pspK acquisition contributes to the loss of capsule in pneumococci: molecular characterisation of non-encapsulated pneumococci.

With the introduction of the pneumococcal conjugate vaccine (PCV), the number of cases of non-vaccine type pneumococci and non-encapsulated Streptococcus pneumoniae (NESp) infection have increased. In order to clarify how pspK-harbouring NESp might have emerged, we characterised NESp and analysed the correlation between transformation and non-encapsulation. A total of 26 NESp strains were used in this study. The genetic backgrounds were compared using multilocus sequence typing (MLST). The ΔpspK::ermB strain, in which pspK was replaced by ermB in NESp, was constructed by homologous recombination. The genomic DNA of the ΔpspK::ermB strain was transformed into two types of encapsulated S. pneumoniae via transformation. The fitness of the parent and non-encapsulated transformants was compared using the growth curve. All NESp had pspK instead of capsular coding regions and were classified into 14 types by MLST, which indicated that NESp had several genetic backgrounds. Transformation of ΔpspK::ermB genomic DNA resulted in 10-4‒10-5 non-encapsulated transformants. Non-encapsulated transformants could grow faster than the encapsulated parent strain. The acquisition of pspK region via transformation contributed to the loss of encapsulation with high frequency. The present results suggest that non-encapsulation through pspK acquisition could be a potential mechanism to evade PCV.

Impact of the introduction of a 13-valent pneumococcal vaccine on pneumococcal serotypes in non-invasive isolates from 2007 to 2016 at a teaching hospital in Japan.

PURPOSE: To prevent severe invasive pneumococcal infection, pneumococcal conjugate vaccines (PCVs) were introduced in Japan in 2010, and in 2013 a pneumococcal 13-valent conjugate vaccine (PCV13) was included in the routine vaccination schedule for infants. In this study, we analysed the antimicrobial susceptibilities and capsular types of pneumococci isolated from non-invasive patient sites from 2007 to 2016 to assess the impact of the introduction of PCV13. METHODOLOGY: A total of 618 pneumococcal isolates collected at a teaching hospital from 2007 to 2016 were used. These isolates were characterized by capsular typing, multilocus sequence typing and antimicrobial susceptibility testing. RESULTS: Capsular typing indicated that, after the introduction of the PCV, the proportion of PCV13 serotypes decreased (P<0.01), while non-PCV13 serotypes became diverse. In particular, increases in 22 F, 15A and 23A were noted among non-PCV13 serotypes. Regarding antimicrobial susceptibility, the non-susceptibility rate to penicillin of pneumococci that showed higher minimum inhibitory concentrations (MICs) than the susceptibility breakpoint decreased, and pneumococci tended to become susceptible. However, all type 23A pneumococci and 77.8  % of type 15A pneumococci showed the reverse trend, with low susceptibility to penicillin. Furthermore, all 15A and 23A isolates had macrolide resistance genes. CONCLUSION: These data suggest that PCVs can prevent infections caused by PCV serotypes. However, since non-PCV13-type pneumococci, in particular 15A and 23A, which have acquired multidrug resistance, have already emerged over time, the development of a novel vaccine targeting a broader spectrum of pneumococci is warranted.