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Auala, T.;  Zavale, B.G.;  Mbakwem, A.�.;  Mocumbi, A.O. Acute Rheumatic Fever and Rheumatic Heart Disease. Encyclopedia. Available online: https://encyclopedia.pub/entry/24858 (accessed on 12 May 2024).
Auala T,  Zavale BG,  Mbakwem A�,  Mocumbi AO. Acute Rheumatic Fever and Rheumatic Heart Disease. Encyclopedia. Available at: https://encyclopedia.pub/entry/24858. Accessed May 12, 2024.
Auala, Tangeni, Ben’lauro Goncalves Zavale, Amam Çhinyere Mbakwem, Ana Olga Mocumbi. "Acute Rheumatic Fever and Rheumatic Heart Disease" Encyclopedia, https://encyclopedia.pub/entry/24858 (accessed May 12, 2024).
Auala, T.,  Zavale, B.G.,  Mbakwem, A.�., & Mocumbi, A.O. (2022, July 06). Acute Rheumatic Fever and Rheumatic Heart Disease. In Encyclopedia. https://encyclopedia.pub/entry/24858
Auala, Tangeni, et al. "Acute Rheumatic Fever and Rheumatic Heart Disease." Encyclopedia. Web. 06 July, 2022.
Acute Rheumatic Fever and Rheumatic Heart Disease
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This entry is adapted from the peer-reviewed paper 10.3390/pathogens11050496

Group A Streptococcus (GAS) causes superficial and invasive infections and immune mediated post-infectious sequalae (including acute rheumatic fever/rheumatic heart disease). Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) are important determinants of global cardiovascular morbidity and mortality. ARF is a multiorgan inflammatory disease that is triggered by GAS infection that activates the innate immune system. In susceptible hosts the response against GAS elicits autoimmune reactions targeting the heart, joints, brain, skin, and subcutaneous tissue. Repeated episodes of ARF—undetected, subclinical, or diagnosed—may progressively lead to RHD, unless prevented by periodic administration of penicillin. The modified Duckett Jones criteria with stratification by population risk remains relevant for the diagnosis of ARF and includes subclinical carditis detected by echocardiography as a major criterion. Chronic RHD is defined by valve regurgitation and/or stenosis that presents with complications such as arrhythmias, systemic embolism, infective endocarditis, pulmonary hypertension, heart failure, and death.

Group A Streptococcus rheumatic fever rheumatic heart disease

1. Introduction

Streptococcus pyogenes, also referred to as Group A Streptococcus (GAS), has been recognized as an important cause of global morbidity and mortality, especially in resource poor settings and is said to be among the top 10 causes of death worldwide [1][2]. GAS causes a wide range of diseases including superficial infection (scarlet fever, impetigo, pharyngitis), invasive infection (cellulitis, necrotizing fasciitis, skeletal infections, sepsis, toxic shock syndrome), and immune mediated post infectious sequalae (acute rheumatic fever/rheumatic heart disease, post-streptococcal glomerulonephritis, and recently paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) [3][4][5].
The traditionally accepted route of transmission of Streptococcus pyogenes is by heavy respiratory droplets. However, there is recent evidence that other routes may play an important role in the transmission: oronasal secretions, small airborne particles, skin-to-skin contact, surfaces, bedding and fabrics, food, and insects [6][7]. Though spread is from infectious individuals, some studies suggest that transmission from carriers may be of epidemiological importance [8][9][10].
Although acute rheumatic fever (ARF) and its sequela rheumatic heart disease (RHD) virtually disappeared in high income settings by late 20th century, they remain major public health concerns in low- and middle-income countries (LMICs) and in vulnerable communities in high income countries [11]. Renewed interest in these diseases resulted in more research, action, and advocacy by groups from affected regions which revealed undeniable evidence that ARF/RHD is the most common acquired heart disease among children and young adults with a female preponderance [12]; it still carries a high risk of death and disability from heart failure, stroke, and infective endocarditis, and constitutes an enormous socioeconomic stress in endemic regions(LMICs) [13][14][15]. In 2013 the World Heart Federation released a position statement on the prevention and control of RHD with a goal to reduce premature deaths caused by RHD in individuals younger than 25 years of age by 25% by the year 2025 [16]. A milestone was achieved in 2018 when ARF and RHD were declared a global health priority for the first time with the passage of a Global WHO Resolution on Rheumatic Fever and Rheumatic Heart Disease. This important resolution establishes key actions, mobilises resources, and renews the global commitment toward the eradication of ARF [17].

2. Epidemiology

Accurate estimates of ARF and RHD disease burden are lacking due to a paucity of comprehensive disease registries, reliance on passive surveillance systems, and the underreporting of both acute and chronic cases from endemic areas for Streptococcus pyogenes infections [18]. Serious GAS disease was previously estimated to affect about 18.1 million people each year, with around 1.78 million new cases and 517,000 deaths annually [19][20]. More recent estimates put the global burden of RHD at 33.4 million and annual mortality around 639,000 [11].
Prevalence of non-invasive GAS infection varies according to the geographical location and seasons; pharyngitis is dominant in temperate regions during the winter months, while impetigo is more common in the tropical zones during summer [21]. Children are both the reservoir of GAS (represent the pool for infection of adults) and the target population for pharyngitis, invasive, and non-invasive infections. The peak age incidence for infections is from 5 to 15 years, with infections in older ages usually occurring in the setting of large gatherings of people in close quarters [21][22].
Developed countries have reported a decreased incidence in invasive GAS disease. Wahl et al. reported a low incidence rate of invasive Streptococcus pyogenes disease between 1996 and 2002 from a voluntary laboratory surveillance system [23]. Germany is classified as a non-endemic country as less than 0.15 deaths per 100,000 population among children 5 to 9 years of age were due to RHD [11]. Despite the reduced incidence of GAS in high income countries, recent resurgences have been reported likely related to changes in circulating strains and/or host susceptibility [24][25]. In 2015, the United States of America reported over 15,000 cases of invasive GAS infection while Canada reported an increase of 5.24 cases over the 2.9 cases/100,000 incidence in 2003 [24][26][27]. A more recent systematic review and meta-analysis on the incidence of sore throat and GAS pharyngitis in children at high risk of developing ARF worldwide found that the pooled incidence rates for sore throat in children at risk of developing ARF in these regions at 82.5 per 100 child-years [28]. This rate is higher than rates reported in developed countries (32.70–40 per 100 child-years); for GAS pharyngitis the incidence rates were 10.8 per 100 child-years (similar to 12.8–14 per 100 years in developed countries) [28]. In East Africa, Bimerwe et al. were able to include 13 research in their systematic review and meta-analysis, finding a pooled prevalence of RHD also considerably higher than the results from developed countries, at 17.9 per 1000 children (95% CI = 11.6–24.2) [29]. Thus, overall GAS infections are worse in socioeconomically disadvantaged groups in developing and developed nations [25][26][27].

3. Natural History

The natural history and progression of ARF and RHD remain incompletely understood. Evidence supports the view that ARF results from an autoimmune response to pharyngeal infection with GAS in genetically predisposed individuals, which is mediated through molecular mimicry [30][31]. About 0.3–3% of people with GAS pharyngitis develop ARF, depending on genetic predisposition and the virulence of the infecting strain [19][32][33]. Whether the finding of more severe forms of RHD at younger ages in Sub Saharan Africa is related to genetic background or repeated GAS infections in the context of health systems challenges is still to be revealed as is the possible role of GAS skin infection causing ARF in LMICs, another important consideration [13][33].

4. Pathogenesis

The initiation of the host-GAS interaction is by avid adhesion of the bacteria via multiple adhesins [1][31][33]. In addition to adhesion and colonisation, intracellular invasion can occur and this requires the expression of M protein and/or fibronectin-binding proteins such as SfbI by GAS [34][35][36]. Internalisation may lead to carriage and persistence as the GAS M protein and hyaluronic acid capsule enables the organism to evade host defence mechanisms (viz opsonization and phagocytosis) [1][35].

4.1. Molecular Mimicry

The transition from a bacterial infection to tissue damage resulting in ARF/RHD is through the immune response to the superficial infections. The antibody and cellular immune response directed against GAS antigens cross reacts with tissues in the heart, joints, brain, skin, and subcutaneous tissues of the susceptible host. This molecular mimicry is due to structural similarity (shared epitopes) between the host tissues and GAS antigens. Studies have demonstrated cross reactive antigens on the GAS cell wall, cell membrane, and hyaluronate capsule that react with three major human host subsets, mainly N-acetyl-glucosamine, myosin, and related molecules and DNA [30][37][38].
The proposed events in rheumatic carditis and valvulitis are both cellular and antibody mediated. The major target of cross-reactive GAS polysaccharide directed antibodies is the valve endothelium and lamina, though there is also reaction with myocardial myosin [34]. This antibody cross reactivity leads to inflammation at the valve surface and expression of increased amounts of the adhesion molecule VCAM-1 (Vascular cell adhesion molecule 1). This promotes the binding, infiltration, and extravasation of cross-reactive T-cells; these T-cells have cross-reactivity with streptococcal M proteins and similar host alpha helical protein antigens (e.g., myosin, laminin, tropomyosin, or vimentin). The T-cells differentiate into CD4+ TH1 cells producing gamma interferon that causes scarring and fibrosis and IL-17A that promotes neovascularization in the normally avascular valve tissue [38][39]. These processes predispose the valve to cellular infiltration through both the activated valve endocardial surface and the neovascularized scar tissue. Antibodies to collagen have also been demonstrated in RHD and may contribute to valve damage, but this pathway will be activated only once the valve is already damaged and underlying collagen is exposed [30]. Aschoff bodies are the typical histopathological lesions in RHD.

Pharyngitis versus Impetigo in Immune Mediated Sequalae

Genetic and epidemiological evidence for skin infection as the event that leads to ARF is mounting, but pharyngeal infection is still considered to be the trigger in most cases [13][40][41][42]. Earlier studies have shown consistent elevation of Anti Streptolysin O (ASO) titres in GAS pharyngitis, while in patients with GAS impetigo inconsistent elevations were seen [40]. Based on the antigenicity of the 3’ terminal repeat region of emm, phage typing with M proteins is classified into I and II; with only class I associated with ARF. The emm chromosomal arrangement was then further classified into 5 patterns responsible for different manifestations: pattern A–C (class I) causing pharyngitis; pattern D (class I) causing impetigo; and pattern E (class II) causing both pharyngitis and impetigo [40][41]. These data, derived from the United States of America, are under debate because in populations from areas with the highest burden of RHD (e.g., native Australians, New Zealanders, and Fijians), GAS impetigo is more frequent than pharyngitis [42][43][44]. The reasons for this could include: the diversity of GAS species between the tropical and temperate regions; possible coinfection by strains causing both impetigo and pharyngitis; and priming by impetigo strain for the immune reaction with a pharyngitis [40]. The possibility of GAS skin infection as the trigger for ARF has great implications for the control programmes for ARF/RHD which have previously only focused on prevention of GAS pharyngitis.

4.2. Genetic Susceptibility

The heritable genetic susceptibility to ARF is demonstrated by the increased risk of concordance among monozygotic twins over dizygotic twins (44% vs. 12%) [19]. The lifetime cumulative incidence of ARF in populations exposed to rheumatogenic GAS infection is consistently 3–6% irrespective of ethnicity or geography [45]. The familial aggregation of rheumatic fever as originally reported by Cheadle, states that the chance of an individual with a family history of ARF acquiring the disease is 5 times greater than that of an individual who has no family history. This has been supported by a study of children raised separately from parents with RHD, who had a relative risk of 2.93 for the development of rheumatic fever compared with children whose parents did not have RHD [46]. Twin studies have evaluated the extent to which the familial occurrence of ARF is due to genetic and environmental factors. Phenotypic concordance among dizygotic twins suggests that ARF has a non-Mendelian inherited component. The risk of rheumatic fever in a monozygotic twin when the co-twin previously had rheumatic fever is more than six times greater than that in dizygotic twins. The heritability of rheumatic fever is 60%, highlighting heredity as a major susceptibility factor of the disease [47].
Several genes responsible for the innate and adaptive immune response, cytokines, and B-cell alloantigens have been associated in the development of ARF and RHD [48][49][50]. A recent multicenter case-control genome-wide association study (GWAS), the Genetics of Rheumatic Heart Disease, studied more than 7 million genotyped and inputted single-nucleotide variations from 4809 African individuals [51]. This demonstrated a new candidate susceptibility locus (11q24.1) which reached genome-wide significance in and exclusive to Black African individuals and thus a heritable component to RHD susceptibility in African individuals [51]. Although significant associations have been found between genetic factors and ARF, study outcomes either contradict each other or are not reproducible. The discovery of the specific genetic and heritable factors for ARF would allow for screening of such variants and identification of individuals who are at high risk and would derive benefit from primary penicillin prophylaxis or vaccination against GAS [52].

4.3. Other Factors

Socioeconomic status (household income, level of education, unemployment) affects multiple potential risk factors for the development of ARF and RHD [53][54][55]. Potential risk/protective factors that have been identified and demonstrated include environmental factors (number of social contacts, household crowding and bed sharing, household resources, laundry, housing conditions); healthcare factors (health literacy, distance to and healthcare access); and health and nutrition factors (health status, oral health status and services, nutrition) [53].

5. Management & Prevention

The management of ARF consists of eradication of the GAS using antibiotic (penicillin or alternative in penicillin allergic individuals) and symptomatic relief with anti-inflammatory drugs, analgesics, and bed rest. Secondary prophylaxis to prevent new episodes of ARF is recommended for patients with previous ARF or established RHD patients, as they are at higher risk of GAS infections [56]. In its advanced stages, RHD causes considerable morbidity and premature mortality mainly related to low awareness of health professionals, low health literacy of patients/parents/carers, long distances to health facilities, low provision diagnostics and drugs, and unavailability of interventions (cardiac catheterization and/or surgery).
Major challenges for the management of ARF and RHD in under-resourced settings include case identification, preoperative assessment, choice of procedure, and postoperative care. Resource allocation toward raising awareness in affected communities and active adequate and continuous training of the health professionals at all levels in the recognition, prevention, and management of GAS infections, ARF, and RHD is essential for any control program. RHD management includes the medical treatment of heart failure and other complications, correction of individual valve lesions through catheter-based Interventions for valve repair or replacement (e.g., commissurotomy for MS), as well as open heart surgery for valve repair or replacement with the performance of minimally invasive surgery wherever available. The decision is determined by several factors viz: age, gender, number, and severity of affected valves, as well as socioeconomic and geographic factors that may influence follow-up, access to anticoagulation, and adherence to long-term prophylaxis.
Anticoagulation is indicated in patients with prosthetic valves and/or atrial fibrillation. Prevention of infective endocarditis in endemic regions is mostly through prevention of skin and oral infections and antibiotic prophylaxis prior to invasive procedures that might cause bacteriemia.
A safe and effective vaccine against ARF would be highly advantageous. Although such developments started in the early 1960s, progression towards a protective vaccine has been hampered by the widespread diversity of GAS strains (numerous emm types), cross-reactivity between streptococcal and host proteins, and lack of relevant animal models for studying the pathogenesis of RHD [57]. The three major types of vaccines are currently in development are those based on cell surface proteins, secreted proteins, and carbohydrates [58].

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Subjects: Cardiac & Cardiovascular Systems
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Tangeni Auala
,
Ben’Lauro Goncalves Zavale
,
Amam Çhinyere Mbakwem
,
Ana Olga Mocumbi
View Times: 298
Revisions: 2 times (View History)
Update Date: 07 Jul 2022
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