Clinical characteristics and risk factor analysis of children with severe Mycoplasma pneumoniae pneumonia complicated by plastic bronchitis

Introduction

Mycoplasma pneumoniae (MP) is the smallest pathogenic microorganism capable of independent self-replication and lacks a cell wall (1). MP infection can cause various respiratory diseases, with Mycoplasma pneumoniae pneumonia (MPP) being the most significant in terms of disease burden. The implementation of coronavirus disease 2019 (COVID-19) prevention measures in 2020 led to a nearly 3-year cessation of MPP outbreaks. However, since 2023, MPP has re-emerged on a large scale across Asia (2,3). Most children with MPP experience mild symptoms and have favorable outcomes; however, effective treatment of severe Mycoplasma pneumoniae pneumonia (SMPP) remains challenging, even with standard anti-infective therapies. SMPP may also lead to complications such as plastic bronchitis (PB), an acute condition characterized by bronchial obstruction due to endogenous bronchial tree-like structures or viscous material. This results in localized or widespread airway blockage, causing partial or complete loss of lung ventilation and atelectasis, ultimately leading to severe respiratory distress. It is a relatively rare respiratory disease in clinical practice PB diagnosis primarily relies on fiberoptic bronchoscopy (FB) and pathological biopsy of plastic materials (4). However, there is a lack of specific clinical identification indicators, which may lead to a high risk of misdiagnosis and missed diagnoses, increasing investment in medical resources and resulting in severe sequelae, such as obstructive bronchitis, posing significant health risks to children and placing a considerable burden on families and society (5). Currently, research on SMPP complicated by PB in this region is limited, highlighting the urgent need to identify high-risk factors associated with PB occurrence. In this study, we retrospectively analyzed the clinical data of 115 pediatric patients with SMPP to explore the clinical characteristics and high-risk factors associated with concurrent PB, aiding the early identification of PB in clinical practice. We present this article in accordance with the STROBE reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-438/rc).

Methods

Patients

Pediatric patients clinically diagnosed with SMPP who underwent FB between January 2023 and March 2024 were recruited. All participants received inpatient care at Chengdu Women’s and Children’s Central Hospital. Inclusion criteria were as follows: (I) age <18 years; (II) clinical condition in accordance with the Guidelines for Diagnosis and Treatment of Mycoplasma Pneumoniae Pneumonia in Children (2023 Edition) (6); (III) patients in the PB group meeting the diagnostic criteria for PB: removal of plastic foreign bodies via FB followed by pathological tissue biopsy (7,8); (IV) signed informed consent for FB. Exclusion criteria included the following: (I) presence of chronic cardiopulmonary disease, rheumatic disease, immunodeficiency disorder, or severe hematological conditions; (II) inhalation of foreign objects; (III) recurrent respiratory infection history. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This retrospective cohort study was approved by the Ethics Committee of the Chengdu Women’s and Children’s Central Hospital [No. 2023 (32)-2] and individual consent for this retrospective analysis was waived.

Diagnostic criteria for MPP and definition of SMPP

The diagnosis of MPP and the definition of SMPP both follow the Guidelines for Diagnosis and Treatment of Mycoplasma Pneumoniae Pneumonia in Children (2023 Edition): (I) clinical manifestations include fever, cough, rhinorrhea, headache, sore throat, and wheezing. Pulmonary auscultation may reveal rhonchi, rales, or diminished breath sounds. (II) Chest X-ray or chest computed tomography (CT) demonstrates peribronchovascular thickening, bronchial wall thickening, with possible ground-glass opacities, tree-in-bud opacities, interlobular septal thickening, reticular opacities, patchy infiltrates, segmental to lobar consolidation; severe cases may show pleural effusions. (III) For patients meeting the above clinical and imaging manifestations, MPP can be diagnosed if one or two of the following are met: Single serum MP-IgM titer ≥1:160 (by particle agglutination method); ≥4-fold rise in MP-IgM titer in paired sera during disease course; Positive MP nucleic acid test. SMPP is defined as meeting MPP diagnostic criteria plus any one of the following: (I) persistent high fever (>39 ℃) for ≥5 days or fever lasting ≥7 days without declining peak temperature trend; (II) presence of wheezing, tachypnea, dyspnea, chest pain, or hemoptysis; (III) resting pulse oximetry (SpO₂) ≤93% on room air; (IV) radiographic evidence showing either ≥2/3 unilateral lobar involvement with homogeneous high-density consolidation or high-density consolidation in ≥2 lobes, potentially accompanied by moderate-to-large pleural effusion; (V) diffuse unilateral or bilateral bronchiolitis affecting ≥4/5 lobes with confirmed mucus plug formation; (VI) occurrence of extrapulmonary complications; (VII) marked elevation in any of C-reactive protein (CRP), lactate dehydrogenase (LDH), or D-dimer levels.

Data collection

Clinical data were extracted from the hospital’s electronic medical records system. The general information included age and sex. Clinical manifestations included fever duration, Hot peak, allergic constitution (history of allergic rhinitis, eczema, food or drug allergies), new rash, and auscultation of the lungs (such as lung rales, lung wheezing, and reduced breath sounds). Laboratory indicators comprised white blood cell count (WBC), neutrophil percentage (N%), neutrophil-lymphocyte ratio (NLR), hemoglobin (HB) levels, platelet (PLT) count, CRP, procalcitonin (PCT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), LDH, and D-dimer levels. Sputum culture, multiplex respiratory nucleic acid testing, and bronchoalveolar lavage fluid next-generation sequencing (NGS) were used to screen for co-infecting pathogens. All molecular detection methods employed are non-microarray-based technologies. Statistical analyses were conducted on macrolide resistance gene profiles in MP and doxycycline utilization patterns. Imaging assessment followed a stepwise protocol: All enrolled children underwent posteroanterior chest radiography within 24 hours of admission. Upon detection of characteristic SMPP imaging findings described in the Methods section, a non-contrast chest CT was subsequently performed to evaluate core features, including laterality of lung involvement (unilateral/bilateral), pleural effusion, and distal bronchial obstruction. Unilateral lung involvement is defined on CT as consolidation occupying ≥2/3 of unilateral pulmonary volume, demonstrating homogeneous opacification with air bronchograms, optionally accompanied by atelectasis. Bilateral lung involvement is defined on CT as diffuse ground-glass opacities and consolidation with centrilobular nodules, interlobular septal thickening, and crazy-paving patterns, exhibiting symmetrically bilateral distribution. Pulmonary function tests were performed to evaluate lung function impairment and fractional exhaled nitric oxide (FENO) levels.

Statistical analysis

Data were processed using SPSS version 26.0. For normally distributed continuous variables, data are presented as mean ± standard deviation and intergroup comparisons were performed using an independent sample t-test. For non-normally distributed continuous variables, data were described using the median [interquartile range (IQR)], with the Mann-Whitney U test used for comparisons between the two groups. Categorical data are expressed as N (%), and the Chi-squared test was used for intergroup comparisons. Indicators that demonstrated both statistical significance and clinical relevance were subjected to binary logistic regression analysis to identify independent risk factors, and receiver operating characteristic (ROC) curve analysis was conducted to assess the predictive value.

Results

General information and clinical manifestations

A total of 115 pediatric patients with SMPP who met the inclusion criteria and completed FB were enrolled. These patients were divided into the PB group (n=74) and the non-PB group (n=41). There were no statistically significant differences in sex or age between the two groups (P>0.05). Fever duration and peak temperature were significantly higher in the PB group than in the non-PB group (P<0.05). However, the two groups did not significantly differ in terms of new rashes, reduced breath sounds, lung rales, lung wheezing, or allergic constitution (P>0.05) (Table 1).

Ancillary tests

Levels of N%, NLR, CRP, PCT, AST, ALT, LDH, and D-dimer were significantly higher in the PB group than in the non-PB group (P<0.05). The differences in the WBC, HB, and PLT counts between the two groups were not statistically significant (P>0.05). The difference in the incidence of coinfection with other pathogens between the two groups was not statistically significant (P=0.75). We further analyzed the specific types of pathogens involved in co-infections within each group. Both groups exhibited cases of single-pathogen coinfection. Among the seven cases of non-PB combined infections, five were associated with viral infections (two cases of adenovirus, one case of bocavirus, one case of influenza A virus, and one case of Epstein-Barr virus), whereas two cases involved bacterial infections (one case of Streptococcus pneumoniae and one case of Haemophilus influenzae). Among the 10 cases with PB combined infections, there were six cases with bacterial infections (four cases of Streptococcus pneumoniae, one case of Haemophilus influenzae, and one case of Staphylococcus aureus), whereas four cases were linked to viral infections (two cases of bocavirus, one case of influenza A virus, and one case of rhinovirus). The difference in the presence of the A2063G mutation gene for MP between the two groups was not statistically significant (P=0.57). Furthermore, a significantly higher proportion of patients in the PB group required doxycycline treatment due to macrolide therapy ineffectiveness than those in the non-PB group (P=0.003). The PB group had significantly higher rates of unilateral lung involvement, distal bronchial obstruction, and pleural effusion than the non-PB group (P<0.05). We selected cases with complete FENO and pulmonary function test results from the 115 children diagnosed with SMPP for statistical analysis. Among these, 29 patients were in the PB group and 35 in the non-PB group. The results showed that the two groups did not significantly differ in terms of FENO values and the extent of pulmonary function impairment (P>0.05) (Table 2).

Independent risk factors for PB in children with SMPP

Binary logistic regression analysis with the stepwise method was performed on indicators that showed statistical significance in the univariate analysis, including fever duration, peak temperature, NLR, C-CRP, PCT, LDH, D-dimer, laterality of lung involvement, distal bronchial obstruction, and pleural effusion. Variable selection strategy adhered to the following principles: statistical principles: to avoid multicollinearity and overfitting, ensuring model robustness. Clinical logic principle: to prioritize aetiological exposure factors rather than treatment outcome indicators. Principle of parsimony: to construct the most concise and clinically applicable model while maintaining predictive performance. The results identified fever duration (X1), LDH (X2), and laterality of lung involvement (X3, unilateral =0, bilateral =1) as independent risk factors for PB. The longer the fever duration, the higher the risk of PB, which was statistically significant [odds ratio (OR) =1.342, 95% confidence interval (CI): 1.083–1.663, P=0.007]; the higher the LDH, the higher the risk of PB, which was statistically significant (OR =1.006, 95% CI: 1.000–1.011, P=0.04); From the perspective of laterality of lung involvement, unilateral large-area consolidation (occupying ≥2/3 of the lung volume, presenting as homogeneous opacification with air bronchograms) is an independent risk factor for the development of PB (OR =0.263, 95% CI: 0.083–0.827; P=0.02) (Table 3). The formula of the prediction model based on logistic regression was Logit (P) =−2.568 + 0.295 * X1 + 0.005 * X2 − 1.337 * X3 (P represents the probability of occurrence of PB). The Hosmer-Lemeshow goodness-of-fit test indicated that the model demonstrated a satisfactory fit (P=0.79). Furthermore, the decision curve analysis (DCA) demonstrated a favorable net clinical benefit of the prediction model, indicating its robust clinical utility for predicting PB in children with SMPP. Notably, the model achieved superior net benefit across most threshold probabilities compared to all three individual predictors (Figure 1).

Figure 1 DCA of the combined predictors. DCA, decision curve analysis; LDH, lactate dehydrogenase.

Predictive value of independent risk factors for PB in children with SMPP

ROC curves were evaluated to assess the predictive value of the above risk factors and the prediction models, as shown in Table 4. The results showed that the area under the curve (AUC) was 0.864 (95% CI: 0.785–0.943), with an optimal cutoff value of 0.648 (at which time the sensitivity was 86% and specificity was 78.8%). Additionally, fever duration, LDH, and laterality of lung involvement had predictive value for PB occurrence, as shown in Figure 2.

Figure 2 The ROC curve analysis indicates the predictive value of three risk factors and the forecasting model for the occurrence of PB in SMPP. LDH, lactate dehydrogenase; PB, plastic bronchitis; ROC, receiver operating characteristic; SMPP, severe Mycoplasma pneumoniae pneumonia.

Discussion

The etiology of PB is complex. International literature often reports a correlation with postoperative outcomes of congenital heart disease, whereas case studies from China primarily associate it with infections caused by respiratory pathogens (9). Recent literature indicates that MP infection is a common cause of PB (10,11). However, the mechanism linking MP infection to PB formation is not fully understood. Previous studies suggest it may involve the following factors: (I) MP infection directly damages respiratory epithelial cells, resulting in significant shedding; (II) airway inflammatory response leads to mucosal congestion and edema, leading to an increase in mucus secretion; (III) concurrently, excessive inflammation damages the pulmonary cilia, impairing their ability to clear shed cells and mucus from the respiratory tract (12,13).

Persistent fever is generally considered to be an important clinical manifestation of severe MP-induced inflammatory response and lung injury. Moreover, persistent fever can cause invisible fluid loss in children, leading to a concentration of mucus secretions in the airway, making it difficult to expel, and increasing PB risk. Our research results show that compared to the non-PB group, the PB group had a longer fever duration (7.5 vs. 4.2 days), and a higher peak temperature (40.0 vs. 39.3 ℃). Zhang et al. analyzed clinical data from children with MPP who underwent FB. Their results indicated that Fever duration and peak temperature in children who developed bronchial mucus plugs were significantly higher than those in the control group, which is largely consistent with our findings (14). A study involving 416 patients with SMPP showed that the duration of fever and peak temperatures were significantly higher in the PB group than in the non-PB group, which is consistent with our findings (15). Zhao and Cheng suggested that the peak temperature can serve as an independent risk factor for the occurrence of PB (12,16). However, unlike their research, we identified fever duration as an independent risk factor for predicting the occurrence of PB in patients with SMPP, with high sensitivity (78.9%) and specificity (72.7%). Compared to a single peak temperature measurement, fever durationfever days provides a more comprehensive reflection of the duration and severity of a child’s illness. A key finding of this study is that despite the presence of definite mechanical airway obstruction in children in the PB group, the incidence of reduced breath sounds showed no significant difference compared to the non-PB group (P=0.27). This finding is inconsistent with the results reported by Yang et al., who observed a significantly higher incidence of decreased breath sounds in the PB group (P=0.009) (17). This discrepancy may stem from differences in study design or auscultation judgment criteria. However, our results align with those of Xu et al., who also found that diminished breath sounds had limited value in distinguishing whether MPP in children was complicated by PB (P=0.055) (4). Potential reasons for this may include: firstly, the sign lacks sufficient sensitivity, as early segmental bronchial obstruction may not cause discernible changes in breath sounds detectable by routine auscultation; secondly, its specificity is low, since both pulmonary consolidation and pleural effusion can produce similar signs, making it ineffective for differentiating between PB and non-PB cases. Therefore, over-reliance on lung auscultation for PB screening may lead to missed or misdiagnosis. Additionally, the subjective variability in physical examination records in retrospective studies might also have influenced the results. Although no intergroup difference was found, this result holds significant clinical implications. It suggests that relying solely on lung auscultation, including reduced breath sounds, for PB screening is insufficiently reliable. Clinical practice should place greater emphasis on comprehensive evaluation incorporating objective clinical indicators (such as duration of fever), laboratory tests, and imaging characteristics.

The results of multiple auxiliary examinations in this study provide objective evidence for further elucidating the pathophysiological process of PB complicating SMPP. Overall, children in the PB group exhibited a more intense systemic inflammatory response, more significant tissue and cellular damage, and more characteristic imaging changes (Table 2).

Firstly, laboratory findings strongly suggest that PB is associated with a more severe systemic inflammatory storm and tissue destruction. Levels of N%, NLR, CRP, and PCT were significantly higher in children with PB compared to the non-PB group, which is consistent with conclusions from previous studies (18,19). The synergistic elevation of these indicators collectively depicts a picture of the body’s intense immune response to pathogens, suggesting that excessive inflammation may be a key driver in the formation of PB. More importantly, markers representing the degree of tissue and cellular damage, such as LDH, AST, and ALT, as well as D-dimer, which reflects coagulopathy, also showed significantly higher values in the PB group. Particularly for LDH, an intracellular enzyme released upon cellular injury, our study, along with research by Zhong et al., confirmed it as an independent risk factor for PB complicating SMPP (20). We speculate that MP infection directly invades respiratory epithelial cells and stimulates the host immune system to produce excessive inflammatory mediators, collectively leading to extensive damage to cell membrane structures and cytolysis, thereby causing a massive release of enzymes like LDH into the bloodstream. This mechanism shares similarities with that of PB secondary to influenza virus pneumonia, indicating that LDH may serve as a universal warning indicator for severe lung injury and PB complications caused by various pathogens (21).

Secondly, the comparison of imaging characteristics provides important clues to the anatomical basis of PB formation. This study found that the proportions of unilateral lung involvement (defined on CT as consolidation occupying ≥2/3 of unilateral lung volume, presenting as homogeneous opacity with air bronchograms, with or without atelectasis), pleural effusion, and distal bronchial obstruction were significantly higher in the PB group than in the non-PB group (P<0.05). The “asymmetry” of inflammatory response suggested by unilateral lung involvement may be closely associated with the risk of PB development. This finding differs from the common impression of MPP typically presenting with bilateral interstitial lesions but aligns with Zheng et al.’s research on Mycoplasma pneumoniae-induced lobar pneumonia (22). We hypothesize that the severe unilateral pulmonary consolidation induced by MP infection creates a favorable local microenvironment for mucus concentration and bronchial cast formation, characterized by more intense localized inflammation, significantly impaired airway drainage, and greater retention of epithelial debris and inflammatory exudates, collectively promoting the development of bronchial casts. In other words, although bilateral diffuse lesions in SMPP can also lead to scattered and limited mucus plugs, severe unilateral focal consolidation acts as a “breeding ground” for the formation of larger, more viscous mucus plugs that are more likely to cause airway obstruction. The imaging feature of distal bronchial obstruction further confirms the consequence of mechanical obstruction caused by PB. It is worth noting that only 37.8% of PB patients in this study showed signs of distal bronchial obstruction on CT. The reasons may include: first, in some patients, the cast had not fully formed or caused complete mechanical obstruction at the time of CT examination; second, some patients may effectively clear secretions through coughing, thereby preventing complete obstruction; third, when obstruction occurs in bronchi smaller than 2 mm in diameter, it may be undetectable due to the limited spatial resolution of CT (23); fourth, even if mechanical obstruction exists, extensive surrounding consolidation may make the obstruction appear atypical on CT.

Furthermore, some negative results and trend-level findings are equally enlightening. Although no statistically significant difference was observed in the overall co-infection rate between the two groups, bacterial co-infections appeared more frequent in the PB group (6/10 vs. 2/7). This suggests that bacterial superinfection may exacerbate tissue damage, thereby potentially promoting PB formation, though this trend requires validation in a larger sample. Notably, while no difference was detected in the rate of the A2063G macrolide resistance gene mutation in MP between the groups, the need for doxycycline treatment was significantly higher in the PB group. This strongly indicates that the clinical treatment response (e.g., non-response to macrolides) serves as a more urgent warning signal for PB than the results of resistance gene testing. When managing children with SMPP presenting persistent high fever and persistently elevated inflammatory markers, clinicians should decisively escalate the treatment regimen rather than await genetic results. Finally, although no intergroup difference was ultimately found in FENO levels measured in this study, this effort aimed to explore the heterogeneity of the inflammatory response in MPP. We hypothesized that some children might exhibit type 2 immune activation associated with MP infection, which could manifest as elevated FENO (24). The negative result suggests that the pathological core of PB may not involve the typical Th2 pathway but is instead closely related to severe epithelial damage and ciliary dysfunction (25). This finding may rule out FENO as a predictive biomarker for PB complicating SMPP and redirects research focus toward other more critical mechanisms.

This study identified fever duration >6 days, LDH >289 U/L, and unilateral lung involvement on CT imaging as independent risk factors for PB complicating SMPP in children. The predictive model constructed based on these indicators integrates information across three dimensions—clinical manifestations, laboratory parameters, and imaging features—overcoming the limitations of single-parameter prediction and providing a more comprehensive risk assessment tool. We propose the following clinical pathway: for children with SMPP, if fever persists beyond 6 days, LDH testing and detailed chest CT evaluation should be promptly performed. If any indicator is abnormal (LDH >289 U/L or imaging suggesting unilateral involvement), a high suspicion of PB should be raised. If the combined model indicates high risk (predicted probability >57.9%), early bronchoscopy and intervention are recommended to improve prognosis. It is important to emphasize that although the model demonstrates good predictive performance, FB remains the gold standard for diagnosing PB. The value of this model lies in its role as an efficient screening tool to optimize the timing and selection of candidates for FB.

There are certain limitations in this study. First, the retrospective design may introduce selection bias. Second, the relatively modest sample size, though sufficient for basic statistical analysis, may affect the stability and statistical power of the model; future studies with larger samples are needed to further verify the reliability of the conclusions. Third, during the construction of the multivariate model, certain variables that were significant in univariate analysis (N%, AST, ALT, and doxycycline use) were intentionally excluded based on clinical relevance and statistical considerations (e.g., to avoid multicollinearity and overfitting). Although this improves the simplicity and interpretability of the final model, it also implies that different variable selection strategies might yield slightly different results. Finally, as a single-center study including only children who underwent bronchoscopy due to disease severity, the study population consisted predominantly of severe SMPP cases, among whom the detection rate of PB (64.3%) was much higher than that in the general MPP population. Therefore, the findings of this study—particularly the predictive model—are primarily applicable to severe cases requiring bronchoscopic evaluation, and caution should be exercised when extrapolating the results to all MPP patients. Future multicenter, prospective studies with larger and more diverse patient cohorts are warranted to validate our conclusions.

Despite limitations inherent in its retrospective design and single-center sample, this study provides valuable evidence for early warning and stratified management of PB complicating SMPP.

Conclusions

This study identified that fever duration >6 days, LDH >289 U/L, and unilateral lung involvement on CT imaging are independent risk factors for PB complicating SMPP in children. The combined predictive model constructed based on these indicators demonstrates high predictive value (AUC =0.864), providing an important tool for the early identification of PB. By integrating clinical manifestations, laboratory parameters, and imaging features, this model overcomes the limitations of single-parameter prediction and exhibits strong clinical utility and generalizability.

Acknowledgments

We would like to thank Editage (www.editage.cn) for English language editing.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-438/rc

Data Sharing Statement: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-438/dss

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-438/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-438/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This retrospective cohort study was approved by the Ethics Committee of the Chengdu Women’s and Children’s Central Hospital [No. 2023 (32)-2] and individual consent for this retrospective analysis was waived.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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