Staphylococcus aureus

Staphylococcus aureus and Coagulase-Negative Staphylococci

Organism

Staphylococci are gram-positive cocci typicallyarranged in irregular and often grape-like clusters.
Facultative anaerobes (def).
Staphylococcus aureus is the most pathogenic species and is implicated in a variety of infections.
Clinically common species of staphylococci other than S. aureus are often referred to as coagulase-negative staphylococci. These staphylococci are normal flora of the skin and, as such, frequently act as opportunistic pathogens, especially in the compromised host.

Habitat

Normal flora of human skin and mucous membranes.

Source

Approximately 30% of adults and most children are healthy nasal carriers of S. aureus. In the majority of S. aureus infections the source of the organism is either the healthy nasal carrier or contact with an abscess from an infected individual. The portal of entry is usually the skin.
Coagulase-negative staphylococci are normal flora of the skin.

Clinical Disease

Staphylococcus aureus causes pus-filled inflammatory lesions known as abscesses. Depending on the location and extent of tissue involvement, the infection is referred to as impetigo (thin walled-vesicles on the skin that become pustular and encrusted), folliculitis (an infected hair follicle), furuncules or boils (inflammation of the subcutaneous layers of the skin), or carbuncles (multiple infection sites with inflammation involving the skin and deeper connective tissue). It may also spread through soft tissues and cause cellulitis. S. aureus frequently causes infections of accidental wounds and postoperative wounds, although it can also infect healthy intact skin.
Less commonly, S. aureus may escape from the local lesion and spread through the blood to other body areas, causing a variety of systemic infections that may involve every system and organ. Such systemic infections include septicemia (def), septic arthritis (def), endocarditis (def), meningitis (def), and osteomyelitis (def), as well as abscesses in the lungs, spleen, liver, and kidneys.
S. aureus pneumonia may also be a secondary respiratory complication of viral infections such as measles and influenza.
S. aureus is frequently introduced into food by way of abscesses or the nasal cavity of food handlers. If it is allowed to grow and produces an enterotoxin (def), it can cause staphylococcal food poisoning.
Some strains also produce TSST-1 (toxic shock syndrome toxin-1) and cause toxic shock syndrome (def), usually associated with tampon use or wounds.
Some strains also produce exfoliatin, an exotoxin that causes scalded skin syndrome (def), an infection usually seen in infants and young children.
Coagulase-negative S. saprophyticus is a relatively common cause of urinary tract infections, especially in young, sexually active women, but is seldom isolated from other sources.
The great majority of infections caused by other coagulase-negative staphylococci, including S. epidermidis, S. haemolyticus, and S. hominis, are associated with intravascular devices (prosthetic heart valves and intra-arterial or intravenous lines) and shunts. Also quite common are infections of prosthetic joints, wound infections, osteomyelitis (def) associated with foreign bodies, and endocarditis (def).

Pathogenesis

A capsule inhibits chemotaxis of phagocytes to the infected area and resists phagocytic engulfment by leukocytes. The capsule also enables the bacterium to adhere to foreign bodies.
Peptidoglygan and teichoic acids stimulate an inflammatory response much like the lipopolysaccharide endotoxin in the gram-negative cell wall (see Fig. 1).
Produces protein A that binds to the Fc portion of antibodies, the portion that normally binds to receptors on phagocytes (see Fig. 2). In this way the bacteria become coated with antibodies in a way that prevents the antibodies from attaching bacteria to phagocytes (see Fig. 3).
Produces a variety of cytotoxins that are toxic for such cells as leukocytes (def), macrophages (def), fibroblasts (def), erythrocytes (def), and platelets (def).
Coagulase causes fibrin clots to form around the bacteria and protects them from phagocytic removal.
Hyaluronidase breals down the hyaluronic acid in connective tissue (def) enabling the bacteria to spread through tissue.
Some strains produce exfoliatin (def), an exotoxin that causes scalded skin syndrome, an infection usually seen in infants and young children.
Some strains produce toxic shock syndrome toxin-1 (TSST-1) that causes toxic shock syndrome (TSS) (def). This exotoxin is a superantigen (def) that causes excessive activation and proliferationion of T-lymphocytes (def). This leads to excessive cytokine (def) production resulting in fever, rash, and shock.
Some strains produce enterotoxins that result in nausea, vomiting, and diarrhea. This exotoxin is a superantigen that causes excessive activation and proliferation of T-lymphocytes. This leads to excessive cytokine production resulting in increased intestinal peristalsis and fluid loss.

Treatment

Treatment is typically with oxacillin or other penicillinase-resistant penicillins or vancomycin for strains resistant to oxacillin* (see antibiotic table).

*Drugs may change with time.

For a more detailed article on Staphylococcus infection, see Staphylococcus Infection , by Thomas Herchline, MD, Associate Professor, Department of Internal Medicine, Division of Infectious Disease, Wright State University. Also Staphylococcus aureus Infection by Elizabeth P. Baorto, MD, MPH, Director, Division of Pediatric Infectious Diseases, Atlantic Health System; and David Baorto, MD, PhD, Medical Knowledge Engineer, Department of Medical Informatics, Columbia University Medical Center.