In this study, drug-resistance gene mutations occurred in 31 of the 48 children with MPP (64.6%). There may be geographical differences, with resistance rates varying from region to region .
It has been reported that children with severe MPP infection may experience encouraging results  when other effective antibiotic alternative treatments, such as quinolones and tetracyclines, are administered. These drugs, which can be a good choice for adults, should carefully be considered when prescribed for children. Drug-related adverse effects should be considered in conjunction with the child’s condition. In this study, 48 children with MPP were eventually treated effectively and recovered well, probably because of the following: ① MPP is a self-limiting disease; ② mutations in drug-resistant genetic loci are not the only possible resistance mechanisms occurring in RMPP, in which autoimmune reactions may be involved. A reliable treatment option, especially for severe MPP infection, is the administration of human immunoglobulin and hormones because they can inhibit excessive immune reactions; ③ the diagnostic and therapeutic value of fibreoptic bronchoscopy and alveolar lavage is high. The advantages are obvious: alveolar lavage prevents further exacerbation and is suitable for treating clinical symptoms and improving lung imaging .
Among the four kinds of mechanisms of MP resistance, the study of 23S rRNA gene mutation leading to the mutation of binding site is a hot spot. In 1995, French scholar Lucier et al.  found mutations at positions 2063 and 2064 in the V region of 23S rRNA in Macrolide resistant strains. Pereyre et al.  also detected 2058,2059 A to G point mutations in V region of 23S rRNA from MP resistant strains isolated in France. Japanese scholar Okazaki et al.  detected A to G point mutation at position 2063 in 15 MP-resistant induced strains isolated from clinic, point mutations at positions 2063 A to G and 2064 A to G or C were also detected in erythromycin-induced strains, and it was inferred that the resistance phenotype was closely related to the site of the point mutation. Chinese scholar Xin et al.  screened 50 strains of MP isolated from children and found 46 strains were resistant to Macrolide. The results of gene sequencing showed that 40 of these strains had mutations at 2063 A to G in V region of 23S rRNA, 5 had mutations at 2064 A to G, and 1 had mutations at 2063 A to C. Liu et al.  reported the presence of 44 resistant strains in 53 MP clinical isolates and all had mutations in the V region of 23S rRNA at positions 2063 A to G.
In this study, logistic multivariate regression analysis led to the conclusion that drug-resistant gene mutations were not correlated with RMPP, which is different from the results reported by Xu et al. . There are more possible mechanisms for the occurrence of RMPP, including drug-resistant gene mutations, immune dysfunction, mixed infections, excessive MP load, a mucus plug, a hypercoagulable state and a community-acquired respiratory distress syndrome toxin. Drug-resistance gene mutation is not the only mechanism. The immune response generated by the organism may also play an important part . The immune dysfunction of the organism after reactive infection with MP leads to a series of inflammatory reactions, resulting in increased lung injury and exacerbation of the disease, suggesting that the immune response of the organism after MP infection may be a factor that cannot be ignored in the development of RMPP.
In this study, we found that the children in the drug-resistant gene mutation group were predominantly five years and older, had a longer duration of fever, hospitalisation, macrolide antibiotic application, fever resolution after application and a higher alveolar lavage fluid MP-DNA load and ultrasensitive C-reactive protein. The findings of Zhan et al.  in 97 children with MPP (80 of whom were children with drug-resistant gene mutations) were consistent with the results of this study but differed from it in terms of age, lactate dehydrogenase, cough duration and pulmonary imaging changes. In this study, the age of children with drug-resistant gene mutation was older (around five years old), which was similar to the MP detection rate in the age group found by Li et al. . The detection rate of the A2063G drug-resistant gene was the highest in the three-year-old ≤ age < seven-year-old group, which was 58.9%, considering that it may be related to the preferred age of children with MPP, with the peak incidence in children who are five to nine years old. There were differences in lactate dehydrogenase, cough duration, and pulmonary imaging changes, which may be because the bronchoalveolar lavage fluid obtained from the experimental samples in this study yielded a higher positive rate than the serum, sputum and pharyngeal wipe test samples. Chen et al.  found a correlation between mycoplasma DNA load and drug-resistance mutations in the lavage fluid of fibreoptic bronchoscopy lavage treatment in children with MPP in the mutation group, which is consistent with the results of this study, suggesting that elevated mycoplasma load may predict the development of drug resistance. In this study, it was observed that mucosal congestion and oedema were present under bronchoscopy in the drug-resistant gene mutation group, the occurrence of sputum emboli was significantly higher than that in the unmutated group, and plastic bronchitis, mucosal folds and erosions that occurred occasionally were found in the unmutated group. This finding was different from the conclusion that there was no difference between both in the previous study. In this study, we found that compared with the non-RMMP group, the RMPP group had longer fever, cough, hospitalisation and macrolide antibiotic duration; longer fever remission time after application; higher ultrasensitive C-reactive protein; more severe pulmonary imaging and bronchoscopic changes; and more extrapulmonary complications. Some findings indicate that a higher MP-DNA load is associated with a greater inflammatory response, more extrapulmonary complications and more severe disease , suggesting a possible association with the development of RMPP. It was observed that children with RMPP showed significantly more microscopic mucosal congestion and oedema, folds, erosions, ductal purulent secretions, sputum emboli, plastic sputum emboli, and ductal occlusion than children with common MPP.
This study has some limitations: it is a small sample study, and it involves only the common loci 2063 and 2064, while the existence of other loci mutations in drug-resistant strains and their resistance mechanisms remain to be explored in depth.