Dr bruetsch in this collection of reprints has demonstrated a well known fact that a late sequel of rheumatic fever is an obliterating endarteritis which may involve the small meningeal and cortical vessels resulting in infarction of parts of the central nervous system. Molecular mimicry between the group a streptococcus heart and brain is supported by evidence from studies of human mabs human t cell clones and serum igg antibodies derived from streptococcal sequelae and rheumatic fever galvin hemric ward cunningham 2000 kirvan swedo heuser cunningham 2003 human mabs derived from rheumatic carditis and sydenham chorea have supported the . Rheumatic fever appears to be a hypersensitivity reaction in which antibodies produced to combat streptococci react and produce lesions at specific tissue sites antigens of group a beta hemolytic streptococci bind to receptors in the heart muscle brain and synovial joints causing an autoimmune response. Rheumatic fever is an inflammatory disease that may develop two to three weeks after a group a streptococcal infection such as strep throat or scarlet fever it is believed to be caused by antibody cross reactivity and can involve the heart joints skin and brain when the brain is damaged due
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