf

MRSA lineage USA300 isolated from bloodstream infections exhibit altered virulence regulation.

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MRSA lineage USA300 isolated from bloodstream infections exhibit altered virulence regulation.