Various pathogenesis of rheumatic heart disease

Etiology And Pathogenesis

The etiologic relationship of group a streptococci to rheumatic fever can be summarized briefly as follows

• Numerous clinical and epidemiologic studies have shown a close association of group a streptococcal infections and rheumatic fever

• Antecedent streptococcal infection can almost always be demonstrated immunologically in the acute stage of rheumatic fever by increased titers of antibodies to streptococcal antigens.

Mover over, in long terms prospective follow up studies rheumatic fever recurs only as a result of intercurrent streptococcal infection

• Both primary and secondary attacks of the disease can be prevent by prompt treatment or prevention of streptococcal infections with antimicrobial therapy.

• The site of infection is critical. The pharyngeal route of infection is necessary of initiate the rheumatic process. Streptococcal skin or soft tissue infections do not do so.

• Not all strains of group A streptococci cause the disease. The so-called skin strains that cause streptococci pyoderma do not cause rheumatic fever, even when infection the throat.

The strains that have been clearly associated with rheumatic fever outbreaks have distinct virulence properties when freshly isolated from the pharynx.

They are very rich in the extractable serotypic surface M protein and contain large hyaluronic acid capsules that are responsible for the formation of mucoid on blood agar plates. Such strains usually belong to certain serotypes notably M types 3,5,18,19,24, and others.

All strains within these serotypes, however, are not always in this phase of virulence and are not always rheumatogenic. The M protein of rheumatogenic strains forms an unusually large, extended molecule consisting of repeating peptide subunits not found in other strains of group A streptococci so far studied.

The mechanism by which the group A streptococci initiates the disease process remains unknown. A relatively small percentage of persons who suffer from streptococci sore throats subsequently develop rheumatic fever.

The organism is not demonstrable in the lesions when rheumatic fever appears after a characteristic latent period of 1 to 5 weeks after the acute pharyngeal streptococcal infection.

No one product of the streptococcus has been incriminated as a cause of the lesions, either as a direct tissue toxin or as an antigen inducting hypersensitivity. Several streptococcus antigens have demonstrated cross-reactivity with cardiac and other tissues. Although the hyaluronic acid of group.

A streptococcal capsules and that of human host tissues are chemically identical, auto antibodies to this substance are demonstrable. Such findings suggest that a “ molecular mimicry “ type of autoimmunity may relate to the pathogenesis of rheumatic fever.

Perhaps induced by the strong Immunologic adjuvant properties of some parts of the M protein molecule that have super antigen-like activity, i.e.,the capability of activating lymphocyte receptors directly.

Such properties may invoke autoimmune responses in susceptible hosts and also may explain the finding that all streptococcal antibodies so far studied tend to be higher in patients with acute rheumatic fever than in those who do not develop the disease following a bout of streptococcal pharyngitis.

Pathology:

The rheumatic fever is disseminated widely through out the body, with special predilection for connective tissues. Focal inflammatory occurs particularly around small blood vessels.

Cardiovascular:

The heart is the site of the most characteristic and consequential involvement, and all its layers endocardium, muocardium, and pericardium may be involved.

This generalized involvement gives rise to the term rheumatic pancarditis. The mast characteristic and specific of rheumatic inflammation is found in the myocardial Aschoff body, a submiliary granuloma.

In many areas the inflammatory lesion is accompanied by swelling and fragmentation of the collagen fibers and alternation in the staining properties of the ground substances of the connective tissues. This change is described as fibrinoid established.

The persistence of is most common in patients who develop sever mitral stenosis. Eventually, the Aschoff body is converted in to a spindle shape or triangular scar lying between the muscle bundles and surrounding blood vessels.

Understanding various pathogenesis of rheumatic heart disease