Rheumatic Fever: Etiology, Pathophysiology, Pathology, and Complications

Rheumatic fever is an inflammatory disease that occurs following an infection with group A Streptococcus bacteria. It primarily affects the heart, joints, brain, and skin.

Etiology

Rheumatic fever develops after an untreated or inadequately treated streptococcal throat infection. It is believed to result from an autoimmune response triggered by bacterial antigens.

Pathophysiology

The disease is characterized by molecular mimicry, where the immune system mistakenly attacks the body's tissues. This immune response leads to widespread inflammation, affecting multiple organ systems.

Pathology: Gross and Microscopic Features

Gross Pathology

• Heart: Endocarditis, myocarditis, and pericarditis.
• Joints: Inflammatory arthritis affecting large joints.
• Skin: Presence of subcutaneous nodules and erythema marginatum.

Microscopic Features

• Heart: Aschoff bodies—granulomatous lesions in the myocardium.
• Joints: Synovial hyperplasia with inflammatory infiltrates.
• Skin: Degenerative changes with inflammatory cells.

Clinical Features

• Cardiac manifestations including murmurs due to valvular damage.
• Polyarthritis affecting large joints in a migratory pattern.
• Neurological symptoms such as Sydenham’s chorea.
• Characteristic skin lesions like erythema marginatum.

Diagnostic Criteria

Diagnosis is based on the modified **Jones Criteria**, including major and minor manifestations such as fever, arthralgia, and prolonged PR interval.

Complications

Rheumatic heart disease is the most severe complication, leading to chronic valvular damage, heart failure, and increased morbidity.