关于 Staphylococcus aureus

Staphylococcus aureus (S. aureus) is a Gram-positive pathogenic bacterium and one of the foremost opportunistic bacterial pathogens of humans, causing major morbidity and mortality globally^[1]. S. aureus colonizes approximately 20–30% of humans persistently in the nose^[2] and frequently in other sites such as the skin, throat, axillae, groin, and intestine. Colonization is harmless but it is a risk factor for developing subsequent infections (often caused by the colonizing strain), which can range from mild skin and soft tissue infections to serious invasive infections, including osteomyelitis and septic arthritis, bacteraemia or septicaemia, pneumonia and endocarditis^[1].

In addition to its protean clinical manifestations, S. aureus is characterized by the ability to acquire resistance to almost any antibiotic. S. aureus secretes an extracellular polymeric substance, known as biofilm, that helps the microbe to resist and minimise the effect of antibacterial drugs. Although penicillin initially revolutionized the treatment of serious S. aureus infections, resistance through the acquisition of the β-lactamase encoding gene blaZ was soon widespread^[3]. The acquisition of resistance to anti-staphylococcal penicillins through the mecA gene has resulted in the global dissemination of diverse lineages of methicillin-resistant S. aureus (MRSA), now considered a global public health threat^[3]. Glycopeptides became the mainstay of therapy for invasive MRSA infections^[4].

Community-acquired MRSA (CA-MRSA) and hospital-acquired MRSA (HA-MRSA) had distinct genotypic and phenotypic characteristics that allowed them to thrive in their ecological niches. For instance, HA-MRSA is more resistant to a broader range of antibiotics^[5]. CA-MRSA, on the other hand, is more sensitive to antibiotics but rather more virulent^[6]. Dissemination of both AMR and virulence factors is mediated by horizontal gene transfer of mobile genetic elements and by mutations^[7]. Other molecular features like SCCmec type and the presence of Panton-Valentine leukocidin toxin genes are classically used to differentiate HA-MRSA from CA-MRSA^[6]. However, a clear-cut between these two types is gradually diminishing due to their increasing shared molecular and epidemiological characteristics^[8]. CA-MRSA strains are increasingly replacing traditional HA-MRSA ones in health care settings blurring their classical definition.

Besides colonizing humans, MRSA had successfully gained a foothold in livestock and companion animals, expanding its host range, and creating additional reservoirs^[9]. MRSA epidemiology and population structure vary with geographical locations. Specific high risk MRSA lineages have spread around the world and become epidemic in MRSA-mediated infections, with different lineages dominating in different parts of the world, at different times^[8].

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