Rheumatic fever is an autoimmune disease that can develop after a streptococcal throat infection. It causes inflammation in connective tissues, especially the heart, joints, blood vessels, and skin. The inflammation is thought to be due to an immune cross-reaction between antigens in the streptococcal bacteria and human tissues. Symptoms vary depending on which tissues are affected but can include heart valve damage, arthritis, neurological disorders like chorea. Treatment involves antibiotics, salicylates like aspirin, and steroids depending on symptoms. Long term prevention requires ongoing antibiotics to prevent future streptococcal infections from triggering recurrences of rheumatic fever.

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Rheumatic Fever
DR.AHEED KHAN
DNB RESIDENT
DEPARTMENT OF PEDIATRICS
MAX HOSPITAL PPG
{aheedk@gmail.com}

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Multisystem Immunological disorder initiated by group
A beta hemolytic Streptococus
It is characterized by an exudative and proliferative
inflammatory lesion of the connective tissue,
especially that of the
 heart
 joints,
 blood vessels and subcutaneous tissue.

3. ETIOLOGY
• An untreated Group- A beta hemolytic streptococcal
infection is the commonest antecedent event that
precipitates an attack of Acute Rheumatic Fever.
 It is a delayed non-suppurative sequelae to URTI with
GABH streptococci.

4. licks the joints; bites
the heart• Acute ARF is an immuno-inflammatory condition that presents as
• carditis
• Arthritis
• chorea
• subcutaneous nodules
• erythema marginatum

5. The portal of entry is usually the fauces.
 Sore throat
 Frank scarlet fever
 Otitis media
 Other streptococcal infection precede the onset of the disease
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6. • Group A streptococcus(e.g., M types-1,
3, 5, 6, 18, 24) are more frequently
isolated from patients with acute
rheumatic fever.
• cross reactive antigens:
• cardiac myofibrillar sm Ag-cell wall/
cell membrane Ag
• heart valve fibroblast Ag- cell membrane
Ag
• subthalamic and caudate nuclei Ag-Gp-
A cell membrane Strep Ag
• heart valve and connective tissue- Gp-A
carbohydrate Ag
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cross
reactivity

7. epidemiology
• The incidence of both initial attacks and recurrences of acute rheu
• India- 0.5-11 per 1000.
• no significant difference in males and females; c
• spring and winter season

8. Predisposing factors -
 low socioeconomic status  overcrowding
 poor nutrition
 poor hygiene
- genetic predisposition.

9. pathogenesis
The cytotoxicity theory -
 streptolysin 0 has a direct cytotoxic effect on
mammalian cells in tissue culture.
The Immunological theory
immunologic cross-reactivity between group A streptococcal co

10. PathologyInflammatory Lesions in
1. Heart
2. Brain
3. Joints
4. Skin
Aschoff bodies in the atrial myocardium-
 Swelling, fragmentation of collagen fibres

11. 2 phases
I.EXUDATIVE PHASE
II.PROLIFERATIVE PHASE

12. aschoff bodies
central necrosis surrounded by ring of plump
histiocytes
aschoff bodies

13. T. Duckett Jones Criteria
for both initial attack and recurrence
5 major and 4 minor+ Evidence of recent GAS
infection
first in 1944; various versions; latest in 2015- risk
groups and lab criteria
low risk-<2 per one lakh school age children;
high risk- >2

14. major criteria
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15. newest
concept of subclinical carditis- silent carditis-
0-53%/isolated arthritis and/or pure chorea without
auscultatory findings of valvular dysfunction

16. MINOR CRITERIAS

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19. expected clinical courseOnly carditis cause permanent cardiac damage.
 S/O mild carditis disappear in weeks.
 Sever carditis may last for 2 to 6 months.
 Arthritis subside within few days to wks & dose not cause perm
 Chorea subsides in 6 to 7 months & dose not cause permanent

20. treatment
Oral salicylates –
Patients with typical migratory polyarthritis and those with
carditis without cardiomegaly or CCF.
•Aspirin -100 mg/kg/24 hr divided qid PO for 3-5 days.
 followed by 75 mg/kg/24 hr divided qid PO for 4 wk.
ANTIBIOTIC THERAPY
 10 days of orally administered penicillin or
erythromycin.
 Single intramuscular injection of benzathine penicillin .

21. Corticosteroids-
Patients with carditis & cardiomegaly or CCF
 Prednisone - 2 mg/kg/24 hr in 4 divided doses for 2-3 wk.
 Followed by a tapering of the dose.
 At the beginning of the tapering of the prednisone dose, aspirin
should be started at 75 mg/kg/24 hr in 4 divided doses for 6 wk.
Chorea-
 Phenobarbitone 15 to 30 mg every 6 to 8 hours.
 Haloperidol (0.01-0.03 mg/kg/ 24 hr divided bid PO)
 Chlorpromazine(0.5 mg/kg q 4-6 hr PO)

22. chemo-prophylaxis

23. duration
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24. thank you