Community-Acquired Pneumonia in Children: Rapid Evidence Review.

In the United States, pneumonia is the most common cause of hospitalization in children. Even in hospitalized children, community-acquired pneumonia is most likely of viral etiology, with respiratory syncytial virus being the most common pathogen, especially in children younger than two years. Typical presenting signs and symptoms include tachypnea, cough, fever, and anorexia. Findings most strongly associated with an infiltrate on chest radiography in children with clinically suspected pneumonia are grunting, history of fever, retractions, crackles, tachypnea, and the overall clinical impression. Chest radiography should be ordered if the diagnosis is uncertain, if patients have hypoxemia or significant respiratory distress, or if patients fail to show clinical improvement within 48 to 72 hours after initiation of antibiotic therapy. Outpatient management of community-acquired pneumonia is appropriate in patients without respiratory distress who can tolerate oral antibiotics. Amoxicillin is the first-line antibiotic with coverage for Streptococcus pneumoniae for school-aged children, and treatment should not exceed seven days. Patients requiring hospitalization and empiric parenteral therapy should be transitioned to oral antibiotics once they are clinically improving and able to tolerate oral intake. Childhood and maternal immunizations against S. pneumoniae, Haemophilus influenzae type b, Bordetella pertussis, and influenza virus are the key to prevention.

Botulinum toxin induces muscle paralysis and inhibits bone regeneration in zebrafish.

Intramuscular administration of Botulinum toxin (BTx) has been associated with impaired osteogenesis in diverse conditions of bone formation (eg, development, growth, and healing), yet the mechanisms of neuromuscular-bone crosstalk underlying these deficits have yet to be identified. Motivated by the emerging utility of zebrafish (Danio rerio) as a rapid, genetically tractable, and optically transparent model for human pathologies (as well as the potential to interrogate neuromuscular-mediated bone disorders in a simple model that bridges in vitro and more complex in vivo model systems), in this study, we developed a model of BTx-induced muscle paralysis in adult zebrafish, and we examined its effects on intramembranous ossification during tail fin regeneration. BTx administration induced rapid muscle paralysis in adult zebrafish in a manner that was dose-dependent, transient, and focal, mirroring the paralytic phenotype observed in animal and human studies. During fin regeneration, BTx impaired continued bone ray outgrowth, morphology, and patterning, indicating defects in early osteogenesis. Further, BTx significantly decreased mineralizing activity and crystalline mineral accumulation, suggesting delayed late-stage osteoblast differentiation and/or altered secondary bone apposition. Bone ray transection proximal to the amputation site focally inhibited bone outgrowth in the affected ray, implicating intra- and/or inter-ray nerves in this process. Taken together, these studies demonstrate the potential to interrogate pathological features of BTx-induced osteoanabolic dysfunction in the regenerating zebrafish fin, define the technological toolbox for detecting bone growth and mineralization deficits in this process, and suggest that pathways mediating neuromuscular regulation of osteogenesis may be conserved beyond established mammalian models of bone anabolic disorders.