Dear Colleagues,

Staphylococcus aureus, a Gram-positive, coagulase-positive pathogen belonging to the family Staphylococcaceae, with a spherical shape that forms grape-like clusters, is a commensal that is often present asymptomatically on parts of the human body. S. aureus is also a major human pathogen able to adapt to diverse hosts and environmental conditions, as well as to cause plenty of infections and is one of the major causes of hospital and community-acquired infections. It can cause infections of the bloodstream, skin and soft tissues, and lower respiratory tract, infections related to medical instrumentation, such as central-line associated bloodstream infection (CLABSI), and some serious deep-seated infections such as osteomyelitis and endocarditis. S. aureus is equipped with a collection of virulence factors and toxins often making it responsible for many toxin-mediated diseases, including staphylococcal toxic shock syndrome, foodborne diseases, and scalded skin syndrome.

A major issue associated with S. aureus is its ability to acquire resistance to most antibiotics. Clinical use of methicillin has led to the emergence of methicillin-resistant S. aureus (MRSA) associated with high morbidity and mortality. MRSA strains produce a new altered penicillin-binding protein (PBP 2a or PBP 2’) associated with decreased affinity for penicillins, encoded by the acquired gene mecA carried on a mobile genetic element (MGE) named staphylococcal cassette chromosome mec (SCCmec) that can be acquired and inserted into the chromosomes of susceptible strains. Another resistance determinant has been rarely identified among MRSA, mecC. MRSA isolates are, therefore, resistant to all available penicillins and most of the other beta-lactam drugs, except ceftaroline and ceftobiprole. Vancomycin has historically been the drug of choice, sometimes considered as the last line for the treatment of serious MRSA infections. However, vancomycin is considered less effective than penicillin, and its increased use has been associated with the rise of vancomycin-intermediate S. aureus (VISA) and vancomycin-resistant S. aureus (VRSA) in some regions.

In the beginning, MRSA was associated only with healthcare settings, the so-called hospital-associated MRSA (HA-MRSA). however, community-acquired MRSA (CA-MRSA) infections have been rising in frequency and now MRSA strains represent a major cause of community-associated infections. CA-MRSA is genetically distinct from HA-MRSA, being resistant to fewer non-beta-lactam antibiotics, carrying a smaller trait of SCCmec, and often producing the Panton-Valentine leukocidin. Moreover, CA-MRSA invading healthcare settings has been also identified as the etiological agent of nosocomial outbreaks. Apart from humans, MRSA colonization and infection have also been reported in animals, for example, in domesticated livestock, companion animals, and wild species. The indiscriminate use of antimicrobial agents in these settings strongly contributed to the spread of MRSA among livestock. Numerous studies have indicated that humans in contact with livestock can be colonized and infected with livestock-associated MRSA (LA-MRSA). Thus, livestock and other animals may become a permanent reservoir for human MRSA infections.

In this Special Issue, we plan to collect original research articles, short communications, or review articles that discuss the pathogenesis of S. aureus infections, and genetic and molecular basis of drug resistance mechanisms in both humans and animals.

Prof. Dr. Giovanni Gherardi
Guest Editor

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