Abstract

Multidrug resistant Acinetobacter baumannii is a serious healthcare threat. In fact, the Center for Disease Control recently reported that carbapenem-resistant A. baumannii is responsible for more than 8,500 infections, 700 deaths, and $281 million in healthcare costs annually in the United States with few, if any, treatment options available, leading to its designation as a pathogen of urgent concern and a priority for novel antimicrobial development. It is hypothesized that biofilms are, at least in part, responsible for the high prevalence of A. baumannii nosocomial and recurrent infections because they frequently contaminate hospital surfaces and patient indwelling devices; therefore, there has been a recent push for mechanistic understanding of biofilm formation, maturation and dispersal. However, most research has focused on A. baumannii pneumonia and bloodstream infections, despite a recent retrospective study showing that 17.1% of A. baumannii isolates compiled from clinical studies over the last two decades were obtained from urinary samples. This highlights that A. baumannii is an underappreciated uropathogen. The following minireview will examine our current understanding of A. baumannii biofilm formation and how this influences urinary tract colonization and pathogenesis.

Highlights

  • Acinetobacter baumannii is a public health menace recently rising to prominence due to the rapid increase in antibiotic resistance and infection rates

  • Infections caused by A. baumannii account for ∼2% of all healthcare-associated infections in the United States and Europe (Sievert et al, 2013; Magill et al, 2014; Lob et al, 2016) and this rate is nearly doubled in Asia and the Middle East (Lob et al, 2016)

  • It is estimated that nearly 45% of all A. baumannii isolates are multidrugresistant (MDR; resistant to ≥3 antibiotics) with rates as eclipsing 70% in Latin America and the Middle East (Giammanco et al, 2017)

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Summary

INTRODUCTION

Acinetobacter baumannii is a public health menace recently rising to prominence due to the rapid increase in antibiotic resistance and infection rates. The prpABCD operon encodes a photoregulated pilus associated with light-regulated motility and biofilm formation in ATCC 17978 (Wood et al, 2018) This operon is conserved in several other A. baumannii strains, including the hyper-biofilm forming MAR002, which displayed a 25-fold increase in the prpD homolog in sessile cells (Alvarez-Fraga et al, 2016). The A1S_2811 deletion mutant displayed a significant reduction in surface motility, pellicle formation and abaI protein (Chen et al, 2017), suggesting a second putative control mechanism associated with QS. Deletion of A1S_0114 displayed an increase in csuAB expression as well as a decrease in other pilin proteins and ompA (Rumbo-Feal et al, 2017) This mutant was unable to form complex 3D biofilm structures on abiotic surfaces and reduced airway epithelial adhesion.

4.94 PSM 33
Findings
PSM 54
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