Streptococcus pneumoniae (S. pneumoniae) is a bacterial species often associated with the occurrence of community-acquired pneumonia (CAP). CAP refers to a specific kind of pneumonia that occurs in individuals who acquire the infection outside of a healthcare setting. It represents the leading cause of both death and morbidity on a global scale. Moreover, the declaration of S. pneumoniae as one of the 12 leading pathogens was made by the World Health Organization (WHO) in 2017. Antibiotics like β-lactams, macrolides, and fluoroquinolones are the primary classes of antimicrobial medicines used for the treatment of S. pneumoniae infections. Nevertheless, the efficacy of these antibiotics is diminishing as a result of the establishment of resistance in S. pneumoniae against these antimicrobial agents. In 2019, the WHO declared that antibiotic resistance was among the top 10 hazards to worldwide health. It is believed that penicillin-binding protein genetic alteration causes β-lactam antibiotic resistance. Ribosomal target site alterations and active efflux pumps cause macrolide resistance. Numerous factors, including the accumulation of mutations, enhanced efflux mechanisms, and plasmid gene acquisition, cause fluoroquinolone resistance. Furthermore, despite the advancements in pneumococcal vaccinations and artificial intelligence (AI), it is not feasible for individuals to rely on them indefinitely. The ongoing development of AI for combating antimicrobial resistance necessitates more research and development efforts. A few strategies can be performed to curb this resistance issue, including providing educational initiatives and guidelines, conducting surveillance, and establishing new antibiotics targeting another part of the bacteria. Hence, understanding the resistance mechanism of S. pneumoniae may aid researchers in developing a more efficacious antibiotic in future endeavors.

Antimicrobial resistance in companion animals is a major public health concern worldwide due to the animals’ zoonotic potential and ability to act as a reservoir for resistant genes. We report on the first use of meta-analysis and a systematic review to analyze the prevalence of vancomycin-resistant Enterococcus (VRE) in companion animals. Databases such as MedLib, PubMed, Web of Science, Scopus, and Google Scholar were searched. The information was extracted by two independent reviewers and the results were reviewed by a third. Two reviewers independently assessed the study protocol using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) checklist and the study quality using the Joanna Briggs Institute (JBI) critical appraisal checklist for prevalence data. OpenMeta analyst and comprehensive meta-analysis (CMA) were used for the meta-analysis. The random effect model was used, and publication bias was assessed using the Eggers test and funnel plot. Between-study heterogeneity was assessed, and the sources were analyzed using the leave-one-out meta-analysis, subgroup analysis and meta-regression. Twenty-two studies met the eligibility criteria, but because some studies reported the prevalence of VRE in more than one companion animal, they were considered as individual studies, and 35 studies were therefore added to the final meta-analysis. Sampling period of the included studies was from 1995–2018. Of the 4288 isolates tested in the included studies, 1241 were VRE. The pooled prevalence of VRE in companion animals was estimated at 14.6% (95% CI; 8.7–23.5%; I² = 97.10%; p < 0.001). Between-study variability was high (t² = 2.859; heterogeneity I² = 97.10% with heterogeneity chi-square (Q) = 1173.346, degrees of freedom (df) = 34, and p < 0.001). The funnel plot showed bias, which was confirmed by Eggers test (t-value = 3.97165; p = 0.00036), and estimates from the leave-one-out forest plot did not affect the pooled prevalence. Pooled prevalence of VRE in dogs and cats were 18.2% (CI = 9.4–32.5%) and 12.3%, CI = 3.8–33.1%), respectively. More studies were reported in Europe than in any other continent, with most studies using feces as the sample type and disc diffusion as the detection method. With the emergence of resistant strains, new antimicrobials are required in veterinary medicine.

Remarkable scientific breakthroughs have been made in the stride towards the development of potent and tolerable hepatitis C regimens within the last three decades. Earlier approaches involved the use of pegylated interferon alfa and ribavirin as standard-of-care treatment. Treating genotype 1a infection with this regimen which was at that time considered the gold standard for hepatitis C virus therapy was rife with challenges; safety and toxicity issues necessitated a rigorous quest for alternative regimens. Deeper understanding of the pathogenesis of hepatitis C virus ushered in the era of direct acting antiviral agents. These agents have been the subject of intensive research in the last two decades, leading to the development of drug classes such as protease inhibitors (e.g., grazoprevir), NS5A inhibitors (e.g., daclatasvir) and NS5B inhibitors (e.g., sofosbuvir). While many are still under development, several have been approved for hepatitis C therapy. A number of studies investigating the combination of direct acting antiviral agents with or without pegylated interferon and/or ribavirin for the treatment of chronic hepatitis have demonstrated sustained virologic response of > 90%. Given the array of direct acting antiviral agents currently available, the present landscape of hepatitis C therapy is now characterized by a gradual transition to all-oral interferon-free regimens. Despite these milestones, the WHO global target of eliminating hepatitis C as a public health problem by 2030 seems uncertain. In this review, we provide a concise account of the evolution and advancements in the development of anti-HCV regimens.