RHEUMATIC FEVER

Rheumatic fever is an inflammatory disease that may develop as a complication of a streptococcus infection, such as strep throat by Streptococcus pyogenes or group A beta-hemolytic streptococcus. If it does develop, it will usually do so two to three weeks after the Group A streptococcal infection. Rheumatic fever mainly affects children aged between 5 and 15 years; however, it can affect adults and younger children. Boys and girls have the same risk of developing the disease; girls and women tend to have more severe symptoms. The disease may cause long term effects on the skin, heart, brain and joints. Rheumatic fever may cause permanent damage to the heart valves in rheumatic heart disease. Rheumatic fever has the potential to cause heart failure, stroke and even death
The disease is caused by bacteria Streptococcus pyogenes (group A) which can affect the skin, brain, and especially the joint and the heart. Rheumatic Fever is an Auto-Immune Disease where the body’s immune system accidentally attacks healthy tissue. Strep bacteria have a protein which is similar to what is found in the body’s tissues. Immune system cells that would normally fight the strep bacteria may handle the body’s own tissues as if they were infectious agents, especially tissues of the heart and joints resulting in attack and inflammation.
If Rheumatic Fever is not treated properly it may persist for several weeks, months, and in some cases much longer, causing the long term problem - Rheumatic Heart Disease. This complication occurs with the mitral value (between the two left chambers) leading to low or wrong direction blood flows, heart failure, arterial fibrillation. Group A streptococcus(GAS) infection is a precursor to Acute Rheumatic Fever(ARF) GAS M proteins share epitomes with proteins found in synovial, heart muscle, and heart valve tissue, molecular mimicry-similarities between foreign and self-peptides that are sufficient to result in the cross-activation of auto reactive T or B cells- contributes to the arthritis, carditis, and valvular damage (2). The antibodies which the immune system generates against the M protein may cross react with cardiac myofiber protein myosin, heart muscle glycogen and smooth muscle cells of arteries (1). Inflammation occurs through direct attachment of complement and receptor-mediated recruitment of neutrophils and macrophages. This is how you get the characteristic inflammation commonly associated with ARF. During a Streptococcus infection, mature antigen presenting cells such as B cells present the bacterial antigen to CD4-T cells, which differentiate into helper T2 cells (2).
Helper T2 cells subsequently activate the B cells to become plasma cells and induce the production of antibodies against the cell wall of Streptococcus. Unfortunately, these antibodies may also react against the host myocardium and synovial joints because of molecular mimicry, producing the symptoms of rheumatic fever. This is referred to as type-II hypersensitivity.
In type II hypersensitivity the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. These cells are now recognized by macrophages or dendrite cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen. Rheumatic fever is a rare, potentially life threatening inflammatory disease that may develop 2 to 3 weeks after the infection of strep throat or scarlet fever. Rheumatic fever occurs worldwide and has caused many cases of damaged heart valves. With the help of antibiotics that treat streptococcus infections, Rheumatic fever has become fairly rare in Western countries since the 60’s. Rheumatic fever is most common in 5 to17 year old children and usually occurs approximately 20 days after developing a strep throat infection (1). The rate of development of Rheumatic fever with an untreated strep throat