Chlamydiae and Mycoplasma Laboratory, Institut Pasteur du Maroc, 20360, Casablanca, Morocco.
Systems & Data Engineering Team, National School of Applied Sciences, Abdelmalek Essaadi University, Tangier, Morocco.
Ann Clin Microbiol Antimicrob. 2021 Sep 3;20(1):59. doi: 10.1186/s12941-021-00465-4.
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.
衣原体是一种能引起人类和动物多种严重疾病的细胞内细菌。治疗衣原体感染的常用方法是使用抗生素。然而，当抗生素被滥用（过度使用或自行用药）时，可能会导致多种衣原体物种产生耐药性，从而在全球范围内引发真正的公共卫生问题。
本研究在以下数据库中进行了全面的文献检索：PubMed、Google Scholar、Cochrane 图书馆、Science Direct 和 Web of Science。主要目的是分析一组描述与抗生素机制相关的衣原体耐药性相关基因和突变的数据。此外，我们对 704 篇检索文章进行了过滤处理，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 和 rplV 基因的突变对大环内酯类药物产生耐药性，通过 rpoB 基因的突变对利福平类药物产生耐药性，通过 gyrA、parC 和 ygeD 基因的突变对氟喹诺酮类药物产生耐药性，通过 rpoB 基因的突变对四环素类药物产生耐药性，通过 murA 基因的突变对磷霉素产生耐药性，通过 secY 基因的突变对 MDQA 产生耐药性。而肺炎衣原体可能通过 rpoB 基因的突变对利福平类药物产生耐药性，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药物产生耐药性，通过 23S rRNA 基因的突变对大环内酯类药物产生耐药性。此外，猪衣原体可以通过 tet(C)基因的突变对四环素类药物产生耐药性。此外，腔室衣原体可能通过 23S rRNA 基因的变异对大环内酯类药物产生耐药性。耐药的相关机制一般为：抑制细菌蛋白质合成、抑制细菌酶的作用、抑制细菌转录过程。
本文献综述揭示了使用分子工具针对衣原体物种基因检测抗生素耐药性相关的多种突变的存在。此外，这些突变与导致耐药性的不同机制有关。在这方面，通过全基因组测序进行更深入的研究，可以显示出更多的突变和信息。当然，这有助于改善对衣原体感染的处理和医疗保健，减少疾病的并发症和医疗费用。
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