Rheumatic Fever

Rheumatic fever occurs as a result of a primary infection with Streptococcus pyogenes. If the infection is not treated, the body's immune system starts to overreact to the presence of the bacteria in the body. Illnesses caused by such overreactions of the immune system are called hypersensitive reactions. Some of the symptoms of rheumatic fever, particularly the involvement of the heart, are thought to be caused by the hypersensitive reactions. Other symptoms may be caused by the release of toxins from the S. pyogenes bacteria that are spread to other parts of the body through the bloodstream.

Not all strains of S. pyogenes cause rheumatic fever; only certain strains of S. pyogenes, called the M strains, have been implicated in cases of rheumatic fever. In addition, not everyone infected with these strains of S. pyogenes will progress to rheumatic fever. Individuals with a specific type of antigen (an immune protein) on their immune cells, called the human leukocyte antigen (HLA), are predisposed to develop rheumatic fever following an untreated strep infection. The specific type of HLA antigen that predisposes a person to develop rheumatic fever is called the class II HLA. These individuals develop their susceptibility during early childhood. Children under two years of age rarely contract rheumatic fever; the incidence of the disease increases during childhood from ages five to 15 and then decreases again in early adulthood. Researchers are not sure about the exact mechanism that leads to susceptibility or the role that the class II antigen plays in susceptibility to rheumatic fever.