Streptococcal Impetigo

A skin infection characterized by pus production is called pyoderma. Pyodermas can result from infection of an insect bite, burn, scrape, or other wound. Sometimes, the injury is so slight that it is not apparent. Impetigo is the most common type of pyoderma (figure 22.5).


Impetigo is a superficial skin infection, involving patches of epidermis just beneath the dead, scaly outer layer. Thin-walled

Streptococcus Pyogenes
Figure 22.5 Impetigo This type of pyoderma is often caused by Streptococcus pyogenes and may result in glomerulonephritis.

Figure 22.6 Streptococcus pyogenes Growing on Blood Agar The colonies are small and surrounded by a wide zone of /¡-hemolysis.

Figure 22.6 Streptococcus pyogenes Growing on Blood Agar The colonies are small and surrounded by a wide zone of /¡-hemolysis.

blisters first develop, then break, and are replaced by yellowish crusts that form from the drying of plasma that weeps through the skin. Usually, little fever or pain develop, but lymph nodes near the involved areas often enlarge, indicating that bacterial products have entered the lymphatic system and an immune response is occurring.

Causative Agent

Although Staphylococcus aureus often causes impetigo, many cases, even epidemics, are due to Streptococcus pyogenes. These Gram-positive, chain-forming cocci are /-hemolytic (figure 22.6) and are frequently referred to as /-hemolytic group A streptococci because their cell walls contain a polysaccharide called group A carbohydrate. A more detailed description of S. pyogenes is found in chapters 23 and 27. ■ hemolysis, p. 94 ■ Streptococcus pyogenes, p. 565

Table 22.5 compares Staphylococcus aureus and Streptococcus pyogenes.


Many different strains of Streptococcus pyogenes exist, some of which can colonize the skin. Infection is probably established by scratches or other minor injuries that introduce the bacteria into the deeper layer of epidermis. In impetigo, even though the infection is limited to the epidermis, streptococcal products are absorbed into the circulation.

As with Staphylococcus aureus, a number of extracellular products may contribute to the virulence of Streptococcus pyo-genes. These products include enzymes such as proteases that degrade protein, nucleases that degrade nucleic acids, and hyaluronidase, which degrades the hyaluronic acid component of host tissues. As with staphylococci, it is probable that such enzymes contribute to streptococcal pathogenicity. None of them appear to be essential, however, since antibody against them fails to protect experimental animals. On the other hand, the surface components of S. pyogenes, notably a hyaluronic acid capsule and a cell wall component known as the M protein, are very important in enabling this organism to cause disease because they interfere with phagocytosis. ■ M protein, p. 470

Acute glomerulonephritis is a serious complication of S. pyogenes pyoderma. This condition may appear abruptly during convalescence from untreated S. pyogenes infections, with fever, fluid retention, high blood pressure, and blood and protein in the urine. Acute glomerulonephritis is caused by inflammation of structures within the kidneys, the glomeruli (singular: glomerulus), small tufts of tiny blood vessels, and the nephrons, responsible for the formation and composition of urine (figure 22.7). Only a few of the many S. pyogenes strains cause the condition. Streptococci are absent from the urine and diseased kidney tissues. Indeed, the bacteria have generally been eliminated from the infection site in the skin by the immune response by the time symptoms of glomerulonephritis appear. Damage to the kidney is caused by immune complexes that are deposited in the glomeruli and provoke an inflammatory reaction. Both streptococcal skin and throat infections can sometimes cause acute glomerulonephritis, but rheumatic fever, a serious complication of strep throat, is not generally a complication of streptococcal pyoderma. ■ immune complexes, p. 448 ■ rheumatic fever, p. 567


Impetigo is most prevalent among poor children of the tropics or elsewhere during the hot, humid season. Children two to six years are mainly afflicted. Person-to-person contact spreads the disease, as do flies and other insects, and fomites—inanimate objects such as toys or towels. Impetigo patients often become throat and nasal carriers of S. pyogenes.

Table 22.5 Streptococcus pyogenes vs. Staphylococcus aureus

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