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Background: There is concern regarding the increasing resistance of Group A streptococcus (GAS) to routinely used antibiotics. GAS is a common cause of bacterial pharyngitis and more severe invasive infections such as septicaemia. Furthermore, GAS pharyngitis is the antecedent for serious conditions such as rheumatic fever and rheumatic heart disease. The study aimed to determine the antimicrobial susceptibility patterns of GAS cultured from patients with invasive and non-invasive infections from Cape Town, as part of the AFRO Strep Registry., Methods: Samples were provided by the AFRO Strep Registry, a continental endeavour aiming to document Streptococcus pyogenes infection in Africa and create the first biorepository of its kind. Ninety-five GAS isolates (invasive, n = 40; non-invasive, n = 55) were evaluated for resistance to a panel of 20 antibiotics using the Sensititre® STP6F system with MICs interpreted by CLSI break points., Results: Amongst all isolates, highest levels of resistance were observed with respect to tetracycline (8.33 %), followed by azithromycin (1.04 %) and erythromycin (1.04 %). No resistance to the remaining antibiotics was detected amongst all isolates. No differences with regard to MIC values were observed between isolates from invasive and non-invasive infections (p-value >0.05 for all antibiotics)., Conclusion: GAS remains susceptible to routine-antimicrobial agents used in our low-resourced setting. Eight percent of the GAS isolates were resistant to tetracycline, and we did not observe macrolide resistance as reported in high income countries. This is the first study to report on the antimicrobial patterns of GAS in South Africa. These results address a critical gap in the available data on GAS in Africa and specifically South Africa and, thus, aid in avoiding therapeutic failures., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors.)

Introduction: It is currently unclear what the role of Group A streptococcus (GAS) virulence factors (VFs) is in contributing to the invasive potential of GAS. This work investigated the evidence for the association of GAS VFs with invasive disease., Methods: We employed a broad search strategy for studies reporting the presence of GAS VFs in invasive and non-invasive GAS disease. Data were independently extracted by two reviewers, quality assessed, and meta-analyzed using Stata®., Results: A total of 32 studies reported on 45 putative virulence factors [invasive (n = 3,236); non-invasive (n = 5,218)], characterized by polymerase chain reaction (PCR) (n = 30) and whole-genome sequencing (WGS) (n = 2). The risk of bias was rated as low and moderate, in 23 and 9 studies, respectively. Meta-,analyses of high-quality studies (n = 23) revealed a significant association of speM [OR, 1.64 (95%CI, 1.06; 2.52)] with invasive infection. Meta-analysis of WGS studies demonstrated a significant association of hasA [OR, 1.91 (95%CI, 1.36; 2.67)] and speG [OR, 2.83 (95%CI, 1.63; 4.92)] with invasive GAS (iGAS). Meta-analysis of PCR studies indicated a significant association of speA [OR, 1.59 (95%CI, 1.10; 2.30)] and speK [OR, 2.95 (95%CI, 1.81; 4.80)] with invasive infection. A significant inverse association was observed between prtf1 [OR, 0.42 (95%CI, 0.20; 0.87)] and invasive infection., Conclusion: This systematic review and genomic meta-analysis provides evidence of a statistically significant association with invasive infection for the hasA gene, while smeZ , ssa , pnga3 , sda1 , sic , and NaDase show statistically significantly inverse associations with invasive infection. SpeA , speK , and speG are associated with GAS virulence; however, it is unclear if they are markers of invasive infection. This work could possibly aid in developing preventative strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Rampersadh, Salie, Engel, Moodley, Zühlke and Engel.)

Background: The prevalence of tuberculosis (TB)-associated pulmonary hypertension (PH) has not previously been quantified, resulting in an underappreciated burden of disease. We aimed to estimate the prevalence of PH in post-TB and active TB populations., Methods: In this systematic review and meta-analysis, we searched PubMed/Medline, Cochrane Library, EBSCOhost, Scopus, African Journals Online and Google Scholar, with no language restriction, for available literature published after 1950. Eligible studies described adult participants (≥16 years), with documented evidence of active or prior TB, diagnosed with PH. Study quality was assessed using a risk of bias tool specifically developed for prevalence studies. Aggregate prevalence estimates with 95% confidence intervals were synthesised using a random-effects meta-analysis model, incorporating the Freeman-Tukey transformation. Subgroup analysis was conducted to ascertain prevalence estimates in specific patient populations., Results: We identified 1452 unique records, of which 34 met our inclusion criteria. 23 studies, with an acceptable risk of bias and where PH was diagnosed at right heart catheterisation or echocardiography, were included in the meta-analysis. In post-TB studies (14/23), the prevalence of PH was 67.0% (95% CI 50.8-81.4) in patients with chronic respiratory failure, 42.4% (95% CI 31.3-54.0) in hospitalised or symptomatic patients and 6.3% (95% CI 2.3-11.8) in nonhealthcare-seeking outpatients (I 2 =96%). There was a lower estimated prevalence of PH in studies of populations with active TB (9.4%, 95% CI 6.3-13.0), I 2 =84%)., Conclusion: Our results highlight the significant burden of PH in post-TB and active TB populations. We emphasise the need for increased recognition of TB-associated PH and additional high-quality prevalence data., Competing Interests: Conflicts of interest: None to declare., (Copyright ©The authors 2024.)