RHEUMATIC FEVER AND RHEUAMTIC HEART DISEASES

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Streptoccocus beta hemolysins bacteria grop- release hemolysins

- Bacteria that causes tonsillitis, pharyngitis

- Belonging to to the lens field group A
- Strep with rheumatogenic strain causes rheumatic fever

-Streptococcus beta hemolytic bacteria when enters the body and causes to(tonsillitis/pharyngitis the macrophages
take up the antigens of the bacteria and present it to the immune system immunse system will respond by producing
antibodies and lymphocytes that attack the bacteria.

-However, in some cases, about 2-3 percent in susceptible population, the immunse reponse may also attack its own
tissues such as the heart(carditis), joints (polyarthritis), skin (erethyma marginatum) , subcutaneous tissues
(subcutaneous nodules), and CNS (motor disturbances).

-Why does this happen? Because some of the bacterial antigens are very similar with our own antigens the
glycoprotein component of the cell wall of the bacteria is similar with that glycoprotein component of the cell walls of
our own tissues

- during the initial infection phase, it takes 2-4 weeks to establish a well immune response, in which systemic
nonsuppurative inflammatory reaction takes place lot of cytokines are produced sensed by the CNS and produces
fever (called rheumatic fever)

-Rheumatic fever- multi system immune mediated acute inflammation, nonsuppurative occurring 2-4 weeks after
infection by streptococcus beta hemolytic bacteria
In the central nervous sytem
- In the wall of the basal ganglia, in the basal nuclei, it contains the neuronal circle and they have a lot of
motor programs  when inflamed, immunically damaged, motor program starts leaking out
inappropriately patient ‘s arm moves purposelessly and involuntarily these purposelessly and jerking
movement is called choreaalso called rheumatic chorea/ sedenham’s chorea /saint vitus dancemore
common in females
In the joints
- Synovial membrane become inflamed (arthritis), pain (arthralgia)
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polyarthritis- multiple joints are inflamed
- In changes over time , it migrate to other joints causing multiple joint inflammation
-Common in 5-15 years of age
-aspirin is given to relieve the symptoms, aspirin should not be given if the migratory stage of arthritis is not established.
- if the child has rheumatic fever, it should take daily antibiotic prophylactically for long period of time to prevent the
progression to valvular heart disease
Note: if the inflammation has subsided and rheumatic fever is gone, then complete recovery is achieved, no long term
complication can arise.

In the skin
- Produce macules which grows in a way that first an inflammed area developed and the inflammation extend
or grows marginally, thus called erythema marginatum

In nthe subcuatenous tissue, fascia under the skin develops nodules which are non tender, painless
In the heart
- If the endometrium is infected(rheumatic endocarditis)
- In the myomnetrium is infected ( rheumatic myocarditis)
- If the endometrium is infected (rheumatic endocarditis)
- If all the heart muscles are affected ( rheumatic pancarditis

Rheumatic pericarditis
In the pericarditis capillaries in it are become highly permeableescapes of blood proteins such as fibrinogen
capillaries shrinks and endothelial gaps are developed when fibrinogen shifts from the vascular to the pericardium
sacit polymerizes and converted into fibrin strands  due to accumulation of fibrin in the pericardium fibrinous
pericarditis cause pericardial pain which sharp(cutting pain0 and localized pain relieved by leaning forward

- When inflamed pericardial layers are rubbing to each other during heart contraction produces a scratchy
sound called pericardial rub
-when the fever resolves , those accumulated firbrins are cut by plasmin and reabsorbed full recovery

Rheumatic myocarditis
-Aschoff bodies- special lesions that could be found in all layers of the myocardium especially in the myocardium
- small pin head size granuloma composed of immune cells  especially found in the pericvascular connective
tissue
- this is a classical lesion of rheumatic myocarditis
- aschoff giant cells- large macrophages that are part of the ashchoff bodies
- myocardium become loose and flabby and become very poorly contractile leads to congestive cardiac
failure  most serious complication of rheumatic fever that can lead to death
Rheumatic endocarditis
- During the acute fever, it attacks the endocardium especially the valves valvular endocardits/rheumatic
valvulitis  the inflamed valves hits its other more frequently than normal because of tachycardia  over
tme, endothelial erosion  on the area of erosion, fibrin and platlets stick to it forms vegetations called
rheumatic vegetations it doesn’t have bacterial component so called sterile vegetations composed of
fibrins and platelets that don’t break away so doesn’t caused emboli the healing is through the fibrotic
process , therby the injured tissue is replace by stiff collagens or fibrins  the valve become distorted and
may lead to long term complication even after the recession of the rheumatic fever during reinfection of
rheumatic fever more and more the valve will become distorted because of the residual damage it
leaves valvualr deformitieschronic rheumatic heart disease.