Innovative Elastomers with Antimicrobial Activity May Decrease Infection Risks during Milking

Abstract

Contagious pathogens are very costly to dairy herds, and they may have zoonotic and reverse-zoonotic potentials and may contribute to the spread of antimicrobial resistance. One of the most important risk factors for spreading these infections is milking, when liner contamination may transfer the pathogens from infected to healthy cows. There is no effective protocol to prevent the transmission of infection without the segregation of infected cows. Recently, the availability of elastomers with patented antimicrobial components in their formulations has allowed the exploration of alternative methods to reduce the risk of infection. Two different types of elastomers (rubber and silicone) and nine different formulations were challenged with three major mastitis pathogens (S. aureus, S. agalactiae, and E. coli). The results that were obtained in this study were interesting and unexpected. Indeed, to our knowledge, this is the first study to show that basic rubber materials have intrinsic antimicrobial activity. Silicone elastomers did not exhibit the same levels of bactericidal activity, although they did exhibit some antibacterial capacity. A significant decrease in bacterial survival curves was observed for all the formulations tested when antimicrobial components were added. The different results observed for the various products are likely due to the different formulations and diverse manufacturing processes. The availability of these new materials that significantly reduce the bacterial load on the liner surface may reduce the risk of spreading intramammary infections during milking. This would be an important step forward in achieving global sustainability of dairy herds, consistent with the objectives of One Health, by reducing the risks of zoonotic diseases and antimicrobial treatments.

Keywords: One Health; antimicrobial resistance; elastomers; liners; mastitis; milking.

Figure 1

Killing activity of elastomer R1 and its control on S. aureus, S. agalactiae, and E. coli at two different initial concentrations (10³ CFU/mL and 10⁴ CFU/mL), measured at two different time points after contact (6 h and 24 h).

Figure 2

Killing activity of elastomer R2 and its control on S. aureus, S. agalactiae, and E. coli at two different initial concentrations (10³ CFU/mL and 10⁴ CFU/mL), measured at two different time points after contact (6 h and 24 h).

Figure 3

Killing activity of elastomers S3 and S4 and its control on S. aureus, S. agalactiae, and E. coli at two different initial concentrations (10³ CFU/mL and 10⁴ CFU/mL), measured at two different time points after contact (6 h and 24 h).

Figure 4

Killing activity of elastomers S5 and S6 and its control on S. aureus, S. agalactiae, and E. coli at two different initial concentrations (10³ CFU/mL and 10⁴ CFU/mL), measured at two different time points after contact (6 h and 24 h).

Figure 5

Killing activity of elastomers S7–S9 and their controls on S. aureus, S. agalactiae, and E. coli at two different initial concentrations (10³ CFU/mL and 10⁴ CFU/mL), measured at two different time points after contact (6 h and 24 h).