S. pyogenes causes a wide variety of infections, most often acute pharyngitis (strep throat) and upper respiratory infection, as well as impetigo (pyoderma). Other manifestations of infection with S. pyogenes include sinusitis, otitis, peritonsillar and retro pharyngeal abscess, pneumonia, scarlet fever, erysipelas, cellulitis, puerperal sepsis, and gangrene. A concern still exists that group A streptococcus may be acquiring greater virulence.

Upper Respiratory Infection

 The clinical manifestations of S. pyogenes–associated upper respiratory infection are age dependent. In an infant or young child, the infection is characterized by an insidious onset of rhinorrhea, coughing, fever, vomiting, and anorexia. Cervical adenopathy may also be present. Rhinorrhea is sometimes purulent. This syndrome is called streptococcosis.

The classic syndrome of streptococcal pharyngitis is seen in children older than 3 years. It begins with a sudden onset of sore throat and fever, which rapidly progress in severity. Pharyngeal erythema with purulent tonsillar exudate and petechiae may be observed on the palate, posterior pharynx, and tonsils. Younger children may have abdominal pain, nausea, and vomiting. Most patients, however, do not manifest the classic syndrome. It is more common for a child with S. pyogenes pharyngitis to have a fever, mild sore throat, and pharyngeal erythema without exudate.

Viral pharyngitis can produce many of the same symptoms and cannot be reliably differentiated from streptococcal pharyngitis on the basis of clinical examination alone.

Impetigo and Cellulitis

 Impetigo is a skin infection that begins as a papule (Fig. 1). The lesion may itch and will eventually crust over and heal. Cellulitis caused by subcutaneous infection with group A streptococci is associated with a warm, red, tender area that may be mildly swollen. Erysipelas, a distinct cellulitis syn drome, usually involves the face and may be associated with pharyngitis. This syndrome is characterized by toxicity and a high fever. If left untreated, erysipelas can be fatal.

Fig1. Impetigo.  Older lesions are dark and encrusted. (From Wehrle PF, Top FH: Communicable and infectious diseases, ed 9, St Louis, 1981, Mosby.)

Scarlet Fever

 Scarlet fever is the result of pharyngeal infection with a strain of group A streptococcus that produces erythrogenic toxin and is responsible for the characteristic rash. The signs and symptoms of scarlet fever are those of streptococcal pharyngitis with the addition of a rash. The rash usually develops on the second day of illness and results in hyperkeratosis with subsequent peeling, similar to the rash of toxic shock syn drome. About 1 week after the onset of illness, the skin of the face begins to peel, which progresses over the next 2 weeks. Exposure to erythrogenic toxin confers specific immunity, limiting to three the number of episodes of scarlet fever in a person.

Complications of Streptococcus pyogenes Infection

 Not all infections with S. pyogenes lead to complications. Acute rheumatic fever, for example, occurs only after upper respiratory tract infection. In contrast, glomerulonephritis occurs after pharyngitis or skin infections (pyoderma). Acute rheumatic fever and poststreptococcal glomerulonephritis are considered nonsuppurative because the organs themselves are not directly infected and a purulent inflammatory response is not present in affected organs (e.g., heart, joints, blood, kidneys).

The pathogenesis of this disease process has not been fully described, but an autoimmune phenomenon may be operational. It is believed that cross-reactive antibodies, originally directed against streptococcal cell membranes, bind to myosin in human heart muscle cells. Other cross-reactive antibodies bind to components of the glomerular basement membrane and form immune complexes at the affected site. These antigen antibody complexes attract reactive host cells and enzymes that ultimately cause the cellular damage.

All M serotypes that infect the throat appear to be capable of causing rheumatic fever. Researchers have identified a few serotypes, however, that cause a much lower proportion of rheumatic fever cases than would be expected from their frequency as a cause of pharyngitis. The incidence of rheumatic fever is directly proportional to the strength of the antibody response to SLO. The prognosis of rheumatic fever is good when carditis is absent during the initial infection.

Glomerulonephritis may follow an infection of the skin or respiratory tract with one of a limited number of nephritogenic M serotypes. These serotypes are defined by antisera against the M protein, which is also associated with virulence. Why these serotypes cause glomerulonephritis is unknown.

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