Staphylococcus aureus

Abstract

Staphylococcus aureus, a natural inhabitant of the human and animal body, is mostly associated with community-acquired and nosocomial infections, which can be fatal in immunodeficient patients. Methicillin and vancomycin-resistant S. aureus can cause serious nosocomial infections in humans. S. aureus also causes mastitis in the cows and joint infection in humans, animals and poultry. Staphylococci are also responsible for food poisoning characterized by severe vomiting and cramping with or without diarrhea. S. aureus produces a large number of toxins and enzymes, of which the enterotoxins (24 serotypes of toxins are identified) are most important in the production of gastroenteritis (vomiting and diarrhea) and superantigen-associated illness. Enterotoxins are heat-stable and are produced when the temperature of food is at or above 46 °C. Consumption of preformed toxins induces vomiting with or without diarrhea within 30 min–8 h (average 3 h). The enterotoxin induces the release of 5-HT (5-hydroxytryptamine) from mast cells, which stimulates vagal nerves in the stomach lining and induces vomiting. Enterotoxins are also called superantigens, because they form a complex with MHC class II molecules on the surface of antigen-presenting cells, activating and proliferating T cells to produce massive amounts of cytokines (IL-2, IFNγ, IL-1, TNF-α) that contribute to fatal toxic shock syndrome. The genes for enterotoxin production are present in pathogenicity islands in the chromosome, in plasmids, in transposons, and in temperate bacteriophages. Toxin production is regulated by a two-component regulatory system called agrAC (accessory gene regulator). Strict hygienic practices are crucial in preventing staphylococcal food poisoning. Skin infection or systemic infection requires antibiotic therapy, while the foodborne intoxication does not require antibiotic therapy since the disease is caused by the toxin and it is mostly self-limiting.