The success of S.

aureus as a pathogen can, in part, be attributed to its vast repertoire of virulence

determinants that enable the bacteria to efficiently extract nutrients from its host and to thwart both
innate and adaptive immune attack by the host.

Professional phagocytes such as macrophages and neutrophils comprise an integral facet of the host
immune response and the interaction of neutrophils with S. aureus has been intensely characterized
(for a recent review see [10])

Remarkably S. aureus can withstand neutrophil mediated killing, an impressive feat considering the
potent microbicidal capacity of the neutrophil.

Like neutrophils, macrophages are professional phagocytes that are equipped with an impressive
armamentarium of antimicrobial effectors and thus represent an important component of the innate
immune response.

The notion that S. aureus is primarily an “extracellular pathogen” has receded, as there exists a
significant body of literature demonstrating that S. aureus can withstand killing after being
phagocytosed by professional phagocytes including neutrophils and macrophages

its genome encodes an armamentarium of immune evasion proteins and toxins that destroy host
cells

pathogens themselves have evolved ways to evade the immune response

An example already mentioned is in Mycobactrium tuberculosis, which has evolved a complex cell
wall that is resistant to the digestive enzymes of the macrophages that ingest them, and thus persists
in the host, causing the chronic disease tuberculosis.

Staphylococcus aureus. S. aureus is commonly found in minor skin infections, such as boils, and some
healthy people harbor it in their nose. One small group of strains of this bacterium, however, called
methicillin-resistant Staphylococcus aureus, has become resistant to multiple antibiotics and is
essentially untreatable.

Different bacterial strains differ in the antigens on their surfaces. The immune response against one
strain (antigen) does not affect the other; thus, the species survives.

Another method of immune evasion is mutation. Because viruses’ surface molecules mutate
continuously, viruses like influenza change enough each year that the flu vaccine for one year may
not protect against the flu common to the next. New vaccine formulations must be derived for each
flu season.

Genetic recombination—the combining of gene segments from two different pathogens—is an

efficient form of immune evasion.