Cardiovascular disorders and hypertension
Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize in Developmental and Adapted Physical Education, 2019
Rheumatic heart disease can occur at any age, but usually occurs in children between 6 and 12 years of age who have had rheumatic fever. Rheumatic fever develops as a reaction to antibodies formed as a defense against streptococcal bacteria. Damage to the heart may often occur from inflammation, which causes scarring that most notably appears in the heart valves over a period of years. After children have contracted rheumatic fever, they are susceptible to repeated attacks, further increasing the probability of inflammation and scarring that may damage the heart. Rheumatic fever may be identified by symptoms such as pain in joints and muscles, poor appetite, uncontrolled movements of arms, legs, or face (twitching of muscles), frequent nosebleeds, fever, streptococcal infection, sore throat, weakness and shortness of breath, and difficulty in swallowing (World Health Organization, 2018). Penicillin and other antibiotics can usually treat strep throat and prevent acute rheumatic fever from developing. Antibiotic therapy has significantly reduced the incidence and mortality rate of rheumatic fever/rheumatic disease. Rheumatic heart disease, often neglected by the media and policy makers, is a major burden in developing countries where it causes most of the cardiovascular morbidity and mortality in young people, leading to about 250,000 deaths per year worldwide (Marijon et al., 2012).
Diagnostics and therapeutics
Lois N. Magner, Oliver J. Kim in A History of Medicine, 2017
Penicillin was also remarkably successful in the battle against rheumatic fever, a leading cause of disease, disability, and death in children during the first half of the twentieth century. In the 1880s, British pediatricians Thomas Barlow and Walter Cheadle described rheumatic fever as a clinical entity characterized by a migratory arthritis, heart disease, chorea, erythematous rashes, tonsillitis, and subcutaneous nodules. Researchers eventually concluded that infection of the tonsils by Group A streptococci caused rheumatic fever. Many doctors thought that other factors—crowding, poverty, damp and cold conditions, and familial susceptibility—were key contributory factors. The bacteriological explanation prevailed when further studies proved that early treatment of “strep throat” with penicillin prevented the development of rheumatic fever. Recognizing the relationship between sore throats caused by streptococcal infections and rheumatic fever was the key to controlling and eliminating rheumatic fever.
Parasite Versus Host: Pathology and Disease
Eric S. Loker, Bruce V. Hofkin in Parasitology, 2015
Various mechanisms have been proposed as an explanation for why self-tolerance is lost. The release of normally sequestered antigen from usually immunologically privileged sites may explain some autoimmune diseases. An example is sympathetic ophthalmia. Trauma to an eye can release antigens normally not encountered by the immune system, resulting in immune system priming and a subsequent attack on the eye. Inappropriately high expression of MHC on the surface of pancreatic islet cells may be involved in the development of insulin-dependent diabetes. In some cases, however, molecular mimicry may be to blame. In this scenario, an individual is infected with a pathogen bearing antigens that are very similar to host antigens. Lymphocytes, activated in response to the pathogen, also direct their immune assault against the similar host antigen, damaging the tissue bearing those antigens. Such molecular mimicry has been difficult to demonstrate; by the time the affected individual starts displaying symptoms of autoimmunity, the offending pathogen is usually long since destroyed. Yet for some conditions, the evidence for such molecular mimicry is strong. Rheumatic fever, for instance, is initiated by a Streptococcus infection. In some individuals, antibodies generated against the bacterium cross-react with antigens on heart valves.
Best management of patients with an acute sore throat – a critical analysis of current evidence and a consensus of experts from different countries and traditions
Published in Infectious Diseases, 2023
Ronny K. Gunnarsson, Mark Ebell, Robert Centor, Paul Little, Theo Verheij, Morten Lindbæk, Pär-Daniel Sundvall
Patients with apparently uncomplicated acute sore throat but with moderate or high risk for rheumatic fever require management focussing on reducing this risk [4]. Clinical judgement alone without the use of POCT to detect GAS is likely to leave a large proportion of patients ill from GAS without antibiotics even in settings with known moderate or high risk for rheumatic fever [53]. Hence, if POCT is available we recommend testing all patients judged to be at moderate or high risk for rheumatic fever, irrespective of clinical scoring for GAS, and to prescribe antibiotics to all patients harbouring GAS [4]. If POCT is unavailable we recommend that all patients with acute sore throat receive antibiotics in settings with a high risk for rheumatic fever [4]. In settings with moderate risk and POCTs are unavailable, antibiotics should be prescribed to patients with a clinical score indicating probability for the presence of GAS such as Centor scores 2–4 or FeverPAIN scores 2–5 [4].
Lack of Association Between TNF-α, IFN-γ, IL-10 Gene Polymorphisms and Rheumatic Heart Disease in South Indian Population
Published in Fetal and Pediatric Pathology, 2018
Maheshkumar Poomarimuthu, Sivakumar Elango, Pravin Raj Solomon, Sambath Soundarapandian, Jayalakshmi Mariakuttikan
Rheumatic fever (RF) is an autoimmune disease caused by cross-reactive immune responses due to molecular mimicry between group A β-hemolytic streptococcus (GAS) antigens and host tissue proteins [1,2]. Proinflammatory cytokines are the key players which mediate prolonged inflammation in valvular tissues thereby increasing the chances of initiation and progression of rheumatic heart disease (RHD) [3,4]. Genes encoding cytokines have numerous single nucleotide polymorphisms (SNPs) in the regulatory region which affect the expression at interindividual level, thus predisposing to RHD [5]. Globally, there are 33 million RHD patients and it accounts for 275,000 deaths annually. RHD is quite profound in developing countries like India and remains as one of the most common causes of acquired heart diseases among children [6].
Concomitant rapidly progressive glomerulonephritis and acute rheumatic fever after streptococcus infection: a case report
Published in Paediatrics and International Child Health, 2022
Suwanna Pornrattanarungsi, Sudarat Eursiriwan, Yupaporn Amornchaicharoensuk, Chutima Chavanisakun, Ornatcha Sirimongkolchaiyakul
Acute post-streptococcal glomerulonephritis (APSGN) and acute rheumatic fever (ARF) are common, non-suppurative disorders which occur after group A streptococcal (GAS) infection, especially acute pharyngitis or skin infection [1,2]. Typical clinical manifestations in acute glomerulonephritis are hypertension, oedema and glomerular haematuria. Acute rheumatic fever may be associated with cardiac lesions together with systemic signs and symptoms such as polyarthritis, chorea, erythema marginatum, fever and increased inflammatory markers. The diagnosis of APSGN or ARF requires laboratory evidence of preceding streptococcal infection. However, the main mechanism underlying both diseases varies. Immune complex formation is the crucial pathogenesis of APSGN whilst ARF can arise as a result of molecular mimicry [3]. Rarely, however, both occur simultaneously.