Bacterial Toxins—Staphylococcal Enterotoxin B

Staphylococcus aureus is a nonmotile, ubiquitous, gram‐positive coccus which is a major human pathogen responsible for a wide range of infections, including skin and soft tissue infections, bacteremia, pneumonia, and several toxin‐mediated diseases. Among many extracellular proteins, S. aureus strains also secrete a variety of potent toxins which include alpha hemolysin, enterotoxins, leukocidins, and exfoliative toxins, all of which are directly associated with particular disease manifestations. To date, more than 33 enterotoxin sequences have been described in various S. aureus genomes. Enterotoxins are heat stable and exert their effect on the epithelium of the intestinal tract when ingested, and thus, they are a common cause of food poisoning. Several enterotoxins are potent superantigens (SAgs) that, in a non‐antigen (Ag)‐dependent way, predominantly activate CD4 + T cells (1) but also activate other immune cells. The SAgs of S. aureus include toxic shock syndrome toxin 1 (TSST‐1), enterotoxin serotypes A to E and I (sea, seb, sec, sed, see, and sei), and enterotoxin‐like serotypes G (selG), H (selH), and J to U (selJ to selU). Of these SAgs, sea to see have the ability to induce emesis in monkeys and are thus referred to as classic enterotoxins. The remaining SAgs either have not been tested for emetic activity or lack emetic activity and are therefore referred to as enterotoxin‐like proteins (selG, selH, and selJ to selU). For the most part, staphylococcal SAgs are encoded by mobile genetic elements, which include extrachromosomal plasmids as well as chromosomal prophages, transposons, and pathogenicity islands. It is noteworthy that a chromosomally carried enterotoxin‐like gene (selX) was recently identified (2). The seb gene is carried on the pathogenicity island SaPI3. The genes of SAgs selG, selI, selM, selO, and selU are located in the enterotoxin gene cluster (egc) and are among the most prevalent SAgs in clinical S. aureus isolates. They are expressed by S. aureus during logarithmic growth and shut off expression once a certain bacterial density is reached. Consequently, they do not induce a humoral response in the human host. In contrast, non‐egc‐associated SAgs (e.g., sea, seb, sec, and tsst‐1) are expressed in late‐logarithmic and stationary growth, induce a specific antibody (Ab) response in the human host, and are a prominent cause of cause toxic shock (3).