肺炎支原体（Mycoplasma pneumoniae，MP）的基因组为双链环状DNA，大小约820 kb，包含超过600个蛋白质编码基因，基因组结构小巧且简单。由于其基因组高度精简，MP无法自主合成氨基酸、核苷酸等必需分子，需依赖与宿主细胞紧密结合以摄取胆固醇等必需物质，其体外培养条件也较为苛刻。基于MP顶端黏附结构中P1蛋白编码基因Rep2/3与Rep4重复序列的差异，MP可划分为P1-1与P1-2型，各型别内部基因组高度保守。MP的流行病学监测数据显示，P1-1型长期占据优势地位且耐药率较高，但自2015年起，多个国家陆续观察到P1-2型菌株，其检出比例逐步上升。
MP被认为是最小的能自我复制的生物体之一，无细胞壁，对β内酰胺类抗生素及所有作用于细胞壁的抗菌药物具有耐药性。在儿童群体中，MP感染约占社区获得性肺炎病例的10%-40%，是导致儿童发病和死亡的主要病原体之一。根据全球疾病负担2021年下呼吸道感染与抗菌药物耐药性协作研究，2021年肺炎支原体属导致2,530万例下呼吸道感染（Lower respiratory tract infections，LRTIs），使其成为全球LRTIs的第三大常见病原体。COVID-19大流行期间，由于采取了广泛的非药物干预措施，MP感染有所下降。但随着防控措施的逐步解除，中国、丹麦、法国、荷兰及西班牙等国均观察到MP感染的再流行态势。
大环内酯类抗生素常被用作儿童MP感染的一线治疗药物。近年来，中国耐大环内酯类MP（Macrolide-resistant MP，MRMP）的检出率持续攀升，其主要耐药机制是23S rRNA V区2063位点发生A→G的突变，从而导致高水平耐药，目前尚未发现其他大环内酯类耐药机制的报道。北京、浙江、武汉、上海、内蒙古及中国东北部等地区监测报告表明，2023年MP感染呈现高发态势。
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