Rheumatic Fever Essay Example

ailments like sore throat and scarlet fever. The emergence of rheumatic fever approximately 20 days after the initial bacterial infection suggests that it is a recurring illness caused by previously infectious bacteria ("Rheumatic Fever," 2008).

Confirmedly, rheumatic fever's beginning is greatly influenced by Streptococcus spp. These cocci are gram-positive and grow in pairs or chains. They can exist with minimal air as they lack mobility (microaerophilic). In 1941, Lancefield sorted this genus into groups according to the serological properties of their cell-wall polysaccharides.

The Lancefield A group bacterium, Streptococcus pyogenes, is accountable for inducing sore throat and scarlet fever. The USFDA (2007) has confirmed that this bacterium has 40 antigenic variations. Furthermore, S. pyogenes can result in rheumatic fever subsequent to producing a sore throat.

Pharyngitis, which is the inflammation of the pharynx and commonly presents with a sore throat, fever, and headache, is primarily caused by Group A ?-hemolytic streptococcus (GABHS). This particular strain of Streptococcus spp. accounts for 15% to 30% of sore throat cases in children and 5% to 15% in adults. However, aside from infectious factors like GABHS, noninfectious causes such as allergies, persistent coughing, smoking, rhinitis with postnasal drip, and gastrointestinal reflux can also lead to pharyngitis (Marcy, 2007).

Streptococcus pyogenes is a common human pathogen that can be found in the throat and on the skin. It has the potential to cause impetigo in skin lesions, including insect bites or abrasions. Additionally, it can lead to serious diseases such as necrotizing fasciitis, puerperal sepsis, acute glomerulonephritis, and rheumatic fever. The management of these life-threatening illnesses caused by Streptococcus pyogenes requires effective antimicrobial drugs (Mayon-White, 2005). Although this extracellular gram-positive bacterium has been known

to trigger rheumatic fever, its mechanism for inducing this disease remains unclear.

Studies are presently centered on the notion that an atypical immune response to streptococcus bacterium antigens is accountable for initiating rheumatic fever, despite the existence of several hypotheses. Additionally, research is being carried out to ascertain if a genetic predisposition influences this immune system reaction. Clinical manifestations of rheumatic fever include arthritis, joint inflammation and pain, abdominal discomfort, Sydenham's chorea, skin rash (referred to as erythema marginatum), nosebleeds or epistaxis, and cardiac complications ("Rheumatic fever," 2007).

Rheumatic fever can manifest in different ways, with the most severe form being carditis. This affects a significant percentage of patients (30-45%) and damages both the mitral and aortic valves. In developing countries, chronic rheumatic heart disease is considered an extension of rheumatic fever according to Guilherme and Jorge (2004). The acute form of rheumatic fever can present as pericarditis, synovitis, myocarditis, or valvulitis.

Chronic rheumatic heart disease is prevalent in developing countries and can lead to death in children and adolescents due to progressive left ventricular dilatation caused by myocardium damage. The damage may be triggered by acute or chronic ventricular volume overload or involvement with rheumatic fever. According to Gentles (2001), the development of left ventricular dilatation during acute rheumatic fever is mainly attributed to volume and pressure overloading, rather than valve regurgitation or contractile dysfunction – unless significant cardiac lesions are present. Additionally, neuropsychiatric disturbances such as hyperactivity, emotional liability, and obsessive-compulsive symptoms are common clinical manifestations during rheumatic fever known as Sydenham's chorea.

Between 10% and 30% of acute rheumatic fever cases may result in Sydenham chorea, which can be a standalone symptom or occur alongside other

clinical manifestations. Typically, it arises within six months of streptococcal pharyngitis or a sore throat (Kirvan, 2003). The cause is thought to involve immune mimicry - a process linked with rheumatic fever and heart disease - although the mechanism remains incompletely understood. A strong correlation exists between prior group A streptococcus infection and subsequent development of Sydenham's chorea through an autoimmune response in the basal ganglia of the brain (Kirvan, 2003).

It is unclear where rheumatic fever originates from, but the predominant theory suggests that it results from a cross-reaction between streptococcal antigens and certain human tissue proteins. Specifically, this reaction appears to involve heart tissue proteins in affected individuals. Molecular mimicry mechanisms are thought to facilitate this cross-reaction, which triggers an inflammatory response responsible for causing lesions associated with rheumatic heart disease. The onset of rheumatic fever is triggered by the antigenic similarity between M-protein epitopes found in streptococcus bacteria's antigens and L.a.K components present in susceptible individuals.

The production of various peptides by antigen presenting cells (APC) in the host occurs during throat infections caused by Streptococcus pyogenes. M proteins constitute a majority of these peptides, which bind to HLA class II molecules and get presented to helper T lymphocytes. This drives a humoral response causing inflammation. If left unattended, the streptococcal infection can prompt an autoimmune reaction from the host's cells leading to rheumatic fever (Guilherme & Jorge, 2004).

K. Guilherme and Jorge (2004) state that acute rheumatic carditis development is a consequence of rheumatic fever which leads to Aschoff’s bodies accumulation in the myocardium or endocardium of the patient. L.F. Guilherme, K. Oshiro, and J. Kalil (2005) explain that the immune response suppression during

infection and molecular mimicry occurring in rheumatic fever and rheumatic heart disease progression is due to similarity between bacterial antigenic M protein and human heart proteins.

Due to the diverse clinical manifestations of rheumatic fever, there is currently no designated diagnostic test available. Diagnosis involves evaluating the joints, skin, and heart for heart sounds, and utilizing electrocardiogram in cardiac examination. Serologic examination is also conducted to identify bacterial infection, specifically Streptococcus species ("Rheumatic Fever," 2008). To address the lack of a definitive diagnostic test, a diagnosis system based on clinical signs and laboratory attributes has been developed.

The Jones criteria, which were established in the 1940s, offer a system for diagnosing rheumatic fever during its acute stages. This system comprises clinical and laboratory aspects. The clinical aspect encompasses major criteria including carditis, pericarditis, chorea, erythema marginatum, and subcutaneous nodules as well as minor criteria such as fever, arthralgia and a history of rheumatic or heart disease. The laboratory aspect includes minor criteria such as inflammation proteins presence, PR segment lengthening in electrocardiogram results evidence of streptococcal infection like antistreptodornase and positive culture for GABHS.

Oliver (2000) suggests that a person with a history of streptococcal infection who meets either two major criteria or one major and two minor criteria likely has the disease. Jones' criteria serves as a guide for identifying those at risk but cannot definitively diagnose rheumatic fever. Even if laboratory tests for rheumatic fever are negative, choreo may still be a definite diagnosis. Furthermore, Meador (2007) notes that Jones' criteria does not cover indolent carditis. The development of technology has led to the creation of an antigen detection test for group A streptococcus (GAS), which

screens rather than diagnoses due to its low sensitivity in detecting the GAS bacterium.

The antistreptococcal antibodies test is a more useful tool for diagnosing rheumatic fever, as it detects high antibody titers which can confirm infection instead of just the presence of the organism. The sensitivity of bacterial culture from a patient’s throat for detecting streptococcal infection is only 25-40%. Rheumatic fever activity can be monitored using acute-phase reactants like C-reactive protein and ESR. Other laboratory tests can also be employed for screening, such as synovial fluid analysis which indicates rheumatic fever if there is a sterile inflammatory reaction and cell count below 20,000 cells/µL without crystals (Meador, 2007).

Managing the clinical symptoms of rheumatic fever is crucial since there is no specific treatment for this autoimmune disease. Aspirin or corticosteroids can alleviate inflammation, while individuals with Streptococcus-induced sore throat are recommended to take antibiotics like penicillin, erythromycin, and sulfadiazine.

"Rheumatic Fever" (2008) suggests administering drugs in low doses over a prolonged period to prevent infection recurrence. Primary prophylactic treatment with penicillin is recommended for cases of pharyngitis or sore throats caused by Streptococcus species. Penicillin G benzathine injections are given as prophylaxis against rheumatic fever reappearance, every 3 or 4 weeks in the years following its initial outbreak. These regimens were supported by a study conducted in the United States during the 1950s (Carapetis, 2007).

Effective management of heart failure varies depending on its severity. Mild cases can be controlled through adequate rest and the administration of corticosteroids. For more severe instances, digoxin may be prescribed with caution due to the potential risk of drug-induced heart blockage. In addition to assisting with nocturnal tachycardia, digoxin can benefit

patients by complementing vasodilators and diuretics. Cases related to Sydenham chorea call for extended antimicrobial prophylaxis (Meador, 2007).

Antirheumatic agents do not alleviate the clinical manifestations of Sydenham chorea, which can be protracted. Haloperidol is a potential treatment option. Managing the syndrome often includes complete physical rest during emotional trauma and adequate sedation. However, salicylates and glucocorticoids are often ineffective for chorea cases (Meador, 2007). Additionally, while the first attack of rheumatic fever typically lasts three months, some cases can last longer (Meador, 2007).

The provision of appropriate treatment is critical for a positive outcome in cases of rheumatic fever. Failure to administer extended low-dose antimicrobial therapy can result in an increased risk of recurrence. The prognosis becomes worse if severe heart complications occur during the illness, particularly when the heart is affected ("Rheumatic Fever," 2008). A greater comprehension of the immune mechanisms implicated in the development of rheumatic fever can assist in creating more efficient therapeutic approaches for managing this autoimmune condition.

Managing autoimmune rheumatic disease, including rheumatic heart disease, can be difficult. To prevent primary infection during Streptococcus spp. and secondary prevention after the onset of rheumatic heart disease, prophylactic therapies are given. The timely identification and treatment of streptococcal infections is essential in preventing episodes of rheumatic fever, particularly caused by Streptococcus pyogenes.