Rheumatic fever is an inflammatory condition that can emerge as a complication of a bacterial infection, affecting the heart, joints, and brain. It is not a direct infection but an autoimmune reaction where the body’s defense system malfunctions. This distinction is why prevention has focused on strategies other than vaccination.
Understanding the Cause of Rheumatic Fever
Rheumatic fever is an autoimmune reaction triggered by an untreated throat infection caused by Group A Streptococcus (GAS) bacteria, the same bacterium responsible for strep throat. The onset of rheumatic fever occurs two to four weeks after the initial streptococcal infection. This condition primarily affects children and adolescents between the ages of 5 and 15.
The development of rheumatic fever is caused by a phenomenon known as molecular mimicry. In its effort to eliminate GAS bacteria, the immune system produces antibodies. However, certain proteins on the bacteria resemble proteins found in human tissues, particularly in the heart, joints, skin, and brain. This similarity tricks the immune system into attacking the body’s own cells.
This autoimmune assault leads to widespread inflammation, causing symptoms like painful joints and, in more severe cases, damage to heart valves. Not everyone with an untreated strep infection develops rheumatic fever, as genetic factors appear to make some individuals more susceptible. This process highlights an error in the immune system’s ability to distinguish between self and non-self.
Challenges in Developing a Vaccine
There is currently no vaccine to prevent rheumatic fever due to a major safety concern. Since the disease is an autoimmune condition, a vaccine introducing parts of the Streptococcus bacterium could trigger the very autoimmune reaction it aims to prevent. This risk of inducing the disease is the central reason for the slow progress in vaccine development.
Early attempts to create a vaccine using whole or fragmented GAS bacteria demonstrated this danger. Some trial participants developed symptoms similar to rheumatic fever, as the vaccine prompted an immune response against their own tissues. This unacceptable risk forced vaccine research to shift its focus toward ensuring safety.
Modern research is concentrated on identifying specific components of the bacterium (antigens) that can stimulate a protective immune response without cross-reacting with human tissues. Scientists are working to isolate bacterial epitopes—the part of an antigen that an antibody attaches to—that are unique to the pathogen. This highly targeted approach is complex and necessary to find a safe and effective candidate.
Current Prevention Strategies
With no vaccine available, preventing rheumatic fever relies on managing Group A Streptococcus infections. The primary strategy is the prompt diagnosis and complete treatment of strep throat with antibiotics like penicillin. Consistent use of these drugs has dramatically reduced the incidence of rheumatic fever worldwide. Completing the full course of antibiotics is necessary to ensure all bacteria are eradicated.
For individuals who have already had rheumatic fever, preventing a recurrence is the focus. They are at a much higher risk of another attack from a subsequent strep infection, with recurrence rates around 50% if untreated. This secondary prevention involves long-term, continuous antibiotic therapy, sometimes for many years or a lifetime, to prevent new strep infections from re-triggering the autoimmune response.
This approach shifts the focus from stimulating immunity to preventing the initial trigger. By treating the root bacterial infection, medical professionals can stop the autoimmune cascade before it begins. This method is a successful public health strategy, significantly lowering the burden of rheumatic fever and its most serious consequence, rheumatic heart disease, which involves long-term damage to the heart valves.