Effective interventions and treatments for complex diseases have been implemented globally, however, coverage in Africa has been comparatively lower due to lack of capacity, clinical applicability and knowledge on the genetic contribution to disease and treatment. Currently, there is a scarcity of genetic data on African populations, which have enormous genetic diversity. Pharmacogenomics studies have the potential to revolutionise treatment of diseases, therefore, African populations are likely to benefit from these approaches to identify likely responders, reduce adverse side effects and optimise drug dosing. This review discusses clinical pharmacogenetics studies conducted in African populations, focusing on studies that examined drug response in complex diseases relevant to healthcare. Several pharmacogenetics associations have emerged from African studies, as have gaps in knowledge.

Background Chlamydiae are intracellular bacteria that cause various severe diseases in humans and animals. The common treatment for chlamydia infections are antibiotics. However, when antibiotics are misused (overuse or self-medication), this may lead to resistance of a number of chlamydia species, causing a real public health problem worldwide. Materials and methods In the present work, a comprehensive literature search was conducted in the following databases: PubMed, Google Scholar, Cochrane Library, Science direct and Web of Science. The primary purpose is to analyse a set of data describing the genes and mutations involved in Chlamydiae resistance to antibiotic mechanisms. In addition, we proceeded to a filtration process among 704 retrieved articles, then finished by focusing on 24 studies to extract data that met our requirements. Results The present study revealed that Chlamydia trachomatis may develop resistance to macrolides via mutations in the 23S rRNA, rplD, rplV genes, to rifamycins via mutations in the rpoB gene, to fluoroquinolones via mutations in the gyrA, parC and ygeD genes, to tetracyclines via mutations in the rpoB gene, to fosfomycin via mutations in the murA gene, to MDQA via mutations in the secY gene. Whereas, Chlamydia pneumoniae may develop resistance to rifamycins via mutations in the rpoB gene, to fluoroquinolones via mutations in the gyrA gene. Furthermore, the extracted data revealed that Chlamydia psittaci may develop resistance to aminoglycosides via mutations in the 16S rRNA and rpoB genes, to macrolides via mutations in the 23S rRNA gene. Moreover, Chlamydia suis can become resistance to tetracyclines via mutations in the tet(C) gene. In addition, Chlamydia caviae may develop resistance to macrolides via variations in the 23S rRNA gene. The associated mechanisms of resistance are generally: the inhibition of bacteria’s protein synthesis, the inhibition of bacterial enzymes’ action and the inhibition of bacterial transcription process. Conclusion This literature review revealed the existence of diverse mutations associated with resistance to antibiotics using molecular tools and targeting chlamydia species’ genes. Furthermore, these mutations were shown to be associated with different mechanisms that led to resistance. In that regards, more mutations and information can be shown by a deep investigation using the whole genome sequencing. Certainly, this can help improving to handle chlamydia infections and healthcare improvement by decreasing diseases complications and medical costs.

Background Chlamydia trachomatis is an obligate intracellular gram-negative pathogen, responsible for diverse affections, mainly trachoma and sexually transmitted diseases. Antibiotics are the commonly used drugs to tackle chlamydiae infections. However, when overused or wrongly used this may lead to strains’ resistance to antibiotics, this phenomenon represents a real health problem worldwide. Numerous studies showed the association of Chlamydia trachomatis resistance with mutations in different genes; these mutations could have a deleterious or neutral impacts on the encoded proteins. The aim of this study is to perform an in silico analysis of C. trachomatis rpoB-encoded proteins using numerous bioinformatics tools and to identify the functional and structural-related effects of the mutations and consequently their impact on the bacteria sensitivity to antibiotics. Results The analysis revealed that the prediction of the damaging impact related to the mutations in rpoB-encoded proteins showed eight mutations: V136F, Q458K, V466A, A467T, H471N, H471Y, H471L, and I517M with big deleterious effects. Among them, six mutations, V136F, Q458K, V466A, A467T, H471N, and I517M, are located in a highly conserved regions decreasing the protein’s stability. Furthermore, the structures analysis showed that the mutations A467T, H471N, I517M, and V136F models had a high deviation compared to the wild type. Moreover, the prediction of protein-protein network indicated that rpoB wild type interacts strongly with 10 proteins of C. trachomatis, which are playing different roles at different levels. Conclusion As conclusion, the present study revealed that the changes observed in the encoded proteins can affect their functions and structures, in addition to their interactions with other proteins which impact the bacteria sensitivity to antibiotics. Consequently, the information revealed through this in silico analysis would be useful for deeper exploration to understand the mechanisms of C. trachomatis resistance and enable managing the infection to avoid its complications. We recommend further investigations and perform deeper experimental analysis with collaboration between bioinformaticians, physicians, biologists, pharmacists, and chemistry and biochemistry scientists.