Community-acquired pneumonia infections by Acinetobacter baumannii

In this issue of Virulence, Asplund et al., provides a proof of principle study indicating that physiological concentrations of alcohol impair macrophage antimicrobial functions against Acinetobacter baumannii (Ab). Thus, this communication delivers seminal evidence that alcohol and macrophages plays a key role the pathogenesis of Ab. Ab is a wide spectrum of intrinsic and acquired multidrug-resistant gram-negative coccobacillus. Ab has the ability to form biofilms on non-viable surfaces, surviving through high temperatures as well as extended periods of desiccation, making it a very resilient pathogen. Therefore, due to its high persistence, pathogenesis, and multidrug resistance, this pathogen has been associated with skin and soft tissue diseases, including necrotizing fasciitis, as well as lethal infections such as pneumonia, which can evolve to septic shock. In addition, in immunosuppressed individuals, Ab is considered a primary causative agent of community-acquired pneumonia (CAP-Ab) especially in association with alcohol abuse resulting in significant high mortality rate >50%. Data around the world indicates that Ab is a leading cause of severe and lethal CAP within various regions of the Asia Pacific such as Taiwan, Hong-Kong, Singapore, and Australia. In the case of biofilm formation, hospital acquired pneumonia caused by Ab (HAP-Ab) is typically acquired by patients in intensive care units via artificial ventilation in which mechanical tubing is Community-acquired pneumonia infections by Acinetobacter baumannii How does alcohol impact the antimicrobial functions of macrophages?