Multiple Roles of Staphylococcus aureus Enterotoxins: Pathogenicity, Superantigenic Activity, and Correlation to Antibiotic Resistance

Abstract

Heat-stable enterotoxins are the most notable virulence factors associated with Staphylococcus aureus, a common pathogen associated with serious community and hospital acquired diseases. Staphylococcal enterotoxins (SEs) cause toxic shock-like syndromes and have been implicated in food poisoning. But SEs also act as superantigens that stimulate T-cell proliferation, and a high correlation between these activities has been detected. Most of the nosocomial S. aureus infections are caused by methicillin-resistant S. aureus (MRSA) strains, and those resistant to quinolones or multiresistant to other antibiotics are emerging, leaving a limited choice for their control. This review focuses on these diverse roles of SE, their possible correlations and the influence in disease progression and therapy.

Characterisation of the Virulence Factors and Genetic Types of Methicillin Susceptible Staphylococcus aureus from Patients and Healthy Individuals

“…This is a cause of concern as enterotoxins are often associated with food poisoning and several allergic and autoimmune diseases [1,3].…”

“…Enterotoxins are short secreted proteins that are usually heat-resistant, and usually resistant to most of the proteolytic enzymes produced by the human body [3]. There are more than 20 different types of enterotoxins (SEA to SEE, SEG to SEI, SEIJ, SEIK-SEIQ, SER to SET, SEW, SEIU) being reported [4].…”

Staphylococcal Enterotoxins, Stayphylococcal Enterotoxin B and Bioterrorism

“…As noted previously, S. aureus is a ubiquitous microorganism with a world-wide distribution, and is responsible for causing large numbers of food poisoning cases throughout the world (Bergdoll, 1989;Le Loir et al, 2003;Ortega, et al, 2010). In its normal environment, the gram-positive cocci and its toxins do not cause disease; however, when introduced into foods such as cream, mayonnaise, or similar foods, the bacteria grow rapidly secreting the exotoxins which then contaminate the food.…”

“…Vaginal epithelial cells were also shown to bind TSST-1 and induce TNF production while treatment of epithelial cells with TSST-1 or SEB induced production of MIP-3 and IL-8 (Brosnahan et al, 2001;Peterson, et al, 2005). SE-induced shock causes severe damage to the endothelial vasculature and vascular leak contributes significantly to TSS pathology (Krakauer, 1994;Ortega et al 2010). Elevated levels of vascular endothelial growth factor are observed in serum from patients with sepsis or septic shock (Karlsson et al 2008).…”

“…However, such interactions do not explain the disease pathophysiology. Patients with SE intoxication can exhibit rather severe gastrointestinal damage including mucosal hyperemia, regional edema, petechiae, and purulent exudates (Ortega et al, 2010;Palmer, 1951). SEs cross the intestinal epithelial barrier and gain access to local and systemic lymphoid tissues, suggesting that activation of local immune tissue may be partially responsible for gastrointestinal damage (Hamad et al, 1997).…”