endocarditis and rheumatic fever

Pathology

Rheumatic fever :
It is a systemic ,post-streptococcal non suppurative inflammatory disease affect the heart,joiant,central nervous system , skin & subcutaneous tissue.

The disease appear in children between 5-15 years & both sex affect equally

It is more common in poor socioeconomic state, living in damp overcrowded places. seen in 3% of patients with acute gp A streptococcal pharyngitis .
Rheumatic fever may cause heart disease during its acute phase (acute rheumatic carditis) or it may cause chronic valvular deformity (chronic rheumatic heart disease ) that may manifest themselves years after the acute phase .

Pathogenesis:

It is suspected that acute Rh.fever is a hypersensitivity reaction induced by gpA streptococci. The antibody which form against m-protien of m.o cross react with normal protein of joint heart brain ,skin &other tissue i.e autoimmune mechanism. .

Morphology.

The lesion of acute rheumatic fever infiltrate many organ characterized by fibrinoid necrosis surround by mixed inflammatory infiltrate which is either diffuse or localize forming granulom a. Fibrosis is common especially in the cardiac tissue.
Acute rheumatic carditis (pancardites) involve the 3 layer of the heart & characterized by the formation of aschoff body which composed of foci of fibrinoid necrosis surrounded by mon onuclear infiltration & occasional large macrophage with vesicular nucleous & basophilic cytoplasm(Antischkow cell) . Aschoff body found near b.v mainly in the myocardium which also show diffuse interstitial inflammatory Infiltrate.
Pericardium manifest grossly & microscopically by fibrinous percarditis sometime associated with pericardial effusion .
Endocardium show inflammation of the valve (mitral & aortic mainly) result in the formation of wart like vegetation at the line of closure of the valve cusp .

Chronic rheumatic heart disease :

Characterized by irreversible deformity of one or more valves result from previous episode of acute valvulitis ,
Usually affect the mitral valve alone or in combination with aortic valve .scaring of the valve either lead to narrow orifice (stenosis ) or incomplete closure of the valve result in (regurgitation) of blood during diastole .


Clinical features of acute rheumatic fever :
Occur 2-3 week often episode of pharyngitis
Fever migrating polyorthritis affect the big joint
Feature of cardiac involvement :pericardial friction , weak heart sound , rapid pulse & arrhythmia .

DX
Major Jones criteria:
Pancarditis
Migrating poly arthritis .
Subcutaneous nodules
Chorea (involuntary movement of trunk & extremities )
Erythema marginatum ( erythematous rash).

Minor Jones criteria

Arthralgia
Fever
Elevated ASO titer (antistreptolysin)
Prolongation of PR interval .

Diagnosis is by 2 major criteria or 1major & 2minor criteria .

Complication of acute & chronic rheumatic heart disease :
SABE
Arrhythmia
Heart failure
Mural thrombi & embolism .

Bacterial endocarditis :

Serious bacterial infection of the valvular & mural endocardium characterized by formation of friable vegetation. It is of 2 types:
1.acute bacterial endocarditis (ABE ) which is fulminating & caused by virulent strain of staph aureus mainly in addition to pneumococci . B-hemolytic streptococci , usually involve normal valve ,it has fatal coarse in a period of 2-6 weeks
2.subacute bacterial endocarditis : caused by less virulent bacteria (streptococcus viridans , staphylococcus epidermides ,E coli , pseudomonas , occur in abnormal valves & it has gradual coarse 6weeks- few months .

Predisposing factors:

condition that initiate transient bactereamia , septicemia , pyaemia
underlying heart disease ( congenital or chronic rheumatic heart disease , prosthetic valve)
impaired host defense ( leukemia , lymphoma, immune suppression)

Pathological changes:

X: the lesion common in the valve of left heart in descending frequency (mitral-aortic- while that of right side is rarely involved)
The vegetation of BE vary in size from few mm to several cm. grey , single or multiple & typically friable . The vegetation of ABE is bulker, globular than that of SABE, may cause ulceration perforation of the leaflet and may produce myocardial abscess in addition to its occurrence in normal valve.
M: Consist of 3 layers :
1-the outer layer consist of eosinophilic material composed of fibrin & platelet.
2-follow by basophilic zone consist of bacteria .
3-the deeper zone consist of non specific inflammatory infiltrate . In case of ABE the inflammatory in is chiefly of neutrophil accompany by tissue necrosis .
In SABE this is mononuclear inflammatory cell infiltrate with evidence of healing in the form of granulation tissue & fibroblast infiltration. In addition histological evidence of pre-existing valvular disease such as RHD
may be seen in SABE.  INCLUDEPICTURE "F:\\JPEG6\\CV041.JPG" \* MERGEFORMATINET 



Clinical feature :
* Fever : In ABE fever, rigor, malaise & weakness. while in SABE: low grade fever, fatigue, loss of wt & flu like symptom.
* spleenomegaly .
* Change in cardiac murmur .
* clubbing fingers .
* systemic emboli is common .

Complication

Cardiac complication:
valvular stenosis or insufficiency
perforation, rupture
myocardial abscess
suppurative pericarditis
heart failure

B: extra cardiac complication

1-emboli originate from left side of the heart enter the systemic circulation & lodge any where causing infarction & abscess .
2-emboli in right side cause pulmonary abscess .
3-petechiae either due to emboli or toxic damage of the capillary
4-in SABE there is painful tender nodule in tip of the finger while in ABE non tender maculo papular lesion on the pulp of the finger.
5-focal glomerulonephritis .