Nanoparticles for treatment of bovine Staphylococcus aureus mastitis

Abstract

Staphylococcus aureus (S. aureus) is one of the most important zoonotic bacterial pathogens, infecting human beings and a wide range of animals, in particular, dairy cattle. Globally. S. aureus causing bovine mastitis is one of the biggest problems and an economic burden facing the dairy industry with a strong negative impact on animal welfare, productivity, and food safety. Furthermore, its smart pathogenesis, including facultative intracellular parasitism, increasingly serious antimicrobial resistance, and biofilm formation, make it challenging to be treated by conventional therapy. Therefore, the development of nanoparticles, especially liposomes, polymeric nanoparticles, solid lipid nanoparticles, nanogels, and inorganic nanoparticles, are gaining traction and excellent tools for overcoming the therapeutic difficulty accompanied by S. aureus mastitis. Therefore, in this review, the current progress and challenges of nanoparticles in enhancing the S. aureus mastitis therapy are focused stepwise. Firstly, the S. aureus treatment difficulties by the antimicrobial drugs are analyzed. Secondly, the advantages of nanoparticles in the treatment of S. aureus mastitis, including improving the penetration and accumulation of their payload drugs intracellular, decreasing the antimicrobial resistance, and preventing the biofilm formation, are also summarized. Thirdly, the progression of different types from the nanoparticles for controlling the S. aureus mastitis are provided. Finally, the difficulties that need to be solved, and future prospects of nanoparticles for S. aureus mastitis treatment are highlighted. This review will provide the readers with enough information about the challenges of the nanosystem to help them to design and fabricate more efficient nanoformulations against S. aureus infections.

Keywords: S. aureus; drug delivery; mastitis; nanogel; nanoparticles; resistance.

Figure 1.

The secreted virulence factors of Staphylococcus aureus. (A) the surface and secreted protein, most of these proteins can be created during the growth phase. (B) and (C) show cross-section in the cell envelope. TSST: toxic shock syndrome toxin.

Figure 2.

Mechanisms of the immune system against S. aureus infection. (A) S. aureus attacks the immune system by various trials as preventing identification, preventing chemotaxis, regulating ROS, Resistance to Amp, and directly lysis of leukocytes. (B) Phagocytosis of bacteria by neutrophil leads to increased ROS and degranulation, which help in killing the ingested microorganism and resulted in apoptosis of neutrophil that can be removed by macrophage to aid in the resolution of infection (Rigby & DeLeo, 2012). Alternatively, bacteria may change in normal neutrophil by accelerating a delay of apoptosis or enhanced neutrophil damage, escaping the pathogen into the tissue and the occurrence of disease (Coxon et al., 1996). Abbreviation: APS: antimicrobial peptide-sensing system; Aur: aureolysin; CHIPS: chemotaxis inhibitory protein of S. aureus; CP: capsular polysaccharide; Hla: α-toxin; HlgABC: γ-hemolysin; LukGH: LukF-G and Luks-H; MprF: multiple peptide resistance factor; PIA: polysaccharide intercellular adhesion; PSMs: Phenol-soluble modulins; PVL: Panton-Valentine leukocidin; Sbi: second binding protein of immunoglobulin; SCIN: staphylococcal inhibitor of complement; SOD: superoxide dismutase; VraFG: vancomycin resistant-associated gene.

Figure 3.

The intracellular parasitism of the S. aureus.

Figure 4.

Strategies in the development and management of the biofilms.

Figure 5.

The cytotoxic effect of the nanoparticles on bacterial cells.

Figure 6.

Physicochemical parameters of nanoparticles that influence on their payloads.