Prior work has shown that S. pneumoniae requires Zn for pathogenesis as deletion of genes for the Zn binding components of its only known Zn acquisition system (adcA and adcAII) abolished pneumococcal virulence in murine nasopharyngeal colonization, septicemia, and pneumonia models [30] and reduced pneumococcal burden in lungs, pleural cavity, and blood of mice fed a Zn depleted or replete diet [31]. Here, PDYN is linked to Sepsis.