Impact of 13-Valent Pneumococcal Conjugate Vaccine on Colonization and Invasive Disease in Cambodian Children

Background Cambodia introduced the 13-valent pneumococcal conjugate vaccine (PCV13) in January 2015 using a 3 + 0 dosing schedule and no catch-up campaign. We investigated the effects of this introduction on pneumococcal colonization and invasive disease in children aged <5 years. Methods There were 6 colonization surveys done between January 2014 and January 2018 in children attending the outpatient department of a nongovernmental pediatric hospital in Siem Reap. Nasopharyngeal swabs were analyzed by phenotypic and genotypic methods to detect pneumococcal serotypes and antimicrobial resistance. Invasive pneumococcal disease (IPD) data for January 2012–December 2018 were retrieved from hospital databases. Pre-PCV IPD data and pre-/post-PCV colonization data were modelled to estimate vaccine effectiveness (VE). Results Comparing 2014 with 2016–2018, and using adjusted prevalence ratios, VE estimates for colonization were 16.6% (95% confidence interval [CI] 10.6–21.8) for all pneumococci and 39.2% (95% CI 26.7–46.1) for vaccine serotype (VT) pneumococci. There was a 26.0% (95% CI 17.7–33.0) decrease in multidrug-resistant pneumococcal colonization. The IPD incidence was estimated to have declined by 26.4% (95% CI 14.4–35.8) by 2018, with a decrease of 36.3% (95% CI 23.8–46.9) for VT IPD and an increase of 101.4% (95% CI 62.0–145.4) for non-VT IPD. Conclusions Following PCV13 introduction into the Cambodian immunization schedule, there have been declines in VT pneumococcal colonization and disease in children aged <5 years. Modelling of dominant serotype colonization data produced plausible VE estimates

Characterizing and measuring tuberculosis stigma in the community: A mixed-methods study in Cambodia

10.1093/ofid/ofaa422Open Forum Infectious Diseases71

The Role of Animal Models in the Study of Epileptogenesis

Epileptogenesis is the process that leads to the development of epilepsy: the propensity to have recurrent, spontaneous seizures. During epileptogenesis, brain excitability increases due to molecular, cellular and network alterations. These changes are thought to be initiated by one or more brain insults which may be naturally occurring events such as traumatic brain injury, but can also be modeled in animals, using insults such as chemically induced status epilepticus (SE: a prolonged seizure). The study of epileptogenesis is critical for (a) identifying patients who are at risk of developing epilepsy and (b) targeting drugs that can modify the epileptogenic process and could therefore prevent the development of the disease