Pathogenesis

Streptococcus pyogenes causes a wide variety ofillnesses, which is not surprising considering its vast arsenal of virulence factors. Some of these disease-causing mechanisms are structural components of the outer cell wall that enable the bacterium to foil host defenses (figure 23.3), while others are destructive enzymes and toxins released by the bacterial cell. Some of the virulence factors of S. pyogenes are listed here and summarized in table 23.2:

■ C5a peptidase is an enzyme released by S. pyogenes. This enzyme destroys the complement component C5a, a substance responsible for attracting phagocytes to the site of a bacterial infection.

■ A capsule composed of hyaluronic acid, present on only some strains of S. pyogenes, inhibits phagocytosis and aids penetration of tissues by causing epithelial cells to separate. Hyaluronic acid is a normal component of human tissue, and its presence as a S. pyogenes capsule may impair recognition of the bacterium by the body's immune system.

■ M protein causes the degradation of complement component C3b, an opsonin that would otherwise promote phagocytosis of the bacteria. M protein is essential for the virulence of S. pyogenes, because antibody

566 Chapter 23 Respiratory System Infections

Figure 23.3 Components of the Cell Envelope of Streptococcus pyogenes The M protein is essential for virulence, while the group carbohydrate helps identify the species. Protein F binds the bacterium to epithelial cells, while protein G helps interfere with phagocytosis by binding to the Fc portion of antibodies. Hyaluronic acid interferes with phagocytosis and may aid penetration of epithelium.

Hyaluronic -acid capsule

Peptidoglycan

Cytoplasmic-

membrane

M protein ^Group carbohydrate

Hyaluronic -acid capsule

Peptidoglycan

Cytoplasmic-

membrane

Protein G

Streptococcus Pyogenes

Streptococci

Protein F

M protein ^Group carbohydrate

Lipoteichoic acid

Protein F

Streptococci to it prevents infection from occurring. Unfortunately, more than 80 different kinds of M protein exist among the many strains of S. pyogenes, and antibody to one type of M protein does not prevent infection by a S. pyogenes strain that has another kind of M protein.

■ Protein F of the cell wall mediates attachment of S. pyogenes to the throat by adhering to a protein found on the surface of epithelial cells.

■ Protein G of the S. pyogenes cell wall has a function like that of the protein A of Staphylococcus aureus in binding the Fc segment of immunoglobulin G. The effect is to prevent phagocytosis mediated by specific antibody against the bacterium.

■ Streptococcal pyrogenic exotoxins (SPEs) are a family of genetically similar exotoxins produced by strains of S. pyogenes that cause severe streptococcal diseases frequently unrelated to strep throat. These diseases include scarlet fever, streptococcal toxic shock syndrome, and "flesh eating" necrotizing fasciitis. Only scarlet fever is usually preceded by strep throat symptoms. These exotoxins are superantigens, causing massive activation of T cells. The resulting uncontrolled release of cytokines is probably responsible for the seriousness of these infections. ■ complement, p. 381 ■ staphylococcal protein A, p. 470 ■ superantigens, p. 474 ■ cytokines, p. 379 ■ opsonins, pp. 383,399

Protein G

Table 23.2 Virulence Factors of Streptococcus pyogenes

Product

Effect

C5a peptidase

Inhibits attraction of phagocytes by destroying C5a

Hyaluronic acid capsule

Inhibits phagocytosis; aids penetration of epithelium

M protein

Interferes with phagocytosis by causing breakdown of C3b opsonin

Protein F

Responsible for attachment to host cells

Protein G

Interferes with phagocytosis by binding Fc segment of IgG

SPEs

Superantigens responsible for scarlet fever, toxic shock, "flesh eating" fasciitis

Streptolysins O and S

Lyse leukocytes and erythrocytes

Tissue degrading enzymes

Enhance spread of bacteria by breaking down DNA, proteins, blood clots, tissue hyaluronic acid

■ Streptolysins O and S are the proteins responsible for /-hemolysis. These hemolysins lyse erythrocytes and leukocytes by making holes in their cell membranes.

■ A number of other enzymes produced by S. pyogenes, including DNase, protease, streptokinase, and hyaluronidase, degrade tissue and probably enhance the spread of the bacterium. The tissue destruction these enzymes cause may trigger the inflammatory response, which in turn leads to the symptoms of strep throat.

Complications of streptococcal pharyngitis can occur during the acute illness. One example, scarlet fever, is due to ery-throgenic toxin, an SPE released from the infection site, that enters the bloodstream and circulates throughout the body, causing a redness of the skin and a whitish coating of the tongue. Another example is quinsy, a painful abscess that develops around one of the tonsils.

Other complications develop days or weeks after the acute illness, often when S. pyogenes has already been eliminated from the body. One of these late complications, acute glomeru-

Aoitic valve is pushed opten when ventricle contracts

Aortic valve

Aoitic valve is pushed opten when ventricle contracts

23.3 Bacterial Infections of the Upper Respiratory System 567

lonephritis, was discussed in chapter 22. Another late complication is acute rheumatic fever. ■ acute glomerulonephritis, p. 540

The symptoms of acute rheumatic fever, including fever, joint pain, chest pain, nodules under the skin, rash, and uncontrollable jerky movements, reflect an inflammatory process involving various tissues, especially the joints, heart, skin, and brain. Heart failure and death can occur during the acute illness, but usually symptoms subside with rest and anti-inflammatory medicines such as aspirin. Chorea, the condition manifest as jerky movements, reflects brain involvement and generally begins after the other symptoms subside. Rheumatic fever often results in damage to the heart valves, causing one or more to leak and lead to heart failure later in life. Significant damage occurs primarily on the left side of the heart (figure 23.4). Normally, oxygenated blood returning from the lungs enters the left ventricle through the mitral, or bicuspid, valve. This valve closes as the heart begins to contract, while the aortic, or semilunar, valve is pushed open as the contracting heart muscle of the left ventricle forces the blood into the circulation. When the heart finishes contracting and begins to relax, the aortic valve closes and the mitral valve opens. If either of the valves fails to open and close properly, the heart muscle has to work hard to deliver enough blood to the circulation. Heart failure results when it can no longer do so. The damaged valves are also subject to

Aortic valve

Als Pathogensis

Normal Heart

Blood enters the left atrium and passes down - through the mitral valve.

Left atrium Mitral valve

Left ventricle err

Bacterial infection, clot

Normal Heart

Leaking aortic valve

Figure 23.4 Rheumatic Heart Disease Damage to the heart valves results from an immune reaction, the nature of which is still controversial.The damaged area sometimes becomes infected by mouth or skin organisms years after acute rheumatic fever, resulting in subacute bacterial endocarditis.

Left ventricle err

Bacterial infection, clot

Leaking aortic valve

Figure 23.4 Rheumatic Heart Disease Damage to the heart valves results from an immune reaction, the nature of which is still controversial.The damaged area sometimes becomes infected by mouth or skin organisms years after acute rheumatic fever, resulting in subacute bacterial endocarditis.

Rheumatic Heart

Rheumatic Heart with Subacute Bacterial Endocarditis

Rheumatic Heart

Rheumatic Heart with Subacute Bacterial Endocarditis

568 Chapter 23 Respiratory System Infections infection, usually by bacteria from the normal skin or mouth flora, causing subacute bacterial endocarditis. ■ inflammation, p. 385 ■ subacute bacterial endocarditis, p. 718

Acute rheumatic fever is a complication of throat, not skin, S. pyogenes infections. Despite many years of study, its pathogenesis is not understood. Symptoms usually begin about 3 weeks after the onset of untreated streptococcal pharyngitis. Cultures of the blood, heart, and joint tissues are negative for S. pyogenes, and antibodies against the bacterium are present in the blood of the patient. One theory is that these antibodies could attack a tissue antigen that is similar to a S. pyogenes antigen, starting an autoimmune process. Another theory is that some streptococcal product, present in only a small percentage of strains, damages the tissue directly or makes it susceptible to attack by the immune system. Genetic factors probably play a role in the development of rheumatic fever, because it occurs more commonly in individuals with certain MHC types. Over-all, the risk of developing acute rheumatic fever after severe, untreated streptococcal pharyngitis is 3% or less. Those with untreated mild pharyngitis have a lower risk. Mild infections result in many cases of rheumatic fever, however, because they are common and much more likely to go untreated. In the United States, rheumatic fever has generally declined in incidence over many years, probably as a result of timely treatment of streptococcal pharyngitis with antibiotics, and a decline in the streptococcal strains associated with the disease. In 1994, the last year in which it was a nationally reportable disease, there were only 112 cases reported, down from about 10,000 in 1961. ■ major histocompatibility complex (MHC), p. 407

Bacterial Vaginosis Facts

Bacterial Vaginosis Facts

This fact sheet is designed to provide you with information on Bacterial Vaginosis. Bacterial vaginosis is an abnormal vaginal condition that is characterized by vaginal discharge and results from an overgrowth of atypical bacteria in the vagina.

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