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. 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. 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. 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.

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与衣原体对抗生素耐药相关的基因和突变概述

衣原体是在人和动物中引起各种严重疾病的细胞内细菌。衣原体感染的常见治疗方法是抗生素。然而，当滥用抗生素（过度使用或自我用药）时，​​可能会导致许多衣原体物种产生耐药性，从而在全球范围内造成真正的公共卫生问题。在目前的工作中，在以下数据库中进行了全面的文献检索：PubMed、Google Scholar、Cochrane Library、Science direct 和 Web of Science。主要目的是分析一组描述衣原体对抗生素机制耐药性的基因和突变的数据。此外，我们对检索到的 704 篇文章进行了过滤，然后重点关注 24 项研究以提取符合我们要求的数据。本研究表明，沙眼衣原体可能通过 23S rRNA、rplD、rplV 基因的突变对大环内酯类药物产生耐药性，通过 rpoB 基因突变对利福霉素产生耐药性，通过 gyrA、parC 和 ygeD 基因突变对氟喹诺酮类药物产生耐药性，通过突变对四环素产生耐药性。在 rpoB 基因中，通过 murA 基因突变到磷霉素，通过 secY 基因突变到 MDQA。然而，肺炎衣原体可能通过 rpoB 基因的突变对利福霉素产生耐药性，通过 gyrA 基因的突变对氟喹诺酮类药物产生耐药性。此外，提取的数据显示鹦鹉热衣原体可能通过 16S rRNA 和 rpoB 基因的突变对氨基糖苷类产生耐药性，通过 23S rRNA 基因的突变对大环内酯类产生耐药性。此外，猪衣原体可通过 tet(C) 基因突变对四环素产生耐药性。此外，豚鼠衣原体可能通过 23S rRNA 基因的变异对大环内酯类产生抗药性。耐药的相关机制一般是：抑制细菌的蛋白质合成、抑制细菌酶的作用和抑制细菌的转录过程。该文献综述揭示了存在与使用分子工具和靶向衣原体基因的抗生素抗性相关的多种突变。此外，这些突变被证明与导致抗药性的不同机制有关。在这方面，可以通过使用全基因组测序的深入调查来显示更多的突变和信息。当然，这可以通过减少疾病并发症和医疗成本来帮助改善衣原体感染和医疗保健的改善。