We established an infant mouse model for colonization and transmission by nonencapsulated Streptococcus pneumoniae (
NESp) strains to gain important information about its virulence among children. Invasive
pneumococcal diseases have decreased dramatically since the worldwide introduction of pneumococcal capsular
polysaccharide vaccines. Increasing prevalence of nonvaccine serotypes, including
NESp, has been highlighted as a challenge in treatment strategy, but the virulence of
NESp is not well understood. Protective strategies against
NESp colonization and transmission between children require particularly urgent evaluation.
NESp lacks capsules, a major
virulence factor of pneumococci, but can cause a variety of
infections in children and older people. PspK, a specific
surface protein of
NESp, is a key factor in establishing nasal colonization. In our infant mouse model for colonization and transmission by
NESp strains,
NESp could establish stable nasal colonization at the same level as encapsulated serotype 6A in infant mice and could be transmitted between littermates. Transmission was promoted by
NESp surface
virulence factor PspK and influenza virus
coinfection. However, PspK deletion mutants lost the ability to colonize and transmit to new hosts. Promotion of
NESp transmission by
influenza was due to increased susceptibility of the new hosts. PspK was a key factor not only in establishment of nasal colonization but also in transmission to new hosts. PspK may be targeted as a new candidate
vaccine for
NESp infection in children.