The damaged valves may result in heart failure and also increase the risk of atrial fibrillation and infection of the valves. Pathophysiology
Rheumatic fever is a systemic disease affecting the connective tissue around arterioles, and can occur after an untreated strep throat infection, specifically due to group A streptococcus (GAS), Streptococcus pyogenes. The similarity between antigens of Streptococcus pyogenes and multiple cardiac proteins can cause a life-threatening type II hypersensitivity reaction. Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation. During a streptococcal infection, mature antigen-presenting cells such as B cells present the bacterial antigen to CD4+T cells which differentiate into helper T2 cells. Helper T2 cells subsequently activate the B cells to become plasma cells and induce the production of antibodies against the cell wall of Streptococcus. However the antibodies may also react against the myocardium and joints, producing the symptoms of rheumatic fever. S. pyogenes is a species of aerobic, cocci, gram-positive bacteria that are non-motile, non-spore forming, and forms chains and large colonies.S. pyogenes has a cell wall composed of branched polymers which sometimes contain M protein, a virulence factor that is highly antigenic. The antibodies which the immune system generates against the M protein  may cross-react with heart muscle cell protein myosin, heart muscle glycogen and smooth muscle cells of arteries, inducing cytokine release and tissue destruction. However, the only proven cross-reaction is with perivascular connective tissue. This inflammation occurs through direct attachment of complement and Fc receptor-mediated recruitment of neutrophils and macrophages.
Conditions which lead to the development of an immunocompromised state make the patient more susceptible to ecthyma gangrenosum and sepsis. In case of sepsis, the bacteria reaches the skin via the bloodstream. Defective humoral or cellular immunity increases risk, as the organism is not cleared from the bloodstream as usual. The main mechanism of the organism that is causing the typical skin lesions is the invasion of the organism into the arteries and veins in the dermis and subcutaneous tissues of the skin. This perivascular invasion leads to nodular formation, ulceration, vasculitis and necrosis due to impaired blood supply. Perivascular involvement is achieved by direct entry of bacteria through the skin or hematogenous spreading in case of sepsis. Diagnosis
Diagnosis is made by clinical observation and the following tests. (1) Gram stain of the fluid from pustules or bullae, and tissue swab. (2) Blood culture
(3) Urine culture
(4) Skin biopsy
(5) Tissue culture
Magnetic resonance imaging can be done in case of ecthyma gangrenosum of plantar foot to differentiate from necrotizing fasciitis. Prevention
The main organism associated with ecthyma gangrenosum is Pseudomonas aeruginosa. However, multi-bacterial cases are reported as well. Prevention measures include practicing proper hygiene, educating the immunocompromised patients for awareness to avoid possible conditions and seek timely medical treatment. Treatments
Treatments involve antibiotics that cover for Pseudomonas aeruginosa. antipseudomonal penicillins, aminoglycosides, fluoroquinolones, third generation cephalosporins or ceftriaxone aztreonam can be given. Usually, the antibiotics are changed according to the culture and sensitivity result. In patients with very low white blood cell counts, granulocyte-macrophage colony-stimulating factor may be given.