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Abstract Objective Mycoplasma pneumoniae is a major causative pathogen in community-acquired pneumonia. Respiratory viral coinfections in children with Mycoplasma pneumoniae pneumonia (MPP) are not uncommon and cause severe clinical manifestations. This study aims to investigate the impacts of viral coinfection in MPP patients and hopes to offer novel insights for discriminating between MPP and MPP coinfection. Methods This study recruited 748 children hospitalized for MP pneumonia between January 2021 and October 2023. Patients were classified into two groups: MPP coinfected with respiratory virus group and MPP group. All children underwent polymerase chain reaction testing for respiratory pathogens. Baseline clinical features and demographic data were obtained retrospectively through medical records. Results The retrospective study included 748 patients, with a viral coinfection rate of 38.75%. Patients in the MPP coinfected with respiratory virus group have a higher disease burden than those in the non-coinfection group. Our findings indicate that patients with Mycoplasma pneumonia co-infected with respiratory viruses had longer hospital stays and prolonged fever post-admission, as well as more severe conditions and a higher incidence of extrapulmonary complications. MPP coinfection was associated with the following factors: patients with extrapulmonary complications of gastroenteritis (OR = 4.474, 95%CI = 1.733–11.554, P = 0.002), longer hospital stay (OR = 1.109, 95%CI = 1.012–1.217, P = 0.027), longer days of fever after admission (OR = 1.215 95%CI = 1.006–1.469, P = 0.043), elevated white blood cell count (OR = 1.332 95%CI = 1.082–1.640, P = 0.007), decreased neutrophil count (OR = 0.768 95%CI = 0.602–0.981, P = 0.035), higher fibrinogen levels (OR = 1.652 95%CI = 1.138–2.398, P = 0.008), and raised lactate dehydrogenase levels (OR = 1.007 95%CI = 1.003–1.011, P = 0.001). Conclusions We determined the clinical significance of respiratory viral coinfection in children with MPP. Timely identification of MPP coinfection and provision of early and comprehensive therapeutic measures are vital in shortening the disease severity and improving prognosis.

ObjectiveTo establish a prediction nomogram for early prediction of neonatal acute respiratory distress syndrome (NARDS).MethodsThis is a retrospective cross-sectional study conducted between January 2021 and December 2023. Clinical characteristics and laboratory results of cases with neonatal pneumonia were compared in terms of presence of NARDS diagnosis based on the Montreux Definition. The NARDS group and non-NARDS group were then compared to establish a prediction nomogram for early prediction of NARDS. The predictive accuracy and compliance of the model were evaluated using subject operating characteristic curves, area under the ROC curve, and calibration curves, and the model performance was estimated by self-lifting weight sampling. The Hosmer–Lemeshow test was used to assess the goodness of fit of the model.FindingsNARDS group consisted of 104, non-NARDS group consisted of 238 newborns in our study. Gestational age, triple concave sign, blood glucose measurement after birth (Glu), Apgar score at the 5th minute (Apgar5), neutrophil count (ANC) and platelet count (PLT) are independent predictors of NARDS in late preterm and term newborns who present with progressive respiratory distress and require varying degrees of respiratory support within the first 24 h of life to minimize work of breathing and restore organismal oxygenation. The area under the ROC curve was 0.829 (95% CI = 0.785–0.873), indicating the model's strong predictive power. In addition, decision curve analysis showed that the model had significantly better net benefits.ConclusionIn this study, a predictive column-line plot was constructed based on six clinically accessible conventional variables. Early application of this model has a better predictive effect on the early diagnosis of NARDS, thus facilitating more timely and effective interventions.

Abstract The plant health status is determined by the interplay of plant-pathogen-microbiota in the rhizosphere. Here, we investigate this tripartite system focusing on the pathogen Fusarium oxysporum f. sp. lycopersici (FOL) and tomato plants as a model system. First, we explore differences in tomato genotype resistance to FOL potentially associated with the differential recruitment of plant-protective rhizosphere taxa. Second, we show the production of fusaric acid by FOL to trigger systemic changes in the rhizosphere microbiota. Specifically, we show this molecule to have opposite effects on the recruitment of rhizosphere disease-suppressive taxa in the resistant and susceptible genotypes. Last, we elucidate that FOL and fusaric acid induce changes in the tomato root exudation with direct effects on the recruitment of specific disease-suppressive taxa. Our study unravels a mechanism mediating plant rhizosphere assembly and disease suppression by integrating plant physiological responses to microbial-mediated mechanisms in the rhizosphere.