scholarly journals Towards developing a vaccine for rheumatic heart disease

2017 ◽  
Vol 2017 (1) ◽  
Author(s):  
Geethanjali Devadoss Gandhi ◽  
Navaneethakrishnan Krishnamoorthy ◽  
Ussama M. Abdel Motal ◽  
Magdi Yacoub

Rheumatic heart disease (RHD) is the most serious manifestations of rheumatic fever, which is caused by group A Streptococcus (GAS or Streptococcus pyogenes) infection. RHD is an auto immune sequelae of GAS pharyngitis, rather than the direct bacterial infection of the heart, which leads to chronic heart valve damage. Although antibiotics like penicillin are effective against GAS infection, improper medical care such as poor patient compliance, overcrowding, poverty, and repeated exposure to GAS, leads to acute rheumatic fever and RHD. Thus, efforts have been put forth towards developing a vaccine. However, a potential global vaccine is yet to be identified due to the widespread diversity of S. pyogenes strains and cross reactivity of streptococcal proteins with host tissues. In this review, we discuss the available vaccine targets of S. pyogenes and the significance of in silico approaches in designing a vaccine for RHD. 

Author(s):  
Ghadeer Turki Aloutaibi ◽  
Abdulrahman L. Al-Malki ◽  
Maha J. Balgoon ◽  
Saud A. Bahaidarah ◽  
Said Salama Moselhy

Acute rheumatic fever (ARF) triggered by Group A streptococcus bacterium due to post-infectious and non-supportive pharyngeal infection. Depending on certain conditions, such as genetic predisposition to the disease, the prevalence of various cases of rheumatism and socioeconomic status in different regions, ARF can have different clinical manifestations. The disease typically manifested by one or more acute episodes, whereas 30-50% of all repeated ARF status can result in chronic rheumatic heart disease (RHD) with gradual and irreversible heart valve damage and also have been found to be correlated with a raised risk of myocardial infarction (MI), cardiovascular disease (CVD) and dyslipidemia. The RHD is the only long-term consequence of ARF and the most serious. The development to chronic RHD is determined by many factors, most notably the frequent episodes of rheumatic fever (RF). The RHD is known socially and economically as being the most frequent heart disease in vulnerable populations. H.pylori infection has been proposed to be involved RHD greater than that of the normal healthy people. H.pylori can be considered as one of the probable risk factor for RHD.It was concluded that patients with H. Pylori should be advised to follow up in cardiology clinics to avoid any complications.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S18-S19
Author(s):  
James Ray Mata Lim ◽  
Bobby L Boyanton ◽  
Julie George ◽  
Matthew Sims

Abstract Background Treatment of Group A Streptococcus (GAS) pharyngitis is imperative to mitigate sequelae such as rheumatic heart disease. The need for treatment of Group C Streptococcus (GCS) and Group G Streptococcus (GGS) pharyngitis is unclear, as rheumatogenic sequelae have not been well documented. Our institution switched from culture to molecular confirmation testing for a negative rapid streptococcal antigen detection test. Cultures reported GAS whereas molecular testing reported GAS, GCS, and GGS. We performed a retrospective chart review to examine the epidemiological differences of GAS, GCS, and GGS pharyngitis. Methods Records were obtained of pharyngeal samples from patients sent for testing at Beaumont Health Laboratory. In all, 92,369 records were analyzed. There were 47,106 records of cultures from May 2012 through December 2014 and 45,263 records of molecular testing from May 2015 to December 2017. Samples positive for either GCS or GGS were reported as positive for Group CG Streptococcus (GCGS). Epidemiological factors were evaluated. If available, electronic records from GCGS positive samples were evaluated for clinical features, antibiotics used, and sequelae or complications reported. Results Molecular testing showed GAS positivity of 9.3% (n = 4,189) and GCGS positivity of 1.5% (n = 687). GCGS pharyngitis was more likely during the summer months and in young adults 13 years and older than children under 13 years. GAS pharyngitis was more likely during spring months and in children aged 4–9 years. Mean age of GCGS pharyngitis was 13 vs. 8.6 years for GAS pharyngitis. Similar results were obtained for GAS between culture and molecular testing records. Amoxicillin was most often prescribed for treatment of GCGS. There were few instances of severe GCGS exudative or recurrent pharyngitis that required hospitalization or tonsillectomy. There were no cases of rheumatic fever or rheumatic heart disease associated with GCGS. Conclusion This is the largest study based on our literature review to evaluate the epidemiology of GAS, GCS, and GGS pharyngitis in children and adults. We found a seasonal and age difference between GAS and GCGS. Complications were rare, and no rheumatogenic sequelae were noted from GCGS infections. Disclosures All Authors: No reported Disclosures.


2000 ◽  
Vol 124 (2) ◽  
pp. 239-244 ◽  
Author(s):  
J. R. CARAPETIS ◽  
B. J. CURRIE ◽  
J. D. MATHEWS

Aboriginal Australians in northern Australia are subject to endemic infection with group A streptococci, with correspondingly high rates of acute rheumatic fever and rheumatic heart disease. For 12 communities with good ascertainment, the estimated lifetime cumulative incidence of acute rheumatic fever was approximately 5·7%, whereas over the whole population, with less adequate ascertainment, the cumulative incidence was only 2·7%. The corresponding prevalences of established rheumatic heart disease were substantially less than the cumulative incidences of acute rheumatic fever, at least in part because of poor ascertainment. The cumulative incidence of acute rheumatic fever estimates the proportion of susceptible individuals in endemically exposed populations. Our figures of 2·7–5·7% susceptible are consistent with others in the literature. Such comparisons suggest that the major part of the variation in rheumatic fever incidence between populations is due to differences in streptococcal exposure and treatment, rather than to any difference in (genetic) susceptibility.


Author(s):  
Herlina Dimiati ◽  
Sofia Sofia ◽  
Gani B

Acute rheumatic fever (ARF) is the body’s immune system reacting to an untreated infection with Group A Streptococcus (GAS) that affects skin, joints, brain, and heart. The heart damage that remains after an occurrence of ARF is called rheumatic heart disease (RHD). The objective of this study was to evaluate the ARF and RHD based on the profile of clinical diagnoses and emerging factors. The data were collected through interviews of the subjects, complete blood counts, the anti-streptolysin titer O analysis, the C-reactive protein Assay, and a statistical analysis. This research was a combination of clinical assessments, the CRP kit, anti-titer O kit, and interviews. The data were analyzed by employing Wilcoxon, Chi-square and Friedman test and also included a correlation analyzed using Spearman’s correlation with significance of (p<0.05. There were 63 samples of ARF and RHD patients involved, consisting of male (50.8%:32) and female (49.9%:31) patients (p<0.05). The factors that triggered ARF and RHD (p<0.05; r=0.88) as well as laboratory diagnosis (p<0.05) of these infections were measured. The ARF caused by residence also caused RHD by the interaction of time with the environment (p<0.05). The population consisted of males (32:50.8%) and females (31:49.2%), and it was not significant (p>0.05), while the streptococcal infection of RHD (63.5%) was much larger than in ARF (36.5%). This was based on the clinical diagnosis of RHD and ARF with a significance of (p<0.05). Also, the residence and the period of interaction with the environment were influences on the RHD and ARF.


ESC CardioMed ◽  
2018 ◽  
pp. 1134-1137
Author(s):  
Liesl Zühlke

This chapter outlines the current best estimates for mortality and morbidity for group A Streptococcus, acute rheumatic fever, and rheumatic heart disease and in particular highlights the disproportionate burden of disease.


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