The Staphylococcus aureus "superbug"

Abstract

There has been some debate about the disease-invoking potential of Staphylococcus aureus strains and whether invasive disease is associated with particularly virulent genotypes, or "superbugs." A study in this issue of the JCI describes the genotyping of a large collection of nonclinical, commensal S. aureus strains from healthy individuals in a Dutch population. Extensive study of their genetic relatedness by amplified restriction fragment typing and comparison with strains that are associated with different types of infections revealed that the S. aureus population is clonal and that some strains have enhanced virulence. This is discussed in the context of growing interest in the mechanisms of bacterial colonization, antibiotic resistance, and novel vaccines.

Figure 1

Schematic diagram illustrating how S. aureus acquires resistance to methicillin and its ability to express different virulence factors. The bacterium expresses surface protein adhesins and WTA and also secretes many toxins and enzymes by activation of chromosomal genes. Adhesins and WTA have been implicated in nasal and skin colonization. Resistance to methicillin is acquired by insertion of a horizontally transferred DNA element called SCCmec. Five different SCCmec elements can integrate at the same site in the chromosome by a Campbell-type mechanism involving site-specific recombination. The mecA gene encodes a novel β-lactam–insensitive penicillin binding protein, PBP2a, which continues to synthesize new cell wall peptidoglycan even when the normal penicillin binding proteins are inhibited. Some virulence factors such as PVL and the chemotaxis inhibitory protein, CHIP, are encoded by genes located on lysogenic bacteriophages.

Figure 2

Principal component analysis of 1,056 S. aureus strains reveals genetic clusters of hypervirulent clones (17). The different cubes, plotted here in a 3D space and colored according to their source, represent each S. aureus strain analyzed in the Melles et al. study. The 5 circles indicate the 3 major (I, II, and III) and 2 minor (IVa and IVb) different phylogenetic clusters identified by AFLP. While strains from each of the genetic clusters are essentially able to cause invasive disease, some clusters contain proportionally more invasive isolates.