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Table 22.2 Some Diseases Often Caused by Staphylococcus aureus

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Carbuncles

p. 536

Endocarditis

p. 718

Folliculitis

p. 536

Food poisoning

p. S12

Furuncles

p. 536

Impetigo

p. 540

Osteomyelitis (bone infection)

p. 53S

Scalded skin syndrome

p. 53S

Toxic shock syndrome

p. 641

Wound infections

p. 693

tion and accumulation of polymorphonuclear leukocytes. If the infection continues, the follicle becomes a plug of inflammatory cells and necrotic tissue overlying a small abscess (figure 22.3). The infectious process spreads deeper, reaching the subcutaneous

Figure 22.3 Pathogenesis of a Boil (Furuncle)

Staphylococcus aureus infects a hair follicle through its opening on the skin surface.The infection produces a plug of necrotic material, a small abscess in the dermis, and, finally, a larger abscess in the subcutaneous tissue.

Epidermis

Dermis

Subcutaneous tissue

Figure 22.3 Pathogenesis of a Boil (Furuncle)

Staphylococcus aureus infects a hair follicle through its opening on the skin surface.The infection produces a plug of necrotic material, a small abscess in the dermis, and, finally, a larger abscess in the subcutaneous tissue.

Epidermis

Dermis

Sebaceous gland

White blood cell

Blood vessel

Sebaceous gland

White blood cell

Blood vessel

Subcutaneous tissue

Table 22.3 Virulence Factors of Staphylococcus aureus

Product

Effect

Capsule

Inhibits phagocytosis

Coagulase

May impede progress of leukocytes into infected area by producing clots in the surrounding capillaries

Exfoliatin

Separates layers of epidermis, causing scalded skin syndrome

Hyaluronidase

Breaks down hyaluronic acid component of tissue, thereby promoting extension of infection

Leukocidin

Kills white blood cells by producing holes in their cytoplasmic membrane

Lipase

Breaks down fats by hydrolyzing the bond between glycerol and fatty acids

Proteases

Degrade collagen and other tissue proteins

Protein A

Binds to Fc portion of antibody, inhibiting phagocytosis (blocks attachment to Fc receptors on white blood cells)

Toxic shock syndrome toxin

Causes rash, diarrhea, and shock

tissue where a large abscess forms. This subcutaneous abscess is responsible for the painful localized swelling that constitutes the boil. Without effective treatment, pressure within the abscess increases, causing it to expand to other hair follicles, causing a carbuncle. If organisms enter the bloodstream, the infection can spread to other parts of the body, such as the heart, bones, or brain. ■ abscess, p. 692

The properties of S. aureus that contribute to its virulence are shown in table 22.3. Virtually all strains possess an unusual cell wall component called protein A. This protein, some of which is released from the cell, prevents the antibody from attaching to Fc receptors on phagocytes. Thus, a major effect of protein A is to interfere with phagocytosis. Many strains of S. aureus growing in body tissues synthesize a polysaccharide capsule that also inhibits phagocytosis. The S. aureus genes responsible for capsule formation are activated following invasion of tissue. Besides producing these cellular components, S. aureus produces numerous extracellular products that might contribute to virulence. These products include leukocidins, which kill white blood cells; hyaluronidase, which degrades hyaluronic acid, a component ofhost tissue that helps hold the cells together; proteases, which degrade various host proteins including collagen, the white fibrous protein found in skin, tendons, and connective tissue; and lipases, which degrade lipids. Lipases may assist colonization of the oily hair follicles by strains of S. aureus that cause follicle infections. ■ protein A, p. 470 ■ Fc receptors, p. 470

Epidemiology

Staphylococcus aureus inhabits the nostrils of virtually everyone at one time or another, each nostril containing as many as 108 bac teria. About 20% of healthy adults have continually positive nasal cultures for a year or more, while over 60% will be colonized at some time during a given year. The organisms are mainly disseminated to other parts of the body and to the environment by the hands. Although the nostrils seem to be the preferred habitat of S. aureus, moist areas of skin are also frequently colonized. People with boils and other staphylococcal infections shed large numbers of S. aureus and should not work with food, or near patients with surgical wounds or chronic illnesses. Staphylococci survive well in the environment, which favors their transmission from one host to another. Since S. aureus is so commonplace and there are many different strains in the population, epidemics of staphylococcal disease can generally be traced to their sources only by precise identification of the epidemic strain. Techniques for characterizing strains of S. aureus include the pattern of susceptibility to multiple antibiotics, bacteriophage typing, and plasmid identification. All of these techniques, however, have their limitations. A more reliable method is to compare the electrophoretic patterns of the DNA fragments produced by treatment with a restriction enzyme.^ bacteriophage typing, p. 257 ■ restriction enzymes, pp. 219,231

Prevention and Treatment

Prevention of staphylococcal skin disease is very difficult. Attempts are made to eliminate the carrier state by applying an antistaphy-lococcal cream to the nostrils, and using soaps containing an anti-staphylococcal agent such as hexachlorophene to bathe the skin. Effective treatment of boils and carbuncles often requires that the pus be surgically drained from the lesion and an antistaphylococcal medicine be given. Antibiotic treatment is complicated by the fact that about 90% of S. aureus strains produce the penicillin-destroying enzyme penicillinase, a ^-lactamase, and so penicillin cannot routinely be used in treatment. Some strains are resistant to multiple antibiotics including ^-lactamase-resistant penicillins, cephalosporins, and vancomycin. ■ cephalosporins, p. 515

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