Staphylococcus aureus

Staphylococcus aureus organisms are pyogenic, nonmotile, Gram-positive cocci that form grapelike clusters. These bacteria cause a myriad of skin lesions (boils, carbuncles, impetigo, and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning, and toxic shock syndrome (TSS).

Staphylococcus aureus organisms are pyogenic, nonmotile, Gram-positive cocci that form grapelike clusters. These bacteria cause a myriad of skin lesions (boils, carbuncles, impetigo, and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning, and toxic shock syndrome.

organ infections are described in other chapters. Staphylococcus epidermidis, a species that is related to S. aureus, causes opportunistic infections in catheterized patients, patients with prosthetic cardiac valves, and drug addicts. Staphylococcus saprophyticus is a common cause of urinary tract infections in young women.

Pathogenesis. S. aureus and other virulent staphylococci possess a multitude of virulence factors, which include surface proteins involved in adherence, secreted enzymes that degrade proteins, and secreted toxins that damage host cells. Staphylococci are distinguished by their large number of plasmids, which encode proteins involved in antibiotic resistance and other virulence factors.

S. aureus expresses surface receptors for fibrinogen (called clumping factor), fibronectin, and vitronectin, and uses these molecules as a bridge to bind to host endothelial cells.

Staphylococci infecting prosthetic valves and catheters have a polysaccharide capsule that allows them to attach to the artificial materials and to resist host cell phagocytosis. The lipase of S. aureus degrades lipids on the skin surface, and its expression is correlated with the ability of the bacteria to produce skin abscesses. Staphylococci also have protein A on their surface, which binds the Fc portion of immunoglobulins.

S. aureus produces multiple membrane-damaging (hemolytic) toxins, including α-toxin, which is a pore-forming protein that intercalates into the plasma membrane of host cells and depolarizes them;76 β-toxin, a sphingomyelinase; and δ-toxin, which is a detergent-like peptide. Staphylococcal γ-toxin and leukocidin lyse erythrocytes and phagocytic cells, respectively.

The exfoliative toxins produced by S. aureus are serine proteases that split the skin by cleaving the protein desmoglein 1, which is part of the desmosomes that hold epidermal cells tightly together.29 This can cause the superficial epidermis to split away from the deeper skin, making the patient vulnerable to secondary infections.

Exfoliation can occur at the site of staphylococcal skin infection (bullous impetigo) or can be widespread, when secreted toxin from a localized infection causes disseminated loss of the superficial epidermis (staphylococcal scalded-skin syndrome).

Superantigens produced by S. aureus cause food poisoning and, of more concern, toxic shock syndrome (TSS). TSS came to public attention because of its association with the use of hyperabsorbent tampons, which became colonized with S. aureus during use. It is now clear that TSS can be caused by growth of S. aureus at many sites, most commonly the vagina and infected surgical sites.

TSS is characterized by hypotension (shock), renal failure, coagulopathy, liver disease, respiratory distress, a generalized erythematous rash, and soft tissue necrosis at the site of infection. If not promptly treated, TSS can be fatal. TSS can also be caused by Streptococcus pyogenes.

Superantigens bind to conserved portions of MHC molecules and to relatively conserved portions of TCR β chains. In this manner, superantigens may stimulate up to 20% of T lymphocytes.

The stimulation of so many T lymphocytes leads to massive T-lymphocyte proliferation and cytokine release. The high levels of cytokines can lead to capillary leak and shock and may cause vomiting by affecting the nervous system in the gut or the central nervous system.

Morphology

Whether the lesion is located in the skin, lungs, bones, or heart valves, S. aureus causes pyogenic inflammation that is distinctive for its local destructiveness.

Excluding impetigo, which is a staphylococcal or streptococcal infection restricted to the superficial epidermis, staphylococcal skin infections are centered around the hair follicles. A furuncle, or boil, is a focal suppurative inflammation of the skin and subcutaneous tissue, either solitary or multiple or recurrent in successive crops. Furuncles are most frequent in moist, hairy areas, such as the face, axillae, groin, legs, and submammary folds.

Beginning in a single hair follicle, a boil develops into a growing and deepening abscess that eventually "comes to a head" by thinning and rupturing the overlying skin. A carbuncle is associated with deeper suppuration that spreads laterally beneath the deep subcutaneous fascia and then burrows superficially to erupt in multiple adjacent skin sinuses.

Carbuncles typically appear beneath the skin of the upper back and posterior neck, where fascial planes favor their spread.

Chronic abscess formation of apocrine gland regions, most frequently of the axilla, is known as hidradenitis suppurativa. Those of the nail bed (paronychia) or on the palmar side of the fingertips (felons) are exquisitely painful. They may follow trauma or embedded splinters and, if deep enough, destroy the bone of the terminal phalanx or detach the fingernail.

Staphylococcal lung infections (Fig. 8-19) have a polymorphonuclear infiltrate similar to that of pneumococcus (see Fig. 8-7) but are much more destructive of lung tissues. S. aureus lung infections usually occur in patients with predisposing conditions such as influenza or hematogenous spread of infected thrombi.

Staphylococcal scalded skin syndrome (SSSS)

Staphylococcal scalded skin syndrome (SSSS), also called Ritter disease, is caused by the exfoliative A and B toxins. It is an exfoliative dermatitis that most frequently occurs in children with staphylococcal infections of the nasopharynx or skin. In staphylococcal scalded skin syndrome, there is a sunburnlike rash that spreads over the entire body and forms fragile bullae that lead to partial or total skin loss. The intraepithelial split in staphylococcal scalded skin syndrome is in the granulosa layer, distinguishing it from toxic epidermal necrolysis, or Lyell’s disease, which is secondary to drug hypersensitivity and causes splitting at the epidermal-dermal junction.

Pathogenesis

S. aureus and other virulent staphylococci possess a multitude of virulence factors, which include surface proteins involved in adherence, secreted enzymes that degrade proteins, and secreted toxins that damage host cells. Staphylococci are distinguished by their large number of plasmids, which encode proteins involved in antibiotic resistance and other virulence factors.

S. aureus expresses surface receptors for fibrinogen (called clumping factor), fibronectin, and vitronectin, and uses these molecules as a bridge to bind to host endothelial cells.

Staphylococci infecting prosthetic valves and catheters have a polysaccharide capsule that allows them to attach to the artificial materials and to resist host cell phagocytosis.

The lipase of S. aureus degrades lipids on the skin surface, and its expression is correlated with the ability of the bacteria to produce skin abscesses.

Staphylococci also have protein A on their surface, which binds the Fc portion of immunoglobulins.

S. aureus produces multiple membrane-damaging (hemolytic) toxins, including α-toxin, which is a pore-forming protein that intercalates into the plasma membrane of host cells and depolarizes them; β-toxin, a sphingomyelinase; and δ-toxin, which is a detergent-like peptide. Staphylococcal γ-toxin and leukocidin lyse erythrocytes and phagocytic cells, respectively.

Cutaneous bullous lesions

The exfoliative toxins produced by S. aureus are serine proteases that split the skin by cleaving the protein desmoglein-1 (DSG1), which is part of the desmosomes that hold epidermal cells tightly together.

This can cause the superficial epidermis to split away from the deeper skin, making the patient vulnerable to secondary infections.

Exfoliation can occur at the site of staphylococcal skin infection (bullous impetigo) or can be widespread, when secreted toxin from a localized infection causes disseminated loss of the superficial epidermis (staphylococcal scalded-skin syndrome or SSSS).

Superantigens

Superantigens produced by S. aureus cause food poisoning and, of more concern, toxic shock syndrome (TSS). TSS came to public attention because of its association with the use of hyperabsorbent tampons, which became colonized with S. aureus during use. It is now clear that TSS can be caused by growth of S. aureus at many sites, most commonly the vagina and infected surgical sites.

TSS is characterized by hypotension (shock), renal failure, coagulopathy, liver disease, respiratory distress, a generalized erythematous rash, and soft tissue necrosis at the site of infection. If not promptly treated, TSS can be fatal. TSS can also be caused by Streptococcus pyogenes.

Superantigens bind to conserved portions of MHC molecules and to relatively conserved portions of TCR β chains. In this manner, superantigens may stimulate up to 20% of T lymphocytes. The stimulation of so many T lymphocytes leads to massive T-lymphocyte proliferation and cytokine release. The high levels of cytokines can lead to capillary leak and shock and may cause vomiting by affecting the nervous system in the gut or the central nervous system.

See also

 methicillin-resistant Staphylococcus aureus (MRSA)