Background
Staphylococcus aureus rosenbach is an important human pathogen that belongs to the genus Staphylococcus and can cause a variety of serious infections. The enterotoxin produced by Staphylococcus aureus is very stable and difficult to be destroyed. Staphylococcus aureus can produce a variety of enterotoxins such as A, B, C, D, E, and F. Enterotoxin type A is the most common cause of Staphylococcus aureus food poisoning. Enterotoxins are extremely resistant to heat and cannot be completely destroyed when heated to 100°C for 30 minutes. They can still make people sick. Type B is the most heat-resistant, followed by type C, and type A is the worst. The cell wall of Staphylococcus aureus contains 90% peptidoglycan and 10% teichoic acid. The peptidoglycan network structure is denser than that of Gram-negative bacteria. When dyeing, crystal violet is not decolorized by alcohol after being attached, so it appears purple. On the contrary, negative bacteria do not have a cell wall structure, so the purple is washed away by alcohol and then attached to sandy red. Staphylococcus aureus is closely related to the discovery of penicillin. Fleming discovered penicillin when he discovered that some cocci were killed in his Petri dish of Staphylococcus aureus. Studies have also shown that penicillin is only effective against Gram-positive bacteria represented by Staphylococcus aureus. This is also caused by the thickness and structure of the peptidoglycan layer. The newly emerged methicillin-resistant Staphylococcus aureus, known as a superbug, is resistant to almost all human drugs, but vancomycin can deal with it. Typical Staphylococcus aureus is spherical, with a diameter of about 0.8 μm, and is arranged in the shape of grape clusters under a microscope.
Figure 1. Expansion of S. aureus in a modified motility assay.(Source: Pollitt EJ, et al., 2015)
Staphylococcus aureus has no spores or flagella, most are non-capsulated, and are Gram stain positive. Staphylococcus aureus does not have high nutritional requirements. It grows well on ordinary culture media and is aerobic or facultatively anaerobic. The optimal growth temperature is 37°C and the optimal growth pH is 7.4. It can survive for several weeks in a dry environment. The colonies on the plate are thick, shiny, round and convex, with a diameter of 1~2mm. A transparent hemolytic ring forms around the colonies on the blood plate. Staphylococcus aureus has a high degree of salt tolerance and can grow in 10~15% NaCl broth. It can decompose glucose, maltose, lactose and sucrose, producing acid but not gas. The methyl red reaction is positive and the VP reaction is weakly positive. Many strains can break down arginine, hydrolyze urea, reduce nitrate, and liquefy gelatin. Staphylococcus aureus has strong resistance and low sensitivity to sulfa drugs, but is highly sensitive to penicillin and erythromycin. It is sensitive to alkaline dyes, and one part per 100,000 of gentian violet liquid can inhibit its growth.
After Staphylococcus aureus contaminates food, it multiplies and produces enterotoxin at 20~30°C for 2 -4 hours. People will develop symptoms of acute gastroenteritis 1~5 hours after eating food containing this toxin, including nausea, vomiting and diarrhea. Food poisoning is mainly caused by enterotoxin and has nothing to do with bacteria. The minimum dose of enterotoxin causing food poisoning is 1~7.2g/kg body weight. The mechanism of action of enterotoxin may be that the toxin interacts with intestinal nerve cell receptors to stimulate the vomiting center, leading to acute gastroenteritis with vomiting as the main symptom. Use kittens or monkeys to conduct animal experiments. Take leftover food containing toxins and inject the toxins into the animals' stomachs or intraperitoneally or intravenously to observe whether the animals have reactions such as nausea, vomiting, diarrhea, chills, etc., or use immune agar diffusion method or indirect hemagglutination. The content of enterotoxin in food can be detected by serological examinations such as reverse indirect hemagglutination method, immunofluorescence method and radioimmunoassay.
Alternative Names
S. aureus Toxoid B
Staphylococcal Enterotoxin B Toxoid
SEB Toxoid
Staphylococcal Enterotoxin B Immunogen
SaTox B Toxoid
Staphylococcal Enterotoxin B Antigen
Staphylococcal Enterotoxin B Immunogen
References
- 1. Pollitt EJ, et al., Staphylococcus aureus forms spreading dendrites that have characteristics of active motility. Sci Rep. 2015, 5:17698.
References
Contribution of Staphylococcal Enterotoxin B to Staphylococcus aureus Systemic Infection
J Infect Dis
Authors: Bae JS, Da F, Liu R, He L, Lv H, Fisher EL, Rajagopalan G, Li M, Cheung GYC, Otto M.
Abstract
Staphylococcal enterotoxin B (SEB), which is produced by the major human pathogen, Staphylococcus aureus, represents a powerful superantigenic toxin and is considered a bioweapon. However, the contribution of SEB to S. aureus pathogenesis has never been directly demonstrated with genetically defined mutants in clinically relevant strains. Many isolates of the predominant Asian community-associated methicillin-resistant S. aureus lineage sequence type (ST) 59 harbor seb, implying a significant role of SEB in the observed hypervirulence of this lineage. We created an isogenic seb mutant in a representative ST59 isolate and assessed its virulence potential in mouse infection models. We detected a significant contribution of seb to systemic ST59 infection that was associated with a cytokine storm. Our results directly demonstrate that seb contributes to S. aureus pathogenesis, suggesting the value of including SEB as a target in multipronged antistaphylococcal drug development strategies. Furthermore, they indicate that seb contributes to fatal exacerbation of community-associated methicillin-resistant S. aureus infection.
Staphylococcus aureus enterotoxin A- and B-specific IgE in chronic obstructive pulmonary disease
Respir Res
Authors: Karakioulaki M, Berkemeier CM, Heijnen I, Grize L, Papakonstantinou E, Goulas A, Tamm M, Stolz D.
Abstract
Sensitization to Staphylococcus aureus enterotoxins A (SEA) and B (SEB) has been associated with asthma severity, exacerbations, and disease control. Our study aimed to investigate if there are differences in serum SEA-IgE and SEB-IgE levels between patients with chronic obstructive pulmonary disease (COPD), asthma, and controls, and to assess the association between SE sensitization and COPD clinical parameters and Th2 inflammation biomarkers in two well-defined COPD cohorts. Our findings suggest that COPD patients do not exhibit higher SEA and SEB sensitization compared to asthma patients and controls. However, in COPD patients, the presence of atopy and allergy is associated with positivity for SEA-IgE and SEB-IgE. Consequently, these allergens may aid in identifying atopic or allergic subgroups within the COPD population, but they are not directly associated with the diagnosis of COPD, elevated circulating blood eosinophils, or fractional exhaled nitric oxide (FENO) levels.