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The waning of vaccine protection may be responsible for outbreaks toward the end of the influenza season. Three of five outbreaks occurred at the beginning of April following an interval of >100 days from the date of vaccination; the reported index case was a nurse or office worker, and >50% of those affected were healthcare workers. The results are consistent with intra-seasonal waning of vaccine immunity that resulted in outbreaks at the end of season.

The cell division‐related gene A (cdrA) of Helicobacter pyloriis dispensable in vivoand unique in having a repressive role on cell division and long‐term survival. To clarify its role, comparisons of the wild‐type HPK5 and isogenic cdrA‐disrupted mutant HPKT510 were examined by ultrastructural morphology, PBP profiles, and susceptibility to β‐lactam antibiotics during long‐term cultivation. Ultrastructural analyses revealed that the shorter rods of HPKT510 had a slightly wider periplasmic space between the inner and the outer membrane than those of HPK5. Cell division of HPKT510 cells was complete even under high‐salt conditions in which HPK5 cells became filamentous due to inhibition of division. The filamentous HPK5 cells constructed an inner membrane without a cell wall at the presumed division site. After 4 days of cultivation (the late stationary phase), most of the HPK5 cells turned into ghosts and aggregates, while some of the HPKT510 cells remained as curved rods, which coincided with the results of cell viability. HPKT510 cells became resistant to ampicillin killing compared to HPK5 cells, although their minimum inhibitory concentrations (MICs) and PBP profiles were not significantly different. These results suggest that the cdrAproduct represses cell division via inhibiting cell wall synthesis at division site. During infection in both mice and humans, inactivation of cdrAeventually gains biological aspects such as increased viability, long‐term survival and tolerance to antibiotics and high‐salt condition, which might enhance a persistent infection.