<P> Molecular mimicry occurs when epitopes are shared between host antigens and Streptococcus antigens . This causes an autoimmune reaction against native tissues in the heart that are incorrectly recognized as "foreign" due to the cross-reactivity of antibodies generated as a result of epitope sharing . The valvular endothelium is a prominent site of lymphocyte - induced damage . CD4 + T cells are the major effectors of heart tissue autoimmune reactions in RHD . Normally, T cell activation is triggered by the presentation of bacterial antigens . In RHD, molecular mimicry results in incorrect T cell activation, and these T lymphocytes can go on to activate B cells, which will begin to produce self - antigen - specific antibodies . This leads to an immune response attack mounted against tissues in the heart that have been misidentified as pathogens . Rheumatic valves display increased expression of VCAM - 1, a protein that mediates the adhesion of lymphocytes . Self - antigen - specific antibodies generated via molecular mimicry between human proteins and streptococcal antigens up - regulate VCAM - 1 after binding to the valvular endothelium . This leads to the inflammation and valve scarring observed in rheumatic valvulitis, mainly due to CD4+ T cell infiltration . </P> <P> While the mechanisms of genetic predisposition remain unclear, a few genetic factors have been found to increase susceptibility to autoimmune reactions in RHD . The dominant contributors are a component of MHC class II molecules, found on lymphocytes and antigen - presenting cells, specifically the DR and DQ alleles on human chromosome 6 . Certain allele combinations appear to increase RHD autoimmune susceptibility . Human leukocyte antigen (HLA) class II allele DR7 (HLA - DR7) is most often associated with RHD, and its combination with certain DQ alleles is seemingly associated with the development of valvular lesions . The mechanism by which MHC class II molecules increase a host's susceptibility to autoimmune reactions in RHD is unknown, but it is likely related to the role HLA molecules play in presenting antigens to T cell receptors, thus triggering an immune response . Also found on human chromosome 6 is the cytokine TNF - α which is also associated with RHD . High expression levels of TNF - α may exacerbate valvular tissue inflammation, contributing to RHD pathogenesis . Mannose - binding lectin (MBL) is an inflammatory protein involved in pathogen recognition . Different variants of MBL2 gene regions are associated in RHD . RHD - induced mitral valve stenosis has been associated with MBL2 alleles encoding for high production of MBL . Aortic valve regurgitation in RHD patients has been associated with different MBL2 alleles that encode for low production of MBL . Other genes are also being investigated to better understand the complexity of autoimmune reactions that occur in RHD . </P> <P> Modified Jones criteria were first published in 1944 by T. Duckett Jones, MD . They have been periodically revised by the American Heart Association in collaboration with other groups . According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre or DNAase . Exceptions are chorea and indolent carditis, each of which by itself can indicate rheumatic fever . An April 2013 review article in the Indian Journal of Medical Research stated that echocardiographic and Doppler (E & D) studies, despite some reservations about their utility, have identified a massive burden of rheumatic heart disease, which suggests the inadequacy of the 1992 Jones' criteria . E & D studies have identified subclinical carditis in patients with rheumatic fever, as well as in follow - ups of rheumatic heart disease patients who initially presented as having isolated cases of Sydenham's chorea . Signs of a preceding streptococcal infection include: recent scarlet fever, raised antistreptolysin O or other streptococcal antibody titre, or positive throat culture . </P> <Ul> <Li> Polyarthritis: A temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards . </Li> <Li> Carditis: Inflammation of the heart muscle (myocarditis) which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur . </Li> <Li> Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons . They commonly appear on the back of the wrist, the outside elbow, and the front of the knees . </Li> <Li> Erythema marginatum: A long - lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake - like appearance . This rash typically spares the face and is made worse with heat . </Li> <Li> Sydenham's chorea (St. Vitus' dance): A characteristic series of involuntary rapid movements of the face and arms . This can occur very late in the disease for at least three months from onset of infection . </Li> </Ul>

When do you say the patient has rheumatic fever based on jones criteria
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