SummaryStaphylococci 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 speciesspecific coagulation activity; however, the SaPIcoded 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.

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. In order 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 natural nucleotide mutation was required and sufficient to convert a human-specific S. aureus strain into one which 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 micro-organism during its evolution highlights the capacity of some pathogens to readily expand into novel host-species populations.

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 2O2 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 2O2 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 H2O2 lethality. Because the vast majority of S. aureus strains are lysogenic, the production of H 2O2 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 2O2. This is apparently because they are resistant to the DNAdamaging 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.hydrogen peroxide ͉ SOS response ͉ Staphylococcus aureus ͉ Streptococcus pneumoniae ͉ bacterial interference

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Infections caused by methicillin-resistant Staphylococcus aureus (MRSA) have been a growing problem in human medicine since the 1960s, and more recently in veterinary medicine with the appearance of livestock-associated MRSA (LA-MRSA). Nevertheless, information about the presence of MRSA in rabbits is quite scarce since only one LA-MRSA identification has been previously reported. The present study aimed to determine genotypic characterization by verifying the presence of resistance determinants, virulence, and toxin genes of different S. aureus strains that cause lesions in rabbits, and their phenotypic traits based on the antimicrobial susceptibility profile. The analysis of 240 S. aureus isolates obtained from different lesion types collected from 89 Spanish and Portuguese rabbit commercial farms in the last 4 years (2014–2017) was performed. The methicillin-resistant gene mecA was found in 11.25% of the studied isolates (27 of 240) from 19 farms (13 Spanish and 6 Portuguese). Staphylococcal cassette chromosome mec (SCCmec) typing predominantly revealed type III (n = 15). Additionally, three MRSA isolates carrying the mecC gen were detected in samples from three different farms (two Spanish and one Portuguese). None of the 30 MRSA isolates was PVL-positive or tst-positive. After the multilocus sequence typing (MLST) procedure, 16 belonged to ST2855, 6 to ST146, 6 to ST398, and 2 ST4774. No ST121 isolate was mec-positive. ST398 and ST4774 isolates lacked the immune-evasion-cluster (IEC) genes. ST2855 strains were associated with the presence only of the sak gene, and ST146 isolates were ascribed to IEC type E. Therefore, this is the first description of LA-MRSA from rabbits belonging to ST2855. Interestingly, one ST2855 and two ST4774 isolates were mecC-positive, which could act as a mecC-MRSA reservoir. More studies are needed to further characterize these isolates and their relationship with humans and other animal species.