Staphylococcus aureus is an important and common pathogen in humans. It is found in the nose or on the skin of many healthy, asymptomatic persons (i.e., carriers) and can cause infections with clinical manifestations ranging from pustules to sepsis and death. Most transmission occurs through the contaminated hands of a person infected with or carrying S. aureus. MRSA infections frequently are encountered in health-care settings (Lowy, 1998).
A common cause of blood-stream infections, pneumonia, endocarditits, skin and soft tissue infections, and bone and joint infections, S. aureus infection is often associated with significant morbidity and mortality.
S. aureus is well adapted to the human body, capable of spreading from person to person, hiding in intracellular compartments and inducing various forms of human disease. During infection the bacterial cells produce a large variety of virulence factors, among which, for instance, are molecules that interfere with the chemotaxis of neutrophils to the site of infection. Adding to the complexity of the infectious process is the fact that the host also responds with a variety of immunological defenses, sometimes producing a certain degree of resistance to infection.
Many healthcare and clinical professionals assume that MSRA is more virulent than its predecessor; however, in control studies, no clear difference has been seen in types of infections, infection severity, and infection-associated mortality caused by MRSA and MSSA (Bradley, 1992). Although not more virulent than MSSA, MRSA infections are significantly more difficult and costly to treat. Treatment generally requires IV antibiotics that are associated with the possibility of increased potential for adverse events compared to those treatable with oral antibiotics and often create the need to move a patient to an acute-care facility.
S. aureus has remained among the top three clinically important pathogens over the past few decades, and a particular worry has been the rise of methicillin resistant strains. In addition to the fact that the organism is not yet completely understood, clinicians worry due to its acquisition of resistance to antibiotics, and how that contributes to its pathoclinical potential. Methicillin resistant S aureus (MRSA) emerged rapidly after the introduction of the antibiotic, with the primary cause of the spread of the MRSA bacteria through clonal dissemination. Although the gene inducing the resistance has been discovered in various genetic backgrounds, colonisation and infection were mainly caused by rapid spread, sometimes even between continents, of relatively small numbers of epidemic bacterial strains (Lowy, 2000).
Since the 1960s, treatment of these infections has become more difficult because S. aureus has progressively acquired resistance to previously effective antimicrobial agents. In 1999, 2,538 (53.5%) of 4,744 intensive care unit patients with hospital-acquired S. aureus-associated infection had MRSA (Center for Disease Control, 2001).
There has been an increasing prevalence of MRSA as a cause of infections in institutional settings, but there is less information about an increasing role of this pathogen in community-acquired infections. Lending to the confusion is that studies in one center may not necessarily reflect patterns of causative organisms and antimicrobial susceptibility elsewhere. Results from antimicrobial susceptibility testing show resistance of S aureus to penicillin has decreased over the past two decades, while resistance to erythromycin increased from 1980 to 1986 and has remained relatively unchanged since (Guttman, 2001).
Risk factors for infection with MRSA in health-care settings include prolonged hospital stay, exposure to multiple or prolonged broad-spectrum antimicrobial therapy, stay in an intensive care or burn unit, proximity to patients colonized or infected with MRSA, use of invasive...