An 8-year-old girl presented to a hospital pediatric emergency department with a 1-week history of cough, fever for 4 days, and dyspnea for 5 h, without any response to oral cephalosporins. When she was admitted to the hospital, she had shortness of breath, 50 beats per minute, fever, 38.3  C, tachycardia, 154 beats per minute, and hypoxemia, 72% in ambient air. Physical examination revealed moist rales in the left lung and diminished breath sounds over the right lung. Leukocyte count was 19 x 109/L, indicating leukocytosis of mainly neutrophils, and C-reactive protein level was 0.2 mg/dl. Blood biochemical analysis showed that the level of alanine aminotransferase was 516 U/L, lactate dehydrogenase was 2113 U/L, and sodium ions was 122 mmol/L. Chest x-ray photograph showed diffuse opacification on the left lung, Atelectasis was observed in the right lung with a large effusion in the right pleural cavity (Figure 1). She received a combination of antibiotics (azithromycin and ceftriaxone) to treat severe pneumonia and was transferred to the pediatric intensive care unit (PICU) for further treatment. There, she was given high-flow warm humidified oxygen through the nose. A computed tomography (CT) scan of the chest showed bilateral lung infection and right lung consolidation density; Multiplelymph nodes in the mediastinum show that the area is slightly larger; Bilateral pleural effusion (Figure 2A). Ultrasonic examination also showed a large amount of pleural effusion in the right lung. Lower chest puncture drainage was performed under ultrasound guidance, and antibiotic therapy was escalated to cefoperazone sodium, sulbactam sodium, and azithromycin. Analysis of pleural effusion showed that a protein level of 38.2 g/L, glucose of 6.57 mmol/L, lactate dehydrogenase of 3082 U/L, and mononuclear phagocyte predominance was observed. Negative bacterial culture results for blood, endotracheal aspirate and pleural effusion. Antigen testing for respiratory pathogens (including adenovirus, respiratory syncytial virus, influenza virus and EB virus) is suggestive of negative results. Polymerase chain reaction (PCR) showed that MP was positive in endotracheal aspirate and pleural effusion. MP-specific IgM and IgG antibodies from blood showed negative results. Acquired mutations on the ribosomal macrolide target were negative, suggesting that it was not a macrolide-resistant strain. Further medical history obtained from family members did not indicate any risk factors for tuberculosis; however, a gamma release assay was also sent for analysis. On the first day of admission, patient was found to have abnormal coagulation function, and bleeding spots appear on the skin the next day. In the coagulation profile, the international normalized ratio was 1.67, with a partial thromboplastin time of 31.5 s and a prothrombin time of 17.5 s. Thrombin time was 60.0 s. The fibrinogen function K value was 18.1 min, the fibrinogen and platelet function (angle) were 27.9, the platelet function was 21.2 mm, and the comprehensive index of coagulation function was -14.5. In order to exclude hematologic diseases, coagulation factors and plasma correction tests were added, and fresh frozen plasma and fibrinogen infusions were given, and the coagulation function was slightly improved. After 48 h, she remained febrile with worsening tachypnea and hypoxic respiratory failure, hemoptysis, and required intubation and ventilation. Blood was visible in the airway, and bronchoscopy and bronchoalveolar lavage revealed DAH. Therefore, a diagnosis of severe MP in conjunction with DAH, severe pediatric acute respiratory distress syndrome (ARDS), and acute hypoxic respiratory failure was established. Human blood immunoglobulin, epinephrine endotracheal instillation, and intravenous application of glucocorticoids were administered.
Because of ongoing hypoxia, she was cannulated onto veno-venous extracorporeal membrane oxygenation (VV-ECMO) on hospitalization day 3. The results of pleural fluid and blood tests for metagenomic next-generation sequencing (mNGS) suggested MP infection, with no other viral or bacterial infections. She was screened for rheumatological conditions, tuberculosis, autoimmune diseases, and tumour. Results did not suggest these situations.The patient stayed on ECMO for 5 d; Due to the significant prolongation of PT and APTT, anticoagulation was given without heparin or low-dose heparin regimen, and the anticoagulation target was gradually adjusted on the basis of fresh frozen plasma supplementation to prevent thrombosis in the extracorporeal membrane lung and pipeline. Laying in the prone position for for 10 h + per day during this period improved oxygenation. Ultrasound was used to assess lung exudation. The patient was ventilated for ten days. During this period, she received methylprednisolone 1-2 mg/kg/d and a 14-day tapering regimen for acute respiratory distress syndrome and azithromycin was given intravenously, for inflammation, three times a week. Simultaneously, further testing revealed that the patient's humoral and cellular immune function was disorder, the TBNK lymphocyte subsets were suggested that CD3 799 x 106/L(normal 960-3640), CD4 344 x 106/L(normal 550-2190), CD8 440 x 106/L(normal 260-1380), CD4/CD8 0.78(normal 0.72-2.88),natural killer cell 60 x 106/L(normal 80-680); Cytokine detection suggested that IL-6 1.33 pg/ml(normal 0-20), IL-10 27.56 pg/ml(normal 0-5.9); Immunoglobulins and complements were shown that IgA0.37 g/L(normal 0.52-2.16), IgM0.46 g/L(normal 6.09-12.85), C3 0.25 g/L(normal 0.79-1.52), C4 0.09 g/L(normal 0.12-0.36). Hemophagocytic lymphohistiocytosis was negative. Mycoplasma DNA continued to test positive on repeat workups.
On the 9th day, the patient had low-grade fever; sputum culture, blood mNGS testing, and G test suggested Candida albicans infection, and fluconazole antifungal therapy was administered for 10 d. Other infectious organism was not found in repeated respiratory tract, blood cultures andpleural cultures. After 8 d of therapy, CT of the chest revealed exudative changes in both lungs, partial consolidation in the right lung, similar to the range of lesions as before, interstitial changes in the right lower lung with multiple bronchial cystic changes, and reactive lymphadenopathy (Figure 2B). After 12 d of therapy, the patient clinically improved and became afebrile. Ventilator use was discontinued, and she was discharged from the hospital 15 d after extubation without supplemental oxygen. Pulmonary CT review 45 days after discharge indicated that the lesion was significantly absorbed compared to the lesion in the previous CT scan (Figure 2C).
Written informed consent to participate in this study was provided by the participant's legal guardian/next of kin. We obtained informed written consent from the patient's parent authorizing the publication of this clinical case and images.