Community-associated methicillin-resistant Staphylococcus aureus immune evasion and virulence

Abstract

Staphylococcus aureus is a significant cause of human infections globally. Methicillin-resistant S. aureus (MRSA) emerged in the early 1960s and is now endemic in most healthcare facilities. Although healthcare-associated MRSA infections remain a major problem in most industrialized countries, those caused by community-associated MRSA (CA-MRSA) are now the most abundant cause of bacterial infections in the community in some parts of the world, such as the United States. The basis for the emergence and subsequent success of CA-MRSA is incompletely defined. However, the ability of the pathogen to cause disease in otherwise healthy individuals is likely attributed, in part, to its ability to circumvent killing by the innate immune system, which includes survival after phagocytosis by neutrophils. In this review, we discuss the role of neutrophils in host defense against S. aureus and highlight progress made toward understanding mechanisms of CA-MRSA virulence and pathogenesis.

Fig. 1

Two possible outcomes of the interaction of PMNs with bacteria. On one hand, bacteria (pink spheres) are ingested, activate PMNs, and are killed, and this process ultimately triggers PMN apoptosis and the removal of these cells by macrophages (Efferocytosis). This phenomenon leads to the resolution of the inflammatory response (RESOLUTION). Alternatively, bacterial pathogens (yellow spheres or red particles) are ingested and either delay normal PMN apoptosis and turnover or cause PMN lysis. Typically, these processes facilitate survival of bacteria and thereby promote disease (DISEASE)