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Staphylococcus aureus (S. aureus) is a major pathogen involved in ruminant mastitis and present worldwide. Clinical signs of S. aureus mastitis vary considerably and are largely dependent on strain-specific factors. A comparison of two S. aureus strains that reproducibly induced either severe (O11) or mild (O46) mastitis in ewes revealed that the transcriptional regulator sigS was mutated in O46 (Le Maréchal et al., 2011. PLoS One. 6 (11) e27354. doi:10.1371/journal.pone.0027354). In the present paper, we analysed the sigS sequence in 18 other S. aureus strains isolated from goat or ewe mastitis and found a 4-bp deletion similar to that of the O46 sigS gene in three strains associated with subclinical ewe mastitis. This sigS gene was disrupted in strain O11 (O11ΔsigS), so our aim was to investigate its involvement in the severity of infections in the context of mastitis. The wild type (wt) and mutant strains were then characterized in vitro to determine the involvement of sigS in the response S. aureus under various stress conditions, and assess its influence on the cytotoxicity of the pathogen, its invasive capacity and biofilm formation. The strains were compared in vivo in an experimental mouse mastitis model in which clinical signs and cytokine production were evaluated at 24 h post-infection. While no significant differences in the effect on bacterial growth between O11 and O11ΔsigS were observed either in vitro or in vivo, a significantly weaker in vivo production of interleukin (IL)-1α, IL-1β, and Tumor Necrosis Factor (TNF)-α was measured in the mammary glands infected with the mutant strain, suggesting that infection with O11ΔsigS induced an attenuated local innate immune response. These results suggest an impact of sigS disruption on S. aureus pathogenesis in a ruminant mastitis context. This disruption is probably involved in, and may partly explain, the milder symptoms previously observed in S. aureus O46-induced mastitis in ewes.

Staphylococcus aureus is an opportunistic pathogen in dairy ruminants where it is found in healthy carriage and can be a major cause of mastitis. A better knowledge of the host-pathogen interactions is needed to tackle this serious animal health problem. This study aimed at identifying S. aureus proteins differentially expressed by S. aureus in nasal colonization versus mastitis. Serological proteome analysis (SERPA) was used to examine protein samples prepared from culture supernatants of S. aureus strains originally isolated from gangrenous mastitis and nasal carriage (O11) or subclinical mastitis (O46) and to compare patterns of immune-reactive proteins. These staphylococcal proteins were revealed by sera obtained from ewes suffering from S. aureus mastitis and by sera obtained from healthy nulliparous ewes (i.e. no lactation and no mastitis or other symptoms) that were nasally colonized by S. aureus. Altogether 49 staphylococcal immune-reactive proteins were identified in this study. Patterns of proteins revealed by sera from infected- or healthy carrier- animals were comparable and analysis singled out one immune-reactive protein, N-acetylmuramyl-L-alanine amidase, which was recognized by each of the 6 sera from infected animals, when tested individually, and not by the sera of healthy carriers. This is the first study that compares the S. aureus seroproteome in colonization versus mastitis context in ruminants. These results open avenues for studies aiming at a better understanding of the balance between infection and commensal lifestyle in this opportunistic pathogen and at new prevention strategies.

The relationship between 10 cell-level descriptors in the first lactation and the risk of clinical mastitis in the second lactation was studied in 10 205 Holstein cows from 1254 commercial herds using logistic regression. These 10 cell descriptors were based on the mean cell level over the whole first lactation, on the cell level at the beginning or at the end of the first lactation or on the proportion of cell counts below or above given thresholds. Separate analyses were also performed for subsets of herds defined according to their clinical mastitis incidence risk and their lactation mean somatic-cell count (SCC). Odds of clinical mastitis in second lactation was highest (lowest) for high- (low-) yielding cows. All cell descriptors provided consistent results. Lower (higher) mean cell level, higher (lower) proportion of low SCC values, and lower (higher) proportion of high SCC values in the first lactation were associated with a lower (higher) risk of clinical mastitis in the second lactation. The same trends were observed in all subgroups of herds. Cows with the lowest mean SCC in the first lactation had the lowest risk for clinical mastitis in the second lactation. This suggests that selection for decreased SCC may effectively reduce clinical mastitis incidence and that the breeding goal should favor cows with the lowest observed SCC.

Individual risk factors for clinical mastitis within the first month of lactation (early clinical mastitis, ECM) were analyzed in 695 Holstein multiparous cows (561 ECM- and 134 ECM+) which were clinical mastitis-free during the previous lactation. They belonged to 44 herds from the French Brittany region and were surveyed for 4 years. Individual biological parameter levels during the last 2 months of gestation, production of the preceding lactation and calving conditions and health were the available explanatory variables. The construction and explanation model used multiple logistic regression run with herd as a fixed effect. High precalving plasma ceruloplasmin oxidase (p < 0.01) and low glutamate dehydrogenase (p < 0.05) activities, high 305-day previous-lactation milk yield (p < 0.001) and milk protein content at the last milk-test day before drying-off (p < 0.01) were the significant risk factors for ECM occurrence. Intensive production and unsatisfactory dietary conditions (energy and antioxidants) would increase ECM risk in the dairy cow. Further studies should be conducted to determine if metabolic and/or genetic factors could explain the relationship between ceruloplasmin and subsequent ECM occurrence.