Streptococcus beta-haemolyticus of Lancefield group A and Rheumatic Fever

12 months ago

Not all sore throats lead to Rheumatic fever, but sore caused by group A Streptococcus which is between 2- 4 weeks after the infection, and it most commonly affects children within the age of 15 and in some cases adults. It can be caused by people who are genetically predisposed or people who have been infected by the Streptococcus bacteria causing sore throat which leads to an autoimmune reaction.

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Rheumatic fever and Rheumatic Heart disease are not far from Streptococcal infection. If a person has a sore throat caused by Streptococcus beta-haemolyticus of Lancefield group A, which produces hemolysins that produce hemolysis of RBC in blood agar. This Streptococcus is of the Reuma Rheumatogenic strains. When this bacteria attacks the mucosa of the pharynx, it causes the larynx to be inflamed as neutrophils and macrophages go to the area of inflammation. These antigens are shown to the immune system which produces antibodies and sensitizes lymphocytes, and a T-streptococcal immune response would be generated to attack the bacteria. In some cases when this process happens and destroys the bacteria, it can also attack the tissues such as the cardiac tissues, joints, skin, subcutaneous tissues, and the central nervous system leading to lesions in these tissues because some foreign antigens are similar to the body's own antigen. While reacting with the cell wall of the bacteria, the antibodies might attack the tissues of organs in the body. It could also be as a result of attacking the proteins of the bacteria cell membrane such as protein-m can also cause the attack on tissues since the proteins are similar.

The immune system of the body would take a while to build and attack the bacteria leading to multi-systemic immune-mediated inflammation. The inflammation causes the production of cytokines which sends a message to the hypothalamus to precipitate fever which would lead to a Multi-system immune-mediated acute non-separative inflammation fever that occurs after pharyngitis caused by Streptococcus beta-hemolytic of Lancefield group A is known as Rheumatic fever. Tissues and systems that are vulnerable are the cardiac systems, the joints, the subcutaneous nodule, the skin, and the Central nervous system. With Rheumatic fever, multiple organs or systems in the body are inflamed which are immune-mediated, with no bacteria in the tissues which are inflamed.

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If the central nervous system is inflamed as a result of the basal nuclei being attacked by the immune system, it will affect the motor movement of the body which is involuntary. This can lead to Rheumatic Chorea (especially in female), Once the patient develop chorea and it subsides, it doesn't cause residual damage to the central nervous system. Rheumatic fever affecting the joint can lead to Arthritis as a result of inflammation of the synovial membrane and the fever can also lead to arthralgia which doesn't accompany swelling, tenderness, or inflammation. When there are multiple inflammations, it can be known as polyarthritis. Pain is very severe with the arthritis during the fever but there is no long-term complication as the joint becomes normal when the fever is over. Rheumatic fever in the skin will cause the skin to produce lesions to become macules which would increase and the margins are inflamed known as Erythema marginatum. This effect becomes clear when the patient's fever is gone. The Subcutaneous tissues can also experience lesions and the production of non-tender subcutaneous nodules on extensor muscles and subcutaneous area. Rheumatic fever can also cause cardiac problems. In acute phases, the cardiac tissue is interacted with as there can be an inflammation of the pericardium leading to Rheumatic pericarditis. It can also involve the myocardium leading to rheumatic myocarditis. It can also interact with the endocardium, leading to rheumatic endocarditis. When the three tissues of the heart are involved, it is known as Pancarditis. If a patient has rheumatic pericarditis, the immune system attacks both the parietal and visceral pericardium developing hypermobility in the capillaries and large intra-endothelial gaps leading to the leakage of proteins such as fibrin strands and fibrinogens known as fibrinous pericarditis which produces pain in the chest that is sharp and localized. When listened to, pericardial rub can be heard as a result of the pericardial layers rubbing against one another. When the fever is over, the fibrin is cut down by plasmin causing the reabsorption of fibrin and not causing any complication.