What question did this study set out to answer?

This research aims to evaluate the association between Staphylococcus aureus virulence genes and the severity of bovine mastitis in dairy cows.

February 9, 2026Open Access

Association of Staphylococcus aureus virulence factors with clinical and subclinical bovine mastitis

Key Points

This research aims to evaluate the association between Staphylococcus aureus virulence genes and the severity of bovine mastitis in dairy cows.
Analyzed 50 S. aureus isolates from subclinical mastitis and 101 from clinical mastitis.
Screened virulence genes related to enterotoxins, biofilm production, toxic shock syndrome, and adhesion.
Used pulsed-field gel electrophoresis to differentiate genetic profiles between disease presentations.
Clinical mastitis isolates showed a higher prevalence of virulence genes (72.7%) compared to subclinical (63.6%).
Most common genes in all isolates included icaD (99.3%), eno (98%), and clfA (78.8%).
Distinct genetic profiles observed; no single cluster included isolates causing both clinical and subclinical mastitis.

Abstract

Staphylococcus aureus is a major pathogen responsible for both clinical and subclinical bovine mastitis. Its ability to persist within the mammary gland and evade host immune responses makes it particularly significant for herd health and dairy production. So, this study aimed to evaluate whether the presence and diversity of S. aureus virulence genes mastitis-causing are associated with the onset and severity of mastitis in dairy cows. We analyzed 50 S. aureus isolates obtained from milk samples of cows with subclinical mastitis (SM) and 101 isolates from clinical mastitis (CM), including 28 from mild and 73 from moderate cases. These isolates were screened for genes encoding enterotoxins (sea, seb, sec, sed, see, seg, seh, sei, and sej), biofilm production (bap, icaA, and icaD), toxic shock syndrome toxin (tsst-1), Panton-Valentine leukocidin (pvl), and microbial surface components recognizing adhesive matrix molecules (fnbA, fnbB, fib, clfA, clfB, cna, eno, and ebpS). In addition, pulsed-field gel electrophoresis (PFGE) was used to differentiate the genetic profiles associated with the various disease presentations. The CM isolates presented 16 out of 22 (72.7%) virulence genes compared with 14 (63.6%) in SM isolates. Regardless of mastitis severity, icaD (99.3%), eno (98%), and clfA (78.8%) were the most frequently observed, and seb and sej were not found. Our results also revealed that the virulence genes significantly associated with CM were fnbA, fib, clfA, clfB, cna, ebpS, seg, seh, sei, bap, and icaA. The PFGE revealed that no single cluster included isolates causing both CM and SM. However, CM clusters contained isolates from both mild and moderate mastitis cases. Although the host is a significant variable in the development of mastitis, our findings demonstrate that the virulence profile can play a crucial role in disease progression, as further supported by PFGE results, which showed a distinct separation between CM and SM clusters.

Demander à l'IA

Bookmark

View Full Paper