The impact of pneumococcal conjugate vaccine on the prevalence and severity of hospitalizations for pneumonia in children.

Pneumococcal conjugate vaccines (PCV) were introduced into the Israeli national immunization plan starting with the heptavalent PCV7 in 2009 and then PCV13 in the late 2010. The objective of this study was to determine the vaccines' impact on hospitalization rates for community-acquired pneumonia on the severity of the pneumonia episodes and upon pneumococcal serotype distribution. We retrospectively reviewed all children hospitalized in our institution with pneumonia, aged between 1 and 16 years, between the years 2006 and 2015. Demographic, clinical, and laboratory data between three time periods: pre-PCV, PCV7, and PCV13, were compared. During the study period, 1375 children were hospitalized with pneumonia. A gradual decline in hospitalization rates due to pneumonia was observed starting in 2006 in the pre-PCV period and continued until after the introduction of PCV13. A similar trend was observed in pneumonias with a culture positive for S. pneumoniae. Pleural effusion was observed in 24% of all pneumonias, and this percentage was stable throughout the study period. The average age at hospitalization increased during the study period, as did the average duration of hospital stay. Pneumococcal serotypes included in the vaccine were isolated less frequently during the study and non-vaccine serotypes tended to appear more frequently. Pediatric pneumonia hospitalization rates continued to decline since the introduction of PCV without increasing the frequency of complications. Pneumococcal serotype distribution shifted in parallel. Our findings confirm the efficacy of PCV and support the evidence to include more serotypes in the next generation of PCV.

Dynamic JUNQ inclusion bodies are asymmetrically inherited in mammalian cell lines through the asymmetric partitioning of vimentin.

Aging is associated with the accumulation of several types of damage: in particular, damage to the proteome. Recent work points to a conserved replicative rejuvenation mechanism that works by preventing the inheritance of damaged and misfolded proteins by specific cells during division. Asymmetric inheritance of misfolded and aggregated proteins has been shown in bacteria and yeast, but relatively little evidence exists for a similar mechanism in mammalian cells. Here, we demonstrate, using long-term 4D imaging, that the vimentin intermediate filament establishes mitotic polarity in mammalian cell lines and mediates the asymmetric partitioning of damaged proteins. We show that mammalian JUNQ inclusion bodies containing soluble misfolded proteins are inherited asymmetrically, similarly to JUNQ quality-control inclusions observed in yeast. Mammalian IPOD-like inclusion bodies, meanwhile, are not always inherited by the same cell as the JUNQ. Our study suggests that the mammalian cytoskeleton and intermediate filaments provide the physical scaffold for asymmetric inheritance of dynamic quality-control JUNQ inclusions. Mammalian IPOD inclusions containing amyloidogenic proteins are not partitioned as effectively during mitosis as their counterparts in yeast. These findings provide a valuable mechanistic basis for studying the process of asymmetric inheritance in mammalian cells, including cells potentially undergoing polar divisions, such as differentiating stem cells and cancer cells.