Methicillin-resistant Staphylococcus aureus: an ever emerging threat

Staphylococcus aureus is an ubiquitous bacterium that is frequently part of the human microflora, causing disease when the immune system becomes compromized. Although S. aureus can be found in different parts of the body, anterior nares are the main ecological reservoir in humans [1]. This versatile pathogen is responsible for a wide variety of diseases, including superficial, systemic and life-threatening infections, and toxinoses [2]. Our capacity to treat S. aureus infection, has been increasingly challenged by the emergence and re-emergence of antibiotic-resistant isolates. This microorganism has a great adaptative power to antibiotics, and little by little, it has acquired resistance to multiple antimicrobial agents. Methicillin-resistant S. aureus (MRSA) was first described in 1961 in England [3] as the result of the acquisition of an exogenous gene (mecA) that probably originated from Staphylococcus sciuri [4]. The mecA gene encodes an additional penicillin-bindingprotein (PBP2a) with low affinity for b-lactam antibiotics. The mecA gene is regulated by the repressor MecI and the transducer MecR1. The mecA gene, which is 2.1 kb in length, is located on a mobile genomic island, that is called staphylococcal cassette chromosome mec (SCCmec). Until now, seven main types of SCCmec (types I–VII) are recognized. SCCmec type I, IV, V, VI and VII only cause b-lactam antibiotic resistance, while SCCmec type II and III cause resistance to multiple classes of anti biotics due to the additional drug resistance genes integrated into SCCmec. Over the last four decades, MRSA has spread throughout the world and has become highly endemic in many geographical areas. This pathogen causes severe morbidity and mortality in hospitals worldwide [5,6]. Initially, MRSA nosoco mial infections were mainly detected in large tertiary hospitals and in intensive care units, where colonized and infected patients, as well as colonized healthcare workers, were a significant source of cross-contamination. Currently, MRSA is one of the most common pathogens in hospitals of all sizes and of different types (acute, chronic and long-term care facilities) worldwide. Until recently, the MRSA problem was limited to hospitals, and MRSA infections were mostly acquired in hospital units. The emergence and dissemination of community-associated (CA)-MRSA producing the Panton–Valentine Among multidrug-resistant bacteria, methicillin-resistant Staphylococcus aureus (MRSA) is of immediate concern, given its potential for pathogenicity and widespread presence in healthcare settings. Over the last four decades, MRSA has spread throughout the world and the global prevalence of MRSA in hospitals (hospital-associated MRSA) continues to increase with the dissemination of a limited number of MRSA clones, each with a specific genetic background and staphylococcal cassette chromosome mec. Measures to control the hospital spread of MRSA have concentrated principally on transmission-based control policies. European surveillance data suggest that the increasing rate of hospital-associated MRSA is not an inexorable trend, and European countries with variable baseline prevalence and infection control policies were able to reverse the MRSA trend. Recently, MRSA strains have emerged and rapidly spread in the community. These so-called community-associated (CA)-MRSA strains are mainly associated with skin and soft tissue infections in previously healthy and young persons. CA-MRSA isolates from different areas of the world have common characteristics: the production of Panton–Valentine leukocidin and the presence of short staphylococcal cassette chromosome mec elements. In the USA, CA-MRSA became more prevalent than methicillin-susceptible S. aureus in community-associated S. aureus infections. In Europe, their prevalence remains below 5%, except for in Greece. The recent emergence of virulent CA-MRSA isolates harboring the tst gene and of MRSA from animal origin is of major concern. Large efforts are necessary to avoid penicillinase-mediated resistance in S. aureus occuring again with MRSA.