Abstract
Acinetobacter baumannii is a nosocomial pathogen that exhibits substantial genomic plasticity. Here, the identification of two variants of A. baumannii ATCC 17978 that differ based on the presence of a 44-kb accessory locus, named AbaAL44 (A. baumannii accessory locus 44 kb), is described. Analyses of existing deposited data suggest that both variants are found in published studies of A. baumannii ATCC 17978 and that American Type Culture Collection (ATCC)-derived laboratory stocks comprise a mix of these two variants. Yet, each variant exhibits distinct interactions with the host in vitro and in vivo. Infection with the variant that harbors AbaAL44 (A. baumannii 17978 UN) results in decreased bacterial burdens and increased neutrophilic lung inflammation in a mouse model of pneumonia, and affects the production of interleukin 1 beta (IL-1β) and IL-10 by infected macrophages. AbaAL44 harbors putative pathogenesis genes, including those predicted to encode a type I pilus cluster, a catalase, and a cardiolipin synthase. The accessory catalase increases A. baumannii resistance to oxidative stress and neutrophil-mediated killing in vitro. The accessory cardiolipin synthase plays a dichotomous role by promoting bacterial uptake and increasing IL-1β production by macrophages, but also by enhancing bacterial resistance to cell envelope stress. Collectively, these findings highlight the phenotypic consequences of the genomic dynamism of A. baumannii through the evolution of two variants of a common type strain with distinct infection-related attributes.