Identification and characterization of a novel peptide from rainbow trout (Oncorhynchus mykiss) with antimicrobial activity against Streptococcus iniae

Streptococcus iniae in aquaculture: a review of pathogenesis, virulence, and antibiotic resistance

“…The reason is that by interacting with the bacterial cell membrane, its charge is neutralized and subsequently induces cell death by penetrating the membrane [ 43 ]. Notably, many of these peptides exhibit low toxicity to organisms [ 44 , 45 ], posing a stable and soluble molecular structure [ 46 ].…”

“… Host Recognition and Adhesion : The first step in the interaction between pathogen and host is adhesion to the host surface [ 45 ]. Key molecules in this process are bacterial adhesins, present as proteins or polysaccharides with some secreted in the form of polysaccharide capsules; adhesins are located on the bacterial cell wall and facilitate the attachment of the microorganism to host cells [ 46 , 49 , 50 ]. This binding triggers complex signalling cascades in both the pathogen and host, which can lead to extracellular colonization and invasion of underlying cells [ 51 ].…”

“…This binding triggers complex signalling cascades in both the pathogen and host, which can lead to extracellular colonization and invasion of underlying cells [ 51 ]. The adherence capacity of S. iniae to fish epithelium is attributed to the production of M-family adhesins, encoded by the simA gene, which are responsible for adhesion, invasion, and resistance to phagocytic destruction [ 46 ]. However, this adhesion capacity is enhanced by the mutant capsule Δ cpsD , where the capsule operon contains the cpsD gene, necessary for capsule polymerization [ 52 ].…”

“…This process occurs without being immediately recognized as cellular damage and takes approximately 30 min. After the penetration of the pathogen in epithelial cells, its dissemination via internalization within fish macrophages may transpire [ 46 ] and facilitate the potential invasion of other tissues or cells, while the nutrients to sustain its metabolism are simultaneously acquired [ 47 ]. Thus, as documented S. iniae strains form biofilms under both in vitro and in vivo conditions, and this may play a crucial role in colonization, invasion, and persistence process of the bacteria in the host [ 17 , 54–56 ].…”

“…Virulence, in turn, is determined by the production of extracellular molecules called virulence factors [ 17 ]. In the case of S. iniae , virulence is governed by various mechanisms, including resistance to phagocytic action, damage inflicted on host cells, and its adhesion and invasion strategies [ 46 ]. These factors trigger responses from both the innate and adaptive immune systems, resulting in an increase in the production of specific serum antibodies [ 64 ].…”