Respiratory syncytial virus infection continues to be one of the most important health problems in infancy. Active prophylaxis against this infection (i.e., vaccination) is not available. Therefore, protection of high-risk infants is possible only by passive prophylaxis with specific antibodies. Palivizumab (Synagis) and respiratory syncytial virus intravenous immune globulin are licensed by the US Food and Drug Administration for the prevention of severe lower respiratory tract infections caused by respiratory syncytial virus in infants with bronchopulmonary dysplasia, infants with a history of premature birth (< or =35 weeks gestational age) and children with hemodynamically significant congenital heart disease. Palivizumab is a humanized monoclonal antibody produced by recombinant DNA technology, directed to an epitope in the A antigenic side of the F-protein of the respiratory syncytial virus. This review discusses the characteristics of this drug in detail.

Early-life respiratory infection with Pseudomonas aeruginosa is common in children with cystic fibrosis or immune deficits. Although many of its clinical manifestations involve neural reflexes, little information is available on the peripheral nervous system of infected airways. This study sought to determine whether early-life infection triggers a neurogenic-mediated immunoinflammatory response, the mechanisms of this response, and its relationship with other immunoinflammatory pathways. Weanling and adult rats were inoculated with suspensions containing P. aeruginosa (PAO1) coated on alginate microspheres suspended in Tris-CaCl(2) buffer. Five days after infection, rats were injected with capsaicin to stimulate nociceptive nerves in the airway mucosa, and microvascular permeability was measured using Evans blue as a tracer. PAO1 increased neurogenic inflammation in the extra- and intrapulmonary compartments of weanlings but not in adults. The mechanism involves selective overexpression of NGF, which is critical for the local increase in microvascular permeability and for the infiltration of polymorphonuclear leukocytes into infected lung parenchyma. These effects are mediated in part by induction of downstream inflammatory cytokines and chemokines, especially IL-1beta, IL-18, and leptin. Our data suggest that neurogenic-mediated immunoinflammatory mechanisms play important roles in airway inflammation and hyperreactivity associated with P. aeruginosa when infection occurs early in life.

Background During the Fall of 2014, numerous children were hospitalized with asthma or respiratory distress related to Enterovirus D68 (EV-D68). A large proportion initially tested positive for rhinovirus. During this period our laboratory noted a cross-reactivity between EV-D68 and the rhinovirus component of the GenMark multiplex respiratory viral panel. Many other laboratories used assays not designed to distinguish these Picornoviridae. Methods To compare the presentation and outcomes of patients with rhinovirus and EV-D68, 103 GenMark rhinovirus positive nasopharyngeal swabs from hospitalized children were retested for EV-D68. Results EV-D68 positive patients vs EV-D68 negative patients were more likely to have a history of asthma (33.3% vs 11.0%, P = 0.02) and to present with acute respiratory illness (66.7% vs 40.2%, P = 0.048), especially status asthmaticus (47.6% vs 2.4%, P < 0.001). On admission they had more wheezing, respiratory distress, and lower respiratory tract involvement, and were more likely to be treated with steroids and discharged home on asthma medications. Respiratory viral coinfection was less common in EV-D68 positive vs EV-D68 negative patients. In patients without a respiratory viral coinfection the overall findings were similar. Conclusion Patients with EV-D68 vs rhinovirus were more likely to have a history of asthma, to present with status asthmaticus, to wheeze on admission, and to receive treatment with asthma medications in hospital and at discharge. The inability of common assays to distinguish EV-D68 from rhinoviruses raises the possibility that the role of EV-D68 as a viral trigger of asthma has been under appreciated.

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Hemoptysis is a serious and potentially life-threatening event. Mortality is estimated at 13% for this chief complaint with age, volume of hemoptysis and receipt of blood products as risk factors for mortality. Hemoptysis is mostly seen in those with underlying congenital cardiac conditions or Cystic Fibrosis. We describe a unique case of a previously healthy 10 year old male who presented to the ED by EMS with a moderate volume episode of hemoptysis. He was admitted to the PICU where a sudden episode of massive hemoptysis precipitated by forced respiratory effort occurred during his examination. He decompensated and was emergently brought to the OR for airway evaluation by ENT and pulmonology. A large clot was found in the RML segment with brisk bleeding following removal of the clot. A 5 Fr bronchial blocker was placed to achieve hemostasis. Bronchial artery angiogram by IR demonstrated extravasation of contrast from right bronchial artery to segmental right lower lobe pulmonary artery shunt. He underwent embolization of the right bronchial artery. He was extubated the following day after no recurrent bleeding was confirmed with bronchoscopy. BA-PA fistulas are rare vascular anomalies in which an anastomosis is formed between systemic and pulmonary arteries. They are most commonly acquired, often described as secondary to chronic inflammatory lung diseases. BA-PA fistulas can also be congenital and have been seldom described in the literature. Our case highlights the importance of this rare diagnosis, which must remain on a pediatric pulmonologist’s differential due to the significant associated mortality.