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The niches encountered during infection vary significantly from the more commonly studied laboratory setting, and consequently, the genes responsible for\n                    <jats:italic>in vivo<\/jats:italic>\n                    pathogenesis have yet to be fully elucidated. This study utilized the\n                    <jats:italic>A. baumannii<\/jats:italic>\n                    AB5075-UW transposon mutant library with unbiased genome-wide transposon sequencing to identify the genetic basis for survival and fitness during pneumonia and septicaemia infections. We identified 128 genes essential for in-host survival, including 22 required for survival in all tissues. Additionally, 302 genes with significantly altered fitness\n                    <jats:italic>in vivo<\/jats:italic>\n                    were also identified. Tissue specificity was observed, highlighting the importance of genes associated with\n                    <jats:sc>aa<\/jats:sc>\n                    biosynthesis in the lungs, cell shape and structure in the kidneys and metal acquisition during septicaemia. The majority (89%) of the genes with aberrant fitness were constituents of the core\n                    <jats:italic>A. baumannii<\/jats:italic>\n                    genome. The findings were validated using a subset of targeted mutants, including those required for infection (\n                    <jats:italic>phoB<\/jats:italic>\n                    ,\n                    <jats:italic>cysI<\/jats:italic>\n                    and\n                    <jats:italic>hom<\/jats:italic>\n                    ) or specifically septicaemia (\n                    <jats:italic>corA<\/jats:italic>\n                    ,\n                    <jats:italic>lepA<\/jats:italic>\n                    and\n                    <jats:italic>purN<\/jats:italic>\n                    ) or pneumonia (\n                    <jats:italic>argC<\/jats:italic>\n                    ,\n                    <jats:italic>hisC<\/jats:italic>\n                    and\n                    <jats:italic>leuD<\/jats:italic>\n                    ), confirming that these observations were a result of specific\n                    <jats:italic>in vivo<\/jats:italic>\n                    fitness defects rather than aberrant\n                    <jats:italic>in vitro<\/jats:italic>\n                    growth. Taken together, these data provide the first global profile of genes required for\n                    <jats:italic>in vivo<\/jats:italic>\n                    fitness of\n                    <jats:italic>A. baumannii<\/jats:italic>\n                    during different disease states and growth in different tissues.\n                  <\/jats:p>","DOI":"10.1099\/mgen.0.001556","type":"journal-article","created":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T17:17:06Z","timestamp":1762881426000},"source":"Crossref","is-referenced-by-count":0,"title":["Gene dependence during mammalian Acinetobacter baumannii pneumonia and septicaemia infections"],"prefix":"10.1099","volume":"11","author":[{"given":"Faye C.","family":"Morris","sequence":"first","affiliation":[{"name":"Centre to Impact AMR, Monash University, Clayton, Victoria, Australia"},{"name":"Infection Program, Monash Biomedicine Discovery Institute, Department of Microbiology, Monash University, Clayton, Victoria, 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