What is behind the epidemiological difference between community-acquired and health-care associated methicillin-resistant Staphylococcus aureus?

One of most striking features of methicillin-resistant Staphylococcus aureus (MRSA) is the strong clonal structure of the bacterial population. MRSA isolates were first reported among hospitalized patients at the beginning of the 1960s, and remain major agents of hospital infections worldwide. Typical lineages (clones) of health care-associated MRSA (HA-MRSA) are ST5 (CC5), ST239 (CC8), ST22 (CC22), and ST36 (CC30). However, these rarely cause infections in healthy individuals who are not hospitalized or attended a healthcare service in the 6–12 months before infection. A biologic consequence of acquiring antimicrobial resistance is the reduction of competitive fitness. This has generally been associated with HA-MRSA failure to efficiently spread in the community. At the end of the 1980s, MRSA isolates were reported to cause typical community-acquired (CA) infections in Oceania; this CA-MRSA clone (ST1-SCCmecIV) was named WA-1, for Western Australia-1. After that, CAMRSA infections were reported on all continents. Generally, typical CA-MRSA strains display important differences from HA-MRSA strains including the production of Panton-Valentine leucocidin (PVL), low-level susceptibility to non-b-lactam antibiotics, and carriage of SCCmec types IV or V. While most CA-MRSA harbor lukSF genes for PVL, exceptions have already been reported. Actually, the majority of WA-1 isolates are PVL negatives. It is also remarkable that some CA-MRSA lineages can prevail in specific geographic regions. For instance, in Europe, ST80 is the predominant CA-MRSA lineage, and it possibly originated from a PVL-positive MSSA ancestor from sub-Saharan Africa. In Australia, 3 different lineages (ST93, ST30, and ST1) are prevailing. The ST30 is also the predominant CA-MRSA in South America. In the USA, a ST8 CA-MRSA (the so-called USA300) is the dominant clone in CA infections. Nevertheless, the factors involved in the local expansion of a specific CA-MRSA lineage and the mechanisms behind the bacterial diversification in HAor CA-MRSA remain unclear. In the 2000s, CA-MRSA emerged in hospital settings to compete with HA-MRSA clones, representing an important epidemiological change. The PVL-positive, CA-MRSA USA300 is now challenging the previously dominant HA-MRSA clone New York/Japan (ST5) in USA hospitals. In Orange County (CA, USA), for example, 38.0% of the MRSA isolates from 30 hospitals were genotyped as USA300, while 36.8% as NY/J clone. In Rio de Janeiro, Brazil, the CA-MRSA ST30 is frequently detected causing typical HA-infections including septicemia. A legitimate concern of the scientific community is related to the possibility that once in hospitals the CAMRSA could exchange DNA with typical HA-MRSA clones and thus acquire multiple-resistant genes. There is also the possibility that the intense CA-MRSA dissemination in health care units might facilitate the acquisition of additional adaptive mutations to increase bacterial fitness and survival despite the costs of antibiotic resistance. Another novel situation regarding to MRSA epidemiology involves intra-lineage diversification/evolution. Here, a PVL-negative clone related to a classical CA-MRSA lineage is largely confined to hospitals. The hospital-restricted and multiresistant ST1SCCmecIV, PVL-negative, related to the USA400 CA-MRSA—a PVL-positive strain previously detected causing CA infections in USA and Canada— emerged in Brazilian hospitals. This is a good example of this epidemiological change that can even further