Staphylococcus aureus is an opportunistic bacterial pathogen that frequently causes chronic and persistent infections in humans and animals. S. aureus is well known for its potential to cause subclinical, persistent bovine intramammary infections (IMI) in dairy cattle, which are difficult to treat by antibiotics and often require premature culling. The adaptation process of S. aureus to the host environments requires complex physiological changes and the emergence of specific host-adapted S. aureus subtypes is thought to be crucial for persistence of S. aureus in the bovine mammary gland. Thus, this project aims to shed light into the mechanisms contributing to S. aureushost-adaptive lifestyles in chronic bovine IMI. Using FTIR spectroscopy as a high throughput metabolic fingerprinting method [1,2], we followed the adaptation of S. aureus to its host during the progression of chronic, subclinical IMI in dairy cattle.
A comparison between the initial and host-adapted isolates showed that host adaptation results in reduced capsule expression but increased biofilm formation. Exoproteome analysis revealed an altered proteolytic cascade of Aur, SspA and SspB resulting in increased enzymatic activity for SspA in the host-adapted isolate, assuming that increased bacterial proteolysis might play an important role in chronicity. Furthermore, in vitro and in vivo studies, employing bovine mammary epithelial (Mac-T) cells and an insect model, revealed significant differences in the pathogenic characteristics of the initial and within-host adapted S. aureus isolates, which will be discussed. In summary, FTIR spectroscopy, used as a biophotonic method to follow S. aureus host adaptation, allowed to generate of a set of host-adapted prototype strains with phenotypic features linked to bacterial chronicity. This strain panel provides not only the basis to decipher the mechanism of host adaptation in detail but could also open new avenues for the development of effective strategies to combat persistent S. aureus IMI infections.