Summary: Staphylococci adapt specifically to various animal hosts by genetically determined mechanisms that are not well understood. One such adaptation involves the ability to coagulate host plasma, by which strains isolated from ruminants or horses can be differentiated from closely related human strains. Here, we report first that this differential coagulation activity is due to animal‐specific alleles of the von Willebrand factor‐binding protein (vWbp) gene, vwb, and second that these vwb alleles are carried by highly mobile pathogenicity islands, SaPIs. Although all Staphylococcus aureus possess chromosomal vwb as well as coagulase (coa) genes, neither confers species‐specific coagulation activity; however, the SaPI‐coded vWbps possess a unique N‐terminal region specific for the activation of ruminant and equine prothrombin. vWbp‐encoding SaPIs are widely distributed among S. aureus strains infecting ruminant or equine hosts, and we have identified and characterized four of these, SaPIbov4, SaPIbov5, SaPIeq1 and SaPIov2, which encode vWbp^Sbo4, vWbp^Sbo5, vWbp^Seq1 and vWbp^Sov2 respectively. Moreover, the SaPI‐carried vwb genes are regulated differently from the chromosomal vwb genes of the same strains. We suggest that the SaPI‐encoded vWbps may represent an important host adaptation mechanism for S. aureus pathogenicity, and therefore that acquisition of vWbp‐encoding SaPIs may be determinative for animal specificity.

A surprising example of interspecies competition is the production by certain bacteria of hydrogen peroxide at concentrations that are lethal for others. A case in point is the displacement of Staphylococcus aureus by Streptococcus pneumoniae in the nasopharynx, which is of considerable clinical significance. How it is accomplished, however, has been a great mystery, because H ₂ O ₂ is a very well known disinfectant whose lethality is largely due to the production of hyperoxides through the abiological Fenton reaction. In this report, we have solved the mystery by showing that H ₂ O ₂ at the concentrations typically produced by pneumococci kills lysogenic but not nonlysogenic staphylococci by inducing the SOS response. The SOS response, a stress response to DNA damage, not only invokes DNA repair mechanisms but also induces resident prophages, and the resulting lysis is responsible for H ₂ O ₂ lethality. Because the vast majority of S. aureus strains are lysogenic, the production of H ₂ O ₂ is a very widely effective antistaphylococcal strategy. Pneumococci, however, which are also commonly lysogenic and undergo SOS induction in response to DNA-damaging agents such as mitomycin C, are not SOS-induced on exposure to H ₂ O _2. This is apparently because they are resistant to the DNA-damaging effects of the Fenton reaction. The production of an SOS-inducing signal to activate prophages in neighboring organisms is thus a rather unique competitive strategy, which we suggest may be in widespread use for bacterial interference. However, this strategy has as a by-product the release of active phage, which can potentially spread mobile genetic elements carrying virulence genes.

José Penadés and colleagues examine host adaptation and specificity for Staphylococcus aureus with analysis of the whole-genome sequences of strains isolated from humans or rabbits. They find that a rabbit-specific clone evolved through a human-to-rabbit host jump, enabled by a single mutation in dltB. The capacity of microbial pathogens to alter their host tropism leading to epidemics in distinct host species populations is a global public and veterinary health concern. To investigate the molecular basis of a bacterial host-switching event in a tractable host species, we traced the evolutionary trajectory of the common rabbit clone of Staphylococcus aureus. We report that it evolved through a likely human-to-rabbit host jump over 40 years ago and that only a single naturally occurring nucleotide mutation was required and sufficient to convert a human-specific S. aureus strain into one that could infect rabbits. Related mutations were identified at the same locus in other rabbit strains of distinct clonal origin, consistent with convergent evolution. This first report of a single mutation that was sufficient to alter the host tropism of a microorganism during its evolution highlights the capacity of some pathogens to readily expand into new host species populations.

The main reasons for culling adult rabbit does on two Spanish rabbit farms were investigated for a year. The most important conditions were mastitis (33·3 per cent), followed by subcutaneous abscesses (9·9 per cent) and pyometra (8·7 per cent). Staphylococcus aureus infections were the most severe problem, the organism being isolated from 69·2 per cent of infected animals. Pasteurella species were more prevalent in cases of pyometra and pneumonia. Two strains of S aureus were identified by using polymorphism of the coagulase gene as the criterion. One of these strains was responsible for the majority of the staphylococcal infections and was isolated from several pathological processes.