The staphylococci are important pathogenic bacteria responsible for a variety of diseases in humans and other animals. They are the most common cause of hospital acquired infection and antibiotic resistant strains (MRSA) have become endemic in hospitals in most countries causing major public health issues. In addition, the incidence of new strains that cause severe community-acquired infections in healthy people is increasing and MRSA strains are emerging in agricultural and domestic animals. In the race to understand staphylococcal pathogenesis the focus has been on genetics, as a bacterium can only do what its genes allow. The publication of the first staphylococcal whole genome sequence in 2001 paved the way for a greater understanding of the molecular basis of its virulence, evolution, epidemiology and drug resistance. Since then the available genomic data has mushroomed and this, coupled with the major advances in genetic know-how and the availability of better genetic tools, has allowed significant advances to be made.

Further reading: Staphylococcus: Molecular Genetics

Whole genome sequences for twelve diverse Staphylococcus aureus isolates are available and their annotation provides enormous insight into S. aureus physiology, capabilities and virulence. Whole genome microarrays, built using the sequences, have enabled whole genome regulatory responses to environmental conditions or global regulators to be investigated. Comparative genomics by sequencing and by multi-strain microarrays have identified the S. aureus population structure and how genomes vary, as well as suggesting that invasive isolates do not carry more virulence genes than carriage isolates.

A large amount of genetic information is available on several examples of this species and this, together with multilocus sequence typing (MLST) data on >1400 isolates from many countries has provided unique insights into the biology of the species and in particular, its ability to exploit a wide variety of niches. These studies show that although the great majority of S. aureus genes share a high degree of homology, virulence and antibiotic resistance genes carried on mobile genetic elements can drastically alter strain characteristics in the short-term giving the species a high degree of adaptability. These allow it to survive in many different human and animal tissues and provide the adaptability necessary to evolve resistance to new antibiotics.

Further reading: Staphylococcus: Molecular Genetics

See also: Plasmids

There is enormous variation between strains of S. aureus. Evolution occurs when genomes vary and the fittest bacteria are selected. Variation occurs in three major ways: single nucleotide polymorphisms (SNP) and other minor changes in conserved core genes; variation in hundreds of genes (particularly those encoding proteins that interact with host) that are associated with lineages of S. aureus; and acquisition and loss of mobile genetic elements (MGE) which often encode virulence and resistance genes. Barriers that block horizontal transfer of DNA, such as restriction modification, influence lineages and MGE. S. aureus MGE have their own complex life-cycles that control their spread and survival. Selection of the fittest bacteria is likely being driven by mammalian host factors and antibiotic use, and new strains of S. aureus are emerging that are increasingly virulent and resistant to antibiotics, causing novel healthcare issues.

Recommended reading: Staphylococcus: Molecular Genetics