Emergence of Respiratory Streptococcus agalactiae Isolates in Cystic Fibrosis Patients

Streptococcus agalactiae is a well-known pathogen for neonates and immunocompromized adults. Beyond the neonatal period, S. agalactiae is rarely found in the respiratory tract. During 2002–2008 we noticed S. agalactiae in respiratory secretions of 30/185 (16%) of cystic fibrosis (CF) patients. The median age of these patients was 3–6 years older than the median age CF patients not harboring S. agalactiae. To analyze, if the S. agalactiae isolates from CF patients were clonal, further characterization of the strains was achieved by capsular serotyping, surface protein determination and multilocus sequence typing (MLST). We found a variety of sequence types (ST) among the isolates, which did not substantially differ from the MLST patterns of colonizing strains from Germany. However serotype III, which is often seen in colonizing strains and invasive infections was rare among CF patients. The emergence of S. agalactiae in the respiratory tract of CF patients may represent the adaptation to a novel host environment, supported by the altered surfactant composition in older CF patients

Improved lung preservation relates to an increase in tubular myelin-associated surfactant protein A

BACKGROUND: Declining levels of surfactant protein A (SP-A) after lung transplantation are suggested to indicate progression of ischemia/reperfusion (IR) injury. We hypothesized that the previously described preservation-dependent improvement of alveolar surfactant integrity after IR was associated with alterations in intraalveolar SP-A levels. METHODS: Using immuno electron microscopy and design-based stereology, amount and distribution of SP-A, and of intracellular surfactant phospholipids (lamellar bodies) as well as infiltration by polymorphonuclear leukocytes (PMNs) and alveolar macrophages were evaluated in rat lungs after IR and preservation with EuroCollins or Celsior. RESULTS: After IR, labelling of tubular myelin for intraalveolar SP-A was significantly increased. In lungs preserved with EuroCollins, the total amount of intracellular surfactant phospholipid was reduced, and infiltration by PMNs and alveolar macrophages was significantly increased. With Celsior no changes in infiltration or intracellular surfactant phospholipid amount occurred. Here, an increase in the number of lamellar bodies per cell was associated with a shift towards smaller lamellar bodies. This accounts for preservation-dependent changes in the balance between surfactant phospholipid secretion and synthesis as well as in inflammatory cell infiltration. CONCLUSION: We suggest that enhanced release of surfactant phospholipids and SP-A represents an early protective response that compensates in part for the inactivation of intraalveolar surfactant in the early phase of IR injury. This beneficial effect can be supported by adequate lung preservation, as e.g. with Celsior, maintaining surfactant integrity and reducing inflammation, either directly (via antioxidants) or indirectly (via improved surfactant integrity)

Impact of Low Social Preference on the Development of Depressive and Aggressive Symptoms: Buffering by Children’s Prosocial Behavior

Holding a low social position among peers has been widely demonstrated to be associated with the development of depressive and aggressive symptoms in children. However, little is known about potential protective factors in this association. The present study examined whether increases in children’s prosocial behavior can buffer the association between their low social preference among peers and the development of depressive and aggressive symptoms in the first few school years. We followed 324 children over 1.5 years with three assessments across kindergarten and first grade elementary school. Children rated the (dis)likability of each of their classroom peers and teachers rated each child’s prosocial behavior, depressive and aggressive symptoms. Results showed that low social preference at the start of kindergarten predicted persistent low social preference at the start of first grade in elementary school, which in turn predicted increases in both depressive and aggressive symptoms at the end of first grade. However, the indirect pathways were moderated by change in prosocial behavior. Specifically, for children whose prosocial behavior increased during kindergarten, low social preference in first grade elementary school no longer predicted increases in depressive and aggressive symptoms. In contrast, for children whose prosocial behavior did not increase, their low social preference in first grade elementary school continued to predict increases in both depressive and aggressive symptoms. These results suggest that improving prosocial behavior in children with low social preference as early as kindergarten may reduce subsequent risk of developing depressive and aggressive symptom