Pulmonary Abscess Caused by Coinfections of Mycoplasma pneumoniae and Prevotella oris in a 4-year-old Child

To the Editors: Prevotella oris, a Gram-negative anaerobic rod, is commonly found in the oral cavity, intestines and vagina.1 However, it is rarely associated with pneumonia or pulmonary abscess due to the aerobic lung environment. Recently, we encountered an exceptionally rare case of pulmonary abscess in a 4-year-old female. This pulmonary abscess was caused by coinfections of Mycoplasma pneumoniae and P. oris. The diagnosis was confirmed through metagenomic next-generation sequencing–based microbial identification and culture of the purulent fluid within the abscess. To our knowledge, this represents the first documented case of combined M. pneumoniae and P. oris infection leading to a pulmonary abscess. A 4-year-old female was admitted to Children's Hospital with a 5-day history of high fever and 3-day history of cough. Her medical history was unremarkable. Notably, the patient exhibited poor oral hygiene, and a recent examination revealed untreated dental caries. Physical examination revealed diminished breath sounds on the right side, absent of crackles or wheezes. Chest computed tomography scan showed consolidation in the right upper lobe. Laboratory tests indicated leukocytosis (white blood cell count 11.6 × 109/L) with neutrophilia (62.1%), elevated C-reactive protein (26 mg/L; normal range, <8 mg/L) and erythrocyte sedimentation rate (35 mm/h; normal range, <20 mm/h). The serologic antibody titer for M. pneumoniae was 1:1280, and the sputum M. pneumoniae RNA test was positive. On days 3 and 10 of hospitalization, the patient underwent bronchoalveolar lavage. During the first lavage, ulceration of the bronchial mucosa in the right upper lobe was observed, along with a tree-like cast (plastic bronchitis). Blood and bronchoalveolar lavage fluid cultures were conducted twice, respectively, and both yielded negative results. The patient received treatment with intravenous (IV) azithromycin, amoxicillin-clavulanate, methylprednisolone and immunoglobulin, resulting in clinical improvement and normalization of inflammatory markers by day 15. However, on day 20, the patient's symptoms worsened, presenting with recurrent high fever and chest pain. Upon reevaluation, the laboratory results showed a white blood cell count of 29.3 × 109/L, with a neutrophil percentage of 77.0%. Additionally, the levels of C-reactive protein and erythrocyte sedimentation rate increased to 77.82 mg/L and 130 mm/h, respectively. A repeat computed tomography scan revealed aggravated pulmonary imaging, including a large lung abscess with an air-fluid level in the right upper hemithorax. Antibiotics were adjusted to IV vancomycin and cefotaxime. The patient underwent a right upper lobectomy via thoracoscopy on day 28. Pathological investigation revealed a large purulent cavity had formed in the apical and posterior segments of the right upper lobe, containing a substantial amount of thick yellow purulent fluid. The metagenomic next-generation sequencing of the purulent fluid identified P. oris as the exclusive pathogen. The patient's antibiotic regimen was adjusted to IV meropenem in combination with metronidazole. Three days after the surgery, her body temperature normalized. Subsequent purulent fluid culture results confirmed the growth of P. oris, and antibiotics were continued until discharge on day 50. The chest radiographic changes observed on days 1, 20 and 40 during hospitalization are depicted in Figure 1.FIGURE 1.: The chest computed tomography changes observed during hospitalization. A: Day 1: consolidation in the right lower lobe. B (coronal view) and C (transverse view): Day 20: a large pulmonary abscess with an air-fluid level manifests in the right upper hemithorax. D: Day 50 (upon discharge): substantial resolution of the pulmonary lesion.P. oris is commonly found in the oral cavity and is considered a commensal bacterium within the human body. As an obligate anaerobe, it does not readily grow in the lungs. To date, only 2 reported pediatric cases of P. oris-related pneumonia have been documented.2 One case involved a 4-year-old child with sickle cell anemia who developed necrotizing pneumonia following infection with influenza A and subsequent P. oris infection. The other case was a 13-year-old child with Glanzmann thrombasthenia and a history of asthma, who developed pneumonia and pleural effusion after P. oris infection. Könönen proposed that the presence of P. oris in the lower respiratory tract is associated with T helper cell 17 activation and differentiation.3P. oris not only exacerbates airway immune responses but also modulates immune reactions induced by other pathogens. In the case we presented, severe M. pneumoniae infection led to necrotizing pneumonia, creating an anaerobic environment within the necrotic lung areas. This environment provides a suitable growth milieu for anaerobic bacteria. Furthermore, the inflammatory response triggered by M. pneumoniae infection may impair lung defenses,4 allowing otherwise nonpathogenic conditionally pathogenic bacteria to invade and cause infection.5 Notably, this patient's poor oral hygiene, untreated cavities and use of glucocorticoids were contributing factors for the development of the pulmonary abscess due to P. oris. In summary, necrotizing pneumonia resulting from severe M. pneumoniae infection not only establishes an anaerobic environment but also impairs lung defense mechanisms due to the inflammatory response. This condition can allow P. oris to invade and cause pulmonary abscess. When antibiotic treatment fails, surgical intervention becomes crucial for improving patient prognosis and reducing morbidity and mortality.