Pediatric Critical Illness Score, Clinical Characteristics and Comprehensive Treatment of Children with Severe Mycoplasma Pneumoniae Pneumonia

Abstract Background A systemic inflammatory response is observed in coronavirus disease 2019 (COVID-19). Elevated serum levels of C-reactive protein (CRP), a marker of systemic inflammation, are associated with severe disease in bacterial or viral infections. We aimed to explore associations between CRP concentration at initial hospital presentation and clinical outcomes in patients with COVID-19. Methods and results Consecutive adults aged ≥18 years with COVID-19 admitted to a large New York healthcare system between 1 March and 8 April 2020 were identified. Patients with measurement of CRP were included. Venous thrombo-embolism (VTE), acute kidney injury (AKI), critical illness, and in-hospital mortality were determined for all patients. Among 2782 patients hospitalized with COVID-19, 2601 (93.5%) had a CRP measurement [median 108 mg/L, interquartile range (IQR) 53–169]. CRP concentrations above the median value were associated with VTE [8.3% vs. 3.4%; adjusted odds ratio (aOR) 2.33, 95% confidence interval (CI) 1.61–3.36], AKI (43.0% vs. 28.4%; aOR 2.11, 95% CI 1.76–2.52), critical illness (47.6% vs. 25.9%; aOR 2.83, 95% CI 2.37–3.37), and mortality (32.2% vs. 17.8%; aOR 2.59, 95% CI 2.11–3.18), compared with CRP below the median. A dose response was observed between CRP concentration and adverse outcomes. While the associations between CRP and adverse outcomes were consistent among patients with low and high D-dimer levels, patients with high D-dimer and high CRP have the greatest risk of adverse outcomes. Conclusions Systemic inflammation, as measured by CRP, is strongly associated with VTE, AKI, critical illness, and mortality in COVID-19. CRP-based approaches to risk stratification and treatment should be tested.

Mycoplasma pneumoniae is an important cause of community-acquired pneumonia in children and young adolescents. Macrolides are recommended as the first-line therapy however, macrolide resistance rates in M. pneumoniae among children have been increasing substantially. Areas covered: This review focused on clinical characteristics and treatment of macrolide-resistant M. pneumoniae pneumonia in children. Expert commentary: Antibiotic choice should be based on in vitro activity, clinical efficacy and in consideration of potential adverse events. Macrolide resistance did not contribute to the clinical severity of M. pneumoniae pneumonia, but resistance may be an aggravating factor. Antibiotics may not be required for treatment in mild cases due to the self-resolving nature of M. pneumonia infection, regardless of macrolide resistance. In contrast, antibiotic treatment of severe cases of M. pneumoniae pneumonia is complicated. The clinical benefit of tetracyclines and fluoroquinolones has been shown in terms of shortening duration of symptoms and rapid defervescence in some reports. However, due to safety concerns regarding these two alternative antibiotics, clinicians should weigh the risks and benefits when choosing treatment options. Alternative antibiotics may be considered when patients remain febrile or when chest x-rays show deterioration at least 48-72 hours after macrolide treatment.

Mycoplasma are the smallest prokaryotic microbes present in nature. These wall-less, malleable organisms can pass through cell filters, and grow and propagate under cell-free conditions in vitro. Of the pathogenic Mycoplasma Mycoplasma pneumoniae has been examined the most. In addition to primary atypical pneumonia and community-acquired pneumonia with predominantly respiratory symptoms, M. pneumoniae can also induce autoimmune hemolytic anemia and other diseases in the blood, cardiovascular system, gastrointestinal tract and skin, and can induce pericarditis, myocarditis, nephritis and meningitis. The pathogenesis of M. pneumoniae infection is complex and remains to be fully elucidated. The present review aimed to summarize several direct damage mechanisms, including adhesion damage, destruction of membrane fusion, nutrition depletion, invasive damage, toxic damage, inflammatory damage and immune damage. Further investigations are required for determining the detailed pathogenesis of M. pneumoniae.