Staphylococcus aureus produces a variety of toxins, including staphylococcal enterotoxins (SEs) and staphylococcal-like (SEl) proteins. SEs, such as SEA to SEE, are potent superantigens with emetic activity, while SEl proteins, like SElL and SElQ, have not been shown to cause emesis in primates. SEs and SEls are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, and the staphylococcal cassette chromosome (SCC). SEs are a major cause of food poisoning, typically occurring after ingestion of contaminated foods like meat and dairy products. Symptoms include rapid onset of nausea, vomiting, and diarrhea, with the illness usually self-limiting. SEA is the most common cause of staphylococcal food poisoning globally, though other SEs have also been implicated. New SE/SEl toxins, such as SEH, have been associated with food poisoning, but many SEl toxins remain untested for emetic activity. SEs are resistant to proteolytic enzymes and heat, allowing them to survive in the digestive tract. SEs are produced during the logarithmic phase of growth and are active in high nanogram to low microgram quantities. They interact with MHC class II molecules and T-cell receptors, leading to T-cell activation and potentially lethal toxic shock syndrome. SEs are found in various foods, including meat, dairy, and salads, and are often linked to food handlers carrying the bacteria. SEs are encoded on mobile genetic elements, such as plasmids, prophages, and pathogenicity islands, and their presence can influence the virulence of S. aureus. The egc gene cluster is a major source of SEs and SEls, with various subtypes identified. SEs and SEls play a significant role in food poisoning outbreaks, with SEA being the most commonly reported. While SEs are well characterized, the role of SEls in pathogenesis remains understudied. The study highlights the importance of understanding SEs and SEls in the context of food poisoning and their potential impact on public health.Staphylococcus aureus produces a variety of toxins, including staphylococcal enterotoxins (SEs) and staphylococcal-like (SEl) proteins. SEs, such as SEA to SEE, are potent superantigens with emetic activity, while SEl proteins, like SElL and SElQ, have not been shown to cause emesis in primates. SEs and SEls are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, and the staphylococcal cassette chromosome (SCC). SEs are a major cause of food poisoning, typically occurring after ingestion of contaminated foods like meat and dairy products. Symptoms include rapid onset of nausea, vomiting, and diarrhea, with the illness usually self-limiting. SEA is the most common cause of staphylococcal food poisoning globally, though other SEs have also been implicated. New SE/SEl toxins, such as SEH, have been associated with food poisoning, but many SEl toxins remain untested for emetic activity. SEs are resistant to proteolytic enzymes and heat, allowing them to survive in the digestive tract. SEs are produced during the logarithmic phase of growth and are active in high nanogram to low microgram quantities. They interact with MHC class II molecules and T-cell receptors, leading to T-cell activation and potentially lethal toxic shock syndrome. SEs are found in various foods, including meat, dairy, and salads, and are often linked to food handlers carrying the bacteria. SEs are encoded on mobile genetic elements, such as plasmids, prophages, and pathogenicity islands, and their presence can influence the virulence of S. aureus. The egc gene cluster is a major source of SEs and SEls, with various subtypes identified. SEs and SEls play a significant role in food poisoning outbreaks, with SEA being the most commonly reported. While SEs are well characterized, the role of SEls in pathogenesis remains understudied. The study highlights the importance of understanding SEs and SEls in the context of food poisoning and their potential impact on public health.